Spirolactone Effect on Postoperative Electrolytes and Adrenal Activity

NOT LONG AFTER intravenous sodium chloride solutions became available for human use, they were administered to surgical patients. It soon became apparent that salt was retained during the postoperative period to such a degree that some patients became edematous and a few developed overt congestive heart failure after sodium chloride administration. In 1945, Coller and associates quantitated postoperative salt retention by the use of a sodium chloride solution infusion. They found that patients retained approximately 50% of an intravenous sodium chloride solution load during the first 30 hours after an abdominoperineal resection.¹ Although stress-induced adrenal cortical hyperactivity was postulated as a cause of postoperative salt retention, the minimal mineralo-corticoid activity of cortisone or cortisol did not appear to account for the marked salt retention. In 1952 aldosterone, a corticosteroid which possesses one thousand times the salt-retaining potency of cortisone, was isolated.² Subsequently the role of aldosterone as