ESSENTIALS OF DIAGNOSIS
Serum concentration of magnesium may be normal even in the presence of magnesium depletion. Check urinary magnesium excretion if renal magnesium wasting is suspected.
Causes neurologic symptoms and arrhythmias.
Impairs release of PTH.
Causes of hypomagnesemia are listed in Table 21–12. Normomagnesemia does not exclude magnesium depletion because only 1% of total body magnesium is in the ECF. Hypomagnesemia and hypokalemia share many etiologies, including diuretics, diarrhea, alcoholism, aminoglycosides, and amphotericin. Renal potassium wasting also occurs from hypomagnesemia, and is refractory to potassium replacement until magnesium is repleted. Hypomagnesemia also suppresses PTH release and causes end-organ resistance to PTH and low 1,25-dihydroxyvitamin D3 levels. The resultant hypocalcemia is refractory to calcium replacement until the magnesium is normalized. Molecular mechanisms of magnesium wasting have been revealed in some hereditary disorders. There is an FDA warning about hypomagnesemia for patients taking proton pump inhibitors. The presumed mechanism is decreased intestinal magnesium absorption, but it is not clear why this complication develops in only a small fraction of patients taking these medications.
Table 21–12.Causes of hypomagnesemia. ||Download (.pdf) Table 21–12. Causes of hypomagnesemia.
Diminished absorption or intake
Malabsorption, chronic diarrhea, laxative abuse
Proton pump inhibitors
Prolonged gastrointestinal suction
Small bowel bypass
Total parenteral alimentation with inadequate Mg2+ content
Increased renal loss
Diuretic therapy (loop diuretics, thiazide diuretics)
Hyperaldosteronism, Gitelman syndrome
Drugs (aminoglycoside, cetuximab, cisplatin, amphotericin B, pentamidine)
Post-parathyroidectomy (hungry bone syndrome)
Common symptoms are those of hypokalemia and hypocalcemia, with weakness and muscle cramps. Marked neuromuscular and central nervous system hyperirritability may produce tremors, athetoid movements, jerking, nystagmus, Babinski response, confusion, and disorientation. Cardiovascular manifestations include hypertension, tachycardia, and ventricular arrhythmias.
Urinary excretion of magnesium exceeding 10–30 mg/day or a fractional excretion greater than 2% indicates renal magnesium wasting. Hypocalcemia and hypokalemia are often present. The ECG may show prolonged QT interval, due to lengthening of the ST segment. PTH secretion is often suppressed (see Hypocalcemia).
Magnesium oxide, 250–500 mg orally once or twice daily, is useful for treating chronic hypomagnesemia. Symptomatic hypomagnesemia requires intravenous magnesium sulfate 1–2 g over 5–60 minutes mixed in either dextrose 5% or 0.9% normal saline. Torsades de pointes in the setting of hypomagnesemia can be treated with 1–2 g of magnesium sulfate in 10 mL of dextrose 5% solution pushed intravenously over 15 minutes. Severe, non–life-threatening deficiency can be treated at a rate to 1–2 g/h over 3–6 hours. Magnesium sulfate may also be given intramuscularly in a dosage of 200–800 mg/day (8–33 mmol/day) in four divided doses. Serum levels ...