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Gastrocystoplasty

Gastrocystoplasty is a form of augmentation cystoplasty that uses a vascularized wedge of gastric body wall to enlarge the bladder. First popularized by Adams, Mitchell, and Rink in 1988, it was developed to address the metabolic complications of enterocystoplasty, particularly hyperchloremic metabolic acidosis, by exploiting the stomach's unique secretory physiology (acid and chloride secretion rather than absorption).[1][2] However, gastrocystoplasty has become increasingly controversial and is no longer favored at many institutions because of two prominent concerns: the hematuria-dysuria syndrome (HDS) and late malignancy risk.[3][4]

Indications​

Gastrocystoplasty shares the general indications for augmentation cystoplasty but is specifically considered when intestinal segments are disadvantageous:[1][2][5]

  • Chronic renal insufficiency. Gastric segment secretes acid and chloride into the urine rather than absorbing them, reducing bowel-mediated hyperchloremic acidosis. Patients with renal insufficiency can develop serious metabolic alkalosis after gastric augmentation.[1][6] Anuria warrants particular caution: two patients in DeFoor's 44-patient series had severe hematuria while anuric from renal failure, and a 2024 dialysis case required gastric-patch resection for refractory hemorrhage.[5][32]
  • Short bowel syndrome or insufficient bowel. Insufficient bowel occurs in cloacal exstrophy and after extensive bowel resections.[1][5]
  • Cloacal exstrophy. This condition often combines renal insufficiency and short bowel.[5][7]
  • Reduced mucus production. The stomach produces significantly less mucus than intestinal segments.[1][3]

For adults with NLUTD considering augmentation, the AUA/SUFU discussion accompanying Statement 51 says the patient or a family member/caregiver must have the hand and cognitive function needed for regular clean intermittent catheterization.[29]

Surgical Technique​

The standard technique harvests a gastric body wedge flap based on the right gastroepiploic artery:[1][8]

  1. Gastric wedge harvest. Excise a wedge-shaped segment of gastric body, preserving the lesser curvature and vagus nerve to minimize postoperative gastric dysfunction. The pedicle is based on the right gastroepiploic artery for blood supply.
  2. Gastric closure. Close the stomach primarily with staples or sutures.
  3. Pedicle tunneling. Tunnel the gastric flap on its vascular pedicle through the transverse mesocolon and into the pelvis. Passing the pedicle through windows in the distal ileal mesentery and securing it to the posterior peritoneum, rather than leaving it free-floating, has been described as a way to reduce pedicle twisting or kinking and limit the chance that small bowel herniates beneath it during later abdominal exploration.[30]
  4. Cystotomy. Bivalve the native bladder.
  5. Anastomosis. Suture the gastric wedge to the opened bladder with the mucosa facing the bladder lumen.[1][8][9]

An alternative flap using the pyloric antrum, carried into the pelvis on an omental pedicle supplied by the left gastroepiploic artery rather than the right, has also been described; no comparison of the two pedicles, functional outcomes, or gastric effects has been reported.[30]

Concomitant procedures: ureteral reimplantation (thick gastric wall facilitates submucosal tunnel), bladder-neck procedures, continent catheterizable channel, and AUS.[2][7][8][10]

Continent gastric tube. Gastric tissue can be fashioned into a continent catheterizable tube from the anterior gastric flap, simultaneously or as a secondary procedure.[9] In a ten-patient series, stomal complications occurred only with flush or protuberant stomas and resolved after revision with recessed skin flaps.[9]

Demucosalized gastrocystoplasty. Gastric mucosa is stripped, leaving only the seromuscular layer, which is placed over an autoaugmented bladder. The aim is to avoid acid-secreting mucosa. Residual mucosa or regrowth and patch contraction remain concerns; in Castellan's series, the one demucosalized patch contracted and was excised.[4] In 11 pediatric patients followed for a mean of 23 months (range 8–33 months), capacity rose from 109 to 236 mL and compliance from 3 to 9 mL/cm H₂O; no metabolic complications were reported, and urine was mucus-free.[11] See autoaugmentation.

Outcomes​

Small retrospective cohorts report variable outcomes, without a pooled gastric-augmentation success estimate. In the initial 13-patient report (ten augmentations and three reservoirs), 11 were continent and ten needed CIC at mean 13 months.[1] Later reports emphasize long-term HDS, reoperation, acid-base complications, and malignancy as well as functional benefit.[2][3][4][12]

In a retrospective long-term renal outcomes study (Hubert, n=35, median 19 yr), the majority preserved or improved renal function; 5/15 patients with stage 3–4 CKD improved to normal eGFR (9 progressed to ESRD); no bladder malignancies in this cohort; nine patients developed HDS.[12]

Advantages Over Enterocystoplasty​

FeatureGastrocystoplastyEnterocystoplasty
Metabolic exchangeAvoids intestinal chloride/ammonium absorption but can cause serious hypochloremic hypokalemic alkalosisHyperchloremic acidosis can occur
Mucus productionOften lower; irrigation needs remain individualMucus and irrigation burden are common
Urinary tract infectionsSymptomatic infection still occurs; clinical superiority is not established—
Bladder stonesInfrequent in small gastric series—
Bladder perforationReported, including peptic-ulcer perforationRecognized long-term risk
Small-bowel preservation and gastric donor morbidityAvoids further small-bowel resection but removes gastric tissue; a five-child renal-failure case series described weight loss, feeding intolerance, dumping, and delayed gastric emptying after gastrocystoplasty[31]Depends on bowel segment and length
Thick muscular wallFacilitates ureteral reimplantationThin wall (ileum)
Complication patternHDS and metabolic alkalosis; late malignancy has been reported[3][20]Late malignancy has also been reported after enterocystoplasty[23]

Hematuria-Dysuria Syndrome (HDS)​

HDS is the signature complication of gastrocystoplasty and one of the main reasons the procedure has fallen out of favor at many centers. It is defined as one or more of the following symptoms in the absence of infection:[14]

  • Bladder spasm or suprapubic / penile / periurethral pain.
  • Coffee-brown or bright-red hematuria without infection.
  • Skin irritation or excoriation (peristomal or periurethral).
  • Dysuria without infection.

Reported frequency: Retrospective cohorts reported HDS in 17/72 (24%) under broad criteria[15], 27% of 47 children[3], and 21 of 57 patients after gastric reconstruction (including three total bladder replacements)[14]; follow-up and case definitions differed. A later 11-patient series reported symptoms in 7/11 after median 17 years.[21] Continuous medication was required in 3/72 (4%) in the Chadwick Plaire cohort.[3][14][15][21]

Risk factors[2][3][14]​

  • Sensate urethra (intact pelvic sensation): HDS in 75% of patients without neurogenic bladder (e.g., exstrophy, PUV) versus only 14% of those with neurogenic bladder.[3]
  • Urinary incontinence: wet patients are more prone to HDS.[14]
  • Renal insufficiency may increase risk.[14]

Pathophysiology​

The gastric segment continues to secrete hydrochloric acid as though it were part of the stomach ("once a stomach, always a stomach"). Acid secretion is stimulated by meals (gastrin release) but not by bladder distention.[14][16] Acidic urine may contribute to bladder and skin irritation.[14][16]

Treatment[7][15][16][17][18]​

  • Acid suppression with an H₂ receptor antagonist such as famotidine or a proton pump inhibitor may help. Small historical series report variable responses without a clear first-line choice.
  • Proton pump inhibitors (omeprazole) are used when H₂ blockers are insufficient. Omeprazole treated severe metabolic alkalosis with persistent hypergastrinemia in one renal-failure patient unresponsive to standard acid inhibition.[18] In Gosalbez's series, a second patient with hypergastrinemia did not respond to maximal H₂ blocker, electrolyte replacement and omeprazole, and underwent removal of three-quarters of the gastric augmentation.[17]
  • Antimuscarinics may be considered for associated bladder spasms; do not rely on them to manage a severe acid-base disorder.
  • Prophylactic H₂ blockers / PPIs were used in 16/23 (70%) in one series to prevent HDS.[7]
  • Gastric-patch excision or reconstruction was needed for different reasons: Leonard reported conversion to another urinary reconstruction in 3/23 patients with medically refractory HDS; in Castellan's mixed 29-patient gastric-segment reconstruction cohort, patch excision for intractable HDS in 1/29 and, separately, excision with enteric re-augmentation for contraction of a demucosalized patch in another patient.[4][7]

Metabolic Disturbances​

Unlike the hyperchloremic acidosis associated with enterocystoplasty, gastrocystoplasty can cause hypochloremic hypokalemic metabolic alkalosis; severe cases have been reported even with normal baseline renal function.[2][3][17]

  • Kurzrock's retrospective series of 47 children (mean follow-up 4.4 years) reported mean serum chloride decreasing by 2.7 mEq/L and bicarbonate increasing by 3.3 mEq/L postoperatively.[3]
  • Serum bicarbonate rose 8 mEq/L in the 3 patients with renal insufficiency.[3]
  • Severe hypochloremic hypokalemic alkalosis can be life-threatening. Gosalbez described two severe cases among 34 children with normal baseline renal function, including seizures and altered mental status or respiratory depression. Urgent monitored correction of volume, chloride and potassium deficits, acid suppression, and specialist management are required; historical rescue regimens should not be copied as a routine order set. Refractory disease may require gastric-patch revision or removal.[17]
  • Experimental: gastrocystoplasty protected healthy rats from acid overload but failed to protect rats with chronic renal failure under the same conditions; the metabolic advantage may be limited in severe CKD.[19]

Malignancy Risk​

The malignancy risk is a major concern and one of the strongest arguments against the procedure:

  • Castellan (n=119): 4 (3.4%) developed carcinoma (3 gastric adenocarcinomas, 1 TCC), all >10 yr after augmentation.[20]
  • Boissier (n=11, median 17 yr): 3 (27%) developed gastric adenocarcinoma on the gastric graft, 2 metastatic at diagnosis; 7/11 ultimately required excision of the gastric patch.[21]
  • Castellan complications series (n=29, mean 13.9 yr): 3 patients developed malignancy at 11, 12, and 14 yr; all 3 died of metastasis. Authors concluded: "We do not recommend the use of gastric segments for reconstruction of the lower urinary tract."[4]
  • Literature review: 14 total cases of gastric adenocarcinoma after gastrocystoplasty; majority presented with hematuria >10 yr postop; 36% died within 5 yr.[22]
  • French nationwide cancer series (n = 16 across augmentation types): adenocarcinomas occurred mainly after gastrocystoplasty, whereas urothelial carcinomas were typical after colocystoplasty. Median cancer latency was 20 years and overall one-year survival was 56% for the full mixed-segment cancer cohort.[23]
  • Experimental rat model: papillary hyperplasia occurred in 14/26 gastrocystoplasty rats (53.8%), versus 9/22 sigmoidocystoplasty rats (40.9%) and 0/18 ileocystoplasty rats. No carcinomas were found over approximately one year, and the lesions' malignant potential was unknown.[24]
  • Periodic histopathologic surveillance in 15 gastrocystoplasty patients with at least 2 years of follow-up found no malignancy and pathological changes (inflammation, metaplasia, hyperplasia) in 9/15 (60%).[13] A later report followed 11 of those 15 gastrocystoplasty patients over a 15-year surveillance period, found no malignancy, and questioned routine cystoscopy or biopsy without suspicious symptoms.[33]

Urodynamic Comparison With Other Segments​

Long-term urodynamic study of 84 patients (18 gastro-, 35 colo-, 31 ileocystoplasty):[25]

  • All three segments produced significant improvements in capacity, maximum intravesical pressure, and compliance (p < 0.001).
  • Pathologic contractions: ileocystoplasty 26%, colocystoplasty 43%, gastrocystoplasty 50%, highest with stomach.[25]

Complications Summary​

IssueEvidence and implication
HDSCommon in long-term series; symptoms require assessment for infection, stones, and malignancy rather than automatic attribution to acid
Metabolic alkalosisCan be severe even with normal preoperative renal function[17]
MalignancyFour tumors among 119 patients in Castellan 2007 and three among 11 in Boissier are different small-cohort observations, not a pooled 3.4–27% risk range[20][21]
Revision/excisionEight of 35 patients required revision in Hubert; seven of 11 had patch excision in Boissier, over different follow-up periods[12][21]
Stones, infection, perforationAll remain possible
MortalitySeven of 35 patients died in Hubert from varied causes[12]

Peptic ulcer disease. Unique complication. Gastric segment can ulcerate, particularly when defunctionalized (not exposed to urine). Urine buffering was proposed as a protective mechanism: in a 12-dog experiment, ulceration was more prominent in the bladder tissue of urine-diverted than urine-exposed segments, with three perforations on the dry side; a separate case report described perforation of a gastric-patch peptic ulcer in a child.[26][27] In a 12-dog experiment, H₂ blockade was associated with less ulceration in functioning (wet) gastrocystoplasties but had less apparent effect on defunctionalized (dry) segments; clinical prevention efficacy remains uncertain.[26][27]

Current Status and Recommendations​

Gastrocystoplasty has become highly controversial, with a clear trend toward abandonment at many centers.

Against continued use:

  • Castellan (n=29, 13.9 yr): "We do not recommend the use of gastric segments for reconstruction of the lower urinary tract due to the high incidence of reoperations and complications."[4]
  • Boissier (n=11, 17 yr): results "question the use of this technique for bladder augmentation, irrespective of the indication"; 7/11 required gastric-patch excision.[21]
  • Mingin (36% late complication rate): data "cast serious doubt on the long-term advantages of using stomach for bladder augmentation."[8]

In favor of selective use:

  • Kurzrock (n=47, mean 4.4 yr): gastrocystoplasty has "significant advantages over intestinal augmentation" but "should be avoided in sensate patients with sufficient bowel."[3]
  • DeFoor (n=44, median 9.8 yr): "remains an important option" specifically in patients with chronic renal insufficiency, metabolic acidosis, or short gut syndrome.[5]
  • Leonard: "may be considered in patients with cloacal exstrophy and/or metabolic acidosis."[7]

Exceptional situations discussed in historical series[2][3][5][7]​

  • Cloacal exstrophy with both short bowel and renal insufficiency (the classic indication).
  • Chronic renal failure where hyperchloremic acidosis from enterocystoplasty would be dangerous, and insufficient bowel for enterocystoplasty.
  • Short bowel syndrome where ileum and colon cannot be sacrificed.
  • The patient should ideally have an insensate urethra (neurogenic bladder) to minimize HDS risk.
  • The procedure should be avoided in patients with normal pelvic sensation and adequate bowel.

Long-Term Surveillance​

Lifelong surveillance is required. For adult NLUTD after reconstruction incorporating a bowel segment, AUA/SUFU advises annual focused history, examination and symptom assessment, a basic metabolic panel and urinary tract imaging , and cystoscopy for gross hematuria or symptomatic recurrent UTI .[29] The companion AUA/SUFU diagnosis guideline recommends against screening or surveillance cystoscopy in adults with NLUTD .[34]

  • Annual ultrasound of bladder and upper tracts.
  • Individualized endoscopic surveillance discussion. Castellan 2007 recommended annual cystoscopy from ten years, with biopsy of suspicious lesions, not routine biopsy of every normal reservoir. In a separate 72-patient cohort, two patients had metastatic cancer without preceding gross hematuria, recurrent UTI, or pain; those authors advocated annual surveillance.[28] New hematuria, unexplained recurrent symptomatic UTI, or pain requires prompt evaluation regardless of elapsed time.
  • At least annual basic metabolic panel in NLUTD bowel reconstruction, with more frequent testing for symptoms, renal disease, or prior acid-base disturbance.
  • Renal function monitoring.
  • HDS symptom assessment at each visit.
  • Patient education about tumor-related symptoms (new hematuria, pain, change in voiding pattern).

Videos​

Total Robotic Augmentation Gastrocystoplasty
Yee CH, et al. Urology Video Journal 2020 (CC BY-NC-ND 4.0)
Open source videoRead the article

References​

1. Adams MC, Mitchell ME, Rink RC. "Gastrocystoplasty: An Alternative Solution to the Problem of Urological Reconstruction in the Severely Compromised Patient." The Journal of Urology. 1988;140(5 Pt 2):1152-6. doi:10.1016/s0022-5347(17)41986-0

2. Kurzrock EA, Baskin LS, Kogan BA. "Gastrocystoplasty: Is There a Consensus?" World Journal of Urology. 1998;16(4):242-50. doi:10.1007/s003450050061

3. Kurzrock EA, Baskin LS, Kogan BA. "Gastrocystoplasty: Long-Term Followup." The Journal of Urology. 1998;160(6 Pt 1):2182-6. doi:10.1016/s0022-5347(01)62289-4

4. Castellan M, Gosalbez R, Bar-Yosef Y, Labbie A. "Complications After Use of Gastric Segments for Lower Urinary Tract Reconstruction." The Journal of Urology. 2012;187(5):1823-7. doi:10.1016/j.juro.2011.12.105

5. DeFoor W, Minevich E, Reeves D, et al. "Gastrocystoplasty: Long-Term Followup." The Journal of Urology. 2003;170(4 Pt 2):1647-9. doi:10.1097/01.ju.0000091220.86291.96

6. Chancellor MB, Erhard MJ, Strup S, Tammela TL. "Bladder Augmentation Using the Stomach in Spinal Cord Injured Patients With Impaired Renal Function." Archives of Physical Medicine and Rehabilitation. 1993;74(11):1222-4. doi:10.1016/s0003-9993(23)00021-7

7. Leonard MP, Dharamsi N, Williot PE. "Outcome of Gastrocystoplasty in Tertiary Pediatric Urology Practice." The Journal of Urology. 2000;164(3 Pt 2):947-50. doi:10.1097/00005392-200009020-00007

8. Mingin GC, Stock JA, Hanna MK. "Gastrocystoplasty: Long-Term Complications in 22 Patients." The Journal of Urology. 1999;162(3 Pt 2):1122-5. doi:10.1016/S0022-5347(01)68092-3

9. Close CE, Mitchell ME. "Continent Gastric Tube: New Techniques and Long-Term Followup." The Journal of Urology. 1997;157(1):51-5. doi:10.1016/s0022-5347(01)65278-9

10. Abdel-Azim MS, Abdel-Hakim AM. "Gastrocystoplasty in Patients With an Areflexic Low Compliant Bladder." European Urology. 2003;44(2):260-5. doi:10.1016/s0302-2838(03)00260-4

11. Nguyen DH, Mitchell ME, Horowitz M, Bagli DJ, Carr MC. "Demucosalized Augmentation Gastrocystoplasty With Bladder Autoaugmentation in Pediatric Patients." The Journal of Urology. 1996;156(1):206-9. doi:10.1016/s0022-5347(01)66001-4

12. Hubert KC, Large T, Leiser J, et al. "Long-Term Renal Functional Outcomes After Primary Gastrocystoplasty." The Journal of Urology. 2015;193(6):2079-84. doi:10.1016/j.juro.2014.12.088

13. Vajda P, Kaiser L, Magyarlaki T, et al. "Histological Findings After Colocystoplasty and Gastrocystoplasty." The Journal of Urology. 2002;168(2):698-701. doi:10.1016/s0022-5347(05)64727-1

14. Nguyen DH, Bain MA, Salmonson KL, et al. "The Syndrome of Dysuria and Hematuria in Pediatric Urinary Reconstruction With Stomach." The Journal of Urology. 1993;150(2 Pt 2):707-9. doi:10.1016/s0022-5347(17)35593-3

15. Chadwick Plaire J, Snodgrass WT, Grady RW, Mitchell ME. "Long-Term Followup of the Hematuria-Dysuria Syndrome." The Journal of Urology. 2000;164(3 Pt 2):921-3. doi:10.1016/s0022-5347(05)67218-7

16. Bogaert GA, Mevorach RA, Kim J, Kogan BA. "The Physiology of Gastrocystoplasty: Once a Stomach, Always a Stomach." The Journal of Urology. 1995;153(6):1977-80. doi:10.1016/s0022-5347(01)67383-x

17. Gosalbez R, Woodard JR, Broecker BH, Warshaw B. "Metabolic Complications of the Use of Stomach for Urinary Reconstruction." The Journal of Urology. 1993;150(2 Pt 2):710-2. doi:10.1016/s0022-5347(17)35594-5

18. Kinahan TJ, Khoury AE, McLorie GA, Churchill BM. "Omeprazole in Post-Gastrocystoplasty Metabolic Alkalosis and Aciduria." The Journal of Urology. 1992;147(2):435-7. doi:10.1016/s0022-5347(17)37261-0

19. de Freitas Filho LG, Carnevale J, Leão JQ, Schor N, Ortiz V. "Gastrocystoplasty and Chronic Renal Failure: An Acid-Base Metabolism Study." The Journal of Urology. 2001;166(1):251-4. doi:10.1016/S0022-5347(05)66139-3

20. Castellan M, Gosalbez R, Perez-Brayfield M, et al. "Tumor in Bladder Reservoir After Gastrocystoplasty." The Journal of Urology. 2007;178(4 Pt 2):1771-4. doi:10.1016/j.juro.2007.05.100

21. Boissier R, Di Crocco E, Faure A, et al. "What Is the Outcome of Paediatric Gastrocystoplasty When the Patients Reach Adulthood?" BJU International. 2016;118(6):980-986. doi:10.1111/bju.13558

22. Tran THT, Melamed J, Deng FM. "Gastric Adenocarcinoma Arising in Gastrocystoplasty." Urology. 2021;148:270-273. doi:10.1016/j.urology.2020.07.003

23. Garnier S, Vendrell J, Boillot B, et al. "Malignancy After Augmentation Enterocystoplasty: A Nationwide Study of Natural History, Prognosis and Oncogene Panel Analysis." The Journal of Urology. 2020;204(1):136-143. doi:10.1097/JU.0000000000000752

24. Buson H, Diaz DC, Manivel JC, et al. "The Development of Tumors in Experimental Gastroenterocystoplasty." The Journal of Urology. 1993;150(2 Pt 2):730-3. doi:10.1016/s0022-5347(17)35599-4

25. Juhász ZS, Kispál Z, Kardos D, Vajda P. "Long-Term Urodynamic Findings Following Colo-, Gastro- And Ileocystoplasty." Pediatric Surgery International. 2024;40(1):131. doi:10.1007/s00383-024-05714-z

26. Castro-Diaz D, Froemming C, Manivel JC, et al. "The Influence of Urinary Diversion on Experimental Gastrocystoplasty." The Journal of Urology. 1992;148(2 Pt 2):571-4. doi:10.1016/s0022-5347(17)36656-9

27. Reinberg Y, Manivel JC, Froemming C, Gonzalez R. "Perforation of the Gastric Segment of an Augmented Bladder Secondary to Peptic Ulcer Disease." The Journal of Urology. 1992;148(2 Pt 1):369-71. doi:10.1016/s0022-5347(17)36600-4

28. Vemulakonda VM, Lendvay TS, Shnorhavorian M, et al. "Metastatic Adenocarcinoma After Augmentation Gastrocystoplasty." The Journal of Urology. 2008;179(3):1094-6. doi:10.1016/j.juro.2007.10.089

29. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-Up. J Urol. 2021;206(5):1106-1113. doi:10.1097/JU.0000000000002239.

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31. Gold BD, Bhoopalam PS, Reifen RM, Harvey E, Marcon MA. "Gastrointestinal complications of gastrocystoplasty." Arch Dis Child. 1992;67(10):1272-1276. doi:10.1136/adc.67.10.1272

32. Yamagiwa S, Yamada H, Morikami H, et al. "A Case of Refractory Bladder Hemorrhage After Gastrocystoplasty." Nihon Hinyokika Gakkai Zasshi. 2024;115(2):90-93. doi:10.5980/jpnjurol.115.90

33. Kardos DJ, Kereskai L, Tornoczky T, et al. "Re-evaluation of histological findings after colocystoplasty and gastrocystoplasty." J Pediatr Urol. 2019;15(6):651.e1-651.e8. doi:10.1016/j.jpurol.2019.10.003

34. Ginsberg DA, Boone TB, Cameron AP, et al. "The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation." J Urol. 2021;206(5):1097-1105. doi:10.1097/JU.0000000000002235