Sodium Homeostasis After Small-Bowel Resection

Abstract

In 16 small-bowel-resected patients, 8 with ileostomy and 8 with at least half of the colon in function, plasma volume, plasma aldosterone concentration, plasma renin activity, and the 4-day excretion of sodium and potassium in urine and stools were determined. Patients with ileostomy had a high faecal loss of sodium: 85-181 (median, 149) mmol/24 h, and were all more or less sodium-depleted with decreased plasma volume of 1.4-2.5 (median, 2.0) 1/175 cm (normal range, 2.3-3.81/175 cm), increased plasma aldosterone of 742-2250 (median, 1131) pg/ml (normal range, 33-220 pg/ ml), and extremely low sodium excretion in the urine of 0-3 (median, 1) mmol/24 h. Patients with similar small-bowel resection but with at least half of the colon in function had a much smaller faecal sodium loss of 1-66 (median, 8) mmol/24 h. They showed significantly higher plasma volume, 2.2-3.7 (median, 2.6) 1/175 cm; normal plasma aldosterone, 25-232 (median, 124) pg/ml; and normal or almost normal sodium excretion in the urine, 49-168 (median, 118) mmol/24 h. Six jejunostomy patients, who sustained a normal or almost normal sodium balance thanks to parenteral saline, had intravenous infusion over 6 h of 1000 ml isotonic sodium chloride with or without aldosterone added. During aldosterone infusion plasma aldosterone increased to the level in the sodium-depleted ileostomy patients. Urinary sodium excretion decreased significantly. Stomal sodium loss did not change. It is concluded that small-bowel resection in ileostomized patients causes excessive faecal sodium loss and results in chronic sodium depletion with severe secondary hyperaldos-teronism. Small-bowel-resected patients with at least half of the colon in function are able to maintain normal sodium balance. The increased plasma aldosterone apparently has no effect on stomal sodium loss.