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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.

GENERAL CONSIDERATIONS

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.

CLINICAL FINDINGS

A. Symptoms and Signs

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.

B. Laboratory Findings

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).

TREATMENT

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 must be monitored ...

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