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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 other compartments. The ECF contains only about 1% of total body Mg. The remainder resides in the intracellular compartment. Normal plasma Mg concentration ranges from 1.4 to 2.1 mEq/L (0.70 to 1.05 mmol/L).

The maintenance of plasma 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 plasma Mg is ultrafiltered by the kidney; the remainder is bound to protein. Protein binding of Mg is pH dependent. Plasma Mg concentration and either total body Mg or intracellular Mg content are not closely related. However, severe plasma hypomagnesemia may reflect diminished body stores of Mg.

Many enzymes are Mg activated or dependent. 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

Hypomagnesemia is plasma 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.

Plasma Mg concentration, even if 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 8: Fluid and Electrolyte Metabolism: Causes of Hypomagnesemia).

Table 8
Causes of Hypomagnesemia Cause Comment Alcoholism Due to both inadequate intake and excessive renal excretion Gl losses Chronic diabetes Steatorrhea Pregnancy-related Pre-eclampsia/eclampsia (see Abnormalities of Pregnancy: Preeclampsia and Eclampsia)   Lactation (increased Mg requirements) Primary renal losses Rare disorder(s). Inappropriately high urinary Mg excretion without apparent cause (eg, Gitelman's syndrome) Secondary renal losses Loop and thiazide diuretics   Hypercalcemia   After removal of parathyroid tumor   Diabetic ketoacidosis   Hypersecretion of aldosterone, thyroid hormones, or ADH   Nephrotoxins ( amphotericin B Some Trade Names ABELCET AMBISOME AMPHOCIN AMPHOTEC Click for Drug Monograph , cisplastin, cyclosporine Some Trade Names NEORAL SANDIMMUNE Click for Drug Monograph , aminoglycosides)

Symptoms, Signs, and Diagnosis

Clinical manifestations are anorexia, nausea, vomiting, lethargy, weakness, personality change, tetany (eg, positive Trousseau's or Chvostek's sign or spontaneous carpopedal spasm), and tremor and muscle fasciculations. The neurologic signs, particularly tetany, correlate with development of concomitant hypocalcemia and/or hypokalemia. Myopathic potentials are found on electromyography but are also compatible with hypocalcemia or hypokalemia. Severe hypomagnesemia may produce generalized tonic-clonic seizures, especially in children.

Hypomagnesemia is diagnosed by a serum Mg level < 1.4 mEq/L (< 0.70 mmol/L). Severe hypomagnesemia usually results in levels of < 1.0 mEq/L (< 0.50 mmol/L). Associated hypocalcemia and hypocalciuria are common in patients with steatorrhea, alcoholism, or other causes of Mg deficiency. Hypokalemia with increased urinary K excretion and metabolic alkalosis may be present. Thus, unexplained hypocalcemia and hypokalemia suggest the possibility of Mg depletion.

Treatment

Treatment with Mg salts (sulfate or chloride) is indicated when Mg deficiency is symptomatic or persistent by < 1 mEq/L (< 0.50 mmol/L). Alcoholics 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. Mg gluconate 500 to 1000 mg po tid is given for 3 to 4 days. Parenteral administration is reserved for patients with severe, symptomatic hypomagnesemia or who cannot tolerate oral drugs. 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 plasma Mg level should be monitored frequently during Mg therapy, particularly when Mg is given parenterally or to patients with renal insufficiency. Treatment is continued until a normal plasma Mg level is achieved.

In severe, symptomatic hypomagnesemia (eg, generalized seizures, Mg < 1 mEq/L [< 0.5 mmol/L]), 2 to 4 g of MgSO₄ IV is given over 5 to 10 min. If seizures persist, the dose may be repeated up to a total of 10 g over the next 6 h. If 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 plasma Mg. When plasma Mg is 1 mEq/L (< 0.5 mmol/L) but symptoms are less severe, MgSO₄ 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 plasma Mg level is normal.

Hypermagnesemia

Hypermagnesemia is a plasma Mg concentration > 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 levels. 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, Signs, and Diagnosis

At plasma 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 plasma Mg level approaches 10 mEq/L (5.0 mmol/L); hypotension, respiratory depression, and narcosis develop with increasing hypermagnesemia. Cardiac arrest may occur when blood Mg levels exceed 12 to 15 mEq/L (6.0 to 7.5 mmol/L).

Hypermagnesemia is diagnosed when serum Mg levels are > 2.1 mEq/L (> 1.05 mmol/L).

Treatment

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 Some Trade Names
LASIX
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can increase Mg excretion if renal function is adequate and volume status is maintained. Hemodialysis may be valuable in severe hypermagnesemia, because a relatively large fraction (about 70%) of blood Mg is not protein bound and thus ultrafilterable. If hemodynamic compromise occurs and hemodialysis is impractical, peritoneal dialysis is an option.

Last full review/revision November 2005

Content last modified November 2005