NDT Advance Access originally published online on March 14, 2008
Nephrology Dialysis Transplantation 2008 23(6):2081-2083; doi:10.1093/ndt/gfn097
© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Hyperkalaemia as a complication of ureteroileostomy: a case report and literature review
Nizar Eskandar and
Jean L. Holley
Nephrology Division, University of Virginia Health System, Box 800133, Charlottesville, VA 22908, USA
Correspondence and offprint requests to: Nizar Eskandar, Division of Nephrology, University of Virginia Health System, Box 800133, Charlottesville, VA 22908, USA. Tel: +1-434-924-5125; Fax: +1-434-924-5848; E-mail: ne9u{at}virginia.edu
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Introduction
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Ureteral diversion in which the ureter is implanted into either
the sigmoid colon or a short loop of ileum is associated with
multiple metabolic complications [
1,2]. Ureterosigmoidostomy
commonly leads to metabolic acidosis due to the presence of
colonic anion exchange pumps that reabsorb luminal chloride
as bicarbonate is secreted across the sigmoid colon. In such
cases, reabsorption of urinary ammonium that contacts the sigmoid
colon may also contribute to metabolic acidosis [
1]. In addition,
sigmoid loops usually lead to hypokalaemia due to colonic potassium
secretion. However, if the intestinal conduit in contact with
ureteral contents is jejunum, hyperkalaemia may occur, presumably
due to absorption of urinary potassium by the jejunum. This
infrequent complication of ureteral diversion has been rarely
reported but should be considered in cases of hyperkalaemia
in patients with ureteroiliostomies. In such cases, jejunal
contact with the ureteral drainage likely is occurring and resulting
in hyperkalaemia via jejunal absorption of potassium. We report
an illustrative case in which enteral feeding repeatedly resulted
in hyperkalaemia in a patient who underwent urinary diversion
with a conduit assumed to be implanted in the low ileum.
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Case
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A 77-year-old man with advanced rectal carcinoma underwent pelvic
exoneration, cystectomy and ileal conduit followed by radiation
treatment
6 years ago. He was hospitalized recently with a 1-week
history of abdominal pain, fever, bleeding per rectum and obstipation.
Colonoscopy revealed ischaemic colitis. He was treated conservatively
and discharged after 5 days. He presented 6 weeks later with
abdominal pain, nausea and vomiting due to bowel obstruction.
He was also noted to have a colonic to urinary tract fistula.
Exploratory laparatomy was performed with extensive lysis of
adhesions, creation of loop ileostomy and revision of the urinary
conduit. His prior surgery and radiation as well as multiple
adhesions complicated the procedure and made bowel segment identification
difficult. Nephrology consultation was called 6 days postoperatively
for hyperkalaemia.
On physical examination, he appeared thin, chronically ill and complained of decreased energy. His blood pressure was 108/63 mmHg, heart rate 56 and temperature 37.5°C. The abdomen was soft, mildly distended and non-tender. He had a PEG tube in place. The ileoconduit was intact and in place. His extremities were well perfused. His medications included codeine on PRN basis, Famotidine 20 mg BID, Heparin 5000 units SQ q 8 h and Metoprolol 25 mg BID. The blood chemistry test results and urine test results at the time of nephrology consultation are shown in Table 1. The calculated Trans Tubular Potassium Gradient (TTKG) was 13.4 indicating normal aldosterone effect. The patient's urine output was 3 L/day.
Postoperatively, the patient received total parenteral nutrition
(TPN) and maintained normal serum electrolytes (Figure
1). On
postoperative day 5, enteral feeding was begun and his plasma
potassium rose to 5 mmol/L. At one point during his hospital
stay, the enteral feeding was discontinued because of nausea
and vomiting and TPN was resumed for 4 days. His electrolytes,
including potassium, were normal during these 4 days (Figure
1). At the time of nephrology consultation, the patient was
on enteral feeding. The subcutaneous heparin was discontinued
but hyperkalaemia persisted (Figure
1).
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Discussion
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Hyperkalaemia rarely occurs in normal subjects due to multiple
mechanisms that prevent the accumulation of potassium in the
extracellular fluid. These mechanisms include the shifting of
potassium in and out of the cellular compartment and increased
urinary excretion of potassium. Thus, increasing potassium intake
does not cause hyperkalaemia unless it occurs very acutely or
in the setting of impaired potassium excretion (e.g. acute kidney
injury or failure). Transient elevation in the serum potassium
level can occur as a result of an increased release of cellular
potassium or decreased cellular potassium entry, but persistent
hyperkalaemia requires an impairment in urinary potassium excretion.
Causes of hyperkalaemia are listed in Table
2.
Urinary diversion procedures using jejunal conduits are less
common than sigmoid or ileal conduits and have been noted to
result in hyperkalaemia although the number of reported cases
are few [
3–8]. A review of the operative report of our
patient in an attempt to delineate the anatomic insertion of
the urinary conduit was unrevealing. Discussion with the surgeon
performing the procedure suggested that the exact bowel segment
used for insertion of the urinary conduit was unknown; the procedure
was complicated by previous pelvic exoneration, cystectomy and
ileal conduit 6 years ago as well as his past radiation treatment.
The urinary conduit surgery involved exploratory laparatomy,
extensive lysis of adhesions, creation of loop ileostomy and
revision of the urinary conduit. The surgeon believed that the
implanted urinary conduit was in the ileum but could not exclude
the possibility of a very high ileal or jejunal segment used
as the conduit. The patient's clinical course of hyperkalaemia
only with higher potassium enteral feeding suggests that the
conduit may be in the jejunum (Figure
1).
Hyperkalaemia in the setting of urinary conduits using jejunum is presumed to occur as a result of jejunal potassium absorption [3–6]. Normal individuals ingest on average 80–100 mEq of K+ daily in the their diet; 90% (90 mEq/day) of the ingested K+ will be absorbed and subsequently excreted in an equivalent amount in the urine. Normal fecal excretion of K+ averages 10% of the ingested K+ (10 mEq/day). The vast majority of intestinal K+ absorption occurs in the small intestine; the colon contribution to net K+ absorption and secretion is trivial, and perhaps the rectum and sigmoid colon have some capacity to actively secrete K+ but the physiologic significance of this active secretion is uncertain. Hyperaldosteronism increases fecal K+ excretion by 3 mEq/day in people with normal intestinal tracts. The absorptive mechanisms of K+ are not disturbed by diarrhoea per se, but fecal K+ losses are increased with diarrhoea due to unabsorbed anions like chloride that ‘obligates’ K+ luminal secretion by electrical gradients [9]. Unlike conduits with sigmoid colon or ileum that usually result in hypokalaemia, the jejunal epithelium is unique in its potassium reabsorption. The exact mechanism of jejunal potassium absorption is unclear and although relatively rare [3–6] does occur. Since our patient became hyperkalaemic only with higher K enteral feeding (Figure 1), jejunal potassium absorption is clearly implicated. Subsequently, our patient was treated with a low-potassium enteral diet 50 mEq/day and his potassium level remained around 4.5 mmol/L.
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Summary
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Although jejunal potassium absorption is recognized, it is rarely
reported and may be misinterpreted as a complication of ileal
diversion [
7,8]. Given the differences in ileal and jejunal
potassium handling and the difficulty of surgically identifying
exact intestinal segments in the setting of multiple past procedures
and adhesions, post-procedure hyperkalaemia should raise suspicion
that the urinary conduit was planted in the high ileum or jejunum.
Controlling potassium intake in such cases is the foundation
of treatment.
Conflicting of interest statement. None declared.
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References
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- McDougal WS. Metabolic complication of urinary intestinal diversion. J Urol (1992) 147:1199–1208.[Web of Science][Medline]
- Mundy AR. Metabolic complication of urinary diversion. Lancet (1999) 353:1813–1814.[CrossRef][Web of Science][Medline]
- Golimbu M, Morales P. Electrolytes disturbances in jejunal urinary diversion. Urology (1973) 1:432–438.[CrossRef][Medline]
- Clark SS. Electrolytes disturbances associated with jejunal conduit. J Urol (1974) 112:42–47.[Web of Science][Medline]
- Mansson W, Lindstedt E. Electrolytes disturbances after jejunal conduit urinary diversion Scand. J Urol Nephrol (1978) 12:17–21.
- Koba K, Furuya R. A case report of complication liked jejunal conduit syndrome induced by reconstruction of ileal conduit. Nippon Hinyokika Gakkai Zasshi (2004) 95:630–633. (Japanese).[Medline]
- Tak PP, Diamant Z. Hyponatremia, hyperkalemia and hypercalcemia after ileal conduit diversion. Scand. J Uro Nephrol (1993) 27:271–274.
- Cuxart M, Matas M. Heart block caused by hyperkalemia as a complication of ureteroileostomy. Actas Urol Esp (1996) 20:757–759. (Spanish).[Medline]
- Agarwal R, Afzalpurkar R, Fordtran JS. Pathophysiology of potassium absorption and secretion by human intestine. Gastroenterology (1994) 107:548–571.[Web of Science][Medline]
Received for publication: 17. 8.07
Accepted in revised form: 1. 2.08
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Introduction
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