POSTOPERATIVE POTASSIUM DEFICIT AND METABOLIC ALKALOSIS. THE PATHOGENIC SIGNIFICANCE OF OPERATIVE TRAUMA AND OF POTASSIUM AND PHOSPHORUS DEPRIVATION 1

Abstract

The metabolic effects resulting from operative trauma and from K and P deprivation were observed in 2 patients. During the postoperative period the 1st patient received no K or P, while the 2d received optimal amts. of these elements. The patients were maintained on constant caloric and protein intakes. Similar metabolic changes were observed in each patient postoperatively, though more pronounced in the patient who received no K or P. These changes were: (a) loss of protoplasm as shown by negative balances of N, P, and K, (b) intracellular depletion of K and P, (c) development of metabolic alkalosis and hypochloremia, (d) eosinopenia, and (e) increased urinary excretion of uric acid, creatine, formaldehydogenic steroids and ketosteroids. These changes bear a striking resemblance to those seen in patients with hyperadrenocorticism, whether spontaneous or induced by ACTH or cortisone. A preoperative period of K and P deprivation in the 2d patient resulted in intracellular losses of these elements, but failed to produce increased N loss or any evidence of increased adrenal cortical function. In spite of substantial and constant intakes of K and P, operative trauma in the 2d patient resulted in marked increases in urinary content, and in intracellular losses, of these elements. These findings suggest that a post-traumatic increase in adrenal cortical steroid production resulted in the metabolic changes observed. However, it has not been established whether similar changes with respect to N and the electrolytes would occur post-traumatically in the absence of a hyperadrenocortical state. A prompt rise in urinary Ca excretion was observed during P deprivation, indicating that in the presence of intracellular P deficit, decalcification of bone provides a small amt. of P for repair purposes.