Causes

Hypomagnesemia is defined as magnesium concentration less than 1.6 mEq/liter (<1.9 mg/dL). Its causes are of three types:48,49

(1) Inadequate dietary intake

(2) Diminished gastrointestinal absorption

  • disorders or bypass of the small bowel (e.g., prolonged parenteral feeding, especially in combination with loss of body fluids via gastric suction or diarrhea)
  • diarrhea
  • malabsorption
  • steatorrhea
  • acute pancreatitis

(3) Wasting from the kidneys50

  • inhibition of sodium reabsorption in those segments in which magnesium transport passively follows that of sodium
  • primary defect in renal tubular magnesium reabsorption
  • alcohol-induced tubular dysfunction
  • use of drugs that promote magnesium wasting from the kidneys:
    • loop and thiazide diuretics
    • aminoglycoside antibiotics
    • amphotericin B
    • cisplatin
    • pentamidine
    • cyclosporine

In neonates, hypomagnesemia is associated with prematurity, DiGeorge syndrome, familial hypoparathyroidism, and exchange transfusions. It may also occur in infants of diabetic mothers or mothers with hyperparathyroidism or magnesium deficiency.

The overall frequency of hypomagnesemia in hospitalized patients is 11%,51 although this may be an underestimate.52 The frequency may be as high as 65% in patients in an intensive care setting, in whom major operations, poor nutrition, diuretics, hypoalbuminemia, and aminoglycosides may be factors.49,53,54

 

Clinical presentation

Magnesium, an essential cation, is involved in many enzymatic reactions and is a cofactor to adenosine triphosphatase. Consequently, magnesium is critical in energy-requiring metabolic processes.49

Symptoms of hypomagnesemia include:

  • irritability
  • agitation
  • confusion
  • anorexia
  • nausea
  • vomiting
  • lethargy
  • weakness
  • tetany (correlates with the secondary development of hypocalcemia or hypokalemia)
  • tremor
  • muscle fasciculations

Seizures, usually tonic-clonic, can occur in neonates and adults in association with severe hypomagnesemia.10

Evaluation

Physical examination may reveal an abnormal mental status and a positive Trousseau's sign, carpal spasm due to regional ischemia to the hand. Trousseau's sign may be observed by inflating a blood pressure cuff on the upper arm above systolic pressure for 2 to 3 minutes. (This sign is present in 6% of healthy persons and is also associated with alkalotic states, hypocalcemia, hypokalemia, and hyperkalemia.)

Once hypomagnesemia is confirmed by measurement of the serum magnesium level, the etiology can usually be obtained from the history. If there is no apparent cause, the distinction between GI and renal losses can be made by measuring 24-hour urinary magnesium excretion or the fractional excretion of magnesium on a random urine specimen.

Other electrolyte disturbances may be found. For example, hypokalemia occurs in 40-60% of patients with hypomagnesemia,52,54 and hypocalcemia and metabolic alkalosis are frequent findings.

Electrocardiogram (ECG) changes, including widening of the QRS wave complex and peaking of T waves, may be seen.

Treatment

Treatment with magnesium salts (e.g., sulfate or chloride) should be given for symptomatic hypomagnesemia. In the setting of seizures, 2-4 g of magnesium sulfate heptahydrate may be given intravenously (as a 10% solution in 20 to 30 mL of 5% dextrose in water) over 5 to 15 minutes and repeated, if seizures persist, to a total of 10 g over the next 6 hours.

During magnesium replacement, calcium gluconate should be available, because apnea from respiratory muscle paralysis can result from transient hypermagnesemia.

In neonates, 0.25-1.00 mL of 50% magnesium sulfate heptahydrate (0.125-0.500 g) can be injected intramuscularly or given intravenously over 10 to 15 minutes with careful ECG monitoring. This dose may be repeated two to three times a day.

Besides magnesium replacement, the underlying disease should also be corrected when possible.

Adapted from: Schachter SC and Lopez MR. Metabolic disorders. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;195?208. 
With permission from Elsevier (www.elsevier.com). 

I<
Reviewed By: 
Steven C. Schachter, MD
on: 
Thursday, April 1, 2004