Radical Retropubic Prostatectomy for Prostate Cancer
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With the evolving techniques and improving knowledge of surgical anatomy, physicians can perform radical retropubic prostatectomy (RRP) with great efficacy and minimal morbidity. The procedure has evolved over the last several decades to remain an important approach for the treatment of prostate cancer.
In 1947, Millin introduced the retropubic approach to prostatectomy. The operation had 2 distinct advantages over radical perineal prostatectomy (RPP):
Walsh deserves much credit for pioneering the technique of nerve-sparing RRP. [1] Before anatomic characterization in the early 1980s and the description and anatomic characterization of the Santorini plexus, the operation was fraught with massive blood loss and morbidity.
Modifications in the technique of RRP and the introduction of the anatomic nerve-sparing method [2] have dramatically decreased the frequency of the most worrisome associated morbidities—incontinence and impotence. As a consequence of these developments, most patients with prostate cancer have a high quality of life after undergoing radical prostatectomy.
RRP has been the standard for the surgical approach. However, the explosion of minimally invasive surgery has led to the search for less invasive treatment options and laparoscopic and robotic appear to provide equally efficacious surgical options in selected patients. [2]
Pure laparoscopic radical prostatectomy has a steep learning curve and currently accounts for fewer than 1% of all prostatectomies in the United States. Laparoscopy was introduced to urology in the early 1990s, with the first series of laparoscopic retropubic prostatectomy reported by Schuessler et al in 1991. [3] Most studies indicate longer operating times for laparoscopic retropubic prostatectomy than for RRP and a longer learning curve, but the former consistently seems to yield significantly decreased estimated blood loss and transfusion rates. Laparoscopic retropubic prostatectomy is well tolerated and provides short-term oncologic and functional results that are comparable with those of RRP in the hands of experienced surgeons.
Robotic technology began to be utilized more broadly after 2005 and the usage of a robot for RP increased from 4.5% in 2003 to 85.2% in 2009. [4] It offers many advantages over conventional laparoscopic retropubic prostatectomy, including 3-dimensional visualization, magnification, increased degrees of freedom, absence of the fulcrum effect, and robotic-wrist instrumentation. Robotic-assisted laparoscopic prostatectomy (RALP) can potentially reduce the learning curve that even experienced surgeons face while performing laparoscopic retropubic prostatectomy. However, there are still situations where open RRP may provide benefit including in patients with previous abdominal or pelvic surgery, and more extensive cancers where tactile information is an advantage.
Functional recovery (potency and continence) after open RRP is high for experienced surgeons. However, the robotic approach provides equivalent outcomes in experienced hands. [5, 6] Oncologic outcomes appear similar in the shorter term for the majority of low and intermediate grade cancers when compared to open RRP. [7]
Minimally invasive approaches provide excellent visualization of the anatomy, cause less pain, permit earlier discharge, and have equivalent oncologic efficacy. Nevertheless, a sound and fundamental knowledge of traditional open radical prostatectomy, with and without nerve sparing, remains a crucial component of the urologist’s armamentarium. When choosing an approach, a major feature is the urologist’s experience and comfort with the robotic or open approach.
Adenocarcinoma of the prostate is the most commonly diagnosed cancer and the second leading cause of death in American males. A surge in the incidence of prostate cancer was noted in the 1980’s due to the wider use of the serum prostate-specific antigen (PSA) test, which has also changed trends in clinical and pathologic aspects of prostate cancer. [8]
Since the advent of serum PSA testing, physicians have detected more prostate cancers at an earlier stage. From 1998 – 2011, there was a twofold increased incidence of low risk prostate cancer from 14 – 28% and more than twofold decrease in the incidence of metastatic prostate cancer form 25% – 11%. During the same time period, the percentage of T1c disease increased from 36 – 71%, PSA levels between 4 and 6 ng/ml increased from 24% to 38%; T2 tumors decreased from 39% to 20% and PSA between 8 and 10 ng/ml decreased from 24% to 15%. [9]
In 2008, the United States Preventive Services Task Force (USPSTF) recommended against PSA-based screening in men aged ≥ 75 years. This recommendation was expanded to include all men in 2012. In 2013, the American Urological Association also issued a guideline statement for not screening men over the age of 70 years. These recommendations had widespread ramifications on age stratified outcomes. The exclusion of PSA screening saw a further increase in aggressive disease and higher mortality rates in men over the age of 70. [10] Since 2012, consequent to USPSTF recommendations, there was a decrease in PSA screening and a decrease in the incidence of early stage prostate cancer in men of all ages. However, there was a stage and grade migration, with more men presenting with advanced disease at presentation. [11] Subsequently the USPSTSF revised its recommendation to screen men between ages 55 to 69 years in 2017 based on physician’s discussion about potential benefits and harms of prostate-specific antigen (PSA)–based screening for prostate cancer. [12]
The incidence of small, lower risk well-differentiated prostate cancer increased in the early PSA era and almost half of the patients with this diagnosis are candidates for active surveillance (AS) in an attempt to avoid overtreatment and morbidity associated with surgery or radiation. [13] The selection of men for AS has been traditionally guided by clinicopathological features that indicate the patient presents with an organ confined, well-differentiated tumor. Using strict selection criteria, patients with a life expectancy > 10 years, T1c, PSA ≤ 10, Gleason ≤ 6, ≤ 2 positive biopsy cores, ≤ 50% cancer in any core, and PSAD < 0.15 would be eligible for AS. Recent studies have shown that including intermediate risk disease for AS (4 or fewer cores with GS 6 cancer and/or only 1 core of Gleason 3+4 cancer <15%) did not adversely affect outcomes. [14] Discussion of risks and benefits of AS with patients and shared decision making is the key to successful surveillance.
15-year mortality of prostate cancer specific mortality rate based on a contemporary multiinstitutional data for pathological Gleason score 6 or less, 3+4, 4+3 and 8-10 was 0.2% to 1.2%, 4.2% to 6.5%, 6.6% to 11% and 26% to 37%. [15] The 15-year prostate cancer specific mortality risk was 0.8% to 1.5%, 2.9% to 10%, 15% to 27% and 22% to 30% for organ confined cancer, extraprostatic extension, seminal vesicle invasion and lymph node metastasis, respectively.
Incidence
In the United States, prostate cancer, which is predominantly a disease of elderly men, is the second-most common malignancy in males. Worldwide, the incidence of prostate cancer varies, but in general, it is higher in Western developed countries. For example, African American men (in whom the incidence of prostate cancer is highest) are 200 times as likely to develop prostate cancer as are Chinese men living in Asia (in whom the incidence of prostate cancer is among the lowest in the world). As worldwide life expectancy increases, the absolute number of prostate cancer cases is expected to grow.
Mortality
The American Cancer Society has estimated that in 2017, approximately 161,360 new cases of prostate cancer would be diagnosed, and approximately 26,730 prostate cancer deaths would occur generating a 1:6 ratio. [15]
Environmental risk factors
Migration studies have revealed increased prostate cancer rates among migrants who move from areas with low prevalence to areas of high prevalence. In one study, the incidence of prostate cancer in emigrants from Japan increased 4-9 times over the disease’s incidence in Japan. [16]
Such studies suggest that environmental factors (eg, diet) play an important role in prostate cancer. Researchers have found a positive correlation between higher consumption of fat, especially animal fat, and a higher prostate-cancer death rate increasing relative risk by a factor of 1.6-1.9.
Experts suggest certain dietary habits to lower the risk of prostate cancer. These include consumption of a low-fat, high-fiber diet, which lowers serum androgen levels. Researchers have investigated other dietary components, including selenium, lycopene, vitamin D, alpha-tocopherol, vitamin E, and large amounts of green tea, and have postulated that consumption of these substances may prevent prostate cancer. However, a recently concluded metaanalysis of 12 international prospective cohort studies concluded that there were no statistically significant associations for advanced prostate cancer or prostate cancer mortality with any food group (including total fruits and vegetables, total fruits, total vegetables, fruit and vegetable juice, cruciferous vegetables, and tomato products), nor specific fruit and vegetables. Pooled multivariable relative risks comparing the highest versus lowest quantiles across all fruit and vegetable exposures and prostate cancer outcomes ranged from 0.89 to 1.09. [17] However, this does not discount the impact that diet may have in subsets of susceptible patients and research on the association of genetics, ethnicity and diet will likely generate impactful findings in the future.
Familial and genetic risk factors
Family history and genetics can play a role in the etiology of prostate cancer. Having a single first-degree relative with prostate cancer increases the risk of prostate cancer by a factor of 2.1-2.8. Having both a first-degree and a second-degree relative with prostate cancer increases the risk by a factor of 6. [18]
Researchers have mapped prostate cancer susceptibility loci including HPC1 (1q24-25), involved in 33% of hereditary prostate cancer cases. [19] Indeed, testing is now available using a number of these susceptibility loci that can help predict an individual’s risk for prostate cancer development. [20] However, the interplay of environment and these loci are complex making use of this test for one individual less reliable.
An estimated 10% of prostate cancer is due to mutations in BRCA1, BRCA2, HOXB13 and Lynch syndrome. [21] BRCA1 and 2 are associated with risk of breast, ovarian, pancreatic, prostate cancers and melanoma. Families with BRCA2 mutations appear to harbor aggressive variants of prostate cancer. Mutations of HOXB13 are associated with 2-8 fold increased risk of hereditary prostate cancer (HPC) among first degree relatives and early onset caner before 55 years of age. Patients with Lynch syndrome have a threefold elevated risk of prostate cancer, apart from colorectal, ovarian, upper tract urothelial and gastric cancers. [22]
At present, genetic testing can be performed for BRCA1 and BRCA2 mutations according to NCCN guidelines which include a personal history of Gleason ≥ 7 prostate cancer at any age with a first degree relative with early onset breast cancer (
Currently, nerve-sparing RRP remains a reasonable treatment option for men with clinically localized prostate cancer who have at least a 10-year life expectancy and low comorbidities. It is a well-tolerated procedure that is associated with low morbidity.
Although RRP is not limited to men younger than a certain age, patients older than 70 years should be carefully selected for prostatectomy. All cases must be judged on an individual basis, and it is difficult to justify a major operation in an elderly patient with prostate cancer who has alternatives to major surgery and in whom a 10-year overall survival is improbable.
Life expectancy calculators give an accurate prediction of mortality rates. Age, Charlson Comorbidity Index (CCI) and the type of treatment were used for predicting 10-year life expectancy after treatment for localized prostate cancer. [23] The model was 84% accurate in 10-year mortality prediction. The Memorial Sloan Kettering Cancer Center (MSKCC) model for predicting 10-year survival probability before treatment of localized prostate cancer is an online tool that is widely used by clinicians. https://www.mskcc.org/nomograms/prostate/pre-op/coefficients
In a large SEER based retrospective study done in 23,338 men with localized prostate cancer, the 10-year cancer specific mortality was only 2.8%, compared to 21% mortality due to other causes. [24] Coronary artery disease, stroke and other cancers were the leading cause of death in this age group.
Optimal management of higher-stage disease remains controversial, but RP is considered a viable treatment option in T3 disease for select patients. Patients with high risk of Extracapsular extension (ECE) and neurovascular bundle invasion are increasingly staged with multiparametric MRI before definitive therapy. A multiparametric MRI consists of a combination of T2 weighted imaging, diffusion weighted imaging and Dynamic Contrast Enhanced imaging and /or MR spectroscopy for functional details. A 3T MR imaging scanner is preferred and if using a 1.5 T MR imaging scanner, combining endorectal coil with an external phased array coil is preferred. [25] Cancer with invasion of the bladder, sphincter or rectum are better served by radiation therapy if clinically localized.
RP is being increasingly employed in patients with clinical T3 disease. The rates of RP vs radiation was 49.8% vs. 37.1% in one retrospective study from 2012. [26] Many studies comparing surgery versus radiation therapy for locally advanced disease have shown a trend towards better oncological outcomes with surgery. [27, 28] However, healthier earlier stage patients are often selected for surgery which may confound these results. An ongoing prospective randomized controlled trial NCT02102477 is expected to clarify the superiority of one modality over the other.
As noted, all patients selected for nerve-sparing RRP should have few to no comorbidities, at least a 10-year life expectancy, and clinically localized disease. Patients with locally advanced disease, detected by MRI or physical exam, may undergo non nerve-sparing RRP; because of the extent of the local tumor burden (especially posteriorly), the nerve-sparing procedure can compromise the adequacy of the operation. In this setting, the radical prostatectomy specimen should include both layers of Denonvilliers fascia, with wide excision of the lateral pelvic fascia and the neurovascular bundle on that side en bloc with the prostate and ejaculatory organs. In patients with obvious extension outside the prostate into the bladder or other structures radiation may be a preferred approach.
Physicians must have a clear understanding of the anatomy pertinent to radical prostatectomy, including not only the gland itself but also the periprostatic anatomy. Such an understanding, coupled with achievement of vascular control and preservation of the neurovascular bundles, allows a safe and anatomic approach to the operation, with reduced morbidity.
The fascial investment of the bladder and the prostate, the endopelvic fascia (ie, pelvic fascia), sweeps down and off the pelvic sidewall, where it covers the levator ani.
The puboprostatic ligaments represent the anterior condensation of the fusion of the parietal and visceral pelvic fascia.
Incising the fascia at this point of fusion exposes the lateral surface of the prostate and the anterolateral rectal wall. At this point, the lateral periprostatic or lateral prostatic fascia becomes evident. This layer continues posteriorly to cover the neurovascular bundles and to become the lateral rectal fascia, and it continues distally over the membranous urethra to become the lateral periurethral fascia.
The lateral periprostatic fascia is continuous with the endopelvic fascia and is fused to the anterior and posterior Denonvilliers fascia. The rectal fascia (ie, posterior Denonvilliers fascia) covers the anterior surface of the rectum. The neurovascular bundles are invested in this posterior layer of Denonvilliers fascia laterally and are posterior and lateral to the prostate.
Anterior and posterior leaflets of the anterior Denonvilliers fascia envelop the seminal vesicles. Entering the posterior aspect of the anterior Denonvilliers fascia is essential for dissection of the seminal vesicles in RRP for localized prostate cancer.
The prostatic plexus of veins (i.e., Santorini plexus) carries the venous return from the deep dorsal vein of the penis and the cavernosal veins. These venous effluents ultimately drain into the internal iliac veins.
The venous drainage may vary greatly and may be asymmetrical. In general, the system trifurcates shortly after exiting under the pubic bone. Accordingly, great care must be taken in the dissection, especially at the prostatic apex, where blood loss can be significant. The superficial branch lies within the retropubic fat, between the puboprostatic ligaments.
Visualization of the prostate and its fascia is critical and complete removal of investing fat is critical for the operation. Using gentle bilateral digital or blunt dissection using scissors through the lateral aspects of periprostatic fascia develops a plane just above the urethra and leads to isolation of Santorini plexus which is then easily ligated and divided. [29]
The periphery of the glandular elements of the prostatic peripheral zone contains a fibromuscular rim referred to as the prostatic capsule. The base and the apex of the prostate have no well-defined capsule; the capsule is deficient as it merges with the smooth muscle of the bladder neck superiorly and with the striated muscle of the urethral sphincter inferiorly.
The striated urethral sphincter is directly beneath the dorsal venous complex and courses anterolaterally, creating a horseshoe-shaped appearance. Because the striated sphincter lies beneath the dorsal venous complex clear visualization is important to avoid injury.
The cavernous nerves originate from the pelvic plexus on either side of the rectum. They travel posterolaterally to the prostate beneath the cover of the lateral periprostatic fascia. At the level of the membranous urethra, these nerves course anteriorly and lie directly lateral to the urethra.
Numerous papers have demonstrated the excellent long-term cancer control and survival data after this operation, however numerous factor impact these outcomes. A significant portion of the outcome is driven by the Gleason Score of the cancer. For organ confined prostate cancer, high grade tumor volume (as predicted by the percentage of cancer in biopsy), Gleason sum, PSA levels, margin positive status and bilateral disease were all significant predictors of outcome after RP. [30]
Clinical stages T1a and T1b
Clinical stages T1a and T1b refer to prostate cancer incidentally detected during transurethral resection of the prostate (TURP). Stage T1a refers to fewer than 5% and T1b refers to greater than 5% cancer in resected chips during TURP. In a series from the Mayo Clinic, T1a and T1b tumors constituted 1.5% and 5.6% of all clinically organ-confined tumors, respectively. [31] Eighty-eight percent of T1a tumors were pathologically organ-confined at the time of radical prostatectomy, as opposed to 68% of T1b tumors.
Several series revealed that the likelihood of finding significant tumor on examination of the radical prostatectomy specimen for T1a disease ranges from 12% to 20%. A substantial portion of these patients harbor cancer in the peripheral zone that can be detected by subsequent peripheral zone biopsy or MRI.
Radical prostatectomy is a viable treatment option for young, healthy patients with a life expectancy of more than 10-15 years and T1a disease. Observation may be a viable option, along with careful follow-up, serial serum PSA testing, digital rectal examination (DRE), peripheral zone biopsy, imaging with MRI and peripheral zone biopsy, when indicated. Significant residual disease (i.e., clinical stage T1b or high-grade T1a disease) may warrant early treatment with radical prostatectomy.
Clinical stages T1c and T2
Overall, 76%, 71%, and 54% of patients with clinical stage T1c, T2a, and T2b/c lesions had organ-confined disease (less than p-T2c) at the time of prostatectomy, respectively. [32] The pathologic stage, Gleason score, and DNA ploidy pattern were comparable in clinical T1c and T2a disease. Progression-free survival (systemic or local and PSA level progression [>0.2 ng/mL]) was also comparable in these 2 groups but was significantly worse in the c-T2b/c group (see the images below).
Certain clinical and pathologic factors of c-T1c tumors closely resemble those of c-T2b/c tumors, especially with regard to preoperative PSA level and margin positivity. The short-term 7-year cause-specific survival rates of 99.9%, 98.6%, and 97.6% in clinical T1c, T2a, and T2b/c prostate cancers, respectively, in the PSA era are a testament to the effectiveness of radical prostatectomy in this group of patients.
Clinical stage T3
The role of radical prostatectomy in patients with locally advanced disease is controversial. Much of the debate is based on earlier series, which reported poor 10-year survivals in patients undergoing RPP. [33, 34] Because of the high incidence of lymph node metastasis and the potential for incomplete excision, many surgeons use combination of surgery with radiotherapy with or without androgen deprivation therapy. Recent retrospective studies have suggested that a multimodality approach is associated with a better cancer specific and overall survival. [35]
Radical prostatectomy in locally advanced prostate cancer is based on the following principles:
In reviewing radical prostatectomy for T3 disease, a prominent feature was inaccurate clinical staging.
Neoadjuvant androgen deprivation does not alter the long-term recurrence rate in men with clinical stage T3 prostate cancer.
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David F Jarrard, MD Professor of Urology and Molecular and Environmental Toxicology, University of Wisconsin School of Medicine and Public Health
David F Jarrard, MD is a member of the following medical societies: American Urological Association
Disclosure: Nothing to disclose.
Shivashankar Damodaran, MB, MCh Fellow in Urologic Oncology, Department of Urology, University of Wisconsin School of Medicine and Public Health
Shivashankar Damodaran, MB, MCh is a member of the following medical societies: American Urological Association
Disclosure: Nothing to disclose.
Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, Sexual Medicine Society of North America, Tennessee Medical Association
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Endo, Avadel.
Reza Ghavamian, MD Professor of Clinical Urology, Albert Einstein College of Medicine; Director of Urologic Oncology, Director of Minimally Invasive and Robotic Urologic Surgery, Montefiore Medical Center
Reza Ghavamian, MD is a member of the following medical societies: American Urological Association, Society of Urologic Oncology
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Dan Theodorescu, MD, PhD Paul A Bunn Professor of Cancer Research, Professor of Surgery and Pharmacology, Director, University of Colorado Comprehensive Cancer Center
Dan Theodorescu, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Urological Association, Medical Society of Virginia, Society for Basic Urologic Research, and Society of Urologic Oncology
Disclosure: Key Genomics Ownership interest Co-Founder-50% Stock Ownership; KromaTiD, Inc Stock Options Board membership
Acknowledgments
Medscape Reference thanks Dennis G Lusaya, MD, Associate Professor II, Department of Surgery (Urology), University of Santo Tomas; Head of Urology Unit, Benavides Cancer Institute, University of Santo Tomas Hospital; Chief of Urologic Oncology, St Luke’s Medical Center Global City, Bonifacio Global City, Philippines, for the video contribution to this article.
Medscape Reference also thanks Edgar V Lerma, MD, FACP, FASN, FAHA, Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC, for his assistance with the video contribution to this article.
Radical Retropubic Prostatectomy for Prostate Cancer
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