Partial Cystectomy
- Author: E Jason Abel, MD; Chief Editor: Bradley Fields Schwartz, DO, FACS more...
Background
Definition
Partial or segmental cystectomy is a bladder-preserving treatment that involves full-thickness surgical removal of the bladder tumor and surrounding bladder wall.[1]
Key points
- Only 5.8-18.9% of patients with muscle-invasive bladder cancer are suitable candidates for partial cystectomy.
- Partial cystectomy is indicated in the patient with a normally functioning bladder with good capacity and a solitary tumor located where a 1-cm to 2-cm resection margin is possible.
- For high-risk tumor in a bladder diverticulum, a multimodal approach with preoperative chemotherapy and possible radiotherapy may be needed.
- Absolute contraindications include carcinoma in situ (CIS) elsewhere in the bladder and multifocal tumors.
- After surgery, ongoing surveillance, including imaging, cystoscopy, and cytology, is important because the local recurrence rate is high (37-78%).
- Patients who have undergone partial cystectomy for bladder cancer should have cystoscopy and urinary cytologic examination every 3 months for at least 2 years. Regular CT scans of the pelvis and abdomen are recommended in the first several years of follow-up.
Partial cystectomy is used to treat both malignant and benign conditions of the bladder. Its primary malignant indication is for solitary, primary, muscle-invasive, or high-grade bladder cancer that does not involve specific regions of the bladder such as the bladder trigone, vesical neck, or posterior urethra and that can be resected with adequate surgical margins (1-2 cm). The classically described indication for partial cystectomy is for the removal of an adenocarcinoma or urachal carcinoma that develops in the dome of the bladder.
A better understanding of the natural history of urothelial carcinoma (transitional cell carcinoma) of the bladder has led to more stringent selection criteria for partial cystectomy; consequently, this procedure is being performed less frequently for malignant conditions (see Table 1). For example, the ideal clinical scenario would be if the bladder tumor was in an easily accessible location in the bladder, small in size (< 2cm) and no tumor(s) existed in the rest of the bladder. Partial cystectomy should only be considered if the cancer has not left its site of origin.
Despite advances in transurethral surgery for bladder tumors, some instances exist when the tumor can not be completely resected and partial cystectomy is not only indicated but the most definitive procedure. For example, the morbidly obese patient with a superficial bladder tumor located in the upper aspect of the posterior bladder wall or dome might require a partial cystectomy because the surgeon was unable to reach the tumor transurethrally. Other indications for partial cystectomy include a need for adequate biopsy of radiation-induced ulcerations, the presence of a tumor in a bladder diverticulum, patient choice, palliation of severe local symptoms, preservation of native bladder function and continence, and poor surgical risk for more aggressive procedures such as radical cystectomy.
A few benign conditions of the bladder can be managed with partial cystectomy. These include resection of bladder diverticula, colovesical fistula repair, vesicovaginal fistula repair and less commonly for cavernous hemangiomas, ulcerative interstitial cystitis, and localized endometriosis of the bladder.
Partial cystectomy has certain advantages over radical cystectomy, such as preserving a functionally continent native urinary reservoir and sparing of potency in males. In addition, because a separate urinary diversion procedure (as is necessary in radical cystectomy) is not performed, some surgeons view partial cystectomy as a less morbid operation, suited for high-risk patients and palliative situations. The main disadvantage of partial cystectomy lies in the high historical local recurrence rates of bladder cancer, with only part of a globally diseased urothelium addressed. Although partial cystectomy plays a limited role in the treatment of bladder cancer, in properly selected patients, similar oncologic results can be achieved as seen in patients treated with radical cystectomy. This review focuses on the current applications and indications for partial cystectomy, with an emphasis on the treatment of bladder cancer.
History of the Procedure
Historically, this operation has been performed since the 19th century, when it was thought that many patients with bladder cancer would be ideal candidates. Little was known about how bladder cancer may affect the entire bladder despite the appearance of a solitary tumor. The widespread use of this operation in the mid 1950s led to high local recurrence rates from 37% to 78%.[2, 3] The advent and technical improvements of transurethral resection (TUR) has made it possible to initially resect most bladder tumors.
Table 1. Proportion of Patients With Bladder Cancer Treated With Partial Cystectomy (Open Table in a new window)
| Source | Total Patients With Bladder Cancer | Patients Treated With Partial Cystectomy (%) |
| Utz et al (1973) | 3454 | 199 (5.8) |
| Brannan et al (1978) | 551 | 49 (7.1) |
| Faysal and Freiha (1979) | 859 | 117 (13.6) |
| Merrell et al (1979) | 585 | 54 (9.2) |
| Ojeda and Johnson (1983) | 397 | 23 (5.8) |
| Jardin and Vallencien (1984) | 475 | 90 (18.9) |
| Hayter et al (2000) | 20,822 | 729 (3.5) |
| Holzbeierlein et al (2004) | 935 | 58 (6.2) |
Epidemiology
Frequency
Based on the National Cancer Institutes SEER Cancer Statistics Review, 70,530 new cases of bladder cancer were estimated to be diagnosed in 2010, and 14,680 persons expected to die from the disease. Currently, the overall male-to-female patient ratio is approximately 4:1. The ratio of bladder cancer in Caucasian Americans compared with African Americans is 1.5-2.1:1. The median age of patients is 73 years at time of diagnosis, with incidence and mortality per pathologic grade increasing as a function of age. Since 1950, the incidence of bladder cancer has increased by 50%, but the overall mortality rate (primarily in men) has decreased by 33%. More than 500,000 people in the United States are survivors of bladder cancer.
Etiology
The etiology of bladder cancer, a frequent indication for bladder resection, is unknown. Postulated theories include environmental carcinogens (eg, chemicals, ultraviolet light, radiation), aberration of normal cell growth regulation (eg, oncogene induction, suppressor gene negation), and abnormalities in the genetic composition of malignant cells.
Chemical exposures that may increase the risk of bladder cancer include aromatic amines, dietary nitrites, and nitrates. These include aniline dyes (eg, 2-naphthylamine, 4-aminobiphenyl, 4-nitrobiphenyl, 4-4-diaminobiphenyl [benzidine], 2-amino-1-naphthol), combustion gases, coal soot, chlorinated aliphatic hydrocarbons, and acrolein dyes. Smoking is associated with an up to 4-fold increase in the risk of bladder cancer. Other implicated factors include coffee and tea, phenacetin (an analgesic), chronic cystitis, the presence of chronic indwelling catheters, bladder calculi, pelvic irradiation, and exposure to cyclophosphamide. Schistosomiasis of the urinary bladder is associated with a higher incidence of squamous cell carcinoma. Currently, no evidence links bladder cancer to heredity.
Recent investigations have addressed the arsenic content of drinking water. International studies in Taiwan, Chile, and Argentina have suggested that as little as 10.1 mcg/L of arsenic in drinking water increases the risk.[4, 5] In Taiwan, population studies of 8102 residents found that concentrations of 10-50, 50-100, and more than 100 mcg/L of arsenic in drinking water (compared with levels < 10 mcg/L) increase the relative risk of developing transitional cell carcinoma to 1.9, 8.2, and 15.3, respectively.[4] In Chile, studies of arsenic levels from 100-570 mcg/L revealed an elevated standardized mortality ratio of bladder cancer of 6 in men and 8.2 in women.[5] In the United States, estimates indicate that 350,000 persons are exposed to arsenic levels of more than 50 mcg/L and that 2.5 million are exposed to levels higher than 25 mcg/L. In one study, the relative risk estimate for an average level of arsenic in US drinking water was 1 in 1000 persons.[6]
Oncogenes and tumor suppressor genes implicated in bladder cancer include TP53, retinoblastoma gene (Rb), p15, and p16. Alterations in TP53, a normal tumor suppressor gene that is found on chromosome 17p and that controls apoptosis, lead to more aggressive bladder cancers. Ongoing studies are exploring the clinical implications of these tumor suppressor genes. Currently, conventional staging and grading are sufficient.
The tumor suppressor gene Rb is found on chromosome 13q. A mutated Rb gene or phosphorylated Rb gene leads to dissociation of its product protein, pRB, from the normally complexed transcription factor, E2F. Dissociated E2F drives the transition from G1 to S phase in cellular mitosis.
Two more protein regulators encoded on chromosome 9p, p15 and p16, inhibit nuclear cyclin-dependent kinases from phosphorylating pRB. When p15 and p16 mutate, they can no longer prevent phosphorylation of pRB, resulting in dissociation of the pRB-E2F complex, and free E2F is allowed to stimulate the cell's G1- to S-phase proliferation. Very aggressive high-grade bladder tumors have been associated with alterations in TP53. Mutations in Rb, p15, and p16 have been associated with low-grade superficial tumors.
Bladder cancer often behaves as a field disease; the entire urothelium, from the renal pelvis to the urethra, is susceptible to malignant transformation. Transitional carcinoma cells may also have the ability to migrate and implant at different sites along the urothelium.
Presentation
A thorough history should be obtained, and a thorough physical examination should be performed. In patients with bladder cancer, the most common presenting symptom is painless hematuria (85%). Hematuria is often intermittent; therefore, a single urinalysis finding may not be significant. Bladder irritability that manifests as urinary frequency, urgency, and dysuria is the second most common symptom. These symptoms rarely occur without hematuria (microscopic or gross). Flank pain due to ureteral obstruction, lower-extremity edema, and pelvic masses are other presenting symptoms. Symptoms of advanced disease, such as weight loss and abdominal or bone pain, are rare because patients usually seek medical attention before these develop.
Indications
Indications for malignancy
Urothelial carcinoma (also called transitional cell carcinoma) accounts for the vast majority of bladder cancer in the United States. However, in some countries, squamous cell carcinoma is the dominant subtype of bladder cancer because of chronic infection with Schistosomiasis hematobium.
Partial cystectomy for urothelial carcinoma is recommended in properly selected cases. Suggested selection criteria include the following:
- No history of multifocal bladder cancer (negative random bladder biopsies)
- No evidence of metastatic disease
- Absence of multiple lesions (including carcinoma in situ)
- A solitary, high grade muscle-invasive tumor located in a position that is amenable to wide resection (ideally achieving 1-2 cm margins)
- Tumor located away from the ureteral orifices (although resection and re-implantation is possible) and not involving bladder neck or prostate
- Expectation that the residual postoperative bladder will have adequate capacity and compliance to ensure functionality
As a result of such strict criteria, relatively few patients with muscle invasive bladder cancer are candidates for bladder-sparing surgery.[7] The most common lesions amenable to partial cystectomy are high-grade tumors located in the lateral walls or dome of the bladder.
Cancer in bladder diverticula
Diverticular cancers comprise 1.5-10% of all bladder cancers and are more likely to penetrate the bladder wall because of the relatively thin nature of the wall and its lack of thick muscular layers. Transurethral resection of the tumor may be an option; however, inadvertent perforation is possible because of the paucity of muscle fibers in the diverticulum, which may lead to dissemination of urothelial cancer cells. Urothelial carcinoma in a bladder diverticulum is a common reason for performing partial cystectomy. Historical series suggested a high rate of recurrence and poor prognosis for diverticular tumors, but more contemporary data suggest that complete tumor resection with partial cystectomy results in 5-year disease-specific survival rates of around 70%.[8]
Partial cystectomy for cancers other than urothelial carcinoma
Squamous cell carcinoma has a poor prognosis and is not responsive to chemotherapy and radiation. Although some series describe feasibility of partial cystectomy, this approach has not been studied extensively because of the low prevalence in the western world (3-7% in the United States).[9] In contrast, 75% of all bladder cancers in Egypt are of squamous cell derivation because of S hematobium infection. In some reports, bilharzial bladder cancer (bladder cancer associated with Schistosomiasis) has a similar prognosis to transitional cell cancer when compared stage-for-stage, but whether this is true for nonbilharzial squamous cell carcinoma is unclear.
Primary adenocarcinoma of the bladder may be treated with partial cystectomy in select cases. Urachal lesions, which represent 20-40% of all primary bladder adenocarcinomas, are thought to arise from residual transitional cells that line the urachal remnant in the dome of the bladder. Historically, the overall, 5-year survival rate associated with urachal adenocarcinoma has been poor (6-15%).
However, recent evidence has shown that extended partial cystectomy with removal of the bladder segment, posterior rectus fascia, peritoneum, and umbilicus offers the best chance for survival. In a study by Dandekar et al, the 5-year survival rate after partial cystectomy for urachal adenocarcinoma was 56.3%.[10] Herr found that contained urachal adenocarcinomas that were completely resected using extended partial cystectomy had a favorable disease-free rate (77%).[11] Following partial cystectomy, cure rates of well-differentiated urachal adenocarcinomas have been reported to approach 100%.
Rectal, colon, prostate, uterus, cervix, or ovarian cancers that are locally advanced can be treated with partial cystectomy in selected cases, although pelvic exenteration may be required. A local recurrence rate of 17% and a 3-year survival rate of 39-74% has been reported with negative surgical margins.[12, 13]
Rhabdomyosarcomas of the bladder comprise 17-50% of all genitourinary rhabdomyosarcomas. These patients have also been successfully treated with partial cystectomy as an alternative to complete, radical cystectomy or chemotherapy. Disease-free survival rates have been reported as high as 78.5% with a 2-16 year follow-up after partial cystectomy with or without neoadjuvant chemotherapy and radiation. Most of these patients were able to retain functional bladders with minimal lower urinary tract symptoms.[14]
Benign conditions
Nonmalignant conditions of the bladder can also be managed with partial cystectomy. These conditions include bladder diverticula, cystic hydatid disease, cavernous hemangiomas, paraganglioma, leiomyomas, refractory interstitial cystitis, colovesical fistula, vesicovaginal fistula and endometriosis of the bladder.[15, 16]
Relevant Anatomy
The adult bladder is located in the anterior pelvis and is enveloped by extraperitoneal fat and connective tissue. It is separated from the pubic symphysis by an anterior prevesical space known as the retropubic space (of Retzius). The dome of the bladder is covered by peritoneum, and the bladder neck is fixed to neighboring structures by reflections of the pelvic fascia and by true ligaments of the pelvis.
The body of the bladder receives support from the external urethral sphincter muscle and the perineal membrane inferiorly and the obturator internus muscles laterally (see the image below).
Gross anatomy of the bladder. For more information about the relevant anatomy, see Bladder Anatomy. See also Female Urethra Anatomy, Female Urinary Organ Anatomy, Male Urethra Anatomy, and Male Urinary Organ Anatomy.
Contraindications
In patients with bladder cancer being considered for partial cystectomy, the entire urothelial tract from the kidneys to the urethra must be evaluated thoroughly. Prior to surgery, no other malignant disease should be anywhere in the urinary tract. The presence of multifocal disease or CIS is considered an absolute contraindication to partial cystectomy.
Other contraindications to partial cystectomy include the following:
- Cellular atypia in random biopsy specimens
- Prostatic invasion
- Trigonal invasion
- Presence of lymphovascular invasion in biopsy specimen
- Inability to achieve adequate surgical margins
- Prior radiation therapy
- Inadequate bladder volume following resection
- Evidence of metastatic disease
- Poor presurgery performance status conveying high surgical risk
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| Source | Total Patients With Bladder Cancer | Patients Treated With Partial Cystectomy (%) |
| Utz et al (1973) | 3454 | 199 (5.8) |
| Brannan et al (1978) | 551 | 49 (7.1) |
| Faysal and Freiha (1979) | 859 | 117 (13.6) |
| Merrell et al (1979) | 585 | 54 (9.2) |
| Ojeda and Johnson (1983) | 397 | 23 (5.8) |
| Jardin and Vallencien (1984) | 475 | 90 (18.9) |
| Hayter et al (2000) | 20,822 | 729 (3.5) |
| Holzbeierlein et al (2004) | 935 | 58 (6.2) |
| Study | Number of Patients | Induction Therapy | % Complete Response | Consolidation Therapy | % Overall Survival (years) | % Overall Survival with Bladder Intact (years) |
| Housset et al | 120 | Bifractionated XRT + concurrent cisplatin + 5-fluorouracil | 77 | Bifractionated XRT + concurrent 5-fluorouracil + cisplatin | 63 (5) | ... |
| Sauer et al | 184 | 45-54 Gy XRT + concurrent cisplatin or carboplatin | 80 | None | 56 (5) | 41 (5) |
| Fellin et al | 56 | 2 cycles MCVa, 40 Gy XRT + concurrent cisplatin | 50 | 24 Gy XRT + concurrent cisplatin | 55 (5) | 41 (5) |
| Tester et al | 49 | 40 Gy XRT + concurrent cisplatin | 66 | 24 Gy XRT + concurrent cisplatin | 60 (4) | 42 (4) |
| Tester et al | 91 | 2 cycles MCV, 39.6 Gy XRT + concurrent cisplatin | 75 | 25.2 Gy XRT + concurrent cisplatin | 62 (4) | 44 (4) |
| Shipley et al | 61 | 2 cycles MCVa, 39.6 Gy XRT + concurrent cisplatin | 61 | 25.2 Gy XRT + concurrent cisplatin | 48 (5) | 36 (5) |
| Shipley et al | 62 | 39.6 Gy XRT + concurrent cisplatin | 55 | 25.2 Gy XRT + concurrent cisplatin | 49 (5) | 40 (5) |
| Kachnic et al | 106 | 2 cycles MCV, 40 Gy XRT + concurrent cisplatin | 66 | 24.8 Gy XRT + concurrent cisplatin | 52 (5) | 43 (5) |
| Zietman et al | 18 | Bifractionated XRT + concurrent cisplatin + 5-fluorouracil | 78 | Bifractionated XRT + concurrent cisplatin + 5-fluorouracil + 3 cycles MCV | 83 (3) | 78 (3) |
| Studies | Recurrence rates |
| Resnick and O'Connor (1973) | 76% |
| Evans and Texter (1975) | 40% |
| Novick and Stewart (1976) | 50% |
| Peress et al (1977) | 54% |
| Cummings et al (1978) | 49% |
| Schoborg et al (1979) | 70% |
| Faysal and Freiha (1979) | 78% |
| Jardin and Vallencien (1984) | 78% |
| Lindahl et al (1984) | 58% |
| Kaneti (1986) | 38% |
| Dandekar et al (1995) | 43% |
| Holzbeierlein et al (2004) | 19% |
| Kassouf et al (2006) | 49% |
| Source | Five-year Survival (%) | Ten-year Survival (%) | ||||
| Grade I | Grade II | Grade III/IV | Grade I | Grade II | Grade III/IV | |
| Magri (1962) | 88 | 33 | 34 | - | - | - |
| Utz et al (1973) | 100 | 48 | 39 | - | - | - |
| Novick and Stewart (1976) | 100 | 75 | 40 | 0 | 67 | 8 |
| Brannan et al (1978) | 50 | 62 | 55 | 50 | 33 | 30 |
| Cummings et al (1978) | 100 | 96 | 32 | - | - | - |
| Schoborg et al (1979) | 75 | 62 | 26 | 50 | 28 | 4 |
| Faysal and Freiha (1979) | 100 | 53 | 30 | 25 | 20 | 8 |
| Merrell et al (1979) | 78 | 56 | 22 | 83 | 32 | 0 |
| Kaneti (1986) | 75 | 46 | 46 | - | - | - |
| Dandekar et al (1995) | 100 | 94.4 | 53.5 | - | - | - |
| Source | Five-year Survival (%) | Ten-year Survival (%) | |||||||||||
| T0 | T1 | T2 | T3 | T4 | Overall | T0 | T1 | T2 | T3 | T4 | Overall | ||
| Magri (1962) | - | 80 | 38 | 26 | 0 | 42 | - | - | - | - | - | - | |
| Long et al (1962) | 80 | 67 | 43 | 9 | 0 | - | - | - | - | - | - | - | |
| Cox et al (1969) | - | - | 20 | 16 | - | - | - | - | - | - | - | - | |
| Resnick and O'Connor (1978) | 75 | 71 | 77 | 12.5 | 20 | 35 | - | - | - | - | - | - | |
| Utz et al (1973) | - | 68 | 47 | 29 | 0 | 39 | - | - | - | - | - | - | |
| Evans and Texter (1975) | - | 69 | 43 | 14 | 0 | 0 | - | - | - | - | - | 21 | |
| Novick and Stewart (1976) | - | 67 | 53 | 20 | - | 46 | - | 67 | 44 | - | - | 36 | |
| Brannan et al (1978) | 100 | 69 | 54 | 33 | 0 | 57 | - | 31 | 36 | 11 | - | 32 | |
| Cummings et al (1978) | - | 79 | 80 | 6 | - | 60 | - | - | - | - | - | - | |
| Schoborg et al (1979) | 69 | 69 | 29 | 12 | 100 | 43 | - | 37 | 0 | 0 | 0 | 12 | |
| Faysal and Freiha (1979) | 75 | 58 | 29 | 7 | 0 | 40 | 21 | 15 | 13 | 7 | 0 | 9 | |
| Merrell et al (1979) | 100 | 100 | 67 | 25 | - | 48 | - | 100 | 33 | 0 | 0 | 32 | |
| Lindahl et al (1984) | - | 59 | 38 | - | - | 42 | - | 48 | 25 | - | 0 | 38 | |
| Kaneti (1986) | - | 68 | 40 | 33 | 0 | 48 | - | - | - | - | - | - | |
| Smaldone et al (2008) | - | - | - | - | - | 70 | |||||||
| a Stage T3a/T3b | |||||||||||||

