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Plate 11.1
Benign prostatic hyperplasia: Histology
Benign prostatic hyperplasia (BPH) is a benign condition of advancing years
and is a common cause of lower urinary tract symptoms (LUTS) in males.
BPH is, however, a completely histologic classification and must be
distinguished from benign prostatic enlargement (BPE), which describes an
enlarged prostate, and clinical LUTS. LUTS is a broad and nonspecific term
to describe the urinary symptoms affecting the bladder and prostate. LUTS
can be separated into storage symptoms such as urgency, frequency,
nocturia, and urge urinary incontinence or voiding symptoms such as
reduced flow and feeling of incomplete emptying and postvoid dribbling.
LUTS are optimally measured by validated questionnaires, such as the
International Prostate Symptom Score or the American Urological
Association symptom score. The pathophysiology leading to chronic male
LUTS is more complex than just BPH/BPE. Despite its high prevalence and
socioeconomic effects, the pathophysiology of BPH is only incompletely
understood.

The histologic prevalence of BPH at autopsy is as high as 60% for males in

their 60s and increases up to 90% for males over 70 years of age. Histologic
studies have demonstrated that the development of BPH is characterized by
both glandular and stromal proliferation. Specifically, periurethral zones
demonstrate stromal nodules, whereas glandular nodular proliferation is
seen within the transition zone. Additionally, fibromuscular stroma

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proliferation is also seen in the central zone and, rarely, in the anterior zone
of the prostate. Hyperplasia is highly unusual in the posterior zone.

Early lesions consist of fibromyomas that represent proliferation of smooth

muscle and connective tissue surrounding the ducts of the urethral and
submucosal glands, which is like that of uterine myomas except that
prostate nodules usually contain epithelial elements arising from invasion of
epithelial buds from adjacent prostatic ducts. The epithelial elements are
composed of hyperplastic columnar cells that form numerous inclosing
papillae and are morphologically like those of the normal prostate, except
with reduced secretory activity rather than the usual periurethral site. The
fibromuscular stroma lacks the elastic tissue present in the normal prostate.
As the nodules grow, they compress the normal acini of the peripheral zone
into a thin rim of tissue between the growing hyperplastic nodule and the
prostatic capsule. On microscopic examination, the ducts and acini of the
peripheral zone are flattened and compressed.

One configuration of BPH that is unique is the development of the median

lobe or bladder neck hyperplasia, which is a growth of fibromuscular tissue
near the bladder outlet. The tissue may be more fibrotic than muscular and
may contain hyperplastic epithelial elements originating from the suburethral
glands of Albarrán beneath the bladder outlet. The diagnosis is confirmed by
direct visualization through the cystoscope.

Plate 11.1

Benign Prostatic Hyperplasia: Histology

Plate 11.2
Benign prostatic hyperplasia: Sites of hyperplasia
and etiology

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The prostatic nodules in BPH usually enlarge in a symmetric manner,

although in some instances one side may predominate. As nodules grow,
they have been termed median, lateral, and anterior lobe hyperplasia,
according to their location cystoscopically. The most frequent types of
prostatic enlargement are bilobular (the two lateral lobes) and trilobular (the
two lateral lobes plus the median lobe) hyperplasia. Rarely, nodules can
originate in the roof of the urethra within the anterior zone and project
downward into the bladder, giving the appearance of a rounded “anterior”
lobe.

With lateral lobe hyperplasia, the nodule growth is confined within the
prostate without projection into the bladder neck. The lateral lobes may grow
to great size, with only a minimal degree of urinary obstruction. When they
extend into the bladder neck, this projection may interfere with the opening
of the bladder neck and result in urinary obstruction. Median lobe
enlargement begins in the posterior urethra and, following the line of least
resistance, projects as a mass up through the bladder neck and into the
bladder. Other nodular enlargement occurs in the vicinity of the Albarrán
glands just beneath the bladder neck and tends to produce intravesical
hypertrophy.

The etiology of BPH is influenced by a wide variety of risk factors in addition

to direct hormonal effects of testosterone on prostate tissue. Although they
do not cause BPH directly, testicular androgens are required in the
development of BPH with dihydrotestosterone (DHT) interacting directly
with prostatic epithelium and stroma. Testosterone produced in the testes is
converted to DHT by 5-alpha-reductase type 2 in prostate stromal cells and
accounts for 90% of total prostatic androgens. DHT has direct effects on
stromal cells in the prostate, paracrine effects in adjacent prostatic cells, and
endocrine effects in the bloodstream, which influence both cellular
proliferation and apoptosis (cell death). However, with aging there is an

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abnormal accumulation of DHT resulting in the loss of homeostasis between

cellular proliferation and cell death, resulting in an imbalance favoring cellular
proliferation and therefore leading to BPH. This process is termed the DHT
hypothesis and results in increased numbers of epithelial and stromal cells in
the periurethral area of the prostate and can be seen histopathologically.

As mentioned previously, aging and testicular androgen are the two

established risk factors for the development of BPH. Other risk factors in the
development of BPH include metabolic syndrome, obesity, hypertension,
and genetic factors. In the Baltimore Longitudinal Study of Aging cohort,
each 1 kg/m 2 increase in body mass index (BMI) corresponds to a 0.4-mL
increase in prostate volume. Participants with obesity (BMI >35 kg/m 2 ) had
a 3.5-fold increased risk of prostate enlargement compared with nonobese
(BMI <25 kg/m 2 ) participants. The presence of metabolic syndrome is
associated with a higher annual BPE, growth rate, increased sympathetic
activity, and LUTS. Genetic predisposition to BPH has been demonstrated in
cohort studies; first-degree relatives in one study demonstrated a fourfold
increase in the risk of BPH compared with controls. These findings have
demonstrated consistency in twin studies looking at the disease severity of
BPH, with higher rates of LUTS seen in monozygotic twins. Additionally,
there are ethnic trends in occurrence, because the condition is more
common in White and Black males than it is in Asian males. However, the
exact pathophysiologic mechanisms involved in the association of metabolic
and genetic factors with BPH/BPE/LUTS are not completely understood, and
further studies are needed.

Plate 11.2

Benign Prostatic Hyperplasia: Sites of Hyperplasia and Etiology

Plate 11.3

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Benign prostatic hyperplasia: Complications and

medical treatment
The most important clinical feature of BPH is the functional effect of bladder
outlet obstruction. Early symptoms of BPH are urinary hesitation, a decrease
in the caliber of the stream, and day and nighttime urinary frequency,
reflecting disturbances in bladder function. As the bladder wall thickens, the
voiding capacity is reduced, resulting in worsening urinary frequency. With
chronic obstruction, compensatory hypertrophy of the bladder wall occurs,
leading to a thickened bladder wall with trabeculations and cellules, and
ultimately, diverticula. With prolonged obstruction, the bladder will dilate and
eventually decompensate and become atonic and flaccid. During this
process of decompensation, residual urine accumulates after urination and
hydrostatic pressure is transmitted through incompetent or obstructed
ureteral orifices to the kidneys, resulting in hydroureter and hydronephrosis,
thus leading to renal failure. In the end-stage condition, the dilated and
acontractile bladder holds large quantities of residual urine, which can lead
to life-threatening urosepsis that may occur from poor bladder emptying in
the setting of infected urine.

Management of males with LUTS is driven by symptom status, objective

parameters such as postvoid residual volume and uroflowmetry, risk of
disease progression, and the presence of BPH-related complications, such
as recurrent urinary retention, bladder stones, or hydronephrosis/decline in
renal function. In those with LUTS, treatment options range from watchful
waiting to medical and surgical intervention. If watchful waiting is not an
option because of symptom severity or compromised urination, oral medical
therapy with 5-alpha reductase inhibitors that block the production of DHT
from testosterone, or α-blockers that relax smooth musculature of the
bladder neck, prostate, and urethra are very effective in most cases. 5-Alpha
reductase inhibitors affect the secretory prostate and slowly shrink the gland
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by one-third of its original volume over 6 months. Accordingly, serum

prostate-specific antigen (PSA) will also fall by 50% from baseline levels
over the same time frame. As such, this treatment is best suited for larger
prostates. Alpha-blockers work more rapidly to improve urination but have
side effects that include dizziness and retrograde ejaculation. With this
therapy, the prostate will continue to grow and may require more medical or
surgical therapy over time. If medical therapy fails, surgical intervention can
be considered, as outlined in Plates 11.8 through 11.11 .

Plate 11.3

Benign Prostatic Hyperplasia: Complications and Medical Treatment

Plate 11.4
Carcinoma of prostate: Epidemiology, prostate-
specific antigen, staging, and grading
Prostate cancer is the second most common cancer after skin cancer in
American males. One in seven males in the United States will be diagnosed
with prostate cancer over their lifetime. An important risk factor is age,
because more than 70% of males diagnosed with prostate cancer are older
than 65 years. Family history plays a large role in risk of developing prostate
cancer. Dietary factors also can mitigate or increase the risk of prostate
cancer.

Although the role of PSA screening has come into debate, PSA is still
undoubtedly the best blood test available for screening of any type of
cancer. PSA is a member of the kallikrein family and is secreted in high
concentrations into the seminal plasma. It is responsible for liquefaction of
the seminal coagulum. It also “leaks” into the serum in low concentrations
and circulates in both “bound” and “unbound,” or free, forms. BPH,
prostatitis, and cancer can all allow PSA to gain access to the bloodstream at
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higher levels. Prostatic manipulation through biopsy, massage, and

transurethral resection can also elevate PSA levels. Therefore elevated PSA
levels are not specific for cancer. PSA levels are reduced by resection or
hormonal manipulation, including 5-alpha reductase inhibitors.

The common method used with PSA is to set a threshold value, which has
commonly been 4.0 ng/mL. However, a lower threshold will detect more
cancers but cause more unnecessary biopsies. PSA density (PSA
level/prostate volume [mL]) and PSA velocity, or the rate of change of PSA
with time (>0.75 ng/mL/year), can both be used to improve the performance
of PSA. A low free PSA ratio is also associated with a higher risk of prostate
cancer.

New blood tests such as the prostate health index and the 4Kscore test use
a combination of factors to determine risk of prostate cancer detection.
Urine tests such as ExoDX can also help inform on presence of significant
prostate cancer.

A major advance is multiparametric magnetic resonance imaging (MRI),

which accurately measures the size of the prostate to improve the PSA
density calculation. More important, the Prostate Imaging Reporting & Data
System stratifies the risk of abnormal-appearing areas according to
standard criteria and grades lesions on a scale of 1 to 5. Those areas that are
deemed to be a Prostate Imaging Reporting & Data System 3 to 5 lesions
usually are recommended to be biopsied.

In general, prostate cancer does not initially cause symptoms. As the cancer
grows, it infiltrates the prostatic stroma and capsule. The cancer can then
become locally invasive into the neurovascular bundles, periprostatic fat,
seminal vesicles, and, if aggressive, the rectal wall. Bulky disease involving
the bladder wall can cause urethral and ureteral obstruction, but these are

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usually late in the disease process.

Most cancers originate in the posterior zone and are clinically staged as
being organ confined (TNM [tumor, node, metastasis] system stages T1 and
T2), palpable beyond the prostate (T3), or fixed to adjacent structures (T4),
such as the bladder, rectum, or levator muscles. In stage T1c cases, the
tumor is nonpalpable and identified on prostate needle biopsy because of
PSA elevation. The figure illustrates an advanced case (TNM stage T4) of
extension into the bladder and peritoneum.

Histologically, prostate cancer is most commonly adenocarcinoma in which

small acini grow in a disorganized pattern amid fibrous stroma. Ductal
subtypes are less common but portend a higher recurrence rate after local
treatment. Mucinous and small cell adenocarcinomas are uncommon, and
sarcomas (see Plate 11.7 ) and transitional cell carcinoma are very rare.
Prostate cancer is most commonly graded according to the Gleason system,
developed in 1974 and based on the glandular patterns identified on low-
power magnification. Both the primary (predominant) and secondary
(second most prevalent) architectural patterns are rated on a scale of 1 (
most differentiated ) to 5 ( most anaplastic ). Because both patterns are
prognostic, a Gleason “sum” or addition of the two scores is also reported.
Genomic testing of biopsy tissues can also help independently stratify risk
and help refine treatment decisions.

Plate 11.4

Carcinoma of Prostate: Epidemiology, Prostate-Specific Antigen, Staging, and Grading

Plate 11.5
Carcinoma of prostate: Metastases
In 10% of patients at presentation, prostatic carcinoma reveals contiguous

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spread to other organs. However, PSA screening has greatly decreased the
percentage of males who are diagnosed with metastatic disease. When
metastasis occurs, prostate cancer has a propensity to metastasize to either
lymph nodes or to bone.

The value of a nuclear bone scan to detect bony metastases is limited to

patients with a Gleason sum score equal to or greater than 7 or a PSA level
greater than 20 ng/mL. A bone scan is also indicated in patients with prostate
cancer who have symptoms suggesting bony metastases, but bone scan
activity may not be observed until 5 years after micrometastases have
developed. The pattern of bony metastases in prostate cancer also occurs in
a characteristic manner, with involvement of both the axial and appendicular
skeletons, typically the pelvis, sacrum, and spine, observed most commonly.
This metastatic distribution may be a consequence of pelvic venous
drainage through the Batson plexus, a network of valveless veins that
connect the deep pelvic veins draining the inferior bladder, prostate, and
rectum to the internal vertebral venous plexuses. Because of their location
and valveless nature, they are thought to provide a route for the spread of
cancer metastases from prostate and colorectal cancers. From this landing
zone, cancer may then spread to the vertebral column or brain. The plexus is
named after anatomist Oscar Vivian Batson, who first described it in 1940.
The sites of bone involvement are illustrated in the frequency with which
they occur.

Bony metastases from prostate cancer, when viewed on plain radiographs,

appear osteoblastic. The metastasis has a “snowy” appearance because of
an increased deposition of calcium. A more destructive osteoclastic process
(osteolytic metastasis) occurs in 2% of cases. Tumor expansion in bone may
cause pain, compression, pathologic fractures, and anemia due to bone
marrow replacement. The pathologic fracture rate from prostate cancer is
relatively low compared with that of other metastatic cancers precisely

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because it induces bone-forming osteoblastic reactions. Elevation of the

serum acid phosphatase level is found in two-thirds of patients with
metastases and is usually increased when osteoblastic metastases are
present.

Prostate cancer involvement of visceral and soft tissue nodal sites is less
common than bony metastases. In patients with hormone-refractory
prostate cancer, bony involvement can be found in 85% of patients, soft
tissue or nodal involvement in 25%, and visceral metastases (mainly to lung
and liver) in 18%. Although not as characteristic as bony metastases, the
approximate sites of visceral and soft tissue nodal involvement are also
illustrated in the frequency with which they occur.

Computed tomographic imaging may also reveal bony involvement or

enlarged lymph nodes. MRI is superior for local staging and for guiding
biopsy. New prostate-specific membrane antigen–targeted positron
emission tomography scans are showing promise for detecting low-volume
metastasis and revealing many more soft tissue metastases than in the past.
Optimal management of these metastasis is evolving.

Treatment for advanced stage includes a combination of androgen

deprivation therapy with or without chemotherapy agents. Newer agents
such as abiraterone or enzalutamide have been successful in improving
length of survival after diagnosis of metastatic disease. Impending fractures
or bony pain can be aided by the addition of targeted radiotherapy.

Plate 11.5

Carcinoma of Prostate: Metastases

Plate 11.6
Carcinoma of prostate: Diagnosis and treatment
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The only way to definitively diagnose prostate cancer is through tissue

biopsy. Historically, transrectal ultrasound (TRUS)-guided prostate biopsy
has been the standard for the diagnosis of prostate cancer. Classic zonal
anatomy is not evident on TRUS, but the peripheral zone, the source of most
cancers, is distinguishable from the transition zone. Hypoechoic foci on
grayscale TRUS are suggestive of cancer, but more recently MRI-ultrasound
(US) fusion biopsy technology has improved the accuracy of prostate
biopsy. This technology relies on a prior MRI that is then superimposed by
computer technology over the live US image during biopsy. Therefore even
very small MRI lesions can be accurately targeted.

Currently, a systematic 12-core biopsy is most commonly taken with three or

four additional biopsies taken from each suspicious MRI lesion.
Complications from biopsies are uncommon, but sepsis is a significant
concern given the increase in antibiotic-resistant organisms. Transperineal
biopsies are becoming more common to address this concern. These can
also be done under MRI-US fusion guidance but require some experience to
properly anesthetize the perineum.

Treatment counseling is based on grade, stage, and patient factors such as

projected longevity. Treatment options include active surveillance, surgery,
radiation, focal therapies, and hormonal and chemotherapies. For organ-
confined cancers, definitive or curative local therapy consists of surgical
extirpation (see Plates 11.15–11.17 ) or radiation.

For males with low-risk prostate cancer, active surveillance is the treatment
of choice. This involves monitoring with serial PSA, biopsies, and imaging.
Disease characteristic changes indicative of higher risk mandate definite
treatment.

Radiation therapy can be administered by either external beam or

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brachytherapy. Intensity modulation radiation therapy is based on inverse

treatment planning reducing radiation to surrounding tissues. Proton therapy
is currently used; however, no compelling advantages have been shown over
intensity modulation radiation therapy. Brachytherapy involves permanent
implants of radioactive seeds and is typically performed transperineally
under TRUS guidance as an outpatient procedure. Unique complications of
radiation therapy for prostate cancer include LUTS, erectile dysfunction,
radiation cystitis and proctitis, and later development of secondary
malignancy.

Focal therapy may be considered in older males with lower risk disease to
treat small tumors while minimizing morbidity by treating just the affected
portion of the prostate. This treatment can be performed though thermal
ablation such as cryosurgery or high-intensity focused US. These cases can
also be done in the outpatient setting, but close follow-up is mandated
because there is a higher risk of recurrence due to potential multifocality and
lack of definitive imaging.

Metastatic prostate cancer is initially treated with androgen deprivation

therapy. Prostate cancer requires androgen, and the lack of androgen
causes marked regression of tumor. Although surgical castration is effective,
medical castration with gonadotropin-releasing hormone agonists or
antagonists in combination with antiandrogens is commonly used.
Combinations with chemotherapy such as docetaxel, abiraterone, or
enzalutamide while the disease is castrate sensitive or castrate resistant can
be effective in prolonging life for several years.

Plate 11.6

Carcinoma of Prostate: Diagnosis, Treatment

Plate 11.7

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Sarcoma of prostate
Sarcoma of the prostate is a rare cancer (<0.1% of prostate malignancies),
with most cases occurring in the first decade of life. Patients present with
symptoms of urinary obstruction or hematuria, and there can be associated
bowel symptoms of constipation, obstipation, or bloody stools. Sources of
mesodermal tissue giving rise to sarcoma are connective tissue, striated and
smooth muscle, and lymphatic or vascular structures. Although many cases
remain unclassified, for practical purposes prostatic sarcomas may be
grouped into the following categories.

Myosarcomas arise from either smooth or striated muscle elements and

comprise 50% to 60% of cases. Leiomyosarcomas are composed of
interlacing bundles of malignant smooth muscle cells. Rhabdomyosarcomas
generally present in childhood (mean age, 5 years) and show cross and
longitudinal striations within the cytoplasm of striated muscle cells. They
may exhibit extreme pleomorphism in which spindle cells, round cells, and
bizarre multinucleated giant cells intermix. These tumors typically grow to a
large size, projecting into the bladder as a large nodular mass.

Malignant fibrous histiocytoma (MFH) occurs in 10% to 15% of cases and is

highly anaplastic, with marked pleomorphism. MFH is more precisely a
morphologic pattern rather than a distinct pathologic entity. It is a synonym
for undifferentiated, pleomorphic sarcomas showing no specific line of
differentiation. Tumors in this group include storiform, angiomatoid, myxoid,
inflammatory, and giant cell sarcomas. A subset of pleomorphic MFH tumors
includes sarcomas that are termed unclassified because they resemble one
or more of the above histologic types.

Lymphosarcomas constitute 5% of prostatic sarcoma cases and originate

from the sparse lymphatics within the prostate. They contain mature and

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immature lymphocytes that obscure the architecture and show a tendency

to form lymphoid follicles. Lymphomatous involvement of the prostate may
also occur as a metastatic manifestation of leukemia, Hodgkin disease, or
lymphosarcoma originating elsewhere in the body.

Carcinosarcoma of the prostate is rare and generally occurs in males

previously treated with androgen deprivation or radiation therapy for
adenocarcinoma of the prostate. It is a tumor that contains mixed elements
of adenocarcinoma and sarcoma and is very aggressive, with a 5-year
survival of <50%. Fibrosarcomas, originating from fibrous tissue and
collagen, are most commonly found in soft tissue of the extremities and
bone but can be found in the prostate. These include both spindle cell and
round cell sarcomas, in which myxomatous degeneration may be present.

Sarcomas of the prostate can invade the bladder wall, seminal vesicles, and
rectum, with obstruction to the bladder outlet and terminal ureters.
Symptoms in the adult are like those associated with benign prostatic
obstruction but progress within weeks or months to stranguria (straining to
urinate). In the infant, symptoms may mimic those of congenital urethral
valves or obstructive ureterocele. If urinary tract infection is superimposed
on obstruction, the symptoms may be accompanied by dysuria, frequency,
and hematuria. Regional spread to surrounding tissues is a constant feature,
with metastases to neighboring lymph nodes, abdominal viscera, and bone
occurring fairly early. Pain is not a characteristic early symptom but may be a
salient feature after the tumor has grown in size. Unlike prostatic carcinoma,
sarcomas do not cause an elevation of the serum acid phosphatase.

Sarcoma may be suspected on rectal examination, because the prostate is

usually replaced by a rubbery mass that can be felt on rectal examination.
The diagnosis is established by either TRUS-guided prostate biopsy (see
Plate 11.6 ) or transurethral resection. The histologic type of prostate

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sarcoma has prognostic significance, because pediatric patients with

rhabdomyosarcoma do better than those with other histologies, with a
median survival of more than 10 years. Tumor grade and tumor size are less
relevant to outcome. The presence of metastatic disease at diagnosis is a
uniformly poor prognostic marker.

The treatment of sarcoma of the prostate involves mainly surgical resection.

In the rare instance of early detection in which the disease is still confined to
the adult prostate, a radical prostatectomy is indicated. In the infant, it is
necessary to remove the prostate, seminal vesicles, and bladder with
diversion of the urinary stream. Multimodality therapy involving
chemotherapy and radiation therapy shows improved outcomes over surgery
alone with most sarcomas.

Plate 11.8
Benign prostate surgery: Suprapubic
Surgical treatment is indicated if observation and medical management of
BPH are not appropriate or have failed, such as in patients with acute urinary
retention, recurrent or persistent urinary tract infections, recurrent gross
hematuria, or bladder calculi. Prior to intervention, the presence of prostate
cancer should be ruled out. Classically, BPH surgery was performed through
either an open (incisional) or endoscopic approach. Over the past 2
decades, a robotic-assisted laparoscopic approach has largely replaced
open approaches in high- and upper-middle-income countries. Robotic BPH
surgery is described elsewhere in this text, and the open and endoscopic
techniques are detailed below (see Plate 11.3 ).

Among open procedures, suprapubic and retropubic prostatectomies are the

most common. If the prostate gland is more than 80 g in weight or if suitable

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landmarks to guide endoscopic surgery are not visible, open prostatectomy

should be considered. Compared with endoscopic approaches, open
prostatectomy offers a lower retreatment rate and a more complete removal
of the adenoma and avoids the risk of dilutional hyponatremia with
transurethral resection techniques. Conversely, open prostatectomy requires
a midline incision with greater potential for intra- and postoperative
hemorrhage as well as a longer hospitalization and convalescence period.
Mortality rate is <1%.

Suprapubic (transvesical) prostatectomy, first performed in 1894, requires

few specialized instruments and involves enucleation of the prostatic
adenoma through an extraperitoneal, lower abdominal incision. This
approach is particularly well suited to handle large intravesical median and
lateral lobes. In addition, bladder pathology, including calculi, diverticula,
tumors, or foreign bodies, can be treated simultaneously.

In this approach, the skin is opened through either a lower midline or

transverse incision. The anterior rectus sheath is divided either vertically or
transversely, and the rectus muscles are retracted laterally. This allows
visualization of the anterior bladder wall within the retropubic space, inferior
to the peritoneal reflection and above the symphysis pubis. The bladder is
opened with care to not expose any more of the prevesical or paravesical
space than necessary. Using electrocautery, an incision is made in the
bladder mucosa around the bladder neck. Using scissors or a forefinger, the
cleavage plane is developed between the hyperplastic adenoma and the
compressed tissue of the peripheral zone lying against the true capsule of
the prostate. With lateral lobe hyperplasia, the finger is swept around the
lateral aspect of each lobe, including the anterior and posterior
commissures. The adenoma is brought into the bladder through the bladder
neck with care, and the paired posterior prostatic arteries are inspected for
bleeding. If a simple median lobe is present, the mucosa of the bladder neck

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is incised on only its posterior surface, and the line of cleavage is developed
between the hyperplastic median lobe and the prostatic capsule. The
operation is usually performed blindly, as illustrated.

Following removal of the adenoma from within the prostatic capsule,

bleeding is usually controlled first by packing the enucleated fossa with
hemostatic gauze and then by fulguration or ligation of the prostatic arteries
near the bladder neck. Inflation of the Foley catheter balloon within the fossa
can also tamponade bleeding. Advancing the bladder mucosa into the
prostatic fossa with absorbable suture at the 5- and 7-o’clock positions may
also help with hemorrhage and possibly prevent subsequent bladder neck
contracture. Pronounced hemorrhage despite these maneuvers is handled
by placement of a purse-string suture of heavy nylon around the bladder
neck, passed out through the skin, and tied firmly, as described by Malamet.
With excessive bleeding, a suprapubic catheter is also left in the bladder,
along with a Foley catheter to allow for continuous bladder irrigation. A
perivesical, pelvic drain may also be placed. The rectus muscles, fasciae,
and skin are then reapproximated. The urethral catheter is removed after 2
to 4 days, and a voiding trial is administered by clamping the suprapubic
tube. The postvoid residual urine is checked with the suprapubic tube over
several days, and this tube is removed if voiding is adequate. Full activity is
allowed after 1 month.

Plate 11.8

Benign Prostate Surgery: Suprapubic

Plate 11.9
Benign prostate surgery: Retropubic
The alternative open surgical approach for removal of obstructing prostate
adenoma is the retropubic approach. This technique was developed in 1945
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and is essentially a variation of the previously described suprapubic

technique.

Unlike the suprapubic approach (see Plate 11.8 ) in which the bladder is
entered, the retropubic prostatectomy involves directly incising the anterior
prostatic capsule instead. Retropubic prostatectomy is technically more
difficult than the suprapubic approach and requires more retraction in a
deeper wound. This approach is suitable for large prostates in which the
hyperplasia involves mainly the lateral lobes and not median lobe extension
into the bladder. If an individual has obesity, retropubic exposure may be
more difficult. If bladder pathology coexists (tumors or stones) the
retropubic approach is less desirable, because visualization of the bladder
cavity is difficult. It is also not recommended for small glands or for prostate
cancer.

The surgical approach through the skin and rectus muscles to the prevesical
retropubic space is like that of the suprapubic procedure. However, instead
of entering the bladder, the anterior surface of the prostatic capsule beneath
the symphysis pubis is exposed. It may be necessary to divide the
puboprostatic ligaments while removing the areolar tissue from the anterior
surface of the prostate. The prostatic capsule is easily identified by the
overlying plexus of Santorini, because these veins arborize over the surface
of the prostatic capsule. After ligating these veins, a transverse (or vertical)
incision is made into the prostatic capsule, exposing the adenoma. Using the
tip of the index finger, a cleavage plane is easily developed between the
adenoma and the surgical (false) capsule formed by the compressed normal
prostatic tissue. Further access can be obtained by insertion of a finger from
the other hand into the rectum to elevate the prostate. The adenoma is
shelled from the capsule and brought up through the prostatic incision,
where it is then peeled and freed from the bladder neck. If the bladder neck
is small, a wedge of tissue is removed and the bladder mucosa is advanced

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into the prostatic fossa to reduce the risk of the development of a secondary
bladder neck contracture.

Visualization of the prostatic fossa following removal of the adenoma allows

control of bleeding under direct vision. To aid hemostasis, a Foley catheter is
inserted per urethra and the balloon inflated in the prostatic fossa. The
prostatic capsule is then tightly closed with a continuous absorbable suture
without the need for a suprapubic catheter. Closure of the lower abdominal
wound is the same as with the suprapubic prostatectomy, with a drain
placed into the retropubic space. The urethral catheter may be removed
after 4 to 7 days.

In general, the retropubic approach has slightly lower morbidity and a faster
recovery than the suprapubic procedure because the bladder is not entered.
Cystotomy is often associated with increased postoperative discomfort,
dysuria, frequency, and urgency. Additionally, excellent anatomic exposure of
the prostate is afforded by the retropubic approach. Because of this,
complete enucleation of the adenoma and precise transection of the urethra
are possible, lowering the recurrence rate and aiding the return of
continence. Secondary hemorrhage is uncommon, and the urine clears
relatively rapidly after the retropubic procedure.

Plate 11.9

Benign Prostate Surgery: Retropubic

Plate 11.10
Benign prostate surgery: Perineal
Perineal prostatectomy is the least common open approach for the surgical
treatment of BPH but has several advantages over the supra- and infrapubic
approaches. The operation is excellent for the removal of very large glands

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and permits complete removal of all adenomatous tissue. Anatomically, the

perineal region varies less dramatically with body habitus than does the
lower abdominal region, reducing operative times. Patients with prior renal
transplantation or mesh inguinal hernia repairs in which the retropubic space
may be scarred or obliterated are particularly well suited for this approach.
Bleeding can be controlled under direct vision, and morbidity and
convalescence time are relatively low with the perineal approach.
Additionally, drainage of fluid after the procedure is surgeon dependent if
there is evidence of infected urine or exudate drains away from the operative
area and is not retained within a cavity.

Conversely, the perineal prostatectomy is technically more difficult than

other open approaches, making an accurate knowledge of perineal
structures important to avoid injury to the rectal wall or external sphincter
muscle. In addition, the operation is not suitable for patients with extreme
obesity or those with limited hip motion because of severe ankylosis of the
hip or spine or those with unstable artificial hips that would limit the need for
exaggerated lithotomy positioning required for the procedure. Common
degenerative disc disease is not a contraindication for perineal
prostatectomy.

With the patient in high lithotomy position, a perineal incision is made in the
shape of an inverted “U” with the apex 3 cm anterior to the anus. The
ischiorectal fossae on each side of the central tendon are opened and
developed bluntly with the index finger. The musculofibrous central tendon
is divided, exposing the anterior rectal wall, which, with the rectal sphincter,
falls backward and away from the superficial transverse perineal muscles.
With gentle dorsal traction on the rectum, the rectal wall is then detached
from the prostatic apex by dividing the rectourethralis muscle; care is taken
to avoid rectal injury with this maneuver. A finger can also be placed into the
anus (using an anal cover to maintain sterility) to aid with dissection. The

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prostate is then delivered into the field and further cephalad separation of
the prostate from the rectum is undertaken with blunt digital dissection until
the entire posterior surface of the prostate is exposed, if necessary to
beyond the ends of the seminal vesicles.

After exposure of the posterior prostate, a transverse incision is made across

the center of the prostatic capsule and into the prostatic urethra halfway
between the apex and base of the prostate. The incision in the prostate in
this location is made directly into the compressed posterior peripheral zone
tissue to expose the adenoma. The lower lip of the incision through the
capsule is reflected backward, exposing the hyperplastic adenoma and the
urethral floor. A Young retractor is inserted through the opening in the
capsule, to provide counterpressure that elevates the adenoma into the
wound. The index finger is then inserted into the cleavage plane between the
adenoma and the surgical (false) capsule, and the two lateral lobes and any
median lobe are easily enucleated. Enucleation performed with care leaves
the bladder neck intact. After hemostasis is achieved in the prostatic fossa, a
Foley catheter is inserted into the bladder and the balloon is inflated within
the fossa. As with other “open” surgical approaches, if the adenoma is
unusually large, excessive bleeding may occur. In such cases the bladder
neck can be pulled down and the prostatic capsular vessels can be ligated
under direct vision. The prostatic capsule is then tightly closed with a
continuous or interrupted absorbable suture. A rubber Penrose drain is
usually placed on one side of the perineum and placed near the sutured
prostatic capsule. The skin is closed with interrupted suture. Most capsules
sutured in this manner will heal in 5 to 7 days, at which time the urethral
catheter is removed.

Plate 11.10

Benign Prostate Surgery: Perineal

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Plate 11.11
Benign prostate surgery: Transurethral resection
Transurethral resection of the prostate (TURP) is the gold standard approach
for the surgical treatment of BPH. It has the advantage of being an
endoscopic procedure that avoids an abdominal or perineal incision and is
associated with earlier ambulation and faster convalescence than the “open”
approaches. It is appropriate for the treatment of small to moderate size
(<80 g) glands. With benign prostatic enlargement, the objective is complete
removal of the adenomatous tissue to the surgical (false) capsule, but in
cases of urethral obstruction due to prostatic cancer, a “channel” TURP can
be performed with the goal of simply reestablishing urethral patency.

TURP was first performed in 1926 by Maximilian Stern, relying on advances

in cystoscopic devices and high-frequency electrical current. Nearly 100
years later, the technique remains largely unchanged despite major
advances in visualization and resection devices.

With the patient in lithotomy position, the penile urethra is calibrated with
urethral sounds or dilators to ensure that it is sufficient in size to accept a
large cystoscope. If the urethra is not amenable to a large scope (∼26 Fr), a
perineal urethrostomy can be created into the more commodious bulbar
urethra through which the resectoscope can be inserted. This procedure is
now almost universally performed with the assistance of video imaging
connected to the resectoscope.

Adenoma resection should be performed in a stepwise, orderly fashion and

typically begins at the bladder neck as described by Nesbitt. The adenoma
is resected at the bladder neck around its circumference until the circular
fibers of this structure are visible. Many surgeons also resect the intravesical

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median lobe at this point (as illustrated), to increase irrigant flow and overall
visibility for the remainder of the procedure. Next, one of the lateral lobes is
chosen for resection. The resectoscope is fixed immediately proximal to the
verumontanum to minimize damage to the external urethral sphincter. Tissue
resection can begin either at the 6- or 12-o’clock position within the
prostatic urethra; if it is begun posteriorly at 6 o’clock, resection may be
facilitated as the prostate adenoma falls into the resection path. The
resection is carried out posteriorly to anteriorly from the 6 o’clock position
progressively up towards 12 o’clock, back and forth between the right and
left lobe, until the obstructing adenoma is resected. With each excursion of
the cutting loop, a C-shaped piece of adenomatous tissue is cut away and
allowed to fall into the bladder. Bleeding is controlled by application of a
hemostatic current through the wire cautery loop. The other lateral lobe is
then similarly approached. The final part of the procedure involves careful
tissue removal from the floor of the prostate and from the prostatic apex
near the external sphincter while preserving the verumontanum. At the end
of the procedure, accumulated tissue in the bladder is aspirated through the
sheath of the instrument, followed by the insertion of a Foley catheter. The
catheter remains in place for 24 to 48 hours, and obstructing blood clots are
minimized with continuous bladder irrigation if needed.

Sequelae of TURP include bleeding requiring transfusion or reoperation,

urethral or bladder neck strictures, retrograde ejaculation, and, rarely,
incontinence and erectile dysfunction. TUR syndrome is a dilutional
hyponatremia that can occur when a large amount of isotonic water,
commonly used as an irrigant during monopolar resection, is systemically
absorbed because of prolonged resection time or early perforation of the
prostatic capsule. The syndrome is characterized by confusion, nausea,
vomiting, bradycardia, and visual disturbance and can be lethal if not
recognized and treated expeditiously. The use of a bipolar resection device

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that uses saline irrigation rather than water can effectively eliminate the risk
of TUR syndrome.

Methods that employ tissue vaporization and desiccation as well as laser-

induced destruction of tissue in lieu of resection and fulguration have also
been developed to reduce hematuria and catheterization time. Other
minimally invasive methods of treating BPH have also been described that
may reduce the adverse effects of TURP but do not appear to offer the same
quality or durability.

An increasingly common alternative transurethral BPH procedure is holmium

laser enucleation of the prostate (see Plate 11.12 ).

Plate 11.11

Benign Prostate Surgery: Transurethral Resection

Plate 11.12
Enucleation of prostate
Laser enucleation of the prostate (LEP) is a minimally invasive endoscopic
technique developed in the 1990s to treat BPH. According to most recent
American Urological Association guidelines for BPH, holmium laser
enucleation of the prostate (HoLEP) is one of two endoscopic techniques
that is a size-independent option for the surgical management of BPH. The
HoLEP technique is currently more commonly used worldwide and has been
more extensively studied compared with the other option, thulium laser
enucleation of the prostate (ThuLEP). The multiple endourologic applications
of the holmium laser, including the treatment for urolithiasis, urothelial
carcinoma, BPH, and urinary strictures, have led holmium to be a more
popular laser than thulium.

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There are several laser enucleation techniques available to treat patients

with BPH. The original enucleation technique described was the three-lobe
technique. Newer strategies, two-lobe and en bloc techniques, have evolved
from the original procedure and are already being used worldwide.
Regardless of technique, the procedure involves retrograde enucleation of
prostatic adenoma using both blunt and laser dissection to completely
release the adenoma into the bladder. A transurethral endoscopic soft tissue
morcellator is used to remove the tissue out of the bladder.

Three-lobe technique
First, two lengthwise prostatic urethral incisions from the bladder neck to the
verumontanum are created at the 5 and 7 o’clock positions and taking the
incisions to the prostatic capsule fibers. A radial incision is then used to
connect the two incisions just proximal to the verumontanum, and
enucleation of the median lobe is performed in a retrograde manner in the
plane between the prostatic adenoma and the capsule. After the median
lobe is released into the bladder, the bladder neck is incised at the 12 o’clock
position from the bladder neck to the level of the verumontanum. Again, the
incisions are connected distally, and each lateral lobe is enucleated in the
same plane as the median lobe, pushed with the endoscope, and freed into
the bladder.

Two-lobe technique
Only one posterior urethral incision is made at either the 5- or the 7-o’clock
position and carried proximal to distal at the level of the verumontanum. The
incisions effectively divide the adenoma in two: a lateral lobe on one side and
the median lobe en bloc with the second lateral lobe on the other. Then a 12-
o’clock incision is made and the anterior and posterior incisions are
connected distally on both sides, followed by retrograde enucleation.

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En bloc technique
First, the external sphincter, distal border of both lateral and median lobes,
and the verumontanum are identified. Two incisions are made on both sides
of the verumontanum and laterally around the lateral lobes, which connect at
the 12 o’clock position. The incisions are connected proximally to the
verumontanum to complete a circumferential incision. The beak of the scope
is used for blunt dissection together with laser fiber for delicate dissection
and hemostasis as the entire adenoma is enucleated en bloc.

During the procedure, hemostasis of the capsular vessels is obtained by

defocusing the laser energy and activating the laser onto the vessel. The
enucleated adenoma is removed via a soft tissue morcellator device that is
placed through the endoscope.

HoLEP is an endoscopic equivalent to an open prostatectomy without any

limitation to size of the prostate. Compared with open prostatectomy, often
reserved for glands greater than 80 g, HoLEP offers lower morbidity rates,
no abdominal incision, shorter recovery time, shorter hospital stays, and
decreased catheterization time (<24 hours). Compared with TURP, HoLEP is
size independent and avoids the potentially fatal TUR syndrome caused by
the absorption of hypotonic solution. In multiple randomized trials, HoLEP
has been more efficient in the removal of prostatic tissue, with improved
short- and long-term outcomes for any size prostate compared with TURP
or open prostatectomy. The limitations to HoLEP include higher initial cost of
surgical equipment, which includes the high-powered laser unit and the
morcellator, and a steep learning curve compared with TURP.

Plate 11.12

Enucleation of Prostate

Plate 11.13
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Robotic simple prostatectomy

For males with very enlarged prostates (>80 g), standard transurethral
resection of the prostate may not be able to effectively relieve obstruction
(see Plate 11.11 ). Open operations such as the suprapubic prostatectomy or
the retropubic prostatectomy (see Plates 11.8 and 11.9 ) can provide
excellent obstruction relief; however, the open approach is associated with a
longer recovery to normal activities. The robotic technology that has been
successfully applied to radical prostatectomy (see Plate 11.17 ) has also been
effectively used, for patients with large benign prostates in the form of a
robotic simple prostatectomy.

The indications for robotic simple prostatectomy are the same as those for a
suprapubic or retropubic prostatectomy; however, due to the improved
convalescence the robotic procedure may be more widely used, especially
for older males. The patient preparation and positioning are the same as
those for robotic radical prostatectomy, as is the port placement.

A transperitoneal approach can be used after insufflation with a Veress

needle. The retropubic space is developed to provide access to the anterior
bladder neck. The bladder neck dissection is done in just the same was as
during robotic radical prostatectomy. The dissection is directed laterally to
separate the lateral aspect of the bladder from the prostate (A). As the
bladder neck is entered anteriorly, any median lobe is visualized and
delivered through this opening (B). The plane of dissection around the
bladder neck is completed to separate the bladder completely thereby
visualizing the obstructing adenoma of the prostate. A subcapsular plane is
established posteriorly to spare the exterior structures outside the prostate,
and this plane is continued as distally as possible (C). Once clearly defined,
this plane can be carried circumferentially left and right along the adenoma
to the apex. This plane is typically rather avascular, and any bleeding vessels

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are easily controlled with spot electrocautery. Once the apex is approached
the anterior commissure is opened, exposing the interior of the prostate, and
the verumontanum is visualized to ensure that the dissection plane is not
carried too distally (D). The prostate is divided at the apex, and a small
amount of apical tissue is left in the bed to help prevent any stress
incontinence. The prostate is delivered and placed into a laparoscopic
entrapment sac. Any residual bleeding can be sutured or cauterized. The
bladder neck is then anastomosed to the distal prostate (E) using a running
3-0 barbed suture, and a new 18-Fr foley catheter is placed. This closure
obviates the need for any continuous bladder irrigation. The anastomosis is
tested for water tightness. A Jackson-Pratt drain may be used but is rarely
required. The prostate is delivered through the midline port, this port is
closed with a running 0 suture. The skin of all port sites is closed with tissue
adhesive.

Patients are then planned for discharge as an outpatient with a planned

Foley catheter removal in 1 week. Due to the minimally invasive approach,
most patients require only acetaminophen or ibuprofen for postoperative
pain and are encouraged to ambulate as much as able the following day.
Patients can resume unrestricted activity by 3 weeks.

An alternative approach to the robotic simple prostatectomy involves

preservation of the retropubic space and an incision in the dome of the
bladder to then approach the prostatovesical junction transvesically. An
incision in the urothelium circumferentially around the median lobe allows
access to the adenoma, and the dissection can then be performed in a
similar fashion as described above. An anastomosis can also then be
performed after removal of the adenoma, and the incision of the bladder is
also closed and tested for watertightness.

Plate 11.13

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Robotic Simple Prostatectomy

Plate 11.14
Interventional prostate artery embolization
A myriad of urologic procedures exists for the treatment of LUTS from BPH.
Most of these treatments are transurethral procedures, and the most
definitive treatment entails a surgical prostatectomy. Since 2010, prostate
artery embolization (PAE) has emerged as an effective minimally invasive
treatment alternative, especially in patients with prostates larger than 80 g,
for which many of the alternative surgical approaches may be associated
with greater morbidity.

Indications and evaluations

The evaluation for LUTS from BPH begins with review of the patient’s
urologic history and symptoms. The International Prostate Symptoms Score
is an eight-question screening tool used to screen, rapidly diagnose, and
track LUTS from BPH. In addition, the Sexual Health Inventory for Men
questionnaire allows the physician to evaluate and track degrees of erectile
dysfunction.

The patient’s medication list should also be carefully screened. It is

important to identify any medications that can cause obstructive-like
symptoms, such as antidepressants, antihistamines, anticholinergics,
bronchodilators, and sympathomimetics that may affect detrusor and
sphincter function and worsen LUTS.

As part of the evaluation for BPH, a urologist must evaluate the patient for
prostate cancer. At this time, PAE for LUTS is not generally recommended in
patients with prostate cancer.

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Uroflowmetry and urodynamics are also an integral part of the evaluation to

ensure that LUTS is caused by BPH rather than neurologic, anatomic, or
pharmacologic etiologies. Uroflowmetry involves measuring maximum urine
flow rates as well as postvoid residual volumes. Urodynamics evaluates the
function of the bladder, sphincter, and urethra via catheters in the rectum
and bladder.

The initial management of LUTS from BPH entails lifestyle changes. This
would include recommendations to avoid drinking fluids prior to bedtime or
traveling and avoiding caffeinated drinks or alcohol, especially prior to
sleeping. Additional recommendations may also include double voiding,
whereby a male urinates and waits several moments to finish urinating.

When lifestyle changes are not enough to mitigate LUTS symptoms,

medications are included as second-line therapy. The most common
medications used are alpha-blockers, which act to relax the smooth muscle
of the prostate, and 5-alpha reductase inhibitors, which halt the production
of hormones that enlarge the prostate. Other less commonly used classes of
medications are phosphodiesterase-5 inhibitors and muscarinic receptor
antagonists.

Procedure
PAE is a minimally invasive procedure typically performed by an
interventional radiologist. The procedure is regularly performed from the
common femoral artery or left radial artery. Arterial access is gained via
modified Seldinger technique, and a sheath is advanced into the artery
through which catheters will be inserted. A series of angiograms is
performed to evaluate the origins of the prostatic arteries as well as identify
any collateral supply to nontarget organs. A microcatheter is necessary to
select the prostatic arteries and to safely position the catheter in the distal

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segment of the artery. Embolization is performed with particles no larger

than 500 micrometers in diameter. If necessary, coils can be used to
prophylactically embolize collateral arteries arising from the prostatic artery
to minimize the risk of nontarget embolization to periprostatic organs such
as the bladder, seminal vesicles, rectum, and penis. A successful procedure
involves the complete embolization of the prostate without nontarget
embolization.

Adverse events
Adverse events include both side effects and complications. Each is defined
by whether a negative event is expected (side effect) or unanticipated
(complication). Side effects that are common to the procedure include
dysuria, acute urinary retention, increased urinary frequency,
hematospermia, and hematuria. Many of the side effects of PAE can be
managed or at least improved with medications such as analgesics, α-
blockers, or phenazopyridine.

Complications primarily involve the sequela of nontarget embolization to

periprostatic organs, resulting in local ischemia. Organs that are at increased
risk due to their shared vascularity with the prostate include the bladder
(hematuria, bladder necrosis), rectum (ulcers, blood in stool), seminal
vesicles (hematospermia, reduction in ejaculatory volume), and penis
(ischemic balanitis, sexual dysfunction).

Plate 11.14

Interventional Prostate Artery Embolization

Plate 11.15
Malignant prostate surgery: Retropubic

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Prostate cancer is the second leading cause of death from cancer in US

males. The definitive treatment of clinically localized prostate cancer with
radical retropubic prostatectomy has been a popular treatment for 100
years. Although a technically formidable procedure, it remains the gold
standard because hormone treatment and chemotherapy are not curative,
and radiation therapy may not eradicate all cancer cells. The advantages of
radical prostatectomy are that it offers cure with minimal collateral damage,
it provides more accurate pathologic staging, and treatment failure is easily
identified. The ideal candidate for the procedure is healthy, less than 75
years old, has a life expectancy of at least 10 years, and has a biologically
significant tumor.

Radical retropubic prostatectomy involves the complete removal of the

prostate gland and seminal vesicles and may include a pelvic lymph node
dissection. The goals of surgery are cancer control and preservation of
urinary control and sexual function. A spinal, epidural, or general anesthetic
is generally used with the patient in the supine or relaxed dorsal lithotomy
position. A midline, extraperitoneal lower abdominal incision from the pubis
halfway to the umbilicus is made after a Foley catheter is placed in the
bladder. The rectus muscles are separated in the midline, the transversalis
fascia is opened sharply, and the retropubic space is developed. Laterally,
the peritoneum is mobilized off the external iliac vessels to the bifurcation of
the common iliac artery. A self-retaining Balfour retractor is then placed, and
a narrow malleable blade provides excellent exposure for lymph node
dissection. Lymph node dissection, if done, is first undertaken on the side
ipsilateral to the prostate tumor and proceeds by dividing the tissue over the
external iliac vein. The lymphatic tissue is excised to the lateral pelvic wall,
inferior to the femoral canal, and superior to the bifurcation of the common
iliac artery. The obturator lymph nodes are also removed by skeletonizing the
obturator vein and artery and sparing the obturator nerve. Frozen section is

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then performed on the excised nodes before prostatectomy.

Exposure for retropubic prostatectomy involves displacing the peritoneum

superiorly and removing the fibroadipose tissue covering the anterior
prostate. These maneuvers expose the pelvic fascia, puboprostatic
ligaments, and superficial dorsal vein. The endopelvic fascia is then entered
where it reflects over the pelvic side wall, allowing palpation of the lateral
prostate. By finger dissection, the levator ani muscles are released from the
lateral prostate and, with sharp dissection, the puboprostatic ligaments are
taken down anteriorly. The dorsal vein complex is then ligated with care to
avoid damage to the striated urethral sphincter. These maneuvers help
optimally expose the prostatic apex for dissection.

The apical dissection is the most complex and critical step in the operation,
because the striated urethral sphincter and the neurovascular bundles that
control erections are nearby, and the prostatic apex is the most common site
for positive surgical margins. With gentle posterior displacement of the
prostate, the prostatourethral junction is visualized. A right-angle clamp is
passed around the smooth muscle of the urethra anterior to the
neurovascular bundles near the prostatic apex and the urethra is transected
sharply. Six interrupted absorbable sutures are then placed in the distal
urethra while the exposure is optimized and the Foley catheter is removed.
The posterior aspect of the prostate is now exposed, allowing its dissection
off the anterior rectal wall superiorly. Denonvilliers fascia is included with the
prostate. In nerve-sparing procedures, the levator fascia is incised on the
lateral prostate but the prostatic fascia must be left intact during the
superior dissection because the neurovascular bundle is located between
the levator fascia and prostatic fascia.

For the remainder of the posterior dissection, the Foley catheter is replaced.
After the prostate has been mobilized completely, the bladder neck is

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incised completely at the prostatovesicular junction. After the posterior

bladder wall is divided, the bladder neck is retracted and the medially
located vasa deferentia are ligated. The paired seminal vesicles are then
dissected free, staying close to these organs to avoid damage to the pelvic
plexus laterally. After the specimen is removed, the operative site is
inspected for bleeding and residual tumor. The bladder opening is closed
with absorbable suture in a “tennis racket” manner to a diameter that
approximates the urethra, and a rosette of mucosa is created to line the
bladder neck opening for a better anastomotic seal. Finally, the bladder neck
is sutured to the distal urethra using the preplaced sutures, a new Foley
catheter is placed, and the incision is closed. The patient is allowed to
ambulate the day after the procedure and is discharged on hospital day 1 or
2. Excellent cancer control is achieved with this operation.

Plate 11.15

Malignant Prostate Surgery: Retropubic

Plate 11.16
Malignant prostate surgery: Perineal
The radical perineal prostatectomy was first described as a surgical cure for
prostate cancer in 1905. Its popularity waned in the late 1970s as the
importance of pelvic lymph node dissection for accurate staging was
elucidated. More recently, there has been renewed interest in this anatomic
approach to prostate cancer as more accurate staging methods have
reduced the need for staging lymph node dissection. In addition, like its
advantages in benign prostate surgery (see Plate 11.10 ), the perineal
approach for prostate cancer treatment offers unmatched visualization of
the apical prostate and urethral dissection, is important for cancer cure, and
is associated with less blood loss. Unlike with the retropubic approach, a full

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bowel preparation is given the day before perineal surgery. After the
induction of anesthesia, the patient is placed in an exaggerated lithotomy
position; severe hip ankylosis or unstable prosthetic hips may thus be a
contraindication to this approach. A curved Lowsley retractor is placed
transurethrally into the bladder and its wings opened. A curvilinear incision is
made around the anus as described for the perineal prostatectomy for BPH
(see Plate 11.10 ). After bluntly developing the ischiorectal fossa on each
side, the central tendon is cut and the longitudinal muscle fibers of the
rectum are identified. With gentle traction on the rectum, dissection is
carried superiorly until the rectourethralis muscle, which connects the
rectum to the perineal body, is identified. The rectourethralis muscle is
divided close to the prostatic apex, allowing the rectum to fall dorsally. The
risk of rectal injury is highest at this point. Ideally, this dissection is between
the leaves of Denonvilliers fascia. With pressure on the Lowsley retractor, the
prostate is delivered into the field, allowing blunt, digital dissection of the
prostate until its base is identified at the vesicoprostatic junction.

Unlike with perineal prostatectomy for BPH, the prostatic capsule is not
incised when the entire gland is to be removed. Instead, the exposed anterior
layer of Denonvilliers fascia is incised vertically in the midline from the base
to the apex of the prostate to preserve the neurovascular bundles. Careful
lateral dissection and gentle traction help preserve the neurovascular
bundles as they course between the leaves of Denonvilliers fascia. At the
prostatic apex, the bundles are also dissected free of the urethra, and the
posterior urethra is incised sharply over the Lowsley retractor. With traction
on the retractor, the anterior urethra is then transected and the prostate
freed to the bladder neck by sharp and blunt dissection. The puboprostatic
ligaments are then transected. Care is needed to avoid injuring the dorsal
venous complex during this dissection of the anterior prostate.

The prostate–bladder neck junction is identified by palpation of the wings of

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the Lowsley retractor. With sharp and blunt dissection, the bladder neck is
preserved. The bladder neck is first incised anteriorly to avoid injury to the
ureteral orifices posteriorly. With traction on the prostate, the bladder neck
incision is continued circumferentially around the prostate base, dissecting
and ligating the lateral pedicles coursing toward the prostate. Ligation of
these pedicles is performed close to the prostate to avoid injury to the
adjacent neurovascular bundles. With further posterior dissection, the paired
vasa deferentia are ligated and transected and the seminal vesicles are
excised with the prostate.

After the specimen is removed, the bladder neck is easily visible.

Occasionally, it may be necessary to reconstruct the bladder neck in a
“tennis racket” fashion with absorbable suture. Accurate anastomotic suture
placement between the bladder neck and membranous urethra is guided by
better visualization of these structures with the perineal method compared
with the retropubic approach. A Penrose drain is placed near the bladder
neck anastomosis and brought out through the skin incision. The levator ani
muscles and central tendon are then reapproximated and the skin is closed
with interrupted vertical mattress sutures. Patients are advised to ambulate
the evening of surgery, and the drain is removed and patients are advanced
to a regular diet the day after surgery. Rectal stimulation and medications are
prohibited. Hospital discharge is on day 1 or 2 after surgery. Unique but
infrequent complications of perineal prostatectomy are transient lower
extremity sensory neurapraxia (<2%) and rectal incontinence (<3%). Rates
of urinary incontinence and erectile dysfunction are comparable to those of
retropubic methods.

Plate 11.16

Malignant Prostate Surgery: Perineal

Plate 11.17
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Malignant prostate surgery: Laparoscopic and

robotic
To decrease the morbidity of open radical prostatectomy, robotic radical
prostatectomy has become preeminent over the past 20 years. This is due to
computer-assisted robotic technology. “Wristed technology” enabled
movement with the facility of the human wrist replacing the difficult
counterintuitive nature of pure laparoscopy. Compared with open
prostatectomy, robotic prostatectomy offers comparable oncologic
outcomes with less pain and blood loss, shorter hospitalization, and fewer
postoperative complications. In the United States, robotic surgery has
replaced open surgery as the most common approach for prostatectomy. In
2017 it was estimated that 83% of prostatectomies were performed
robotically, compared with 40% in 2007.

The indications for robotic prostatectomy are identical to those for open
surgery. The contraindications remain the same: bleeding diathesis and
inability to undergo general anesthesia. Relative precautions remain morbid
obesity, prior complicated abdominal surgery, pelvic irradiation, or whole
gland high-intensity focused ultrasound (see Plate 11.11 ). The surgical
principles for radical prostatectomy are similar for pure laparoscopic and
robotic approaches.

The surgical robot requires four working arms, a console surgeon, and a
bedside laparoscopic assistant. The remote console has control of the
three-dimensional high-definition camera, and the robotic arms allow natural
wrist movements duplicated by the robot. In the classic transperitoneal
approach the pneumoperitoneum is at 8 to 12 mm Hg. The robotic ports are
all transverse with the transverse camera port above or below the umbilicus.
The prostate is removed through this incision. Transverse incisions have a
10-fold risk reduction for incisional hernia compared with vertical ones.

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Secondary trocars are placed under direct vision as needed.

Initially, the bladder is dissected from the anterior abdominal wall after
dividing the urachus, and the retropubic space is developed. The anterior
prostate is defatted and the endopelvic fascia and puboprostatic ligaments
are divided, exposing the levator ani muscle fibers on the lateral prostate.
These fibers are carefully dissected, exposing the prostate-urethral junction.
The anterior and posterior bladder neck are divided. The vas deferens are
isolated and divided. The seminal vesicles are dissected free. With anterior
displacement of the seminal vesicles, Denonvilliers fascia is incised, and
under direct vision the space between the prostate and rectum is developed,
with minimal risk of rectal injury.

Next, the prostatic pedicles are controlled. The course of the subsequent
antegrade or descending dissection of the neurovascular bundle is guided
by the lateral “groove.” Once the nerve sparing has been completed,
dissection of the apex is critical for continence. This is acheived by
maintaining maximal membranous urethral length. Managing the dorsal
venous complex is facilitated by temporarily increasing pressure for a few
minutes (18–20 mm Hg) to reduce bleeding. The urethra is then divided after
preserving urethral length. The specimen is put in an entrapment sac.

Anastomosis is the final step. If the aperture of the bladder neck is large, it
can be reduced by placing running sutures at the 3 and 9 o’clock positions
to better approximate the bladder neck, reducing postoperative issues with
blood clots. A Rocco stitch is recommended because it facilitates the
anastomosis, reduces bladder neck contracture risk, and is hemostatic. The
van Velthoven vesicourethral anastomosis is the most commonly used
anastomotic technique. Two barbed 3-0 sutures are looped to each other.
Initially, one arm is placed starting from the outside through the bladder neck
at the 6-o’clock position and run up one side. The second attached looped

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suture is run up the opposite side and ligated to the other. A Foley catheter is
placed and irrigated to ensure watertightness. If not watertight, the
anastomosis should be repaired.

Finally, the specimen is delivered through an extension of the transverse

umbilical port and the fascia is closed. The smaller trocar sites do not require
fascial closure. Patients are generally discharged the same day or on
hospital day 1. Operative times are typically 2 to 3 hours. Postoperative pain
is well controlled and best managed with nonsteroidal antiinflammatory
drugs rather than opioids. The Foley catheter is typically removed on
postoperative day 5 to 7.

Plate 11.17

Malignant Prostate Surgery: Laparoscopic and Robotic

Plate 11.2
Benign prostatic hyperplasia: Sites of hyperplasia
and etiology
The prostatic nodules in BPH usually enlarge in a symmetric manner,
although in some instances one side may predominate. As nodules grow,
they have been termed median, lateral, and anterior lobe hyperplasia,
according to their location cystoscopically. The most frequent types of
prostatic enlargement are bilobular (the two lateral lobes) and trilobular (the
two lateral lobes plus the median lobe) hyperplasia. Rarely, nodules can
originate in the roof of the urethra within the anterior zone and project
downward into the bladder, giving the appearance of a rounded “anterior”
lobe.

With lateral lobe hyperplasia, the nodule growth is confined within the
prostate without projection into the bladder neck. The lateral lobes may grow

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to great size, with only a minimal degree of urinary obstruction. When they
extend into the bladder neck, this projection may interfere with the opening
of the bladder neck and result in urinary obstruction. Median lobe
enlargement begins in the posterior urethra and, following the line of least
resistance, projects as a mass up through the bladder neck and into the
bladder. Other nodular enlargement occurs in the vicinity of the Albarrán
glands just beneath the bladder neck and tends to produce intravesical
hypertrophy.

The etiology of BPH is influenced by a wide variety of risk factors in addition

to direct hormonal effects of testosterone on prostate tissue. Although they
do not cause BPH directly, testicular androgens are required in the
development of BPH with dihydrotestosterone (DHT) interacting directly
with prostatic epithelium and stroma. Testosterone produced in the testes is
converted to DHT by 5-alpha-reductase type 2 in prostate stromal cells and
accounts for 90% of total prostatic androgens. DHT has direct effects on
stromal cells in the prostate, paracrine effects in adjacent prostatic cells, and
endocrine effects in the bloodstream, which influence both cellular
proliferation and apoptosis (cell death). However, with aging there is an
abnormal accumulation of DHT resulting in the loss of homeostasis between
cellular proliferation and cell death, resulting in an imbalance favoring cellular
proliferation and therefore leading to BPH. This process is termed the DHT
hypothesis and results in increased numbers of epithelial and stromal cells in
the periurethral area of the prostate and can be seen histopathologically.

As mentioned previously, aging and testicular androgen are the two

established risk factors for the development of BPH. Other risk factors in the
development of BPH include metabolic syndrome, obesity, hypertension,
and genetic factors. In the Baltimore Longitudinal Study of Aging cohort,
each 1 kg/m 2 increase in body mass index (BMI) corresponds to a 0.4-mL
increase in prostate volume. Participants with obesity (BMI >35 kg/m 2 ) had

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a 3.5-fold increased risk of prostate enlargement compared with nonobese

(BMI <25 kg/m 2 ) participants. The presence of metabolic syndrome is
associated with a higher annual BPE, growth rate, increased sympathetic
activity, and LUTS. Genetic predisposition to BPH has been demonstrated in
cohort studies; first-degree relatives in one study demonstrated a fourfold
increase in the risk of BPH compared with controls. These findings have
demonstrated consistency in twin studies looking at the disease severity of
BPH, with higher rates of LUTS seen in monozygotic twins. Additionally,
there are ethnic trends in occurrence, because the condition is more
common in White and Black males than it is in Asian males. However, the
exact pathophysiologic mechanisms involved in the association of metabolic
and genetic factors with BPH/BPE/LUTS are not completely understood, and
further studies are needed.

Plate 11.2

Benign Prostatic Hyperplasia: Sites of Hyperplasia and Etiology

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