Clinical Manifestations of Variations in Blood Magnesium— Hypomagnesaemia and Hypermagnesaemia. ∗

Abstract

Serles and one of us reported 1 , 2 that, contrary to the usual conceptions, a large part of the magnesium ingested orally as magnesium sulphate is absorbed from the intestine and in normal animals and normal human beings about 40% of the ingested magnesium passes out in the urine in 24 hours, without causing any significant rise in plasma magnesium. The determinations of magnesium were facilitated by the introduction of a modification of Kolthoff's colorimetric method 3 for determining the magnesium in the oxalated Ca-free plasma and in oxalated Ca-free urine, after precipitation of the phosphate by uranyl acetate. We then found that in nephrectomized or nephrotic animals, oral administration of magnesium sulphate caused the plasma magnesium to rise significantly, a single dose bringing it to about 10 mg. per 100 cc. plasma, larger doses to above the coma producing level (which is about 17 mg. per 100 cc.).

Extending these studies to human beings we have obtained similar results.

1. High blood magnesium. This was found especially in nephritics after the administration of Epsom salts. In normal individuals 20-30 gm. MgSO₄, 7 H₂O by mouth does not significantly raise the blood magnesium and about 40% is excreted in the urine in 24 hours. In nephritics less of the ingested Mg is excreted in the urine, and the blood magnesium rises.

20-30 gm. MgSO₄, 7 H₂O administered to 9 patients with acute and chronic glomerulo nephritis raised blood magnesium from near normal to 9.8-11.3 mg. All these patients were definitely more drowsy when at these levels. Two nephritics with blood magnesium 8.9-9.0 without administration of MgSO₄ were definitely drowsy and unresponsive.

Coma is induced in animals when the blood magnesium approaches 17 mg. Mg per 100 cc. Elevation of blood magnesium to about two thirds of the coma-producing level thus seems to be accompanied by a tendency to somnolence.