SERUM ELECTROLYTE STUDIES IN NORMAL AND PATHOLOGICAL CONDITIONS: PNEUMONIA, RENAL EDEMA, CARDIAC EDEMA, UREMIC AND DIABETIC ACIDOSIS

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Abstract
Serum electrolyte par-titions have been made in normals, in pneumonia, during cardiac diuresia, in nephritic edema (nephrosis) and in nephritic and diabetic acidosis. The accuracy and reliability of the various methods have been discussed. The so-called "undetermined acids" sink to negligible figures if bicarbonate, chloride, protein, phosphate, sulphate and ketones are estimated in these conditions. The mean total base of 18 determinations on normals is 151.9 m. Eq. and the total acid 151.7 m. Eq. Organic acids and sulphates are present in such small quantities as to be entirely unimportant. In pneumonia there is a decrease in total base, chloride, phosphate and protein with a very slow and roughly parallel return to normal after the crisis. These changes received no elucidation from the authors'' data. There is no increase in undetermined acid. Patients with renal edema showed invariably a low protein % and usually a low fixed base. Serum chlorides were often very high and increased as the result of chloride administration more strikingly than normals. A partial explanation of the behavior of the chlorides is offered by citing the effect of a decreased serum protein upon the Donnan equilibrium between serum and the fluids in tissue spaces. Studies of diuresis in cardiac patients demonstrated the ability of the body to eliminate large amounts of chloride and water without parallel decrease in total base. The acidosis of advanced nephritis was followed in several cases and the factors chiefly responsible seem to be: (1) decrease in total base dependent on loss of the base-conserving power of the kidney due to failure of ammonia formation; and (2) retention of phosphate and sulphate because of renal insufficiency. No significant ketosis was observed. BC1 [apparently blood chloride] is a valuable source of base for neutralizing retained acids. Observations on a group of patients suffering from severe diabetic acidosis showed (1) dehydration with high serum protein; (2) loss of base, due probably to urinary excretion in combination with ketones; (3) great drop in bicarbonate dependent on neutralization of ketones; and (4) decrease in serum chlorides dependent in part on vomiting, but nevertheless a real aid in furnishing base for ketones. Shock plays an extraordinarily important role in treatment and prognosis. A return of total base to normal is not necessarily parallel to the clinical recovery.