RESUMEN
Colonoscopy is an important procedure in preventing colon cancer. The risk of colonic perforation during colonoscopy at the Baylor University Medical Center (BUMC) Gastrointestinal Laboratory was chosen as a surrogate marker for the safety of colonoscopy. A recent 2-year experience at BUMC was examined and compared with reports in the medical literature. The results are presented here along with a discussion of problems inherent with different health care systems and their ability to accurately track complications. It was concluded that colonoscopy at BUMC is as safe as that reported by comparable health care systems. The risk of perforation at BUMC was 0.57 per 1000 procedures or 1 in 1750 colonoscopies. Continued efforts to make colonoscopy safer are needed.
RESUMEN
BACKGROUND & AIMS: Secretory diarrhea is caused by inhibition of intestinal active sodium absorption and stimulation of active chloride secretion. The resulting increase in fecal sodium salts causes an isotonic increase in fecal water output. Abnormalities in potassium transport are not known to be a cause of secretory diarrhea. The aim of our report is to describe a patient with secretory diarrhea that was mediated by excess intestinal secretion of potassium. METHODS: A 78-year-old woman developed colonic pseudo-obstruction, complicated by severe diarrhea and hypokalemia. Her stools were collected quantitatively on 11 occasions and analyzed for electrolyte concentrations. Rectosigmoid potential difference was measured. RESULTS: The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low sodium concentration (4-15 mEq/L). Stool potassium losses were as high as 256 mEq/day (normal, 9 mEq/day), and fecal sodium losses were never higher than 13 mEq/day. Potential difference between colonic lumen and a peripheral reference electrode was -14 mV (lumen side negative). CONCLUSIONS: Fecal potassium salts were the exclusive driving force for severe secretory diarrhea in a patient with colonic pseudo-obstruction. The high fecal output of potassium was due to stimulation of active colonic potassium secretion, possibly because of changes in autonomic nervous system activity and distention of the colon in association with colonic pseudo-obstruction. The extremely low fecal excretion of sodium indicates that active sodium absorption was not inhibited. This case study reveals an ion transport mechanism of secretory diarrhea that has not been previously appreciated.