Ogilvie's syndrome, or acute colonic pseudo-obstruction, is characterized by massive dilation of the colon without mechanical obstruction. Water and electrolytes often can be sequestered in the dilated intestinal loops resulting in profuse and watery diarrhea as well as hypokalemia. We report an anuric, end-stage renal disease (ESRD) patient undergoing peritoneal dialysis (PD) who developed acute colonic pseudo-obstruction causing a prolonged hospitalization. He also developed severe hypokalemia with a serum potassium (K++) as low as 2.4 mEq/L and required 180 - 240 mEq of potassium chloride per day for more than a month to correct it. While PD K++ losses often contribute to hypokalemia, the PD K++ loss was estimated to be only 39 mEq/day. Therefore, PD could only contribute modestly to the recalcitrant hypokalemia observed during the episode of pseudo-obstruction. It has been shown, however, that patients with colonic pseudo-obstruction have enhanced colonic K++ secretion. In addition, experimental studies in patients with chronic kidney disease (CK+D) have demonstrated that colonic K++ excretion can be up to 3 times greater than in individuals with normal renal function. This increase may involve an upregulation of the large conductance K+ + channel (maxi-K+), also known as the BK+ channel, in the apical border of the colonocytes. We suggest that ESRD may have placed our patient at a greater risk of developing hypokalemia as his colon may have already adapted to secrete more K++. Clinicians should be aware of this extrarenal K++ wasting etiology in patients with colonic pseudo-obstruction, particularly in those with CK+D where such a severe K++ deficit is not anticipated and, therefore, may inhibit more rigorous K++ replacement.
- Colonic pseudo-Obstruction
- Gastrointestinal potassium losses
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