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.

Key Words:

• Aldosterone
• ileostomy
• short-bowel syndrome
• sodium