Hypomagnesemia

Magnesium depletion usually results from inadequate intake plus impairment of renal conservation or gastrointestinal absorption. There are numerous causes of clinically significant magnesium deficiency (see table Causes of Hypomagnesemia). Hypomagnesemia is common among patients who are hospitalized and frequently occurs with other electrolyte disorders, including hypokalemia and hypocalcemia. Hypomagnesemia is related to decreased intake in patients with undernutrition or long-term alcohol use disorder. Decreased oral intake is frequently compounded by increased urinary excretion exacerbated by diuretic use, which increase urinary excretion of magnesium.

acute kidney injury. The risk of each of these is increased with duration of therapy with amphotericin B and concomitant use of another nephrotoxic agent. Liposomal amphotericin B is less likely to cause either kidney injury or hypomagnesemia. Hypomagnesemia generally resolves with cessation of therapy.

cisplatin. Discontinuation of cisplatin is still recommended if signs of renal toxicity occur during therapy.

Some patients are asymptomatic. Clinical manifestations include anorexia, nausea, vomiting, lethargy, weakness, personality change, tetany (eg, positive Trousseau or Chvostek sign or spontaneous carpopedal spasm, hyperreflexia), tremor, and muscle fasciculations.

Trousseau sign is the precipitation of carpal spasm by reduction of the blood supply to the hand with a tourniquet or blood pressure cuff inflated to 20 mm Hg above systolic blood pressure applied to the forearm for 3 minutes.

Chvostek sign is an involuntary twitching of the facial muscles elicited by a light tapping of the facial nerve just anterior to the exterior auditory meatus.

The neurologic signs, particularly tetany, correlate with development of concomitant hypocalcemia, hypokalemia, or both. Myopathic potentials are found on electromyography but are also compatible with hypocalcemia or hypokalemia.

Severe hypomagnesemia may cause generalized tonic-clonic seizures, especially in children.

• Serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L)

Hypomagnesemia is diagnosed by measurement of serum magnesium concentration. Severe hypomagnesemia usually results in concentrations of < 1.25 mg/dL (< 0.50 mmol/L). Associated hypocalcemia and hypocalciuria are common. Hypokalemia with increased urinary potassium excretion and metabolic alkalosis may be present.

• IV or IM magnesium sulfate for severe hypomagnesemia or inability to tolerate or adhere to oral therapy

< 1.25 mg/dL (< 0.50 mmol/L). Patients with alcohol use disorder are treated empirically. In such patients, deficits approaching 12 to 24 mg/kg are possible.

Parenteral administration is reserved for patients with severe, symptomatic hypomagnesemia who cannot tolerate oral medications. Sometimes a single injection is given in patients with alcohol use disorder who are unlikely to adhere to ongoing oral therapy. When magnesium must be replaced parenterally, a 10% magnesium sulfate solution (1 g/10 mL) is available for IV use and a 50% solution (1 g/2 mL) is available for IM use. The serum magnesium concentration should be monitored frequently during magnesium therapy, particularly when magnesium is given to patients with renal insufficiency or in repeated parenteral doses. In these patients, treatment is continued until a normal serum magnesium concentration is achieved.

In severe, symptomatic hypomagnesemia (eg, magnesium < 1.25 mg/dL [<

When serum magnesium is ≤ 1.25 mg/dL (<

Concurrent hypokalemia or hypocalcemia should be specifically addressed in addition to hypomagnesemia. These electrolyte disturbances are difficult to correct until magnesium has been repleted. Additionally, hypocalcemia can be worsened by isolated treatment of hypomagnesemia with intravenous magnesium sulfate because sulfate binds ionized calcium.