C.: Postoperative potassium deficit and metabolic alkalosis. The pathogenic significance of operative trauma and of potassium and phosphorus

Patients maintained postoperatively on parenteral fluids or a dietary intake low or lacking in potassium may develop a syndrome characterized by apathy, lethargy, muscular weakness, abdominal distension and ileus, cardiac arrhythmias and edema; and occasionally by confusion, delirium, muscular twitching and tetany. A clinical description of the syndrome as observed in 32 postoperative patients has appeared elsewhere (1). Evidence was found in these patients for the existence of potassium deficit, namely: 1) the presence of hypopotassemia, hypochloremia and metabolic alkalosis, 2) electrocardiographic changes consistent with potassium deficit, 3) extensive expansion of the radiosodium space beyond the confines of the bromide space, suggesting that sodium had migrated into the cells to replace lost potassium, 4) lowering of erythrocyte potassium and increase of erythrocyte sodium concentrations in several patients, and 5) prompt reversal of the clinical and blood chemical abnormalities upon administration of adequate amounts of potassium. Two factors were thought to be of primary importance in the pathogenesis of the potassium deficit in the group studied: 1) adrenal cortical hyperfunction resulting from trauma ("alarm reaction") and leading to increased renal excretion of potassium and 2) a low potassium intake with poor renal conservation of potassium. The first facto