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Bladder-sparing multimodality treatment of muscle-invasive bladder cancer: a five-year follow-up.

OBJECTIVES: To determine the long-term results of a bladder-sparing approach in the treatment of muscle-invasive bladder cancer. METHODS: Ninety-four patients with invasive transitional cell carcinoma of the bladder were treated by transurethral resection followed by 2 or 3 cycles of cisplatin-based chemotherapy. Patients were then treated with 6480 cGy of radiation in 49 patients, segmental cystectomy in 8, or surveillance only in 7. Patients who failed to respond to chemotherapy or radiation therapy, or who developed recurrent muscle-invasive disease in follow-up, underwent salvage cystectomy. Patients were then carefully followed for a median follow-up of more than 5 years. RESULTS: After initial therapy, 53 patients (56%) were alive with their bladder preserved. Thirty of those 53 (57%) developed a local recurrence in follow-up. After a median follow-up of more than 5 years, the ultimate relapse-free survival is 49% (Stage T2, 84%; T3, 53%; and T4, 11%; P < 0.01). Of all patients enrolled, 53% had bladder preservation; however, of the currently surviving patients, 16 of 39 (41%) have their bladders intact (T2, 50%; T3, 37%; T4, 0%). Only 18% of the initially enrolled population is alive with a preserved bladder. The 5-year survival of patients who had cystectomy at some point during the study, compared with those who have had their bladders preserved, was 65% versus 40%, respectively (P < 0.01). CONCLUSIONS: Our long-term results with multimodality therapy with attempted bladder preservation showed no definitive improvement in survival compared with modern series of cystectomy alone, and a disappointingly low rate of disease-free bladder preservation. We found a high rate of locally recurrent disease in the preserved bladders. We also noted a decrease in survival in our patients with bladder preservation compared with those without preservation. Bladder preservation, although possible, should be limited to a very select group of patients.

Aged↗

Excess risk of bladder cancer in spinal cord injury: evidence for an association between indwelling catheter use and bladder cancer.

OBJECTIVES: To evaluate whether the risk of bladder cancer is greater in individuals with spinal cord injury (SCI) than in the general population and whether indwelling catheter (IDC) use is a significant independent risk factor for bladder cancer. DESIGN: Historical cohort study in which subjects with SCI were stratified according to bladder management method and followed for the development of bladder cancer. SETTING: A large rehabilitation hospital in the Spinal Cord Injury Model Systems. PARTICIPANTS: A total of 3670 patients with SCI who were evaluated for bladder cancer on at least 1 occasion by cystoscopy over a period of 1 to 47 years. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Bladder cancer occurring after SCI determined by diagnosis at our facility, by subject report, or by report of next of kin. RESULTS: Twenty-one cases of bladder cancer were found in the 3670 study participants. The risk of bladder cancer for subjects with SCI using IDC is 77 per 100,000 person-years, corresponding to an age- and gender-adjusted standardized morbidity ratio (SMR) of 25.4 (95% confidence interval [CI], 14.0--41.9) when compared with the general population. After controlling for age at injury, gender, level and completeness of SCI, history of bladder calculi, and smoking, those using solely IDC had a significantly greater risk of bladder cancer (relative risk [RR] = 4.9; 95% CI, 1.3--13.8) than those using nonindwelling methods. Mortality caused by bladder cancer in individuals with SCI was significantly greater than that of the US population (SMR = 70.6; 95% CI, 36.9--123.3). CONCLUSIONS: Bladder cancer risk and mortality are heightened in SCI compared with the general population. IDC is a significant independent risk factor for the increased risk of and mortality caused by bladder cancer in the SCI population.

Adolescent↗

M2 and M3 muscarinic receptor activation of urinary bladder contractile signal transduction. II. Denervated rat bladder.

Normal rat bladder contractions are mediated by the M(3) muscarinic receptor subtype. The M(2) receptor subtype mediates contractions of the denervated, hypertrophied bladder. This study determined signal transduction mechanisms mediating contraction of the denervated rat bladder. Denervated bladder muscle strips were exposed to inhibitors of enzymes thought to be involved in signal transduction in vitro followed by a cumulative carbachol concentration-response curve. Outcome measures were the maximal contraction, the potency of carbachol, and the affinity of darifenacin for inhibition of contraction. Inhibition of phosphoinositide-specific phospholipase C (PI-PLC) with 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphorylcholine (ET-18-OCH(3)) has no effect on denervated bladder contractions, whereas inhibition of phosphatidyl choline-specific phospholipase C (PC-PLC) with O-tricyclo[5.2.1.02,6]dec-9-yl dithiocarbonate potassium salt (D609) attenuates the carbachol maximum and potency. Inhibition of rho kinase with (R)-(+)-trans-4-(1-aminoethyl)-N-(4-pyridyl)cyclohexanecarboxamide dihydrochloride (Y-27632) reduces carbachol maximum, carbachol potency, and increases darifenacin affinity. Inhibition of rho kinase, protein kinase A (PKA), and protein kinase G (PKG) with 1-(5-isoquinolinesulfonyl)-homopiperazine.HCl (HA-1077) reduces the carbachol maximum and potency. Inhibition of PKC with chelerythrine increases darifenacin affinity, whereas inhibition of rho kinase, PKA, PKG, and protein kinase C (PKC) with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine.2HCl (H7) reduces the carbachol potency while increasing darifenacin affinity. Inhibition of rho kinase, PKA, and PKG with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide.2HCl (H89) increases darifenacin affinity. This study demonstrates that different signal transduction mechanisms mediate the contractile response in the denervated rat bladder than in normal rat bladder. In normal rat bladder, PI-PLC and PC-PLC mediate the contraction, but in denervated bladder only PC-PLC is involved. In the denervated bladder, the rho kinase pathway is more dominant than in normal bladders. PKA seems to mediate a contractile response in normal bladders, whereas it seems to inhibit contraction in denervated bladders.

Animals↗

Exogenous glycosaminoglycans coat damaged bladder surfaces in experimentally damaged mouse bladder.

BACKGROUND: Interstital cystitis is often treated with exogenous glycosaminoglycans such as heparin, chondroitin sulphate (Uracyst), hyaluronate (Cystistat) or the semi-synthetic pentosan polysulphate (Elmiron). The mechanism of action is presumed to be due to a coating of the bladder surface to replace the normally present chondroitin sulphate and heparan sulphate lost as a result of the disease. This study used fluorescent labelled chondroitin sulphate to track the distribution of glycosaminoglycans administered intravesically to mouse bladder that had been damaged on the surface. METHODS: The surfaces of mouse bladders were damaged by 3 mechanisms -- trypsin, 10 mM HCl, and protamine sulphate. Texas Red-labeled chondroitin sulphate was instilled into the bladders of animals with damaged bladders and controls instilled only with saline. Bladders were harvested, frozen, and sectioned for examination by fluorescence. RESULTS: The normal mouse bladder bound a very thin layer of the labelled chondroitin sulphate on the luminal surface. Trypsin- and HCl-damaged bladders bound the labelled chondroitin sulphate extensively on the surface with little penetration into the bladder muscle. Protamine produced less overt damage, and much less labelling was seen, presumably due to loss of the label as it complexed with the protamine intercalated into the bladder surface. CONCLUSION: Glycosaminoglycan administered intravesically does bind to damaged bladder. Given that the changes seen following bladder damage resemble those seen naturally in interstitial cystitis, the mechanisms proposed for the action of these agents is consistent with a coating of damaged bladder.

Animals↗

Mitochondrial DNA mutations in chemical carcinogen-induced rat bladder and human bladder cancer.

Mitochondrial (mt) DNA mutations have been described recently in different tumors, whereas similar studies focusing on bladder cancer are scarce. In an effort to understand the significance of mtDNA mutations in bladder cancer, we investigated the mtDNA alterations in both clinical human bladder cancer and in a carcinogen-induced rat bladder cancer model. Human bladder cancer tissues were obtained by radical cystectomy and transurethral resection of bladder tumors. Rat bladder tumors were induced in SD rats by treatment with N-butyl-N-(4-hydroxybutyl) nitrosamine in drinking water for 24-28 weeks. Genomic DNA was extracted from tumor specimens and microdissected normal bladder mucosae. Mitochondrial genes and D-loop region were amplified by PCR. The amplified PCR fragments were either cloned into plasmid vector or used for direct DNA sequencing. The results of DNA sequence revealed numerous point mutations in the non-coding D-loop region and different mtDNA genes in both human and rat bladder cancers. In addition, we also detected deletions of variable lengths in mononucleotide repeats in the D-loop region, ND2, ATPase 8 and COIII genes in human bladder cancer samples. Our results show that mtDNA exhibits a high rate of mutations in both human and rat bladder cancers. We also demonstrate that the repetitive sequences of mononucleotides within the mt genome are unstable and subjected to deletions. The high incidence of mtDNA mutations in bladder cancer suggests that mtDNA and mitochondria could play an important role in the process of carcinogenesis and also mtDNA could be valuable as a marker for early bladder cancer diagnosis.

Animals↗

Effects of urinary bladder distention on location of the urinary bladder and urethra of healthy dogs and cats.

Evaluation of the anatomic location of the distended and empty urinary bladders and urethras of healthy adult male and female dogs and cats by retrograde urethrocystography revealed substantial variations. In 15 dogs in lateral recumbency with empty bladder lumens, the caudal portion of the urinary bladder was within the pelvic canal in 5 of 7 male and 5 of 8 female dogs. In female dogs examined in ventrodorsal recumbency, only 4 of 8 had the empty urinary bladders in part within the pelvic canal. After luminal distention, 3 of 7 male and 3 of 8 female dogs, while in lateral recumbency, had the urinary bladders in part intrapelvically. However, when female dogs were placed in ventrodorsal recumbency, only 1 of 7 urinary bladders was in part within the pelvis. The urinary bladders of 14 cats were consistently within the abdominal cavity, irrespective of whether the bladder lumen was distended or empty. Urethral flexures occurred in dogs with intrapelvic bladders that were distended or empty. Urethral flexures were not found in cats. The urethras of dogs and cats in lateral recumbency were generally closer to the floor of the pelvis after urinary bladder distention than when the bladder was empty. The urethra of the dogs and cats in ventrodorsal recumbency was to the left or right of or on the midsagittal plane, whether the urinary bladder was empty or distended. A greater degree of lateral displacement was encountered in ventrodorsal recumbency after urinary bladder distention.

Animals↗

Correlation of upper and lower urinary tract function in patients with neurogenic bladder: evaluation using simultaneous measurement of cystometry and diuresis renography with full and empty bladder.

Diuresis renography and water filling cystometry were simultaneously performed with the bladder full and with the bladder empty. The findings of diuresis renography with a full bladder were compared with those of diuresis renography with an empty bladder, in 9 patients (4 male and 5 female, mean 24.4 years old) with neurogenic bladder dysfunction. According to O'Reilly's classification, the findings of diuresis renography with a full bladder were significantly worse than those of diuresis renography with an empty bladder, regardless of cystometry patterns and bladder compliance. These results suggest that in patients with neurogenic bladder dysfunction, a full bladder in itself can cause deterioration of the upper urinary tracts, regardless of bladder pressure and bladder compliance.

Adolescent↗

99mTechnetium-mercaptoacetyltriglycine scintigraphy with full bladder in patients with severe bladder dysfunction.

PURPOSE: We evaluated 99mtechnetium-mercaptoacetyltriglycine scintigraphy for detecting threshold bladder volume at which upper tract obstruction occurs in patients with bladder dysfunction. MATERIALS AND METHODS: A total of 24 patients 19 to 74 years old with severe bladder dysfunction who underwent 99mtechnetium-mercaptoacetyltriglycine scintigraphy and videocystometrogram in a 4-year period were selected for retrospective study. 99mTechnetium-mercaptoacetyltriglycine scintigraphy was done with a full bladder with a mean instilled volume of more than 850 ml saline. In patients in whom an obstructed renal outflow pattern was observed saline was drained at a rate of 100 ml every 5 minutes while dynamic imaging was performed. If results were abnormal, the study was repeated with an empty bladder. Differential function, parenchymal transit time index and outflow efficiency were calculated. RESULTS: Of the 24 patients 15 had an obstructed outflow pattern with a full bladder, which was relieved at a bladder volume of less than 390 ml (median 300, range 250 to 600). Only 2 of these 15 patients had a normal vesical end filling pressure of less than 20 cm H2O. There was no obstruction in 9 patients, of whom 5 had increased vesical end filling pressures. Followup in patients who had normal tracer outflow on a full bladder showed no decrease in renal function, while a small decrease was seen in patients who had obstructed outflow on a full bladder. CONCLUSION: This novel, full bladder 99mtechnetium-mercaptoacetyltriglycine scintigraphic technique provides the ability to detect bladder volumes at which obstructive outflow patterns develop in patients with severe bladder dysfunction.

Adult↗

Bladder shape impact on the accuracy of ultrasonic estimation of bladder volume.

OBJECTIVE: Variations in bladder shape can lead to errors in ultrasonic estimation of the bladder volume. The purposes of this study were to compare the accuracies of various formulas to estimate bladder volume from sonographic measurements and to assess the impact of bladder shape on the accuracy of bladder volume estimation. STUDY DESIGN: Twenty-four healthy volunteers (13 men, 11 women) and 55 spinal cord injury patients (48 men, 7 women) underwent ultrasonographic measurements of dimensions before and after voiding. Bladder shape was classified as cuboid, ellipsoid, or triangular prism. Ten formulas from the literature were applied to estimate bladder volume, using the volume voided or catheterized as the standard, and then linear regression was used to obtain optimal correction coefficients for the whole data set as well as each of the three bladder shapes. SETTING: Rehabilitation hospital affiliated with a medical college. RESULTS: The most accurate of the 10 formulas tested was height (H) X transverse depth (Dt) x weight (W) x 0.7 (mean error 17.4%+/-11.6%). Linear regression analysis yield optimal correction coefficients of .72 for the whole data set and .89, .81, and .66 for cuboidal, ellipsoid, and triangular prism-shaped bladders, respectively. The mean error for the estimation of bladder volume using .72 as the correction coefficient was 16.9%+/-11.9% and decreased to 12.7%+/-10.1% (p < .0001, paired t test) when the bladder shape was taken into account. CONCLUSION: Using bladder shape for reference and applying the corresponding correction coefficient to volume calculations will improve the accuracy of the estimation.

Adult↗

A large animal model of bladder exstrophy: observations of bladder smooth muscle and collagen content.

PURPOSE: The development of adequate bladder capacity is not ensured in all patients with bladder exstrophy despite successful bladder closure and reconstruction. To determine the factors leading to the development and maturation of the exstrophic bladder we created a large animal model of exstrophy. We compared biopsies obtained from a cohort of experimentally induced exstrophic neonatal sheep bladders to those of normal control bladders and related the findings to a previously reported comparison of human neonatal normal and exstrophic bladders. MATERIALS AND METHODS: Bladder specimens of 7 newborn lambs with experimentally induced exstrophy were compared to specimens of 10 newborn control lamb bladders. All specimens were stained with Masson's trichrome as well as with specific monoclonal antibodies to types I and III collagen. Stained sections were then analyzed using a morphometric image analysis system to quantify the amounts of smooth muscle and collagen present. RESULTS: A significant increase in the ratio of collagen-to-smooth muscle was noted in exstrophic versus normal control bladders (p <0.05). This difference was similar to that in the previous study of neonatal human bladders. There was no significant difference in the ratios of types I and III collagen in the 2 groups of sheep bladders. This finding is different from that reported in the previous human studies. CONCLUSIONS: Overall changes in the ratio of smooth muscle-to-collagen in the sheep exstrophy model are similar to those in humans. However, the differences in collagen types I and III do not seem to be present.

Animals↗

Functional bladder capacity after bladder biofeedback predicts long-term outcome in children with nocturnal enuresis.

OBJECTIVE: We previously reported a 70% cure rate for bladder biofeedback in children with primary nocturnal enuresis associated with small bladder capacity and detrusor instability. In this paper we report on bladder capacity and incidence of enuresis after 60 months of follow-up and discuss the role of decreased bladder capacity in nocturnal enuresis. MATERIAL AND METHODS: We prospectively evaluated 21 boys and 3 girls (mean age 10.4 years) treated with bladder biofeedback between October 1993 and July 1995. Baseline bladder capacity and capacity at the end of treatment and at 60 months follow-up were determined from a micturition chart. RESULTS: At the end of primary treatment 17/24 patients had stopped bedwetting. In 4/17 responders and 4/7 non-responders the bladder capacity was <90% of normal for age. At 60 months, 4 patients had been lost to follow-up, 15 were dry at night and 4 continued bedwetting. One patient underwent surgery and was excluded from the study. Only 2/15 dry patients but 3/4 patients with persistent nocturnal enuresis had a bladder capacity of <90% of normal. CONCLUSIONS: Bladder biofeedback can be successfully used to treat children with refractory nocturnal enuresis associated with small bladder capacity and unstable detrusor. Normalization of bladder capacity and continuous growth of the bladder in order to keep the capacity normal would seem to be crucial to the long-term resolution of bedwetting in this select patient population.

Biofeedback, Psychology↗

Giant bladder diverticula causing bladder outlet obstruction in children.

PURPOSE: Congenital giant diverticulum of the bladder is a consequence of deficiency in the detrusor musculature and has been reported in male infants as a rare cause of bladder outlet obstruction. MATERIALS AND METHODS: A 10-year retrospective review revealed 4 patients (3 boys and 1 girl) with bladder outlet obstruction due to a giant bladder diverticulum. Prenatal and postnatal clinical and imaging records were reviewed. RESULTS: Prenatal sonography was unremarkable in all patients. Three males (ages 4 months, 10 months and 3 years) had no medical history of voiding dysfunction, and 1 female (11 years) had the Ehlers-Danlos syndrome. While the girl presented with urinary tract infection, all patients presented with progressively decreasing urinary stream and urinary retention. Each patient underwent voiding cystourethrography (VCUG) and ultrasound. In each patient VCUG showed a giant (greater than 7 cm) bladder diverticulum that descended below the bladder neck and compressed the urethra during voiding. Vesicoureteral reflux was seen in 2 patients. Ultrasonography demonstrated moderate unilateral hydronephrosis in 2 patients. Bladder diverticulectomy was successfully performed in all patients, with ureteral reimplantation in 3. CONCLUSIONS: A giant congenital bladder diverticulum, when noted on VCUG to descend below the bladder neck, may lead to bladder outlet obstruction. To our knowledge we report the first case of a female presenting with bladder outlet obstruction due to a giant bladder diverticulum. Children with connective tissue disorders may be predisposed to this disorder, which must be excluded, regardless of gender, in all patients presenting with voiding abnormalities. Surgical diverticulectomy, often with ureteral reimplantation, is the preferred treatment, with excellent long-term results.

Child↗

The use of combined bladder and epispadias repair in boys with classic bladder exstrophy: outcomes, complications and consequences.

PURPOSE: Despite widespread use of modern staged reconstruction for classic bladder exstrophy, there remains a role for combined bladder closure and epispadias repair when primary closure is delayed or initial reconstruction has failed. The principle of combining bladder and urethral closure in 1 operation was first proposed more than 40 years ago, and represents a demanding technical procedure. We recount our experience to date with this approach. MATERIALS AND METHODS: A total of 38 boys underwent combined bladder and epispadias repair using pelvic osteotomies. Five cases were delayed primary closures owing to a bladder template unsuitable for newborn closure. A total of 30 cases were previous failed bladder closures, with concurrent epispadias repair in 6. The 3 remaining cases were staged closures where the epispadias repair failed, leading to bladder prolapse via the posterior urethra. Overall, there was a major bladder prolapse in 25 cases, and separation of the pubic symphysis with dehiscence of anterior abdominal wall structures and bladder in 8. RESULTS: Mean age at surgery was 26.5 months for the 33 reclosures. A total of 10 boys had development of a urethrocutaneous fistula and 4 had development of strictures. A total of 19 patients required additional procedures of the bladder neck (endoscopic), urethra or penis. A later bladder neck reconstruction was undertaken in 19 boys, of whom 12 are continent. Seven boys underwent continent diversion and 5 are considering the procedure. A total of 14 boys are awaiting adequate capacity for bladder neck reconstruction. Ureteral reimplantation was performed in 22 patients, and no patient was rendered hypospadiac. CONCLUSIONS: When combined closure is applied to failed previous exstrophy repair one can expect at best a 50% continence rate without continent diversion. Furthermore, based on the experience at this institution the majority of patients require ureteral reimplantation, and many require additional surgery to the penis or urethra. However, with the application of modern reconstructive techniques continence and a cosmetically pleasing phallus can be expected in most cases, although at the expense of multiple surgical procedures.

Bladder Exstrophy↗

The role of nitric oxide in bladder urothelial injury after bladder outlet obstruction.

OBJECTIVE: To investigate the role of nitric oxide (NO) in the pathogenesis of injury to the bladder mucosa after bladder outlet obstruction (BOO). MATERIALS AND METHODS: The response of bladder mucosa to BOO consists of thickening with fibrous connective tissue; NO is a multipurpose messenger important in blood vessel relaxation, neuronal communication and inflammatory activities of macrophages, and is synthesized by NO synthase (NOS), with three distinct isoforms; inducible (iNOS), endothelial (eNOS) and neuronal (nNOS). Fifteen male guinea pigs had a silk ligature placed around the bladder neck to induce BOO; controls included five sham-operated animals. The animals were killed at 2, 4, 6, 8 and 12 weeks after BOO. NADPH-diaphorase staining was used as a nonspecific method to determine NOS isoform distribution. Single- and double-label immunofluorescence histochemistry for iNOS, eNOS, nNOS and macrophage colony stimulating factor (M-CSF) were used, with laser scanning confocal microscopy to assess the results. The relative amount of iNOS mRNA was evaluated using reverse-transcription-polymerase chain reaction (RT-PCR), and a standard method to determine the degree of apoptosis. RESULTS: Bladder mucosa had a markedly increased intensity of NADPH-diaphorase staining 2 weeks after BOO. iNOS immunoreactivity was markedly greater in the bladder mucosa 2 weeks after BOO than in controls. The immunolocalization of iNOS and M-CSF was identical in bladder mucosa after BOO. RT-PCR showed stronger iNOS mRNA expression in the obstructed bladder mucosa 2 weeks after BOO than in controls. eNOS and nNOS expression was detected only 8 weeks after BOO, with markedly more immunoreactivity 12 weeks after initiating BOO. Increased eNOS and nNOS immunoreactivity strongly correlated with the induction of apoptosis in the bladder mucosa. CONCLUSION: There was overexpression of iNOS by activated macrophages in the early stages of BOO. This overexpression did not induce apoptosis in the iNOS-expressing cells of bladder mucosa in the early stages. After long-term BOO bladder mucosa showed strong eNOS and nNOS immunoreactivity, correlating with apoptosis. Thus we suggest that eNOS and nNOS, by triggering cell death, may be important in eliminating hyperplastic urothelial cells, reflecting the plasticity of the bladder response to obstructive stimuli.

Animals↗

A gap junction blocker inhibits isolated whole bladder activity in normal rats and rats with partial bladder outlet obstruction.

We examined the effect of 18alpha-glycyrrhetinic acid (18alpha-GA), a gap junction blocker, or propiverine hydrochloride on the activity of isolated whole bladders obtained from intact rats and rats with partial bladder outlet obstruction (BOO). Thirty-two female Sprague-Dawley rats were divided into an intact group and a BOO group. The whole bladder was harvested from each rat and isovolumetric cystometry was performed in Krebs solution. Changes of bladder activity were recorded after addition of 18alpha-GA or propiverine hydrochloride to the perfusate. Propiverine hydrochloride inhibited the amplitude and duration of contraction in both intact and BOO groups. Propiverine hydrochloride also reduced the baseline bladder pressure in the BOO group, but not in the intact group. In contrast, 18alpha-GA inhibited the amplitude and duration of bladder contraction, and also reduced the baseline pressure, in both intact and BOO groups. BOO bladders showed inhibition of the amplitude and duration of bladder contraction at lower concentrations of 18alpha-GA than intact bladders. A gap junction blocker suppressed the in vitro activity of BOO bladders more effectively than that of intact bladders. Therefore, inhibition of intercellular communication in the bladder via gap junctions may be useful for treating detrusor overactivity, as well as propiverine hydrochloride.

Animals↗

Pharmacological studies of the uninhibited neurogenic bladder. III. The influence of adrenergic excitatory and inhibitory drugs on the cystometrogram of neurological patients with normal and uninhibited neurogenic bladder.

In order to elucidate the sympathetic activity of the uninhibited neurogenic bladder, controlled cystometry before and during the influence of alpha- and beta-adrenergic agonists and antagonists was performed on patients with normal and uninhibited neurogenic bladder. Alpha-agonist increased the pathological findings in the cystometrogram of the uninhibited bladder with increase in intravesical pressure, decrease in capacity and increase in the amplitude of the uninhibited contraction, but had no effect whatsoever on the normal bladder. Alpha-antagonists improved the uninhibited bladder with decrease in intravesical pressure, increase in capacity and decrease in amplitude of the uninhibited contraction, and decrease in intravesical pressure in normal bladder. Beta 2-agonist improved the uninhibited bladder too, but was proved to be inactive on the normal bladder. Unselective beta- and selective beta 1-antagonists deteriorated the uninhibited bladder and had only minor effect on the normal bladder. The decreased capacity and forcible uninhibited detrusor contraction seem to be due to a reduction of inhibitory beta-adrenergic impulses as well as an increased contractile alpha-adrenergic action on the bladder wall in uninhibited neurogenic bladder.

Adrenergic Fibers↗

What is the need for additional bladder surgery after bladder augmentation in childhood?

PURPOSE: Bladder augmentation has revolutionized the care of children with a neuropathic bladder but it remains a major surgical procedure. However, the need for subsequent bladder surgery has not been well defined in a large series with long-term followup. MATERIALS AND METHODS: We retrospectively reviewed the records of the first 500 bladder augmentations performed from 1978 to 2003 at our institution. Charts were reviewed for complications requiring additional surgery, including malignancy, bladder perforation, repeat augmentation, bowel obstruction and bladder calculi. Mean and median followup was 13.3 years. RESULTS: Complications occurred in 169 patients (34%) resulting in a total of 254 surgeries. The cumulative risk of further surgery at the bladder level was 0.04 operations per patient per year of augmentation. Three patients (0.6%) had transitional cell carcinoma, of whom all presented with metastatic disease and died. Bladder perforation occurred in 43 patients (8.6%) with a total of 53 events. Of the patients 16 (3.2%) required laparotomy for bowel obstruction and 47 (9.4%) required repeat augmentation. Bladder stones were treated in 75 patients (15%), who required a total of 125 surgeries. CONCLUSIONS: Bladder augmentation provides immeasurable improvements in quality of life but it requires lifelong dedication from the patient, family and health care providers. While the requirements for additional surgery are not trivial, 66% of our patients have not required any further surgery in the augmented bladder.

Child↗