Postoperative Potassium Deficit and Metabolic Alkalosis. The Pathogenic Significance of Operative Trauma and of Potassium and Phosphorus Deprivation 1

Abstract

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. was suggested by the fact that muscular weakness, hypopotassemia, hypochloremia, and metabolic alkalosis are often observed in patients with Cushing's syndrome or in patients receiving ACTH (adrenocorticotropic hormone) or cortisone (1, 2); the second by the fact that all the postoperative patients but one were on a low potassium intake when the syndrome developed. The two studies described in this paper were undertaken to evaluate the relative roles of low potassium intake and operative trauma in the production of the syndrome. Adrenal cortical hyperfunction, as estimated by several criteria, developed following the operative trauma in each case but was not separately evaluated in these studies. Hyperadrenocortical states have been induced in patients with neoplastic and other diseases by administration of adrenocorticotropic hormone (ACTH) or cortisone (1l-dehydro-17-hydroxycorticosterone); and the resulting metabolic effects have been reported in detail (24).The first study (case 1, N. M.) was designed to reproduce approximately the conditions under which the syndrome had been observed to develop, namely, simultaneous deprivation at the time of operation of potassium and phosphorus. These elements were later restored one at a time. In the second study (case 2, M. B.) a period of potassium and phosphorus deprivation was imposed preoperatively, while the operation was performed during a period when these elements were provided in adequate amounts. Both patients underwent major surgery for suspected or proved neoplasms.5 6 We are indebted to Dr. Gordon McNeer and the Gastric and Mixed Tumor Service of Memorial Center, for the opportunity to study these patients. LE...

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

“…With the administration of DCA the renal excretion of acid increased sharply above the expected level of excretion (Figure 2), the additional acid excretion being secondary to an increase in sodium reabsorption with an attendant increase in hydrogen ion secretion. Certainly in the presence of evidence of increased adrenal cortical activity very definite metabolic alkalosis may develop with modest potassium losses (32). A striking demonstration of the effect of DCA in precipitating metabolic alkalosis in the face of small potassium deficits and chloride loss was 1163 presented by Moore and associates (16), who suggested the importance of DCA in the blockade of renal correction of alkalosis.…”

NBCe1-A is required for the renal ammonia and K+response to hypokalemia

“…Hypokalemia stimulates renal ammonia 1 metabolism despite the frequent simultaneous occurrence of metabolic alkalosis (18,33,65,73). This is counterproductive from an acid-base homeostasis perspective, as increased ammonia excretion increases renal bicarbonate generation and can lead to further systemic alkalinization rather than to correction of the metabolic alkalosis that is often seen with hypokalemia.…”

Studies on the Interdependent Effects of Stress and the Adrenal Cortex on Carbohydrate Metabolism in Man 1

“…The abnormality in glucose tolerance in ill subjects likewise is indicative of an alteration in carbohydrate metabolism well-known to occur in response to stressful stimuli (9,27,28,29). Hayes and Brandt (27) have shown that despite the impaired glucose tolerance curves seen in postoperative patients, the fall in serum phosphate is normal, a response which is comparable to that reported by Forsham and Thorn in subjects receiving ACTH or cortisone (26).…”