The seminal vesicles were first described by Fallopius in 1561 (Brewster, 1985) as paired male organs.

Primary pathology within the seminal

vesicles is rare, but secondary lesions are more common. In the past, insufficient imaging methods led to infrequent definition of either
primary or secondary seminal vesicle pathology. The use of ultrasonography, computed tomography (CT), and magnetic resonance
imaging (MRI) has improved diagnostic visibility and facilitated the diagnosis and treatment of seminal vesicle pathology. The necessity
of surgical intervention is rare but includes congenital cysts with infection and/or obstruction causing infertility, ureteral ectopy into a seminal
vesicle with resultant obstruction or dysplasia of the ipsilateral kidney, and primary tumors, either benign or malignant. Surgical access to the
seminal vesicles is mostly via routes familiar to the urologic surgeon, but surgery on the seminal vesicles alone (without adjacent organ removal) is
a unique challenge.

Embryology
Normal Development
An understanding of the normal embryologic development of the seminal vesicles is necessary for the diagnosis and treatment of diseases
involving these structures. The seminal vesicle, a strictly male organ (no female homologue), develops as a dorsolateral bulbous swelling
of the distal mesonephric duct at approximately 12 fetal weeks (Arey, 1965; Brewster, 1985). Initially, the cloaca is subdivided by downward
growth of the urorectal septum into the posterior anal canal and the anterior urogenital sinus (Fig. 1091A). The division is completed around the
seventh week. The mesonephric duct (wolffian duct) is thus included in an area called the vesicourethral canal within the urogenital sinus. The
ureter is a bud originating from the mesonephric duct at 4 weeks that eventually attains a separate opening into the bladder by absorption and
cranial migration (Fig. 1091B). The mesonephric duct becomes the vas deferens, which normally drains into the urethra at the ejaculatory duct
where it is surrounded by the prostatic glands. Separate symmetrical buds extend from the distal mesonephric duct just proximal to the
ejaculatory duct at approximately 12 weeks to form the seminal vesicles (Fig. 1091C).

Embryologic Abnormalities
Developmental anomalies form by alteration of this orderly process. If the ureteral bud arises too far cranially on the mesonephric duct, it will be
absorbed late. This results in failure to meet the metanephric blastema, thus leading to renal dysplasia or agenesis and causing the ureter to enter
ectopically anywhere along the vas deferens or posterior urethra (Tanagho, 1976; MacDonald, 1986). Gordon and Kessler (1972) showed that
50% of ectopic ureters in males enter the posterior urethra, whereas 30% join the seminal vesicle. The remainder enter the vas deferens
or the ejaculatory ducts. Because formation of the seminal vesicles occurs at week 12 of embryogenesis, an alteration in ureteral bud
development from the mesonephric duct may have an impact on formation of the seminal vesicles. There is an association between absence of
the seminal vesicle and ipsilateral renal anomalies. This is discussed later.

Physiology
The physiologic role of the seminal vesicle is not entirely known; however, the secreted fluid is important in the motility and metabolism of
ejaculated sperm. The secretions from the seminal vesicle contribute approximately 50% to 80% of the ejaculate volume, with an average
volume of 2.5 mL and a pH in the neutral to alkaline range. Seminal vesicle secretions primarily contain carbohydrates such as fructose, a
necessary component for sperm motility, and prostaglandins E, A, B, and F, as well as a coagulation factor (Tauber et al, 1975, Tauber et al,
1976). A 52-kDa protein, semenogelin 1, has been identified. It is postulated that this is a sperm motility inhibitor and is cleaved by a proteolytic
enzyme, prostate-specific antigen (PSA), after ejaculation (Robert and Gagnon, 1999).

Anatomy
General Description

The normal adult seminal vesicle is 5 to 10 cm in length and 3 to 5 cm in diameter. The volume capacity of the seminal vesicle averages 13 mL.
The right gland is slightly larger than the left in one third of men, but the size of both decreases with advancing age (Redman, 1987). There are
three major anatomic types; the most common type contains one central canal with minimal tortuosity and only a few side branches (Aboul-Azm,
1979). The major canalof the seminal vesicle empties into the ejaculatory duct (average length of 2.2 cm) at the terminal portion of the vas
deferens within the prostate. Histologically, the ejaculatory ducts are a continuation of the seminal vesicles. However, the thick muscle wall of the
seminal vesicle is not present within the ejaculatory duct. Normal ejaculatory duct luminal and wall dimensions are remarkably uniform among
men. Statistically, a luminal diameter of greater than 2.3 mm defines a dilated system (Nguyen et al, 1996).

Vasculature and Innervation

The blood supply to the seminal vesicle is from the vesiculodeferential artery, a branch of the umbilical artery (Braithwaite, 1952).
Occasionally, the inferior vesicle artery provides a communicating vessel. Venous drainage is from the vesiculodeferential veins and the
inferior vesical plexus. The seminal vesicles are innervated by the pelvic nerve and the hypogastric nerve. The hypogastric nerve sends both
adrenergic and cholinergic fibers to the seminal vesicles (Mawhinney and Tarry, 1991). Lymphatic drainage is via the internal iliac nodes.

Diagnosis
The diagnosis of seminal vesicle neoplasms can be difficult because they often do not cause symptoms until late in their course.
General symptoms that may occur include urinary retention, dysuria, hematuria, or hematospermia. A mass is often palpable above the prostate
and is usually not tender. Transrectal ultrasound (TRUS) is usually the next step in diagnosis and may be accompanied by needle aspiration or
biopsy for diagnosis. CT or MRI would then be appropriate to stage the patient. Because prostate cancer may be mistaken for primary seminal
vesicle cancer, serum PSA and prostatic acid phosphatase (PAP), as well as tissue immunohistochemical stains for both enzymes, should, if
positive, help define the prostate as the site of primary malignancy.

Physical Examination and Laboratory Testing

Physical diagnosis and vasography were once the only diagnostic tools available for studying the seminal vesicle. TRUS, CT, and MRI
have each added substantially to examination and diagnosis of pathologic conditions of the seminal vesicle.
The normal seminal vesicle and adjacent ducts are not palpable in the normal male. On rectal examination, the area directly craniad to the
base of the prostate where the seminal vesicles reside is soft and nondescript. The seminal vesicles lie anterior to the surrounding relatively thick
and inelastic two layers of Denonvilliers' fascia, but no anatomic detail of the vesicles or ducts is usually appreciated by palpation even if the
glands are asymmetric. The area immediately above the prostate on rectal examination may be enlarged and relatively compressible in the
presence of a seminal vesicle cyst or solid and firm if there is a seminal vesicle tumor. These lesions may compress the bladder base anteriorly
instead and, thus, may not be readily palpable. Secondary involvement of the seminal vesicle from prostate or bladder pathology is palpated as
hard areas above the prostate but may not be absolutely definable on physical examination.
Laboratory examination of seminal vesicle fluid requires obtaining a semen sample and testing directly for exclusively seminal vesicle excretions,
such as fructose, and indirectly by measuring the volume and observing liquefaction of the semen sample. A low semen volume and a lack of
both fructose and liquefaction implies either absent seminal vesicles or ejaculatory duct obstruction. Although the terminal portion of the
ejaculate originates from the seminal vesicles, split ejaculate bacterial cultures are more likely contaminated by multiple other sites along the lower
urinary tract and, thus, are not useful for localizing the site of infection (Stamey, 1980). TRUS-guided perineal aspiration cultures and abscess
drainage have been successful, however (Lee et al, 1986).

Ultrasound
Ultrasound (US), by either the transabdominal or the transrectal (preferred) route, has become one of the most accurate methods of
evaluating the seminal vesicle. The advent of probes with high resolution at short focal lengths has allowed rapid, noninvasive, inexpensive, and
accurate seminal vesicle examination in an outpatient setting.
The normal seminal vesicle on TRUS is an elongated, flat, paired structure between the rectum and the bladder just superior to the
prostate (Fig. 1092 ). The seminal vesicle appears predominantly symmetrical and is smooth with apparent saccularity. The center of the
seminal vesicle is echopenic, with occasional areas of increased echogenicity relating to luminal folds within the vesicle itself (Carter et al, 1989).
The ampulla of the vas can usually be seen, particularly near the prostate, as a tortuous tube on sagittal scans. The ejaculatory duct may also be
seen within the substance of the prostate. The verumontanum is characteristically seen as a more densely echoic structure in the midline at the
termination of the ejaculatory ducts. Although sagittal images are best for examining the length of seminal vesicles and adjacent ductular
anatomy, transaxial scans are best for detecting symmetry and volume. TRUS of the seminal vesicles does not require any special
preparation, although a half-full bladder allows easier differentiation of the vesicles and adjacent structures.

Abnormal findings on TRUS include seminal vesicle aplasia, atrophy, obstruction, or cyst formation. Aplasia and atrophy are commonly
associated with infertility in up to 2.5% of infertile men (Carter et al, 1989). TRUS-guided seminal vesiculography is a technique that couples US
with radiography to evaluate male-factor infertility secondary to obstruction. Seminal vesiculography helps image the distal male reproductive tract
(vas deferens, seminal vesicles, ejaculatory ducts) and has been found to be an improvement over standard vasography (Jones et al, 1997).
Findings consistent with obstruction include anteroposterior diameter more than 15 mm, length longer than 35 mm, andlarge anechoic areas
containing sperm on aspiration (Jarow, 1996; Colpi et al, 1997).
Cysts, although quite rare, may be congenital and associated with an ipsilateral ectopic ureter and/or an aplastic kidney, or acquired as a result of
obstruction after transurethral prostatectomy. However, in one study, 5% of men screened for prostate cancer were found to have asymptomatic
cystic dilation of the seminal vesicles (Wessels et al, 1992). The majority of patients with a seminal vesicle cyst are asymptomatic; however, they
may present with urinary tract symptoms including dysuria, painful ejaculation, hematospermia, or recurrent epididymitis. US reveals these cystic
lesions to be anechoic masses within the substance of the seminal vesicle or larger anechoic saccular lesions that might rise out of the pelvis and
displace the bladder and other pelvic structures (Steers and Corriere, 1986). Ultrasonography can be used to guide needle placement for drainage
or contrast studies to more fully delineate the lesion (Shabsigh et al, 1989). US has also been used to attempt to differentiate inflammatory
conditions of the seminal vesicle; however, other than calcifications with chronic bilharziasis, TRUS findings in patients with chronic
prostatourethritis or prostatodynia are relatively nonspecific (Littrup et al, 1988).
Sonographic findings of a tumor within the seminal vesicle depend on whether the tumor is primary or secondary. Primary tumors are
usually unilateral, whereas secondary tumors more likely involve both seminal vesicles and may be difficult to distinguish as to their origin (i.e.,
from the rectum, bladder, or prostate). The TRUS image of a solid tumor is isoechoic to the prostate but relatively hyperechoic with respect to the
normal seminal vesicle. There are no image characteristics indicative of benign versus malignant or primary versus secondary tumors,
except that primary tumors are commonly unilateral and tend not to be contiguous with the prostate, whereas prostate cancer invading the seminal
vesicle may be at the base of both seminal vesicles and contiguous with the prostate tumor. US-guided transrectal or perineal aspiration
cytologies or core biopsies can be useful to pathologically diagnose a seminal vesicle neoplasm.

Computed Tomography
CT is a considerable improvement over conventional radiography for evaluation of the pelvis. Evaluation of seminal vesicle pathology by CT,
however, has not been systematically studied. Silverman and colleagues (1985) reviewed a group of 50 patients with normal seminal vesicles by
CT and determined that mean length was 3.1 cm, width 1.5 cm, and overall area 3.6 cm. The volume tended to decrease with age, and the shape
varied from ovoid (70%) to tubular (20%) to rounded (10%). The seminal vesicles were symmetrical in 67% of those studied. The seminal
vesicles themselves are medium contrast structures (similar to muscle) routinely seen directly below the bladder. The surrounding
Denonvilliers' fascia is not discernible on CT. Goldstein and Schlossberg (1988) studied CT in patients who had absent vas deferens and found
that not all had absent seminal vesicles; they concluded that CT was accurate for detection of the presence of seminal vesicles. CT has been
used to detect congenital anomalies, and perhaps this may be its best use in seminal vesicle diagnosis (Fig. 1093 ). Cystic structures
have CT attenuation numbers (Hounsfield units) from 0 to 10 like most clear fluid-filled structures, although the density may be higher secondary
to debris, pus, or hemorrhage.
Tumor within the seminal vesicle is readily seen on CT as an enlarged vesicle with a higher CT attenuation number in the area of the
tumor mass than in normal seminal vesicle and with a normal bladder and prostate (Fig. 1094). The lesion may be cystic, however, as a
result of tumor necrosis (King et al, 1989). CT cannot distinguish between benign and malignant tumors and cannot routinely distinguish
between primary and secondary tumors, although tissue planes are usually obliterated by secondary tumors invading from prostate or rectum
(Sussman et al, 1986). Inflammatory masses in the seminal vesicles, such as tuberculosis or old bacterial abscesses, can be calcified (Patel and
Wilbur, 1987; Schwartz et al, 1988; Birnbaum et al, 1990) and thus distinguished from tumors, although a history of infection and related
symptoms can usually be elicited. A long-term history of diabetes mellitus has also been associated with seminal vesicle calcification (King et al,
1989).

Magnetic Resonance Imaging

Although MRI is not, in general, more sensitive than CT or US for diagnosis, the anatomic relationships are more clearly seen, multiplanar
imaging is readily available, and the minimal amount of fat in the pelvis and the characteristics of the MR phenomenon (T1- and T2-weighted
image) allow for more definitive diagnosis of cystic lesions and more accurate staging of solid neoplasms in the pelvis. Normally, the
anatomic relationships of the seminal vesicles are similar to those shown on CT except that on T1-weighted images, seminal vesicles are of
low signal intensity, which increases substantially on T2-weighted images (Fig. 1095 ). This is thought to be secondary to the secretions
present in the ductular lumen of the seminal vesicle. The surrounding Denonvilliers' fascia is of low intensity on both T1- and T2-weighted images.
In general, T2-weighted images have signal intensities that are lower than that of fat in prepubertal children, similar to or higher than that of fat in
adults, and similar to or lower than that of fat in patients older than 70 years. Endocrine and radiation therapy influence the size and intensity of the
seminal vesicles (Secaf et al, 1991). Seminal vesicle cysts are similar to cysts in other locations in that the T1-weighted image is of low intensity
but the T2-weighted image is that of a unilocular smooth wall with a uniform high intensity and well-defined margin (Gevenois et al, 1990; Hihara et
al, 1993). Hemorrhagic cysts have highintensity signal on both T1- and T2-weighted images (Sue et al, 1989). Seminal vesiculitis shows
decreased signal intensity on T1-weighted image, whereas T2-weighted image intensity is higher than that of both fat and the normal seminal
vesicle.
MRI of seminal vesicle tumors shows a heterogeneous mass with a medium intensity on T1-weighted image and a heterogeneous intensity on T2weighted image. There has been no systematic MRI study of seminal vesicle tumors, and MRI cannot distinguish between benign and malignant
solid masses within the seminal vesicle.
Patients with a suspected seminal vesicle abnormality or mass felt on rectal examination should first have TRUS. If the mass is solid and
noncystic, a transperineal or TRUS-guided biopsy is a reasonable next step. If the tumor is confirmed, a CT scan should be done next for staging
purposes; MRI is necessary only to confirm the hemorrhagic nature of the mass or to more definitively stage the extent of the mass to contiguous
organs within the pelvis. Definitive treatment for most seminal vesicle lesions, however, can be appropriately determined without MRI.

Vasography
Vasography, accomplished either by transurethral contrast injection at the seminal colliculus or by surgical exposure of the scrotal vas followed by
contrast injection, was once the preferred means to image the seminal vesicles (Fig. 1096 ). Transurethral routes of injection were often
unsuccessful owing to the length of time, special equipment, and expertise required. Antegrade injection through the surgically exposed vas is
highly successful, particularly in evaluating duct obstruction in azoospermic individuals or those with prior surgical trauma (Al-Omari et al, 1985).
Vasography does not, however, provide accurate demonstration of the pathology of the seminal vesicles in patients with vesiculitis,
cysts, or tumors (Dunnick et al, 1982; King et al, 1989). Direct transrectal needle seminal vesiculography has also been reported as a method for
diagnosis or drug delivery but is not recommended for routine cases (Meyer et al, 1979; Fuse et al, 1988).

Pathology
Congenital Lesions
Agenesis of the Seminal Vesicles
Unilateral agenesis of the seminal vesicles is not uncommon, with an incidence of 0.6% to 1%. It may be associated with unilateral
absence of the vas deferens, as well as ipsilateral renal anomalies (Fig. 1097 ). This is thought to result from an embryologic insult before
the separation of the ureteral bud from the mesonephric duct, which typically occurs at 7 weeks' gestation. It is felt that if the insult occurs after 7
weeks' gestation, then the seminal vesicle anomaly may not be associated with renal agenesis (Hall and Oates, 1993). The frequency of
associated renal anomalies varies, but in one series, 79% of patients with absence of a seminal vesicle and/or vas deferens had ipsilateral renal
agenesis, 12% ipsilateral renal abnormalities, and only 9% had normal kidneys bilaterally (Donohue and Fauver, 1989).
Bilateral absence of the seminal vesicles is frequently found in association with congenital bilateral absence of the vas deferens
(CBAVD). This is commonly associated with a mutation of the cystic fibrosis transmembrane receptor (CFTR). Seventy to eighty percent of men
with bilateral absence of the vas and/or seminal vesicles are carriers for the genetic mutation associated with cystic fibrosis (Anguiano et al, 1994;
Chillon et al, 1995). Conversely, 80% to 95% of men with cystic fibrosis have bilateral absence of the vas deferens or seminal vesicles (Holsclaw
et al, 1971; Boat et al, 1989). In men who have genitourinary anomalies with CBAVD/seminal vesicle agenesis, the incidence of CFTR mutation is
extremely low (de la Taille et al, 1998). However, lack of a vas deferens does not necessarily imply an absent seminal vesicle unless the ipsilateral
ureter is also not present (Goldstein and Schlossberg, 1988). Seminal vesicle agenesis requires no treatment.

Obstruction of the Seminal Vesicles

Whereas absence of the seminal vesicles may be asymptomatic, obstruction is frequently associated with symptoms. Unilateral obstruction may
be due to entrance of an ectopic ureter, leading to infection of the obstructed organ. The kidney associated with the ectopic ureter is frequently
dysplastic. Obstruction may also be due to local invasion of bladder or prostate cancer (Fig. 1098). Bilateral obstruction (Fig. 1099) is frequently
associated with infertility (Donohue and Fauver, 1989; Hall and Oates, 1993). Several authors have described diagnosis of obstruction with the
use of TRUS and aspiration/injection of the seminal vesicles (Jones et al, 1997; Orhan et al, 1999; Seifman et al, 1999). This is covered in further
detail in the chapter on male infertility.

Infection
Vesiculitis
Infection of the seminal vesicles is an uncommon problem in the United States. In less developed countries, tuberculosis and schistosomiasis
remain common causes of seminal vesicle masses, abscesses, and calcification. Chronic bacterial vesiculitis is rare and difficult to diagnose;
however, transrectal/perineal needle aspiration for diagnosis or treatment of abscesses has been successful. Bacterial infections are commonly
due to colonic flora and are thought to be secondary to bacterial prostatitis. In the distant past, bilateral seminal vesiculectomy was used as
treatment for infections of the seminal vesicle, but today, selected systemic antibiotics are usually curative, obviating surgery (Gutierrez et al,
1994). Occasionally, chronic bacterial seminal vesiculitis may require surgical removal to eliminate symptoms and to prevent recurrent septicemia.
Any of the surgical approaches to be described subsequently would be appropriate (Indudhara et al, 1991).

Abscess
Abscesses of the seminal vesicles usually have an unknown etiology, although predisposing factors include diabetes mellitus, chronic
indwelling catheter, and endoscopic manipulation. Signs and symptoms vary but are typically related to inflammation. Conservative drainage
via a percutaneous route is occasionally successful, but most abscesses of the seminal vesicles require open drainage (Gutierrez et al, 1994;
Kore et al, 1994). Imaging of the abscess is best accomplished with MRI, owing to the high fluid content of the seminal vesicles. In contrast to the
normal hypointense T1-weighted image, inflammation results in a less intense image. The normally hyperintense signal found on a T2-weighted
image is increased further with inflammation. The use of systemic gadolinium/diethylenetriamine pentaacetic acid offers better enhancement and
visualization (Chandra et al, 1991; Doringer et al, 1991).

Calculi
Stones within the seminal vesicles are usually related to obstruction, infection, or both (Li, 1991; Wilkinson, 1993). Patients usually present
with either pain or infection related to the stone, although hematospermia or infertility can be the presenting complaint. Treatment requires
removal of the stone, usually through an open vesiculectomy. Adjuvant treatment with antibiotics may be necessary, particularly in cases of
systemic infection.

Masses
Most masses within the seminal vesicles are not neoplastic. Tumors of the seminal vesicles are extremely rare. Benign primary tumors
are the most common, including papillary adenoma, cystadenoma, fibroma, and leiomyoma (Mostofi and Price, 1973; Lundhus et al, 1984;
Narayana, 1985; Mazur et al, 1987; Bullock, 1988). Simple cysts of the seminal vesicle are seen not uncommonly and may be associated with
other genitourinary anomalies, such as ipsilateral renal agenesis or malformation (Lynch and Flannigan, 1992; Sheih et al, 1993).

Seminal Vesicle Cysts

Cysts of the seminal vesicles (see Fig. 1099) may be either congenital or acquired (King et al, 1991) and are felt to be due to obstruction
of the ejaculatory duct (Heaney et al, 1987; Conn et al, 1992). Numerous authors have reported an association between seminal vesicle
cysts and other abnormalities, including renal agenesis (Kimchi and Wiesenfeld, 1963; Roehrborn et al, 1986), infertility (Nazli et al, 1994),
hematospermia (Mayersak and Viviano, 1992; Wang et al, 1993), and genitourinary infection (Beeby, 1974; Roehrborn et al, 1986; Lynch and
Flannigan, 1992).
Others have reported an association between seminal vesicle cysts and adult polycystic kidney disease (Alpern et al, 1991; Hihara et al, 1993;
Hendry et al, 1998). In contrast to typical benign cysts, some feel that the pathogenesis of these cysts associated with polycystic kidney disease is
due to a general defect in the basement membrane of multiple organs, including the seminal vesicles. One report cited the presence of seminal
vesicle cysts in 60% of patients with polycystic kidney disease (Danaci et al, 1998). These authors, as well as others, recommend that all patients
with cysts of the seminal vesicles have imaging of their kidneys to rule out polycystic kidney disease (Alpern et al, 1991; Danaci et al, 1998;
Hendry et al, 1998).
Unless these cystic lesions are symptomatic, treatment is not usually necessary (Surya et al, 1988). If the lesion causes symptoms,

percutaneous transperineal drainage of the cysts with TRUS guidance can be successful (Kirkali et al, 1991; Wang et al, 1993); if not, open
surgical excision may be necessary. If an ectopic ureter is present, a nephroureterectomy, including removal of the seminal vesicle, should be
curative.

Benign
Papillary Adenoma/Cystadenoma
These may mimic simple seminal vesicle cysts in their presentation and imaging. They generally occur in middle-aged men and involve one side;
only one case of bilateral involvement has been reported (Mazur et al, 1987). Some feel that it originates from embryologic remnants (Tock et al,
1991; Mazzucchelli et al, 1992; Ranschaert et al, 1992). Open surgical removal is the treatment of choice because preoperative diagnosis is rarely
made.
Amyloid of the Seminal Vesicles
Subepithelial deposits of amyloid in the seminal vesicles have been reported in 4% to 17% of male autopsies, with an incidence up to
20% in men older than 76 years (Pitkanen et al, 1983; Ramchandani et al, 1993). Because of increased incidence in the older population, it is
frequently present concomitant with other conditions, such as bladder or prostate cancer. Therefore, it is possible to misinterpret enlargement of
the seminal vesicles from senile amyloidosis as carcinomatous invasion. MRI of the pelvis can usually distinguish tumor invasion, although not
with complete accuracy (Kaji et al, 1992). In contrast to senile amyloidosis, the systemic form of amyloidosis may involve multiple organ systems
with amyloid deposits in the blood vessels and muscle cells as opposed to the subepithelium (Coyne and Kenly, 1993). If patients are
asymptomatic, no treatment is necessary.

Malignant
The main difficulty encountered with seminal vesicle neoplasms is determining that they are, in fact, primary within the seminal
vesicles. Indeed, it is more common for carcinoma of the bladder, adenocarcinoma of the prostate, lymphoma, or rectal carcinoma to secondarily
involve the seminal vesicle (Mostofi and Price, 1973; Jakse et al, 1987; Ro et al, 1987).
Very few primary tumors of the seminal vesicles have been reported. This is due in part to the paucity of symptoms and the lack of detection on
physical examination for small, benign tumors; it was also once due to the lack of diagnostic imaging capable of accurately depicting the seminal
vesicles. It is surprising that a tumor arising from an analogue similar to that of the prostate and responding to similar hormonal influences has so
few recognized pathologic conditions. Perhaps the extremely low proliferative activity of seminal vesicle epithelium partly accounts for this (Meyer
et al, 1982).
Adenocarcinoma
Characteristics of a primary seminal vesicle adenocarcinoma include (1) occurrence in patients older than 50 years; (2) tumor usually extending
locally into prostate and bladder and/or rectum; (3) commonly, prostatic and/or ureteral obstruction; (4) pathology revealing a mucin-producing
papillary or anaplastic carcinoma that may also contain lipofuscin in a patient with no other pelvic primary tumor; (5) normal serum markers for
prostate cancer (PSA, PAP); and (6) elevated serum carcinoembryonic antigen (Mostofi and Price, 1973; Benson et al, 1984; Tanaka et al, 1987;
Chinoy and Kulkarni, 1993). Positive staining for cancer antigen 125 has been reported and may be useful to distinguish this from other
adenocarcinomas, such as that of the prostate or bladder (Ohmori et al, 1994; Ormsby et al, 2000).

Sarcoma
Sarcomas of the seminal vesicles have been reported by various authors and are extremely rare. They are usually diagnosed late in the
course of the disease. There are no distinguishing features except for biopsy findings (Benson et al, 1984; Chiou et al, 1985; Schned et al, 1986;
Tanaka et al, 1987; Davis et al, 1988; Kawahara et al, 1988). These include leiomyosarcoma (Amirkhan, 1994) and angiosarcoma (Lamont et al,
1991), as well as mllerian adenosarcoma-like tumor (Laurila et al, 1992). These all display aggressive behavior. Treatment is similar to that for
carcinoma, with radical extirpation yielding varying results.

Other Pathology
Other pathology includes hydatid cyst (Kuyumcuoglu et al, 1991) and carcinoid (Soyer et al, 1991). Other primary malignant tumors of the
seminal vesicles that have been reported include cystosarcoma phyllodes (Fain, 1993) and primary seminoma (Adachi et al, 1991). Hydatid
disease affecting the seminal vesicles can cause hematospermia, infertility, infection, or pain. Carcinoid of the seminal vesicle appears
homogeneous with intense enhancement on CT. On MRI, hypointense images are demonstrated on both T1- and T2-weighted images, with T2weighted images demonstrating heterogeneity (Soyer et al, 1991).

Treatment
If a solid lesion identified in the seminal vesicle shows no evidence of local spread and is benign on biopsy, treatment depends on
symptoms. If the patient is asymptomatic, close follow-up consisting of repeat rectal examination and TRUS to determine subsequent growth of
the tumor is reasonable, although it may be difficult to be certain the tumor is not malignant. If the mass enlarges or if the patient has symptoms
referable to the mass, simple seminal vesiculectomy is advisable. This may be accomplished through one of several routes described later.
If the mass is quite large, is solid, and has questionable margins, or if the biopsy shows malignant columnar or poorly differentiated carcinoma
cells, the treatment of choice is quite different. Because fewer than 10 cases of primary tumors of the seminal vesicles have been treated at
any one institution, it is difficult to define optimal treatment with any degree of certainty. Radical excision, which usually includes a
cystoprostatectomy with pelvic lymphadenectomy, is the treatment of choice unless the tumor is extremely small. This recommendation is
based on the extensive nature of the majority of the cancers when detected. The excision may include the rectum (total pelvic exenteration) if it is
thought to be invading the surrounding structures. Adjuvant therapy has no proven efficacy, although the only long-term survivors in the literature
had radical surgery with subsequent pelvic radiation therapy or androgen deprivation therapy. No chemotherapeutic regimen is known to be
efficacious.

Surgery
Surgical approaches to the seminal vesicle have varied considerably since the first seminal vesicle was removed by Ullmann in 1889 (de Assis,
1952). Descriptions of large series (up to 700 by one surgeon) of seminal vesiculectomies have been describedmost for tuberculosis or
suspected inflammation. Today, seminal vesiculectomy is rarely necessary. The most useful open surgical methods include transperineal,
similar to radical perineal prostatectomy; transvesical, achieved by incising through the posterior bladder wall; paravesical; retrovesical; or
transcoccygeal. The choice of surgical approach depends partly on the characteristics of the lesion to be treated but probably more on the
experience and expertise of the surgeon. For the most part, congenital lesions require an abdominal approach so that the ipsilateral kidney
can be dealt with concomitantly, if necessary. Benign or very small malignancies could be approached perineally; however, the risk of
impotence is high even if a nerve-sparing approach is attempted. Larger benign tumors or cysts are best handled by an anterior abdominal
approach, although a transcoccygeal method may be as useful. Patients with malignancy require radical extirpation, which commonly includes
cysto-prostato-seminal vesiculectomy and pelvic lymphadenectomy. This operation is no different from a routine procedure for bladder cancer and,
thus, is not described here.

Indications
Most surgeries on seminal vesicles are in conjunction with radical surgical treatment of pelvic neoplasms such as bladder, prostate, or
urethral cancer and, occasionally, with treatment of rectal cancer. The indications and surgical principles entailed for treatment of these conditions
are detailed in other chapters in this book.
Treatments of conditions of the seminal vesicles alone are limited to (1) transperineal/transvesical aspiration of seminal vesicle cysts or
abscesses, (2) transurethral unroofing of seminal vesicle cysts or abscesses, (3) laparoscopic dissection, and (4) open resection of one or both
seminal vesicles.

Preoperative Preparation
Preoperative preparation for open seminal vesicle surgery depends on the extent of the pathology and the planned incision.
Transperineal, transcoccygeal, and transvesical approaches should be prefaced by a complete bowel preparation. We use a mechanical
preparation with GoLYTELY orally the evening before surgery, followed by the standard antibiotic regimen, including oral neomycin/erythromycin.
This is in anticipation of the uncommon, but not unlikely, possibility of a rectal laceration. A prophylactic systemic antibiotic of choice is
administered perioperatively (i.e., immediately before surgery and for 36 hours after). Some method of attempted prevention of phlebothrombosis
in the legs, such as use of intermittent compression stockings during and immediately after surgery, is advisable. The blood loss expected from
seminal vesicle surgery depends on the surgical approach used. One to two units should be prepared for perineal and transcoccygeal approaches
and two to three units for an anterior approach. Autologous blood can be obtained because these operations are rarely emergencies.

Open Surgical Techniques

Indications for an open technique are uncommon; however, we include the following descriptions for historical interest as well as completeness of
this chapter.
Patients with chronic seminal vesiculitis or a small benign tumor of the seminal vesicle can have a seminal vesiculectomy via the
perineal route, similar to a radical perineal prostatectomy. Large benign tumors or cysts require removal through either an anterior incision
or a transcoccygeal approach because the perineal route limits the ability to reach more than a few centimeters craniad to the bladder neck or to
physically remove large masses through the relatively small opening.
Patients with an ectopic ureter into a seminal vesicle cyst require an anterior approach so that the kidney, ureter, and seminal vesicle can
be removed completely. We prefer a midline incision so that the kidney and ureter can be approached transperitoneally after mobilizing the colon.
The ureter can then be followed and dissected from the bladder in a paravesical approach, similar to performing a nephroureterectomy for
urothelial cancer.

Transperineal Approach
The transperineal approach follows the standard positioning and incision described for a radical perineal prostatectomy. To find the
seminal vesicles above the prostate, the rectal wall needs to be dissected free and released higher on the base of the prostate and seminal
vesicles than is usually necessary for initiation of radical prostatectomy. The incision in Denonvilliers' fascia is then made either transversely, just
above the level of the base of the seminal vesicles on the prostate (Fig. 10910), or vertically, if attempting to save the neurovascular bundles
responsible for potency (Weldon and Tavel, 1988). In this latter case, Denonvilliers' fascia is carefully dissected laterally away from the underlying
seminal vesicle and ampulla of the vas so as not to tear the longitudinal tissue carrying the neurovascular bundle. The dissection at the base of
the seminal vesicle may be enhanced by posterior traction on a Lowsley tractor placed through the urethra into the bladder, thus elevating the
prostate and putting tension on Denonvilliers' fascia. The two ampullae of the vas deferens should easily be dissected directly above the prostate
and just under Denonvilliers' fascia. They are somewhat friable but can be clipped with metal clips (not placed too tightly) if necessary. In the case
of a simple seminal vesicle cyst or small adenoma, the vas can be spared, and the dissection then proceeds to the vesicle of concern . If the
reason for surgery is cancer or recurrent infection, a wider resection, including the ampulla of the vas, may be advisable. If the diagnosis
is benign, the dissection can begin directly on the seminal vesicle. There is usually an easily dissected plane that can be found along the seminal
vesicle, surrounding retroperitoneal tissue, and Denonvilliers' fascia. After dissection around the seminal vesicle at the base of the prostate, it is
usually possible to pass a right-angle clamp around the seminal vesicle and use an absorbable 20 suture to ligate the stump of the seminal
vesicle directly on the prostate. A second tie or clip on the distal seminal vesicle will keep the secretions from obscuring the field after the vesicle is
cut across, which is the next step. Although some surgeons may prefer to attempt to dissect out the seminal vesicle completely before ligating its
entry into the prostate, this makes the operation more difficult and lengthy and serves no useful purpose when the seminal vesicle is being
removed for a benign condition. Once the seminal vesicle has been ligated and cut across at the base, an Allis clamp can be used on the cut edge
to put counter-traction on the seminal vesicle so that spreading dissection with Metzenbaum scissors can free the seminal vesicle from the
surrounding tissue. The vascular pedicle is usually encountered within 1 cm of the distal tip, and, after it is ligated with metal clips and cut across,
the organ can be removed. The wound is then closed in layers exactly as outlined for a radical perineal prostatectomy. A Penrose drain is left in
the bed of the seminal vesicle and removed within 24 hours if no drainage is noted.
The perineal approach is extremely well tolerated by patients and affords them minimal blood loss, early ambulation, and minimal
postoperative pain. Because there is no urethral anastomosis, patients may be ready for discharge within 24 to 48 hours. Intraoperative
complications primarily entail inadvertent rectal wall laceration, although it is possible to lacerate the trigone area of the bladder or the ipsilateral
ureter during deep dissection of the distal tip of the seminal vesicle. If an adequate bowel preparation has been given preoperatively and no gross
fecal contamination is seen, a two-layer closure of the rectum using a running mucosal layer of 30 absorbable suture and a submucosal layer of
interrupted 40 silk is usually sufficient. Anal dilation before awakening the patient may be useful. A large laceration and/or fecal contamination
should cause consideration of a temporary colostomy, although such a measure has not been necessary in our experience. If a bladder injury is
noted, it should be closed in two layers with absorbable suture as in any bladder incision and a urethral catheter left indwelling for 7 to 10 days
postoperatively. If a ureteral injury occurs, an attempt to place a self-retaining (double-J) catheter should be made and the ureter then repaired
with absorbable suture. If the ureter cannot be catheterized, flexible cystoscopy and retrograde placement of a ureteral stent should be performed
on the table with the stent left in place for 10 to 14 days postoperatively.

Transvesical Approach

The transvesical approach to the seminal vesicle has been described by numerous authors (Walker and Bowles, 1968; Politano et al,
1975). A midline extraperitoneal suprapubic incision is made up to the umbilicus, and the rectus muscles are separated on the midline. Retzius'
space is opened by downward displacement of the transverse fascia on the pubis, and an Omni retractor is placed to expose the anterior bladder
wall. Care is taken during this dissection to not injure the epigastric vessels on either side of the pubis. The bladder is opened longitudinally
approximately 7 to 10 cm, ending 2 to 3 cm away from the bladder neck. Moist 4 8 sponges are placed on the bladder wall laterally and at the
dome of the bladder, and specialized blades are placed to put the open bladder on stretch. Although it is not absolutely necessary, it is preferable
to place long 8 F feeding tubes in the ureters at this point for definition of the orifices and to help with identification of the subtrigonal ureters to
prevent their injury later in the dissection. Using a Bovie cutting stylet, a vertical incision is made through the trigone on the posterior midline
approximately 5 cm in length (Fig. 10911A). Alternatively, a transverse incision just above the bladder neck can be used, but it is not preferred
(Fig. 10911B). The vertical incision is deepened through the bladder muscle, and the ampullae of the vas should be recognized directly beneath
the bladder neck. They can be dissected by scissors down to their entrance into the prostate and then either ligated and divided or left intact
depending on the pathology, as described in the perineal approach. Just lateral to the ampullae on the prostate base, the seminal vesicles should
be identified and the plane surrounding them entered easily unless there has been prior inflammatory disease. The seminal vesicles should be
encircled and dissected completely free. Metal clips should be placed on the vascular pedicle and a 20 chromic tie on the distal end at the
prostate. A clip is placed across the proximal end of the vas to prevent seminal vesicle contents from obscuring the field, and then the vesicle is
transected and removed. If there is a moderate-sized cyst, the dissection is more involved but is usually made simple because the perivesical
plane is usually more pronounced. The plane may be very difficult to establish if there was prior vesiculitis, and in this instance the ureteral
catheters are a welcome safeguardcare must be taken not to dissect completely through Denonvilliers' fascia posteriorly and into the rectum.
The posterior bladder incision is then closed with a running 20 absorbable suture in the muscle layer followed by a running 40 absorbable
suture in the mucosal layer. The ureteral stents and 4 8 sponges are removed, a 20-F uretheral catheter is placed, and the anterior bladder wall
is closed as the posterior wall was. Suprapubic tube placement is an option, but is not necessary. A suction drain is placed through a separate
stab incision and positioned in the prevesical space away from the suture line. The drain is left for 2 to 3 days and then removed when the
drainage has proved not to be urine and is less than 50 mL/day. The urethral catheter is removed in 5 to 7 days. Early ambulation is the rule, and
the patient is usually discharged within 3 to 5 days after surgery.
This approach is more prone to blood loss and ureteral injury than the perineal approach, but a rectal laceration is much less likely.
These complications are handled as described previously.

Paravesical Approach
The paravesical incision is used in children, when there is a large unilateral cyst that lies lateral to and above the bladder, and when
nephroureterectomy is required. A midline or Pfannenstiel's extraperitoneal suprapubic incision is made. The bladder is finger-dissected away
from the lateral pelvic sidewall on the affected side. The vas deferens is identified, placed on tension, and dissected down toward the base of the
bladder. If the seminal vesicle mass is distended, it should be visible rather quickly as the vas comes close to the bladder posteriorly. Placing a
catheter in the bladder and emptying it usually allows the plane between the bladder and the cyst to be readily identified. The plane is incised with
scissors, and the seminal vesicle cyst is carefully dissected away sharply. When the tip of the cyst is clearly identified, a 10 chromic suture is
placed into it to provide traction, making further dissection easier. As the dissection proceeds, it must be remembered that the ureter crosses the
vas and must be identified to prevent its injury. In addition, the superior vesicle artery and perhaps the inferior vesicle artery may be sacrificed to
gain access to the base of the seminal vesicle. This will cause no harm and should be done without major concern. As the dissection proceeds,
the bladder is progressively rolled over medially, and the mass is dissected away from the bladder laterally. The plane is easily maintained with
sharp dissection. Any vessels feeding the seminal vesicles should be suture ligated or metal clipped. As the prostate is approached, caution
must be used to stay directly on the mass so as not to injure the neurovascular bundle lying just lateral to the seminal vesicle. At the
prostate base, the neck of the seminal vesicle is encircled and ligated with a 20 absorbable suture. A clamp is placed across just distal to the tie,
and the seminal vesicle is severed. There may be no need to clip the vas. A suction drain is placed in the bed of the seminal vesicle and brought
out through a separate stab incision. The wound is then closed in layers. Postoperative care is as previously described, except with this approach,
the drain can be removed within 24 hours if there is no drainage, and the urethral catheter can be removed within 24 hours. The patient may be
discharged within 2 to 3 days. Complications include ureteral injury and excessive blood loss. If the principles outlined earlier are followed, these
are unlikely events.

Retrovesical Approach
The retrovesical approach should be considered in patients requiring bilateral excision of small seminal vesicle cysts or benign masses
(de Assis, 1952). A midline suprapubic incision is made into the peritoneal space. A catheter is placed, and the urine is evacuated. The reflection
of the peritoneum over the rectum at the posterior bladder wall is incised transversely, with care taken not to incise into the rectum (Fig. 10912A).
The bladder is peeled back from the rectum progressively with sharp dissection until the ampullae of the vasa and the tips of the seminal vesicles
come into view (Fig. 10912B). The seminal vesicles are dissected down to the base of the prostate, much as described in the transvesical
approach, and the neck of the seminal vesicle is ligated and divided bilaterally. The ampullae are usually not taken unless necessary (Fig.
10912C). A suction drain is left in the area posterior to the bladder and brought out as before. Postoperative care is as per the description for a
paravesical resection. Complications include rectal injury, bladder laceration, and hemorrhage. In this situation, a rectal injury would be within the
peritoneum well above the levator ani muscles. After a two-layer closure as before, strong consideration should be given to placement of omentum
over the closure between the bladder base and the rectum, as well as to a temporary colostomy.

Transcoccygeal Approach

The transcoccygeal approach may not be familiar to most urologic surgeons and is unlikely to be a common choice owing to fear of rectal injury
and impotence . In individuals for whom the perineal or supine position may be difficult to maintain, or who have had multiple
suprapubic or perineal surgeries, the transcoccygeal approach may be very useful. The patient is placed on the table, ventral side down
(prone) and in a relative jackknife position (Kreager and Jordan, 1965). The incision is made in an "L" shape from midway on the sacrum (10 cm
from the tip of the coccyx) and angled at the tip of the coccyx down the gluteal cleft within 3 cm of the anus (Fig. 10913A). The incision is carried
down to the lateral side of the coccyx, which is dissected free from the underlying rectum and eventually totally removed (Fig. 10913B). The
gluteus maximus muscle layers are moved aside, and the rectosigmoid is encountered and dissected carefully from the underside of the sacrum.
With careful dissection, the lateral wall of the rectum on the side of the lesion is dissected medially from the levator ani muscle and surrounding
tissue until the prostate is encountered (Fig. 10913C). It is possible that the neurovascular bundle will be recognized from this approach; if the
dissection is unilateral, injury may be of little consequence. Once the prostate is palpated, dissection of the tissue directly superior to the base on
the midline should reveal the ampulla of the vas and, lateral to it, the seminal vesicle (Fig. 10913D). If difficulty dissecting the rectum away from
the prostate is encountered, a finger in the anus via an O'Connor sheath will allow the correct plane to be determined. Dissection and removal of
the seminal vesicles should follow the principles outlined previously. A Penrose drain should be left in the area, exiting through a separate stab
incision at closure. The rectum should be carefully scrutinized for injury, and, if found, closed in two layers as previously described. The wound is
closed in layers as well. Postoperative care does not differ from that previously described; similar to the perineal approach, the patient should have
a rapid and easy recovery. The drain should be removed within 2 to 3 days if there is no drainage.

Endoscopic Treatment
Transurethral Resection
If the cyst or abscess is adjacent to the prostate (not in the middle or distal end of the seminal vesicle), it may be possible to unroof the
cavity with a deep transurethral resection into the prostatic substance just distal to the bladder neck at the 5- or 7-o'clock position (Frye and
Loughlin, 1988; de Lichtenberg and Hvidt, 1989). However, urinary reflux, with resultant postvoid dribbling, and infection are potential
complications (Goluboff et al, 1995). Several groups have reported on endoscopic treatment of seminal vesicle abscesses using semirigid
ureteroscopes (Razvi and Denstedt, 1995; Shimada and Yoshida, 1996; Okubo et al, 1998). Another report detailed drainage of a seminal vesicle
cyst cystoscopically with an incision using a Collins knife (Gonzalez and Dalton, 1998).

Laparoscopic Surgery
Most laparoscopic surgery performed on seminal vesicles has been in conjunction with radical prostatectomy. The laparoscopic
approach allows for greater visualization, particularly of the vasculature and the tip of the seminal vesicle. Drawbacks include the need for a
transperitoneal approach and the increase in operative time (Kavoussi et al, 1993). More recently, laparoscopic radical retropubic prostatectomies
have been accomplished (Guillonneau and Vallancien, 1999). Although there is a steep learning curve, those who have used this method
extensively suggest that operative times, blood loss, and catheter removal times have all decreased (Guillonneau et al, 2000; van Velhoven et al,
2000). This approach allows for complete excision of the seminal vesicles with minimal posterior dissection. Excision of benign symptomatic
seminal vesicle cysts has been accomplished laparoscopically inboth adults and children (Carmignani et al, 1995; Ikari et al, 1999).

Medical/Radiologic Treatment
Small seminal vesicle cysts obstructing ejaculatory ducts or causing local symptoms should undergo an initial attempt at transperineal
or TRUS-guided aspiration. If this is not successful because the cyst reaccumulates, consideration could be given to reaspiration with injection of
a sclerosing solution such as tetracycline. Similarly, an abscess in the seminal vesicle could be aspirated for culture and drained, perhaps even
with a short-term indwelling catheter via a transperineal or transvesical percutaneous route using TRUS or CT guidance (Frye and Loughlin, 1988;
Shabsigh et al, 1989; Gutierrez et al, 1994). Direct irrigation of the cavity and subsequent antibiotic injection may be curative (Fox et al, 1988;
Fuse et al, 1988).

Conclusion
The seminal vesicles are difficult organs to access, but they fortunately have a small number of primary pathologic conditions. There are very few
reasons to operate solely on the seminal vesicles, but when the indications are appropriate, the approach and surgical principles are not
particularly different from those of other pelvic conditions more frequently encountered by the urologic surgeon.

REFERENCES
1. Aboul-Azm TE: Anatomy of the human seminal
vesicles and ejaculatory ducts. Arch Androl 1979;3:287292.
2. Adachi Y, Rokujyo M, Kojma H, et al: Primary
seminoma of the seminal vesicle: Report of a case. J Urol
1991;146:857859.
3. Al-Omari H, Girgis SM, Hanna AZ: Diagnostic value of
vaso-seminal-vesiculography. Arch Androl 1985;15:187192.
4. Alpern MB, Dorfman, RE, Gross BH, et al: Seminal
vesicle cysts: Association with adult polycystic kidney disease.
Radiology 1991;180:7980.
5. Amirkhan RH, Molberg KH, Wiley EL, et al: Primary
leiomyosarcoma of the seminal vesicle. Urology 1994;44:132135.
6. Anguiano A, Oates RD, Amos JA, et al: Congenital bilateral absence
of the vas deferens: A primarily genital form of cystic fibrosis. JAMA
1994;267:17941797.
7. Arey LB: The urinary system. In Developmental Anatomy.
Philadelphia, WB Saunders, 1965, p 313.
8. Beeby DI: Seminal vesicle cyst associated with
ipsilateral renal agenesis: Case report and review of literature. J Urol
1974;112:120122.
9. Benson RC Jr, Clark WR, Farrow GM: Carcinoma of
the seminal vesicle. J Urol 1984;132:483485.
10. Birnbaum BA, Friedman JP, Lubat E, et al: Extrarenal
genitourinary tuberculosis: CT appearance of calcified pipe-stem ureter
and seminal vesicle abscess. J Comput Assist Tomogr
1990;14:653655.
11. Boat TF, Welsh MJ, Beaudet AL: Cystic fibrosis. In Scriver CR,
Beaudet AL, Sly WS, Valle D (eds): The Metabolic Basis of Inherited
Disease, 6th ed, vol 2. New York, McGraw-Hill, 1989, pp 26492680.
12. Braithwaite JL: The arterial supply of the male urinary bladder. Br J
Urol 1952;24:6471.
13. Brewster SF: The development and differentiation of
human seminal vesicles. J Anat 1985;143:4555.
14. Bullock KN: Cystadenoma of the seminal vesicle. J R
Soc Med 1988;81:294295.
15. Carmignani G, Gallucci M, Puppo P, et al: Video
laparoscopic excision of a seminal vesicle cyst associated with
ipsilateral renal agenesis. J Urol 1995;153:437439.
16. Carter SS, Shinohara K, Lipshultz LI: Transrectal
ultrasonography in disorders of the seminal vesicles and ejaculatory
ducts. Urol Clin North Am 1989;16:773790.
17. Chandra I, Doringer E, Sarica K, et al: Bilateral
seminal vesicle abscesses. Eur Urol 1991;20:164166.
18. Chillon M, Casals T, Mercier B, et al: Mutations in the
cystic fibrosis gene in patients with congenital absence of the vas
deferens. N Engl J Med 1995;332:14751480.
19. Chinoy RF, Kulkarni JN: Primary papillary
adenocarcinoma of the seminal vesicle. Indian J Cancer
1993;30:8284.
20. Chiou RK, Limas C, Lange PH: Hemangiosarcoma of
the seminal vesicle: Case report and literature review. J Urol
1985;134:371373.
21. Colpi GM, Negri L, Nappi RE, et al: Is transrectal
ultrasonography a reliable diagnostic approach in ejaculatory duct subobstruction? Hum Reprod 1997;12:21862191.
22. Conn IG, Peeling WB, Clements R: Complete
resolution of a large seminal vesicle cyst: Evidence for an obstructive
aetiology. Br J Urol 1992;69:636639.
23. Coyne JD, Kealy WF: Seminal vesicle amyloidosis:
Morphological, histochemical and immunohistochemical observations.
Histopathology 1993;22:173176.
24. Danaci M, Akpolat T, Bastemir M, et al: The

62. Kirkali Z, Yigitbasi O, Diren B, et al: Cysts of the

prostate, seminal vesicles, and diverticulum of the ejaculatory ducts.
Eur Urol 1991;20:7780.
63. Kore RN, McLoughlin J, Kabala J, et al: Seminal
vesicle abscess. Br J Urol 1994;73:331332.
64. Kreager JA Jr, Jordan WP Jr: Transcoccygeal approach to the
seminal vesicles. Am Surg 1965;31:126127.
65. Kuyumcuoglu U, Erol D, Germiyanoglu C, et al:
Hydatid cyst of the seminal vesicle. Int Urol Nephrol 1991;23:479483.
66. Lamont JS, Hesketh PJ, de las Morenas A, Babayan
RK: Primary angiosarcoma of the seminal vesicle. J Urol
1991;146:165167.
67. Langman J: Medical Embryology, 4th ed. Baltimore, Williams &
Wilkins, 1981, pp 234267.
68. Laurila P, Leivo I, Makisalo H, et al: Mullerian
adenosarcomalike tumor of the seminal vesicle. Arch Pathol Lab Med
1992;116:10721076.
69. Lee SB, Lee F, Solomon MH, et al: Seminal vesicle
abscess: Diagnosis by transrectal ultrasound. J Clin Ultrasound
1986;14:546549.
70. Li YK: Diagnosis and management of large seminal
vesicle stones. Br J Urol 1991;68:322323.
71. Littrup PJ, Lee F, McLeary RD, et al: Transrectal US
of the seminal vesicles and ejaculatory ducts: Clinical correlation.
Radiology 1988;168:625628.
72. Lundhus E, Bundgaard N, Sorensen FB:
Cystadenoma of the seminal vesicle. Scand J Urol Nephrol
1984;18:341342.
73. Lynch MJ, Flannigan GM: Seminal vesicle cyst, renal
agenesis, and epididymitis in a 50 year old patient. Br J Urol
1992;69:98.
74. MacDonald GR: The ectopic ureter in men. J Urol
1986;135:12691270.
75. Mawhinney MG, Tarry WF: Male accessory sex organs and
androgen action. In Lipshultz LI, Howards SS (eds): Infertility of the
Male. New York, Churchill Livingstone, 1991, pp 129137.
76. Mayersak JS, Viviano CJ: Unilateral seminal vesicle cyst
presenting as hematospermia; diagnosis established by transrectal
prostatic ultrasound. Wis Med J 1992;1:629631.
77. Mazur MT, Myers JL, Maddox WA: Cystic epithelialstromal tumor of the seminal vesicle. Am J Surg Pathol
1987;11:210217.
78. Mazzucchelli L, Studer UE, Zimmermann A:
Cystadenoma of the seminal vesicle: Case report and literature review.
J Urol 1992;147:16211624.
79. Meyer JJ, Hartig PR, Koos GW, McKinley CR:
Transrectal seminal vesiculography. J Urol 1979;121:129130.
80. Meyer JS, Sufrin G, Martin SA: Proliferative activity of
benign human prostate, prostatic adenocarcinoma and seminal vesicle
evaluated by thymidine labeling. J Urol 1982;128:13531356.
81. Mostofi FK, Price EB: Tumors of the seminal vesicle. In Mostofi FK,
Price EB (eds): Tumors of the Male Genital System. Washington, DC,
Armed Forces Institute of Pathology, 1973, p 259.
82. Narayana A: Tumors of the epididymis, seminal vesicles, and vas
deferens (spermatic cord). In Culp DA, Loening SA (eds):
Genitourinary Oncology. Philadelphia, Lea & Febiger, 1985, pp
385398.
83. Nazli O, Apaydin E, Killi R, et al: Seminal vesicle cyst,
renal agenesis, and infertility in a 32-year-old man. Br J Urol
1994;73:467.
84. Nguyen HT, Etzell J, Turek PJ: Normal human
ejaculatory duct anatomy: A study of cadaveric and surgical
specimens. J Urol 1996;155:16391642.

prevalence of seminal vesicle cysts in autosomal dominant polycystic

kidney disease. Nephrol Dial Transplant 1998;13:28252828.
25. Davis NS, Merguerian PA, DiMarco PL, et al: Primary
adenocarcinoma of seminal vesicle presenting as bladder tumor.
Urology 1988;32:466468.
26. De Assis JS: Seminal vesiculectomy. J Urol 1952;68:747753.
27. de la Taille A, Rigot JM, Mahe P, et al: Correlation
between genito-urinary anomalies, semen analysis and CFTR
genotype in patients with congenital bilateral absence of the vas
deferens. Br J Urol 1998;81:614619.
28. de Lichtenberg HM, Hvidt V: Transurethral,
transprostatic incision of a seminal vesicle cyst. Scand J Urol Nephrol
1989;23:303305.
29. Donohue RE, Fauver HE: Unilateral absence of the
vas deferens. A useful clinical sign. JAMA 1989;261:11801182.
30. Doringer E, Chandra I, Sarica K: MRI of bilateral
seminal vesicle abscesses. Eur J Radiol 1991;12:6062.
31. Dunnick NR, Ford K, Osborne D, et al: Seminal
vesiculography: Limited value in vesiculitis. Urology 1982;20:454457.
32. Fain JS, Cosnow I, King BF, et al: Cystosarcoma
phyllodes of the seminal vesicle. Cancer 1993;71:20552061.
33. Fox CW Jr, Vaccaro JA, Kiesling VJ Jr, et al: Seminal
vesicle abscess: The use of computerized coaxial tomography for
diagnosis and therapy. J Urol 1988;139:384385.
34. Frye K, Loughlin K: Successful transurethral drainage
of bilateral seminal vesicle abscesses. J Urol 1988;139:13231324.
35. Fuse H, Sumiya H, Ishii H, et al: Treatment of
hemospermia caused by dilated seminal vesicles by direct drug
injection guided by ultrasonography. J Urol 1988;140:991992.
36. Gevenois PA, Van Sinoy ML, Sintzoff SA Jr, et al:
Cysts of the prostate and seminal vesicles: MR imaging findings in 11
cases. AJR Am J Roentgenol 1990;155:10211024.
37. Goldstein M, Schlossberg S: Men with congenital
absence of the vas deferens often have seminal vesicles. J Urol
1988;140:8586.
38. Goluboff ET, Kaplan SA, Fisch H: Seminal vesicle
urinary reflux as a complication of transurethral resection of the
ejaculatory ducts. J Urol 1995;153:12341235.
39. Gonzalez CM, Dalton DP: Endoscopic incision of a
seminal vesicle cyst. Urology 1998;51:831.
40. Gordon HL, Kessler R: Ectopic ureter entering the
seminal vesicle associated with renal dysplasia. J Urol
1972;108:389391.
41. Guillonneau B, Cathelineau X, Barret E, et al: Morbidity of
laparoscopic radical prostatectomy: Evaluation after 210 procedures. J
Urol 2000;163:140.
42. Guillonneau B, Vallancien G: Laparoscopic radical
prostatectomy: Initial experience and preliminary assessment after 65
operations. Prostate 1999;39:7175.
43. Gutierrez R, Carrere W, Llopis J, et al: Seminal
vesicle abscess: Two case reports and a review of the literature. Urol
Int 1994;52:4547.
44. Hall S, Oates RD: Unilateral absence of the scrotal
vas deferens associated with contralateral mesonephric duct
anomalies resulting in infertility: Laboratory, physical and radiographic
findings, and therapeutic alternatives. J Urol 1993;150:11611164.
45. Heaney JA, Pfister RC, Meares Jr EM: Giant cyst of
the seminal vesicle with renal agenesis. Am J Radiol
1987;149:139140.
46. Hendry WF, Rickards D, Pryor JP, et al: Seminal
megavesicles with adult polycystic kidney disease. Hum Reprod
1998;13:15671569.
47. Hihara T, Ohnishi H, Muraishi O, et al: MR imaging of

85. Ohmori T, Okada K, Tabei R, et al: CA125 -producing

adenocarcinoma of the seminal vesicle. Pathol Int 1994;44:333337.
86. Okubo K, Maekawa S, Aoki Y, et al: In vivo
endoscopy of the seminal vesicle. J Urol 1998;159:20692070.
87. Orhan I, Onur R, Cayan S, et al: Seminal vesicle
sperm aspiration in the diagnosis of ejaculatory duct obstruction. Br J
Urol Int 1999;84:10501053.
88. Ormsby AH, Haskell R, Jones D, et al: Primary
seminal vesicle carcinoma: An immunohistochemical analysis of four
cases. Mod Pathol 2000;13:4651.
89. Patel PS, Wilbur AC: Cystic seminal vesiculitis: CT
demonstration. J Comput Assist Tomogr 1987;11:11031104.
90. Pitkanen P, Westermark P, Cornwell GG 3rd, et al:
Amyloid of the seminal vesicles. A distinctive and common localized
form of senile amyloidosis. Am J Pathol 1983;110:6469.
91. Politano VA, Lankford RW, Susaeta R: A transvesical
approach to total seminal vesiculectomy: A case report. J Urol
1975;113:385388.
92. Ramchandani P, Schanll MD, LiVolsi VA, et al: Senile
amyloidosis of the seminal vesicles mimicking metastatic spread of
prostatic carcinoma on MR images. AJR Am J Roentgenol
1993;161:99100.
93. Ranschaert ER, Van Mulders P, Usewils R, et al: An
unusual low-abdominal tumor: Cystadenoma of the seminal vesicle. J
Belg Radiol 1992;75:105109.
94. Razvi HA, Denstedt JD: Endourologic management of seminal
vesicle cyst. J Endourol 1995;8:429431.
95. Redman JF: Anatomy of the genitourinary system. In Gillenwater
JY, Grayhack JT, Howards SS, Duckett JW (eds): Adult and Pediatric
Urology, 2nd ed. St. Louis, MosbyYear Book, 1987, pp 362.
96. Ro JY, Ayala AG, el-Naggar A, Wishnow KI: Seminal
vesicle involvement by in situ and invasive transitional cell carcinoma
of the bladder. Am J Surg Pathol 1987;11:951958.
97. Robert M, Gagnon C: Semenogelin I: A coagulum
forming, multifunctional seminal vesicle protein. Cell Mol Life Sci
1999;55:944960.
98. Roehrborn CG, Schneider HJ, Rugendorff EW,
Hamann W: Embryological and diagnostic aspects of seminal vesicle
cysts associated with upper urinary tract malformation. J Urol
1986;135:10291032.
99. Schned AR, Ledbetter JS, Selikowitz SM: Primary
leiomyosarcoma of the seminal vesicle. Cancer 1986;57:22022206.
100. Schwartz ML, Kenney PJ, Bueschen AJ: Computed
tomographic diagnosis of ectopic ureter with seminal vesicle cyst.
Urology 1988;31:5556.
101. Secaf E, Nuruddin RN, Hricak H, et al: MR imaging
of the seminal vesicles. AJR Am J Roentgenol 1991;156:989994.
102. Seifman BD, Ohl DA, Jarow JP, et al: Unilateral
obstruction of the vas deferens diagnosed by seminal vesicle
aspiration. Tech Urol 1999;5:113115.
103. Shabsigh R, Lerner S, Fishman IJ, Kadmon D: The
role of transrectal ultrasonography in the diagnosis and management
of prostatic and seminal vesicle cysts. J Urol 1989;141:12061209.
104. Sheih CP, Liao YJ, Li YW, Yang LY: Seminal vesicle
cyst associated with ipsilateral renal malformation and hemivertebra:
Report of 2 cases. J Urol 1993;150:12141215.
105. Shimada M, Yoshida H: Ex vivo ultrathin endoscopy of the
seminal vesicles. J Urol 1996;156:1338.
106. Silverman PM, Dunnick NR, Ford KK: Computed
tomography of the normal seminal vesicles. Comput Radiol
1985;9:379385.
107. Soyer P, Rougier P, Gad M, Roche A: Primary
carcinoid tumor of the seminal vesicles: CT and MR findings. J Belg
Radiol 1991;74:117119.

seminal vesicle cysts associated with adult polycystic kidney disease.

Radiat Med 1993;11:2426.
48. Hinman F Jr: Seminal vesiculectomy. In Atlas of Urologic Surgery.
Philadelphia, WB Saunders, 1989, pp 379382.
49. Holsclaw DS, Perlmutter AD, Jockin H, et al: Genital
abnormalities in male patients with cystic fibrosis. J Urol
1971;106:568574.
50. Ikari O, Castilho LN, Lucena R, et al: Laparoscopic
excision of seminal vesicle cysts. J Urol 1999;162:498499.
51. Indudhara R, Das K, Sharma M, et al: Seminal
vesiculitis due to Mycobacterium gastri leading to male infertility. Urol
Int 1991;46:99100.
52. Jakse G, Putz A, Hofstadter F: Carcinoma in situ of
the bladder extending into the seminal vesicles. J Urol
1987;137:4445.
53. Jarow JP: Transrectal ultrasonography in the
diagnosis and management of ejaculatory duct obstruction. J Androl
1996;17:467472.
54. Jones TR, Zagoria RJ, Jarow JP: Transrectal USguided seminal vesiculography. Radiology 1997;205:276278.
55. Kaji Y, Sugimura K, Nagaoka S, et al: Amyloid
deposition in seminal vesicles mimicking tumor invasion from bladder
cancer: MR findings. J Comput Assist Tomogr 1992;16:989991.
56. Kavoussi LR, Schuessler WW, Vancaillie TG, et al:
Laparoscopic approach to the seminal vesicles. J Urol
1993;150:417419.
57. Kawahara M, Matsuhashi M, Tajima M, et al: Primary
carcinoma of seminal vesicle. Urology 1988;32:269272.
58. Killi RM, Pourbagher A, Semerci B: Transrectal
ultrasonography-guided echo-enhanced seminal vesiculography. Br J
Urol Int 1999;84:521523.
59. Kimchi D, Wiesenfeld A: Cyst of seminal vesicle associated with
ipsilateral renal agenesis: Case report. J Urol 1963;89:906907.
60. King BF, Hattery RR, Lieber MM, et al: Seminal
vesicle imaging. Radiographics 1989;9:653676.
61. King BF, Hattery RR, Lieber MM, et al: Congenital
cystic disease of the seminal vesicle. Radiology 1991;178:207211.

108. Stamey TA: Urinary infections in males. In Stamey TA (ed):

Pathogenesis and Treatment of Urinary Tract Infections. Baltimore,
Williams & Wilkins, 1980, pp 342429.
109. Steers WD, Corriere JN Jr: Case profile: Seminal
vesicle cyst. Urology 1986;27:177178.
110. Sue DE, Chicola C, Brant-Zawadzki MN, et al: MR
imaging in seminal vesiculitis. J Comput Assist Tomogr
1989;13:662664.
111. Surya BV, Washecka R, Glasser J, Johanson KE:
Cysts of the seminal vesicles: Diagnosis and management. Br J Urol
1988;62:491493.
112. Sussman SK, Dunnick NR, Silverman PM, Cohan
RH: Case report: Carcinoma of the seminal vesicle: CT appearance. J
Comput Assist Tomogr 1986;10:519520.
113. Tanagho EA: Embryological basis for lower ureteral
anomalies: A hypothesis. Urology 1976;7:451464.
114. Tanaka T, Takeuchi T, Oguchi K, et al: Primary
adenocarcinoma of the seminal vesicle. Hum Pathol 1987;18:200202.
115. Tauber PF, Zaneveld LJD, Propping D, et al:
Components of human split ejaculate. J Reprod Fertil
1975;43:249267.
116. Tauber PF, Zaneveld LJD, Propping D, et al:
Components of human split ejaculate II. Enzymes and proteinase
inhibitors. J Reprod Fertil 1976;46:165171.
117. Tock EP, Hoe J, Foo KT: Haemorrhagic papillary
cystadenoma of the seminal vesicle mimicking giant seminal vesicle
cyst: MRI appearances. Ann Acad Med Singapore 1991;20:792794.
118. Van Velhoven R, Peltier A, Hawaux E, et al: Transperitoneal
laparoscopic anatomic radical prostatectomy, preliminary results. J
Urol 2000;163:141.
119. Walker WC, Bowles WT: Transvesical seminal vesiculotomy in
treatment of congenital obstruction of seminal vesicles: Case report. J
Urol 1968;90:324326.
120. Wang TM, Chuang CK, Lai MK: Seminal vesicle
cyst: An unusual cause of hematospermia: A case report. Chang Keng
I Hsueh Tsa Chih 1993;16:275278.
121. Weldon VE, Tavel FR: Potency-sparing radical
perineal prostatectomy: Anatomy, surgical technique and initial results.
J Urol 1988;140:559562.
122. Wessels EC, Ohori M, Granthyre JE, et al: The prevalence of
cystic dilatation of the ejaculatory ducts detected by transrectal
ultrasound (TRUS) in a self-referred (screening) group of men. J Urol
1992;147:456.
123. Wilkinson AG: Case report: Calculus in the seminal
vesicle. Pediatr Radiol 1993;23:327.

Top