Physiologic and clinical aspects of magnesium metabolism

Abstract

Magnesium is among the principal cations in extracellular and especially intracellular fluids. It appears to have an activating action on a wide variety of enzymatic reactions essential to metabolism. The ion has a number of systemic pharmacologic actions, most notable being depression of nervous and cardiovascular systems. Nevertheless the importance of disturbances in magnesium metabolism to clinical medicine has been difficult to determine for a variety of reasons. These include (1) lack of easy and accurate analytic methods; (2) its occurrence in several forms including a protein-bound fraction and its preponderant location in the skeleton or within body cells; and (3) the similarity of probable manifestations of hypo- and hypermagnesemia to symptoms and signs of other disorders also likely to be present in the same patients. Magnesium deficiency may be responsible for a type of tetany distinguishable only by chemical determinations from the tetany of hypocalcemia. Other patients may show less specific findings such as muscular twitching, anxiety, agitation, delirium, or psychotic behavior. Conditions likely to be associated with magnesium deficiency include that of postoperative or other patients on prolonged parenteral fluids especially if associated with large losses of gastric fluid, diabetic acidosis during insulin and fluid therapy, chronic alcoholism and delerium tremens, and chronic renal disease without renal failure especially when daily urinary output is large. Although definite confirmation of a causal relation between hypomagnesemia and clinical manifestations is lacking in such patients, experience suggests that many will benefit from parenteral therapy. Magnesium salts must be given slowly and in dilute concentrations if the intravenous route is used. Magnesium should not be administered to patients with severe oliguria. Magnesium excess may be responsible for drowsiness, loss of deep tendon reflexes, prolonged P-R interval in the electrocardiogram, and, in severe cases, coma and hypotension. In experimental animals, death occurs most often following respiratory arrest. Magnesium excess is most likely in patients with acute or chronic renal failure with oliguria and in those who have received injudicious magnesium therapy. Calcium salts are useful in treatment for their antagonistic action. Dialysis has been effective in reducing hypermagnesemia in patients with acute renal failure.