Mg is the 4th most plentiful cation in the body. A 70-kg adult has about 2000 mEq of Mg. About 50% is sequestered in bone and is not readily exchangeable with Mg in other compartments. The ECF contains only about 1% of total body Mg. The remainder resides in the intracellular compartment. Normal serum Mg concentration ranges from 1.4 to 2.1 mEq/L (0.70 to 1.05 mmol/L).

The maintenance of serum Mg concentration is largely a function of dietary intake and effective renal and intestinal conservation. Within 7 days of initiation of a Mg-deficient diet, renal and stool Mg excretion each fall to about 1 mEq/day (0.5 mmol/day).

About 70% of serum Mg is ultrafiltered (filtered through minute pores) by the kidney; the remainder is bound to protein. Protein binding of Mg is pH dependent. Serum Mg concentration is not closely related to either total body Mg or intracellular Mg content. However, severe serum hypomagnesemia may reflect diminished total body Mg.

Many enzymes are activated by or are dependent on Mg. Mg is required by all enzymatic processes involving ATP and by many of the enzymes involved in nucleic acid metabolism. Mg is required for thiamine pyrophosphate cofactor activity and appears to stabilize the structure of macromolecules such as DNA and RNA. Mg is also related to Ca and K metabolism in an intimate but poorly understood way.


Hypomagnesemia is serum Mg concentration < 1.4 mEq/L (< 0.70 mmol/L). Causes include inadequate Mg 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 Mg replacement.

Serum Mg concentration, even when free Mg ion is measured, may be normal even with decreased intracellular or bone Mg stores. Mg depletion usually results from inadequate intake plus impairment of renal conservation or GI absorption. There are numerous causes of clinically significant Mg deficiency (see Table 10: Electrolyte Disorders: Causes of Hypomagnesemia).
Table 10

Causes of Hypomagnesemia


Due to inadequate intake and excessive renal excretion

GI losses
Chronic diarrhea


Small-bowel bypass

Preeclampsia/eclampsia (see Abnormalities of Pregnancy: Preeclampsia and Eclampsia)

Lactation (increased Mg requirements)

Primary renal losses
Rare disorders that cause inappropriately high Mg excretion (eg, Gitelman's syndrome)

Secondary renal losses
Loop and thiazide diuretics


After removal of parathyroid tumor

Diabetic ketoacidosis

Hypersecretion of aldosterone, thyroid hormones, or ADH

Nephrotoxins (eg, amphotericin B

cisplastin, cyclosporine


Symptoms and Signs

Clinical manifestations are anorexia, nausea, vomiting, lethargy, weakness, personality change, tetany (eg, positive Trousseau's or Chvostek's 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 Mg concentration < 1.4 mEq/L (< 0.70 mmol/L)

Hypomagnesemia is diagnosed by a serum Mg concentration. Severe hypomagnesemia usually results in concentrations of < 1.0 mEq/L (< 0.50 mmol/L). Associated hypocalcemia and hypocalciuria are common. Hypokalemia with increased urinary K excretion and metabolic alkalosis may be present. Mg deficiency should be suspected even when serum Mg concentration is normal in patients with unexplained hypocalcemia or refractory hypokalemia. Mg deficiency should also be suspected in patients with unexplained neurologic symptoms and alcoholism, with chronic diarrhea, or after cyclosporine

, cisplatinum-based chemotherapy or prolonged therapy with amphotericin B

or aminoglycosides.


Oral Mg salts

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

Treatment with Mg salts is indicated when Mg deficiency is symptomatic or persistently < 1 mEq/L (< 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 Mg is excreted in urine. Oral Mg salts (eg, Mg 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 Mg must be replaced parenterally, a 10% Mg sulfate (MgSO4) 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 Mg concentration should be monitored frequently during Mg therapy, particularly when Mg 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, Mg < 1 mEq/L [< 0.5 mmol/L] with seizures or other severe symptoms), 2 to 4 g of MgSO4 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 Mg. When serum Mg is ≤ 1 mEq/L ( 2.1 mEq/L (> 1.05 mmol/L). The major cause is renal failure. Symptoms include hypotension, respiratory depression, and cardiac arrest. Diagnosis is by serum Mg concentration. Treatment includes IV administration of Ca gluconate and possibly furosemide; hemodialysis can be helpful in severe cases.

Symptomatic hypermagnesemia is fairly uncommon. It occurs most commonly in patients with renal failure after ingestion of Mg-containing drugs, such as antacids or purgatives.

Symptoms and signs include hyporeflexia, hypotension, respiratory depression, and cardiac arrest.


Serum Mg concentrations > 2.1 mEq/L (> 1.05 mmol/L)

At serum Mg concentrations of 5 to 10 mEq/L (2.5 to 5 mmol/L), the ECG shows prolongation of the PR interval, widening of the QRS complex, and increased T-wave amplitude. Deep tendon reflexes disappear as the serum Mg concentration approaches 10 mEq/L (5.0 mmol/L); hypotension, respiratory depression, and narcosis develop with increasing hypermagnesemia. Cardiac arrest may occur when blood Mg concentration is > 12 to 15 mEq/L (6.0 to 7.5 mmol/L).


Ca gluconate

Diuresis or dialysis

Treatment of severe Mg toxicity consists of circulatory and respiratory support with administration of 10% Ca gluconate 10 to 20 mL IV. Ca gluconate may reverse many of the Mg-induced changes, including respiratory depression. Administration of IV furosemide

increase Mg excretion when renal function is adequate; volume status should be maintained. Hemodialysis may be valuable in severe hypermagnesemia, because a relatively large fraction (about 70%) of blood Mg is not protein bound and thus removable with hemodialysis. When hemodynamic compromise occurs and hemodialysis is impractical, peritoneal dialysis is an option.

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