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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.

Medications can cause hypomagnesemia. Examples include chronic (> 1 year) use of a proton pump inhibitor and concomitant use of diuretics. Amphotericin B can cause hypomagnesemia, hypokalemia, and 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 can cause increased magnesium losses by the kidneys as well as generalized decrease in kidney function. Magnesium loses can be severe and persist despite discontinuation of 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.

Magnesium deficiency should be suspected even when serum magnesium concentration is normal in patients with unexplained hypocalcemia or refractory hypokalemia. Magnesium deficiency should also be suspected in patients with unexplained neurologic symptoms and alcohol use disorder, with chronic diarrhea, or after cyclosporine use, cisplatin-based chemotherapy, or prolonged therapy with amphotericin B or aminoglycosides.

• Oral magnesium salts

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

Treatment with magnesium salts is indicated when magnesium deficiency is symptomatic or the magnesium concentration is persistently < 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.

About twice the amount of the estimated deficit should be given in patients with intact renal function because about 50% of the administered magnesium is excreted in urine. Oral magnesium salts (eg, magnesium gluconate 500 to 1000 mg orally 3 times a day) are given for 3 to 4 days. Oral treatment is limited by the onset of diarrhea.

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 [< 0.5 mmol/L] with seizures or other severe symptoms), 2 to 4 g of magnesium sulfate IV is given over 5 to 10 minutes. When seizures persist, the dose may be repeated up to a total of 10 g over the next 6 hours. In patients in whom seizures stop, 10 g in 1 L of 5% dextrose in water can be infused over 24 hours, followed by up to 2.5 g every 12 hours to replace the deficit in total magnesium stores and prevent further drops in serum magnesium.

When serum magnesium is ≤ 1.25 mg/dL (< 0.5 mmol/L) but symptoms are less severe, magnesium sulfate may be given IV in 5% dextrose in water at a rate of 1 g/hour as slow infusion for up to 10 hours. In less severe cases of hypomagnesemia, gradual repletion may be achieved by administration of smaller parenteral doses over 3 to 5 days until the serum magnesium concentration is normal.

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.