About 50% of total body magnesium exists in the insoluble state in bone. Only 5% is present as extracellular cation; the remaining 45% is contained in cells as intracellular cation. The normal plasma concentration is 1.5–2.5 meq/L, with about one-third bound to protein and two-thirds existing as free cation. Excretion of magnesium ion is via the kidney.

Magnesium is an important activator ion, participating in the function of many enzymes involved in phosphate transfer reactions. Magnesium exerts physiologic effects on the nervous system resembling those of calcium. Magnesium acts directly upon the myoneural junction.

Altered concentration of Mg2+ in the plasma usually provokes an associated alteration of Ca2+. Hypermagnesemia suppresses secretion of parathyroid hormone with consequent hypocalcemia. Severe and prolonged magnesium depletion impairs secretion of PTH with consequent hypocalcemia. Hypomagnesemia may impair end-organ response to PTH as well.

Nearly half of hospitalized patients in whom serum electrolytes are ordered have unrecognized hypomagnesemia; in critically ill patients, arrhythmias and sudden death may be complications. Common causes include use of large volumes of intravenous fluids, diuretics, cisplatin in cancer patients (with concomitant hypokalemia), and administration of nephrotoxic agents such as aminoglycosides and amphotericin B.

A. Symptoms and Signs: Common symptoms are weakness, muscle cramps, and tremor. There is marked neuromuscular and central nervous system hyperirritability, with tremors, athetoid movements, jerking, nystagmus, and a positive Babinski response. There may be hypertension, tachycardia, and ventricular arrhythmias. Confusion and disorientation may be prominent features.

B. Laboratory Findings: In addition to hypomagnesemia, hypocalcemia and hypokalemia are often present. The ECG shows a prolonged QT interval, particularly due to lengthening of the ST segment.

Treatment consists of the use of intravenous fluids containing magnesium as chloride or sulfate, 240–1200 mg/d (10–50 mmol/d) during the period of severe deficit, followed by 120 mg/d (5 mmol/d) for maintenance. Magnesium sulfate may also be given intramuscularly in a dosage of 200–800 mg/d (8–33 mmol/d) in four divided doses. Serum levels must be monitored and dosage adjusted to keep the concentration from rising above 2.5 mmol/L. K+ and Ca2+ may be required as well. Magnesium oxide, 250–500 mg by mouth two to four times daily, is useful for repleting stores in those with chronic hypomagnesemia.

A. Symptoms and Signs: Muscle weakness, mental obtundation, and confusion are characteristic manifestations. Weakness—even flaccid paralysis—and fall in blood pressure are evident on examination. There may be respiratory muscle paralysis or cardiac arrest.

B. Laboratory Findings: Serum Mg2+ is elevated. In the common setting of renal insufficiency, concentrations of BUN and of serum creatinine, phosphate, and uric acid are elevated; serum K+ may be elevated. Serum Ca2+ is often low. The ECG shows increased PR interval, broadened QRS complexes, and elevated T waves, probably related to associated hyperkalemia.