1988 Volume 37 Issue 4 Pages 365-378
In an attempt to elucidate the etiology of postoperative metabolic alkalosis in surgical patients, the exogeneous bicarbonate load as an etiologic factor was assessed in a prospective study. Also, the renal handling of bicarbonate was studied in postoperative patients. Seventeen patients who had a stomach cancer were randomly divided into two groups before operation. During the postoperative days zero through seven after gastrectomy, bicarbonate was continuously infused through intravenous fluid in group A, while no bicarbonate was given in group B. Citrate in fresh frozen plasma was interpreted as being a bicarbonate load with its nature of metabolic change to bicarbonate. Seven (78.5%) of the nine patients in group A exhibited postoperative metabolic alkalosis, which might have been caused by the retention of exogenous bicarbonate in the kidneys. On the other hand, no incidence of postoperative metabolic alkalosis occurred in group B. With regard to the renal handling of bicarbonate after operation, the rate of renal tubular bicarbonate reabsorption correlated closely to the bicarbonate retention in the kidneys, and was further regulated by sodium-cation exchange in the renal tubules. The blood aldosterone concentration had little effect on the tubular bicarbonate reabsorption. On the contrary, the rate of urinary bicarbonate excretion was indicated as not being determined by a homeostatic mechanism which responded to the systemic pH or blood bicarbonate level. Thus, the increased retention of exogenous bicarbonate followed by an enhanced renal sodium reabsorption under surgical stress was strongly suggested as the mechanism of uostoperative metabolic alkalosis induced by exonenous bicarbonate load. This implies that reevaluation is needed on the routine use of alkalinizing agents in intravenous fluid administration following surgery.
