Formats:
| ||||
Copyright
© Indian Journal of Urology
Bladder augmentation: Review of the literature and
recent advances
Gazi University School of Medicine, Department of
Urology, Section of Pediatric Urology, Ankara, Turkey
*Pediatric Urology Centre Nijmegen,
Department of Urology, Radboud University Nijmegen Medical Centre, The
Netherlands
For correspondence:
Serhat Gurocak, Gazi University School of Medicine, Department of Urology,
Section of Pediatric Urology, 06500, Besevler, Ankara, Turkey. E-mail:
sgurocakmd/at/yahoo.com
This is an
open-access article distributed under the terms of the Creative Commons
Attribution License, which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly
cited.
This article has been cited
by other articles in PMC. Abstract Bladder augmentation is an important tool
in the management of children requiring reconstructions for urinary
incontinence or preserving of the upper urinary tract in congenital
malformations. We reviewed the literature and evaluated the long-term
results of enterocystoplasty in the pediatric age group and summarized
techniques, experimental options and future perspectives for the treatment
of these patients. For this purpose, a directed Medline literature review
for the assessment of enterocystoplasty was performed. Information gained
from these data was reviewed and new perspectives were summarized. The
ideal gastrointestinal (GI) segment for enterocystoplasty remains
controversial. The use of GI segments for enterocystoplasty is associated
with different short and long-term complications. The results of different
centers reported in the literature concerning urological complications
after enterocystoplasty are difficult to compare because of the
non-comparable aspects and different items included by different authors.
On the other hand, there are more and more case reports about cancer
arising from bowel segments used for bladder augmentation in recent
publications.
Although bladder reconstruction with GI
segments can be associated with multiple complications, such as metabolic
disorders, calculus formation, mucus production, enteric fistulas and
potential for malignancy, enterocystoplasty is unfortunately still the
gold standard. However, there is an urgent need for the development of
alternative tissues for bladder augmentation.
Keywords: Bladder
augmentation, children, enterocystoplasty, future perspectives, large
bowel, review, small bowel, stomach Bladder augmentation (BA) with GI tissue
is an important tool in the armamentarium of the urologist in the
management of children requiring reconstruction for urinary incontinence,
preserving the upper urinary tract and in reconstructions for severe
congenital malformations. The goal of BA is to create a reservoir with an
adequate functional capacity with a low end-filling pressure. By achieving
this, the low intravesical pressure will not interfere with ureteral
delivery of the urine to the bladder and preserve the upper urinary tract
from high pressure damage by vesico-ureteral reflux.
To the best of our knowledge, Simon first
reported the use of tissues other than urothelial tissues to achieve this
goal 150 years ago.[1] He clinically applied a ureterosigmoidostomy to a child
with bladder exstrophy. Mikulicz was the first who described the use of
small intestine to augment the bladder in 1899.[2] Yeates described the use of detubularized small
intestine and this method has since been shown to be an effective method
of providing a compliant reservoir.[3] However, this was not a general practice at that time,
because enterocystoplasty was known to result in urinary retention. So,
most pediatric patients were generally diverted from augmentation
procedures due to the retention problems, until Lapides et al.,
proved the efficiency of clean intermittent catheterization (CIC) to empty
the bladder.[4] After this important cornerstone, augmentation
cystoplasty with various intestinal segments grew rapidly and changed the
management of pediatric and adult patients with abnormal bladder function.
The current techniques for pediatric BA are cystoplasty with stomach,[5–6] large bowel,[7–8] small bowel,[9–13] ileocaecal,[14] ureter[15] and engineered tissue[16] with or without urinary continence procedures.
Neuropathic dysfunction (myelomeningocele) and bladder exstrophy are the
main underlying conditions for pediatric patients requiring an
enterocystoplasty. Major postoperative complications like metabolic
disorders, hematuria syndrome, calculus formation, mucus production,
enteric fistulas, bladder rupture, intestinal obstruction and the
potential for developing a malignancy are associated with the use of GI
tissues in the bladder.[17–28] Although bladder reconstruction with GI is associated
with several complications, as well as the morbidity of harvesting the
segment of bowel, enterocystoplasty is still considered to be the best of
all alternatives. The aim of this review is to discuss the details of BA
which include the indications, type of material, the long-term outcome,
alternative options, experimental and future options. AUGMENTATION WITH GASTRIC TISSUE, SMALL AND LARGE BOWEL Technique
Gastrointestinal segments from the
stomach to the sigmoid have been used for an enterocystoplasty. Only the
jejunum quickly fell into disrepute because of salt losses and acidosis.
Augmentation enterocystoplasty is performed using a detubularized segment
of ileum (10), caecum (14) or sigmoid (7). Gastric tissue
Gastric tissue has been used as
donor tissue for bladder augmentation for over 30 years. It was
popularized by Adams et al., in 1984 for use in children who had
no other bowel available (e.g. cloacal exstrophy and after pelvic
irradiation) or in patients who could not tolerate metabolic acidosis from
resorption of chloride.[5] He noted an 85% success rate in their study group. They
found after gastrocystoplasty comparable results to other bowel segments.
Although gastric augmentation usually results in an improvement in bladder
volume and compliance, the stomach segment continues to act as a gastric
secreting organ, which may predispose to hyperchloremic hypokalemic
metabolic alkalosis, hematuria, dysuria syndrome and gastrinemia.[6] Chronic electrolyte imbalance may also lead to
abnormalities in calcium homeostasis, resulting in bone
demineralization.[27] This might compromise growth and development of
children.[28] Mingin et al., found a complication rate of
36% after a mean follow-up of six years.[6] They conclude, considering the major metabolic and
physiological complications of gastrocystoplasty, that the stomach should
be limited to patients who have undergone bowel irradiation and those at
risk for short bowel syndrome, as in cloacal exstrophy. This was also
mentioned by Adams before.[5] Small and large intestine
Many urologists hold bladder augmentation
with small intestine as the procedure of choice when conservative
managements fails. In 1982 Goodwin[9] first described this procedure, which was popularized
later by Mundy and Stephenson.[11] Mundy et al., reported a 90% success rate in
augmentation cystoplasty performed in 40 patients with neuropathic bladder
dysfunction with a mean follow-up of one year. Several other reports have
consequently confirmed the high success rate to achieve a low-pressure,
high-capacity urinary reservoir. Krishna et al., studied 39
children with spina bifida and reported 91.7% reduction in upper tract
dilatation, which was distended preoperatively.[12] Riedmiller et al., used ileum for bladder
augmentation and accomplished large compliant bladders with moderate mucus
production.[13] In addition, they found a low complication rate with
this technique.
On the other hand, augmentation procedures with
the integration of bowel segments into the urinary tract have numerous
disadvantages. It is clear that intestinal segments used in the urinary
tract retain their native function of secreting or reabsorbing salt and
water from the urine. This can result in a multitude of metabolic
disturbances.[25,26] Resection of large parts of the distal small bowel can
result in chronic B12 and folate deficiency.[27] Long-term follow-up of hematological laboratory tests
are needed. The use of bowel in the urinary tract has been associated with
chronic bladder infections and a tendency for bladder stone formation.[22] In addition, it must be kept in mind that
enterocystoplasty is a major intraperitoneal surgery with various
complications and patients should be counseled about the significant
probability of the need for CIC postoperatively ranging from 15%–75%.[28] The possible surgical complications of these
procedures are anastomotic leakage, stricture, intestinal obstruction or
bladder rupture.[17–21]
The ideal bowel segment for enterocystoplasty
remains controversial. Kilic et al.,[29] conclude that ileocystoplasty is the procedure of
choice to achieve a low-pressure, high-capacity urinary reservoir. In
addition, they found a low complication rate in this technique. Others
found more complications after ileocystoplasty in comparison to
sigmoidocystoplasty.[17] We found a comparable complication rate of 7/14
sigmoidocystoplasty patients in comparison to 13/27 in the ileocystoplasty
group by Nuininga et al.[30] The ileum is used most frequently, preferably as an
ileal conduit, possibly due to the accumulated experience with this
technique because of other pathological conditions.
The results of different centers reported
in the literature concerning urological complications after
enterocystoplasty are difficult to compare because of the non-comparable
aspects and different items included by different authors (e.g. with or
without including urinary tract infections, pyelonephritis, renal
transplantation). Many studies report on pediatric and adult patients
together with different follow-up periods. Sometimes only a brief referral
is given about these complications in publications about
enterocystoplasties. Bladder perforation
Rupture of the augmented bladder is
an uncommon but one of the most serious and life-threatening complications
of enterocystoplasty. Factors that are thought to contribute to the risk
of perforation include choice of bowel segment, high bladder pressures,
configuration of the bowel segment, traumatic catheterization, chronic
infection and ischemic necrosis of the intestinal segment. Several studies
evaluated these risk factors for spontaneous bladder perforation after
augmentation cystoplasty. DeFoor et al., found a low incidence of
spontaneous bladder perforation of 5% in 107 children.[31] They explained this by the large number of patients
with gastrocystoplasty, as well as their strict adherence to a
postoperative incremental catheterization program. All patients
postoperatively got temporary cystostomy tubes for four to six weeks and
then patients started intermittent catheterization on a regular or
incremental schedule according to surgeon preference. Metcalfe et
al., reported one of the largest series of bladder augmentations and
found a perforation rate of 8,6% in 500 enterocystoplasty patients.[32] This large and comprehensive series of patients gives
valuable insight into this serious complication. A significant increased
risk of perforation was observed with the use of sigmoid colon and bladder
neck surgery. A decreased risk was associated with the presence of a
continent catheterizable channel. Reservoir perforation must be considered
in patients with sudden lower abdominal pain or peritonitis associated
with low-grade fever. Stone formation
The incidence of calculi in
augmented bladders is high, but varies between published studies. In most,
it is observed in 2–18% of all patients. In one report of children, an
extraordinary 52.5% had formed a stone at a mean follow-up of four
years.[33] In enterocystoplasties one important factor in the
formation of bladder calculi is the production of mucus. The mucus may
probably enhance stone formation directly by acting as a heterogeneous
nucleator or indirectly by facilitating bacterial growth. This was
confirmed by the fact that the frequency of stone formation seems to
depend on the frequency with which the patients irrigate the bladder free
of mucus.[34] But others found no correlation between the frequency
of bladder irrigations and stone formation.[22,35] They found urinary tract infection an independent risk
factor for stone formation. The care should include clear emphasis on the
role of treating symptomatic urinary tract infections. Another risk factor
for stone formation is foreign bodies, such as staples, in the
reservoir.[36] This increases the risk of stone formation from 13% to
43%. Neoplasia
Cancer following augmentation
cystoplasty is a recognized risk factor. In recent publications there are
more and more case reports about cancer arising from bowel segments used
for bladder augmentation. The majority of tumors have been adenocarcinoma
but transitional cell carcinoma (TCC) has also been reported. The majority
of reported cases of post augmentation malignancy have occurred in adults
with other multiple potential risk factors.[23] It is difficult to determine the exact independent
risk associated with bladder augmentation. Recently, Soergel reported
three cases (1.2%) of transitional cell carcinoma (TCC) following
augmentation cystoplasty in a unique population of 260 augmentations with
at least 10 years of follow-up with no additional risk factors for bladder
cancer.[24] No patient had a history of smoking exposure or other
known risk factors for bladder cancer. Mean time from bladder augmentation
to TCC was 19 years. This study supports the hypothesis that bladder
augmentation appears to be an independent risk factor for TCC. They
recommend endoscopic surveillance of all patients with a history of
bladder augmentation beginning 10 years after initial
surgery. ALTERNATIVE OPTIONS Minimally invasive options
Oxybutinin and CIC
Many investigators have attempted
to use alternative materials and tissues for replacement of the
gastrointestinal tissue. An alternative minimal invasive treatment might
be conservative management with anticholinergic therapy and clean
intermittent catheterization (CIC). This conservative management was
performed by many authors and recently by Dik et al.,[37,38] in a prospective study. Fifteen spina bifida patients
were all on a regime of CIC and anticholinergic therapy shortly after
birth. They found that detrusor overactivity recurred immediately after
the cessation of the oxybutinin and concluded that no long-lasting
suppressive effect should be expected from these drugs because of a
primary neuropathic origin. Botulinum-A toxin
Another alternative therapeutic
option might be the use of Botulinum-A toxin injection to the detrusor in
patients with a neuropathic bladder. Schurch et al., were the
first to apply the toxin into the neuropathic overactive detrusor and
achieved increased bladder capacity and decreased pressures.[39] Riccabona et al., operated 15 patients with
myelomeningocele.[40] All patients were injected with 10U/kg of botulinum
toxin-A at 25–40 sites in the detrusor. The urodynamic evaluation of the
efficacy and durability of Botulinum toxin-A was done at three, nine and
12 months. They found significant improvement in bladder compliance,
bladder capacity and decline in maximum bladder pressure at nine months.
But at 12 months the encouraging results reverted to preoperative results.
Although this study showed the safety of this minimal invasive operation,
the need for recurrent treatment each nine months is a big disadvantage.
But this might be better than the several complications with augments.
Future studies including randomization, controls and long-term follow-up
are mandatory before this treatment in patients with a neuropathic bladder
is taken into daily clinical use. Invasive options
Ureterocystoplasty
Ureterocystoplasty might be
indicated in patients who have poor compliance. In a typical case,
function of one kidney in a patient is affected and the affected kidney
has poor renal function with a massively dilated collecting system. In
this procedure, the dilated ureter is used for bladder augmentation and
therefore it avoids the complications associated with intestinal
mucosa.[41] Perovic et al. have performed
ureterocystoplasty in 16 patients and they used the distal part of the
megaureter for bladder augmentation and implanted the proximal part into
the bladder using extravesical tunneling ureteroneocystostomy. With this
technique, they provided an increased bladder capacity between 296 to
442ml (mean 371) and an increase in bladder compliance without any further
worsening of renal function.[42] Nahas et al., assessed clinical and surgical
results in renal transplantation candidates with voiding dysfunction and
end stage renal disease who underwent bladder augmentation with
ureterocystoplasty technique. They analyzed eight patients and they found
that the bladder capacity was increased and intravesical pressure was
decreased in these patients after the surgery with a mean serum creatinine
of 1.65mg/dl. This study shows that ureterocystoplasty can also be used
with confidence in end stage renal disease because it combines the
benefits common to all enterocystoplasties without adding any
complications.[43] In a larger study, Husmann et al., found
similar results such as increased bladder capacity and compliance in 64
patients who underwent ureterocystoplasty.[44] Dewan et al., described the use of
ureterocystoplasty in bladder extrophy[45] and Clento Jr et al., performed
laparoscopically assisted ureterocystoplasty safely in five patients.[46] These studies show us that this technique is a safe
and reliable procedure. Demucosalized enterocycstoplasty
An alternative technique for
providing urothelium-lined bladder to avoid the complications of bowel
mucosa contact with urine including malignancy, mucus and stone formation,
metabolic acidosis and reduced linear growth in children, is augmentation
demucosalized enterocystoplasty. In this technique denuded intestinal
muscle is used for bladder augmentation.[47] Lima et al., presented long-term results on
the use of demucosalized intestine for reconstructive surgery of the
bladder which was performed in 129 bladder augmentations on 123 patients
with 10 years of follow-up. They used sigmoid in 104 cases and ileum in 25
cases. They found a 329% increase in bladder capacity and sevenfold
increase in compliance after surgery. Thirteen cases were considered as
failure and they performed reaugmentation for 11 of these patients. These
data shows that demucosalized intestinal flaps are appropriate for bladder
reconstruction for the same indications as total flaps.[48] In another study by Lima et al.,
demucosalized ileum was used for augmentation of the bladder in 11
patients and a Foley catheter with inflated balloon was used for
dissection of the mucosa from the muscle. They provided a significant
increase in bladder compliance in all patients. They supported this study
with an animal model and good-shaped bladders were obtained in these
animal models.[49] In addition, Lima et al., performed another
animal model with 12 female dogs which underwent total cystectomy and
bladder replacement by neobladder composed of demucosalized ileal segment
and they divided their study population into two groups. In the first
group, an intravesical silicone modeler was used for preventing graft
retraction in contrast to the second group. They found a significant
difference in bladder capacity between the groups after surgery. The
bladder capacity was significantly larger in Group I.[50] In another animal study by Vates et al., they
declared that preservation of the submucosa of the demucosalized colonic
segment is essential to prevent fibrosis and a balloon stent is crucial to
prevent graft contraction. Treatment of the demucosalized segment with
protamine sulfate and urea results in better urothelial expansion and less
colonic mucosal regrowth.[51] The main problem of this technique is the tissue
contracture frequently encountered in demucosalized segments. This
phenomenon might show us the importance of vascular supply contribution of
the colonic mucosa to all segments of the intestine. Animal models like
silicone balloons which are mainly maneuvers to prevent contraction might
be intractable in human being. Autoaugmentation
A number of strategies have been
devised to avoid the use of bowel in the urinary tract. Cartwright and
Snow described the first autoaugmentation technique in dogs in 1989.
Although the follow-up time was short, they reported in their first
clinical study a subjective success of good in three (43%) and excellent
in four (57%) of the seven patients. They declared that autoaugmentation
could be an alternative to enterocystoplasty in a select group of patients
whose compliance is poor based on abnormal pressures. These same workers
declared in a subsequent report with a longer follow-up period that 80% of
patients were continent although a significant increase in bladder
capacity was not observed.[52] Although the results of the aforementioned studies
were promising, doubts remain about the reliability and long-term efficacy
of this technique. Marte et al., reviewed their autoaugmentation
results in myelodysplastic children and found that this procedure failed
in seven of 11 patients after 6.6 years.[53] They concluded that patient selection seemed to be
crucial for the success of autoaugmentation. Macneily et al.,
found that clinical outcome did not appear to be durable.[54] Four of 17 patients (23,5%) required enterocystoplasty
and 12 (71%) patients were considered to be clinical failures due to upper
tract deterioration and ongoing incontinence. The disadvantage of
autoaugmentation is limitation in the postoperative bladder expansion when
compared to conventional enterocystoplasty. In addition, Gurocak et
al.,[55] reviewed autoaugmentations and concluded that
achievement of better compliance after autoaugmentation procedures seems
to be less pronounced and of shorter duration than that of conventional
enterocystoplasty. On the other hand, the low morbidity and lack of
side-effects of bowel integration into the urinary tract are the definite
advantages of this technique. It was concluded that it is the
responsibility of the physician to determine the balance between the
limited efficacies of the procedures versus the definite
advantages. Experimental options
During the last few decades many
investigators have directed their attention to alternatives for bladder
augmentation or reconstruction. Studies in animals with biocompatible and
biodegradable biomatrices are promising.[56,57] Currently, the two most common tissue engineering
techniques for bladder reconstruction are regeneration with unseeded or
seeded biodegradable biomatrices. The unseeded technique, involves
reconstruction of the bladder with a biocompatible and biodegradable
matrix. The success of this repair depends on the natural regeneration
capacity of the bladder. The seeded technique involves in vitro
cell culture techniques to create a biomatrix with primary cultured
epithelium on one side and smooth muscle cells on the other side. This
in vitro prepared ‘bladder wall’ is used in the host for bladder
repair. Reconstruction of the urinary tract using the principles of tissue
engineering now face the challenge of determining which of these
techniques can be applied for clinical use. The unseeded biomatrix has the
advantage of being available to surgeons at any time of a reconstructive
operation. The development of a readymade bioactive biomatrix with
predefined characteristics promoting tissue growth of the bladder would
significantly improve the reconstructive possibilities of the urologist.
Different biodegradable biomatrices have been used for preclinical
studies. Amongst these, SIS, an acellular collagen matrix harvested from
porcine small intestine, is one of the most thoroughly studied biomaterial
used for the unseeded grafts. Bladder reconstruction with SIS has
demonstrated regeneration of transitional epithelium, smooth muscle and
nerves in various different animal models.[58,59] Although the initial results have been promising,
long-term results have been poor. This is due to the complications such as
fibrosis resulting in graft shrinkage, graft incrustation or
infection.
Recently, Atala et al.,
published the first human clinical study with engineered bladders.[16] Seven patients with myelomeningocele and resultant
dysfunctional bladders underwent bladder augmentations with autologous,
smooth muscle and urothelial cell seeded scaffolds. These scaffolds were
made of biodegradable collagen and polyglycolic acid composite. The
engineered tissue improved overall bladder function in all patients, with
mean follow-up of almost four years. All three patients who had composite
scaffolds and omental wrap had better outcomes than earlier decellularized
bladder submucosa scaffold cystoplasties. It seems appropriate to conclude
that the omental wrap (vascular supply) had an important role in the
success of the engineered bladders in the study by Atala et al.
This aforementioned report is a milestone in tissue engineering of the
bladder, but further studies and improvements are needed for widespread
clinical implementation. CONCLUSION Gastrointestinal tissue used for
enterocystoplasty is associated with different short and long-term
complications. Reservoir perforation must be considered in patients with
acute abdominal pain or peritonitis and long-term follow-up of renal
function is needed. In addition, one has to be aware of the long-term risk
of malignancy in these procedures which has come to the attention of the
urologists recently. Regarding these complications, there is a current
necessity to develop alternative tissues for bladder augmentation by the
help of tissue engineering protocols that will replace the integration of
bowel segments into the urinary tract. Until then, intestinal cystoplasty
still seems to be the gold standard due to the lack of promising
alternative options. Acknowledgments This study is sponsored by The Netherlands
Organisation for Health Research and Development
(ZonMW). Footnotes Source of Support:
The Netherlands Organisation for Health Research and Development
(ZonMW)
Conflict of
Interest: None declared. REFERENCES 1. Simon
J. Extropia vesicae (absence of the anterior walls of the bladder and
rubic abdominal parietes): Operation for directing the orifices of the
ureters into the rectum: Temporary success: Subsequent death. autopsy.
Lancet. 1852;2:568.
2. Mikulicz
J. Zur Operation der Augeborenen blasenspate. Zentrabl
Chir. 1889;26:641.
3. Yeates
WK. A technique of ileocystoplasty. Br J
Urol. 1956;28:410.
4. Lapides
J, Diokono AC, Silber SJ, Lowe BS. Clean intermittent self-catheterization
in the treatment of urinary tract disease. J Urol. 1972;107:458–61.[PubMed]
5. Adams
MC, Mitchell ME, Rink RC. Gastrocystoplasty. An alternative solution to
the problem of urological reconstruction in the severely compromised
patient. J Urol. 1988;140:1152–6.[PubMed]
6. Mingin
GC, Stock JA, Hanna MK. Gastrocystoplasty: Long-term complications in 22
patients. J Urol. 1999;162:1122–5.[PubMed]
7. Winter
CC, Goodwin WE. Results of sigmoidocystoplasty. J
Urol. 1958;80:467–72.[PubMed]
8. Arikan
N, Turkolmez K, Budak M. Outcome of augmentation sigmoidocystoplasties in
children with neurogenic bladder. Urol
Int. 2000;64:82–5.[PubMed]
9. Goodwin
WE, Winter CC, Baker WF. Cup-patch technique of ileocystoplasty for
bladder enlargement or partial substitution. Surg
Gynecol Obstet. 1959;108:240–4.[PubMed]
10.
Bramble
FJ. The treatment of adult enuresis and urge incontinence by
enterocystoplasty. Br J Urol.
1982;54:693–6.[PubMed]
11.
Mundy
AR, Stephensons TP. ‘Clam’ ileocystoplasty for the treatment of refractory
urge incontinence. Br J Urol.
1985;57:641–6.[PubMed]
12.
Krishna
A, Gough DC, Fishwick J, Bruce J. Ileocystoplasty in children: assessing
safety and success. Eur Urol.
1995;27:62–6.[PubMed]
13.
Riedmiller
H, Thuroff J, Stockle M, Schofer O, Hohenfellner R. Continent urinary
diversion and bladder augmentation in children: the Mainz procedure.
Pediatr Nephrol. 1989;3:68–74.[PubMed]
14.
Mayo
ME, Chapman WH. Ileocaecal bladder augmentation in myelodysplasia.
J Urol. 1988;139:786–9.[PubMed]
15.
Dewan
PA, Anderson P. Ureterocystoplasty: The latest developments. BJU Int. 2001;88:744–51.[PubMed]
16.
Atala
A, Bauer SB, Soker S, Yoo JJ, Retik AB. Tissue-engineered autologous
bladders for patients needing cystoplasty. Lancet. 2006;367:1241–6.[PubMed]
17.
Gough
DC. Enterocystoplasty. BJU Int.
2001;88:739–43.[PubMed]
18.
Shekarriz
B, Upadhyay J, Demirbilek S, Barthold JS, González R. Surgical
complications of bladder augmentation: comparison between various
enterocystoplasties in 133 patients. Urology. 2000;55:123–8.[PubMed]
19.
Herschorn
S, Hewitt RJ. Patient perspective of long-term outcome of augmentation
cystoplasty for neurogenic bladder. Urology. 1998;52:672–8.[PubMed]
20.
Hendren
WH, Hendren RB. Bladder augmentation: experience with 129 children and
young adults. J Urol. 1990;144:445–53.[PubMed]
21.
Bertschy
C, Bawab F, Liard A, Valioulis, Mitrofanoff P. Enterocystoplasty
complications in children. A study of cases. Eur
J Pediatr Surg. 2000;10:30–4.[PubMed]
22.
Mathoera
RB, Kok DJ, Nijman RJ. Bladder calculi in augmentation cystoplasty in
children. Urology. 2000;56:482–7.[PubMed]
23.
Austen
M, Kalble T. Secondary malignancies in different forms of urinary
diversion using isolated gut. J Urol.
2004;172:831–8.[PubMed]
24.
Soergel
TM, Cain MP, Misseri R, Gardner TA, Koch MO, Rink RC. Transitional cell
carcinoma of the bladder following augmentation cystoplasty for the
neuropathic bladder. J Urol.
2004;172:1649–52.[PubMed]
25.
Gilbert
SM, Hensle TW. Metabolic consequences and long term complications of
enterocystoplasty in children: A review. J
Urol. 2005;173:1080–6.[PubMed]
26.
Feng
AH, Kaar S, Elder JS. Influence of enterocystoplasty on linear growth in
children with exstrophy. J Urol.
2002;167:2552–5.[PubMed]
27.
Steiner
MS, Morton RA, Marshall FF. Vitamin B12 deficiency in patients with
ileocolic neobladders. J Urol.
1993;149:255–7.[PubMed]
28.
Hasan
ST, Marshall C, Robson WA, Neal DE. Clinical outcome and quality of life
following enterocystoplasty for idiopathic detrusor instability and
neurogenic bladder dysfunction. Br J Urol.
1995;76:551–7.[PubMed]
29.
Kilic
N, Celayir S, Elicevik M, Sarimurat N, Soylet Y, Buyukunal C, et al.
Bladder augmentation: Urodynamic findings and clinical outcome in
different augmentation techniques. Eur J
Pediatr Surg. 1999;9:29–32.[PubMed]
30.
Nuininga
JE, de Gier RP, Feitz WF. Urological complications after paediatric
bladder reconstructions. Dutch J Urol.
2006;8:222.
31.
DeFoor
W, Tackett L, Minevich E, Wacksman J, Sheldon C. Risk factors for
spontaneous bladder perforation after augmentation cystoplasty.
Urology. 2003;62:737–41.[PubMed]
32.
Metcalfe
PD, Casale AJ, Kaefer MA, Misseri R, Dussinger AM, Meldrum KK, et al.
Spontaneous bladder perforations: A report of 500 augmentations in
children and analysis of risk. J Urol.
2006;175:1466–71.[PubMed]
33.
Palmer
LS, Franco I, Kogan S, Reda E, Bhagwant G, Levitt S. Urolithiasis in
children following augmentation cystoplasty. J
Urol. 1993;150:726–9.[PubMed]
34.
Hensle
TW, Bingham J, Lam J, Shabsigh A. Preventing reservoir calculi after
augmentation cystoplasty and continent urinary diversion: The influence of
an irrigation protocol. BJU Int.
2004;93:585–7.[PubMed]
35.
DeFoor
W, Minevich E, Reddy P, Sekhon D, Polsky E, Wacksman J, et al. Bladder
calculi after augmentation cystoplasty: Risk factors and prevention
strategies. J Urol. 2004;172:1964–6.[PubMed]
36.
Woodhouse
CR, Robertson WG. Urolithiasis in enterocystoplasties. World
J Urol. 2004;22:215–21.[PubMed]
37.
Amark
P, Bussman G, Eksborg S. Follow-up of long time treatment with
intravesical oxybutinin for neurogenic bladder in children. Eur Urol. 1998;34:148–53.[PubMed]
38.
Dik
P, Klijn AJ, van Gool JD, de Jong-de Vos van Steenwijk CC, de Jong TP.
Early start to therapy preserves kidney function in spina bifida patients.
Eur Urol. 2006;49:908–13.[PubMed]
39.
Schurch
B, Stohrer M, Kramer G, Schmid DM, Gaul G, Hauri D. Botulinum toxin A for
treating detrusor hyperreflexia in spinal cord injured patients: a new
alternative to anticholinergic drugs. J
Urol. 2000;164:692–7.[PubMed]
40.
Riccabona
M, Koen M, Schindler M, Goedele B, Pycha A, Lusuardi L. Botulinum-A toxin
injection into the detrusor: A safe alternative in the treatment of
children with myelomeningocele with detrusor hyperreflexia. J Urol. 2004;171:845–8.[PubMed]
41.
Dewan
PA, Anderson P. Ureterocystoplasty: The latest developments. BJU Int. 2001;88:744–51.[PubMed]
42.
Perovic
SV, Vukadinovic VM, Djordjevic ML. Augmentation ureterocystoplasty could
be performed more frequently. J Urol.
2000;164:924–7.[PubMed]
43.
Nahas
WC, Lucon M, Mazzucchi E, Antonopoulos IM, Piovesan AC, Neto ED, et al.
Clinical and urodynamic evaluation after ureterocystoplasty and kidney
transplantation. J Urol. 2004;171:1428–31.[PubMed]
44.
Hussmann
DA, Snodgrass WT, Koyle MA, Furness PD, Kropp BP, Cheng EY, et al.
Ureterocystoplasty: Indications for a successful augmentation. J Urol. 2004;171:376–80.[PubMed]
45.
Dewan
PA, Erdendtsetseg G, Zhao ZG, Anderson P. Ureterocystoplay as part of
primary closure of bladder exstrophy. BJU
Int. 2003;92:146–9.[PubMed]
46.
Cliento
BG, Jr, Diamond DA, Yeung CK, Manzoni G, Poppas DP, Hensle TW.
Laparoscopically assisted ureterocystoplasy. BJU
Int. 2003;91:525–7.[PubMed]
47.
Dewan
PA. Autoaugmentation demucosalized enterocystoplasy. World
J Urol. 1998;16:255–61.[PubMed]
48.
Lima
SV, Araújo LA, Vilar FO. Nonsecretory intestinocystoplasty: A 10-year
experience. J Urol. 2004;171:2636–40.[PubMed]
49.
Lima
SV, Araújo LA, Vilar FO, Mota D, Maciel A. Experience with demucosalized
ileum for bladder augmentation. BJU Int.
2001;88:762–4.[PubMed]
50.
Vilar
FO, de Ara´jo LA, Lima SV. Total bladder replacement with
de-epithelialized ileum. Experimental study in dogs. Int
Braz J Urol. 2004;30:237–44.[PubMed]
51.
Vates
TS, Denes ED, Rabah R, Shapiro E, Suzer O, Freedman AL, et al. Methods to
enhance in vivo urothelial growth on seromuscular colonic segments in the
dog. J Urol. 1997;158:1081–5.[PubMed]
52.
Snow
BW, Cartwright PC. Bladder autoaugmentation. Urol
Clin North Am. 1996;23:323–31.[PubMed]
53.
Marte
A, Di Meglio, Cotrufo AM, Di Iorio g, de Pasquale M, Vesella A. A
long-term follow-up of auto-augmentation in myelodysplastic children.
BJU Int. 2002;89:928–31.[PubMed]
54.
MacNeily
AE, Afshar K, Coleman GU, Johnson HW. Autoaugmentation by detrusor
myotomy: Its lack of effectiveness in the management of congenital
neuropathic bladder. J Urol.
2003;170:1643–6.[PubMed]
55.
Gurocak
S, de Gier RP, Feitz W. Bladder augmentation without the integration of
intact bowel segments: Critical review and future perspectives.
J Urol. 2007;177:839–44.[PubMed]
56.
Kropp
BP. Small intestinal submucosa for bladder augmentation: A review of
preclinical studies. World J Urol.
1998;16:262–7.[PubMed]
57.
Nuininga
JE, van Moerkerk H, Hanssen A, Hulsbergen CA, Oosterwijk-Wakka J,
Oosterwijk E, et al. A rabbit model to tissue engineer the bladder.
Biomaterials. 2004;25:1657–61.[PubMed]
58.
Wang
DS, Anderson DA, Fretz PC, Nguyen TT, Winfield HN. Laparoscopic
augmentation cystoplasty: A comparison between native ileum and small
intestinal submucosa in the porcine model. BJU Int. 2007;99:628–31.[PubMed]
59.
Zhang
Y, Frimberger D, Cheng EY, Lin HK, Kropp BP. Challenges in a larger
bladder replacement with cell-seeded and unseeded small intestinal
submucosa grafts in a subtotal cystectomy model. BJU
Int. 2006;98:1100–5.[PubMed] |
PubMed related articles
Your browsing activity is empty. Activity recording is turned off. |
J Urol. 1972 Mar; 107(3):458-61.
[J Urol. 1972]J Urol. 1988 Nov; 140(5 Pt 2):1152-6.
[J Urol. 1988]J Urol. 1999 Sep; 162(3 Pt 2):1122-5.
[J Urol. 1999]J Urol. 1958 Dec; 80(6):467-72.
[J Urol. 1958]Urol Int. 2000; 64(2):82-5.
[Urol Int. 2000]J Urol. 1988 Nov; 140(5 Pt 2):1152-6.
[J Urol. 1988]J Urol. 1999 Sep; 162(3 Pt 2):1122-5.
[J Urol. 1999]J Urol. 1993 Feb; 149(2):255-7.
[J Urol. 1993]Br J Urol. 1995 Nov; 76(5):551-7.
[Br J Urol. 1995]Surg Gynecol Obstet. 1959 Feb; 108(2):240-4.
[Surg Gynecol Obstet. 1959]Br J Urol. 1985 Dec; 57(6):641-6.
[Br J Urol. 1985]Eur Urol. 1995; 27(1):62-6.
[Eur Urol. 1995]Pediatr Nephrol. 1989 Jan; 3(1):68-74.
[Pediatr Nephrol. 1989]J Urol. 2005 Apr; 173(4):1080-6.
[J Urol. 2005]J Urol. 2002 Jun; 167(6):2552-5; discussion 2555.
[J Urol. 2002]J Urol. 1993 Feb; 149(2):255-7.
[J Urol. 1993]Urology. 2000 Sep 1; 56(3):482-7.
[Urology. 2000]Br J Urol. 1995 Nov; 76(5):551-7.
[Br J Urol. 1995]Eur J Pediatr Surg. 1999 Feb; 9(1):29-32.
[Eur J Pediatr Surg. 1999]BJU Int. 2001 Nov; 88(7):739-43.
[BJU Int. 2001]Urology. 2003 Oct; 62(4):737-41.
[Urology. 2003]J Urol. 2006 Apr; 175(4):1466-70; discussion 1470-1.
[J Urol. 2006]J Urol. 1993 Aug; 150(2 Pt 2):726-9.
[J Urol. 1993]BJU Int. 2004 Mar; 93(4):585-7.
[BJU Int. 2004]Urology. 2000 Sep 1; 56(3):482-7.
[Urology. 2000]J Urol. 2004 Nov; 172(5 Pt 1):1964-6.
[J Urol. 2004]World J Urol. 2004 Sep; 22(3):215-21.
[World J Urol. 2004]J Urol. 2004 Sep; 172(3):831-8.
[J Urol. 2004]J Urol. 2004 Oct; 172(4 Pt 2):1649-51; discussion 1651-2.
[J Urol. 2004]Eur Urol. 1998 Aug; 34(2):148-53.
[Eur Urol. 1998]Eur Urol. 2006 May; 49(5):908-13.
[Eur Urol. 2006]J Urol. 2000 Sep; 164(3 Pt 1):692-7.
[J Urol. 2000]J Urol. 2004 Feb; 171(2 Pt 1):845-8; discussion 848.
[J Urol. 2004]BJU Int. 2001 Nov; 88(7):744-51.
[BJU Int. 2001]J Urol. 2000 Sep; 164(3 Pt 2):924-7.
[J Urol. 2000]J Urol. 2004 Apr; 171(4):1428-31.
[J Urol. 2004]J Urol. 2004 Jan; 171(1):376-80.
[J Urol. 2004]BJU Int. 2003 Jul; 92(1):146-9.
[BJU Int. 2003]World J Urol. 1998; 16(4):255-61.
[World J Urol. 1998]J Urol. 2004 Jun; 171(6 Pt 2):2636-39; discussion 2639-40.
[J Urol. 2004]BJU Int. 2001 Nov; 88(7):762-4.
[BJU Int. 2001]Int Braz J Urol. 2004 May-Jun; 30(3):237-44.
[Int Braz J Urol. 2004]J Urol. 1997 Sep; 158(3 Pt 2):1081-5.
[J Urol. 1997]Urol Clin North Am. 1996 May; 23(2):323-31.
[Urol Clin North Am. 1996]BJU Int. 2002 Jun; 89(9):928-31.
[BJU Int. 2002]J Urol. 2003 Oct; 170(4 Pt 2):1643-6; discussion 1646.
[J Urol. 2003]J Urol. 2007 Mar; 177(3):839-44.
[J Urol. 2007]World J Urol. 1998; 16(4):262-7.
[World J Urol. 1998]Biomaterials. 2004 Apr; 25(9):1657-61.
[Biomaterials. 2004]BJU Int. 2007 Mar; 99(3):628-31.
[BJU Int. 2007]BJU Int. 2006 Nov; 98(5):1100-5.
[BJU Int. 2006]Lancet. 2006 Apr 15; 367(9518):1241-6.
[Lancet. 2006]