Not Found

Find information on medical topics, symptoms, drugs, procedures, news and more, written for the health care professional.


By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham

Click here for
Patient Education

Hypomagnesemia is serum magnesium concentration< 1.8 mg/dL (< 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or drugs such as furosemide. Clinical features are often due to accompanying hypokalemia and hypocalcemia and include lethargy, tremor, tetany, seizures, and arrhythmias. Treatment is with magnesium replacement.

Serum magnesium concentration, even when free magnesium ion is measured, may be normal even with decreased intracellular or bone magnesium stores.


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

Drugs can cause hypomagnesemia. Examples include chronic (> 1 yr) 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 kidney 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.

Causes of Hypomagnesemia




Due to inadequate intake and excessive renal excretion

GI losses

Chronic diarrhea


Small-bowel bypass

Chronic proton pump inhibitor use


Pregnancy (especially 3rd trimester; excessive renal excretion, other factors; usually physiologic)

Lactation (increased magnesium requirements)

Primary renal losses

Rare disorders that cause inappropriately high magnesium excretion (eg, Gitelman syndrome)

Secondary renal losses

Loop and thiazide diuretics


After removal of parathyroid tumor

Diabetic ketoacidosis

Hypersecretion of aldosterone, thyroid hormones, or vasopressin

Nephrotoxins (eg, amphotericin B, cisplastin, cyclosporine, aminoglycosides)

Symptoms and Signs

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


  • Considered in patients with risk factors and with unexplained hypocalcemia or hypokalemia

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

Hypomagnesemia is diagnosed by a 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 alcoholism, with chronic diarrhea, or after cyclosporine use, cisplatinum-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 persistently < 1.25 mg/dL (< 0.50 mmol/L). Patients with alcoholism are treated empirically. In such cases, 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 po tid) 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 drugs. Sometimes a single injection is given in patients with alcoholism 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 Mg 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 min. When seizures persist, the dose may be repeated up to a total of 10 g over the next 6 h. In patients in whom seizures stop, 10 g in 1 L of 5% D/W can be infused over 24 h, followed by up to 2.5 g q 12 h to replace the deficit in total Mg 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% D/W at a rate of 1 g/h as slow infusion for up to 10 h. 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.

Key Points

  • Hypomagnesemia may occur in alcoholics, in patients with uncontrolled diabetes, and with hypercalcemia or use of loop diuretics.

  • Symptoms include anorexia, nausea, vomiting, lethargy, weakness, personality change, tetany (eg, positive Trousseau or Chvostek sign, spontaneous carpopedal spasm, hyperreflexia), tremor, and muscle fasciculations.

  • Treat with magnesium salts when magnesium deficiency is symptomatic or persistently < 1.25 mg/dL (< 0.50 mmol/L).

  • Give oral magnesium salts unless patients have seizures or other severe symptoms, in which case, give 2 to 4 g of magnesium sulfate IV over 5 to 10 min.

Resources In This Article