Hypomagnesemia

12% of all hospitalized pts as well as 44–60% of all pts admitted to medical/surgical and pediatric ICUs, are hypomagnesemic.

Associated with

• Poor nutrition.

• GI losses: Diarrhea and severe vomiting; malabsorption (steatorrhea, bowel resection, intestinal fistulas, celiac disease); acute pancreatitis; medications (proton pump inhibitors, laxatives).

• Renal losses: Medications (loop/thiazide diuretics, aminoglycosides, amphotericin B, cisplatin, foscarnet, cyclosporine); familial renal Mg ²⁺ wasting syndromes; uncontrolled diabetes mellitus; metabolic acidosis; alcohol abuse.

• Miscellaneous: Prolonged IV therapy; massive blood transfusions; digitalis.

Arrhythmias (atrial, ventricular, prolonged QT, and torsades de pointes). Hypomagnesemia should be corrected prior to elective procedures due to the potential for malignant arrhythmias.

Worsening cardiac ischemia and CHF.

Increased susceptibility to seizures, bronchoconstriction, and vasospasm.

Refractory hypokalemia and hypocalcemia.

Resistance to vasodilators.

Aggravates insulin resistance in the diabetic pt.

Weakness, lethargy, paresthesias, muscle spasms.

Seizures (especially in preeclampsia).

Arrhythmias (especially torsades de pointes).

During treatment of hypomagnesemia: Burning at IV site, overall sense of warmth and flushing. Transient and mild hypotension may occur if MgSO ₄ is given too fast. Administration of Mg ²⁺ will also potentiate the neuromuscular blockade with all nondepolarizing drugs.

Normal range of plasma Mg ²⁺ is 1.7–2.4 mg/dL. Most symptomatic pts have levels <1 mg/dL.

Mg ²⁺ levels are not routinely checked in screening tests. Hypomagnesemia should be suspected, especially in chronic diarrhea, alcoholism, malnutrition, long-term hospitalization, and hypoalbuminemia.

Mg ²⁺ is primarily an intracellular ion. Plasma levels may not reflect the true magnitude of deficit. Intracellular shift may occur with the administration of insulin and thyroid hormone.

Normomagnesemic Mg ²⁺ depletion has been described; if clinical suspicion of hypomagnesemia is present, Mg ²⁺ should be administered, even with normal plasma levels.

If it is unclear from the pt’s history, a 24-h urine sample may help to differentiate renal from nonrenal causes. Mg ²⁺ loss of less than 3–4 mEq/d supports a renal etiology.

Alternatively, a fractional excretion of Mg ²⁺ can be calculated in a spot urine sample.

• FE _Mg = [(U _Mg × P _Cr )/(0.7 × P _Mg ) × U _Cr ] × 100, where U _Mg /U _Cr and P _Mg /U _Cr denotes urinary and plasma concentrations of Mg ²⁺ and Cr.

• Usually, FE _Mg greater than 2% indicates renal Mg ²⁺ wasting.