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The Prostate & Seminal Vesicles

The prostate is a single gland, and the seminal vesicles are paired accessory glands behind the bladder. Their ducts meet the vasa deferentia to form the ejaculatory ducts, and their dissection lies close to the pelvic autonomic plexus and cavernous nerves.[5][6][7]

Gray's Anatomy Fig. 1160 — Prostate with seminal vesicles and vas deferens, viewed from in front and above.

Gray's Anatomy Fig. 1160 — Prostate with seminal vesicles and vas deferens, viewed from in front and above.

The Prostate​

Gross and zonal anatomy​

The prostate is a walnut-sized fibromuscular exocrine gland immediately below the bladder, encircling the prostatic urethra, resting on the urogenital diaphragm, and bounded anteriorly by the pubic symphysis and posteriorly by the rectum (separated by Denonvilliers' fascia). McNeal's zonal anatomy partitions the gland into four regions with distinct disease predispositions and operative relevance:[1][2][3]

Zone% of glandular volumeOrigin / notesDisease predilection
Peripheral zone (PZ)~70%Urogenital-sinus origin68% of 88 cancers with identifiable zonal origin in a prostatectomy series arose here[21]; target of systematic and MRI-guided biopsy
Central zone (CZ)~25%Proposed Wolffian-duct origin; has some histologic and immunohistochemical features in common with the seminal vesicles[4]Relatively cancer-resistant; occasionally invaded by posterior PZ tumors at the base
Transition zone (TZ)Small (enlarges with age)Periurethral, proximal to verumontanumPrincipal site of BPH enlargement, together with periurethral tissue; the adenoma is removed in enucleation procedures
Anterior fibromuscular stroma (AFS)Not applicable (non-glandular)Forms much of the anterior surfaceThe stroma itself is non-glandular; distinguish it from adjacent anterior glandular tissue during imaging and dissection

Surface landmarks used in the operating room:

  • Base. Superior surface, contiguous with the bladder neck.
  • Apex. Inferior, continuous with the membranous urethra through the rhabdosphincter.
  • Anterior surface. AFS; retropubic / Retzius access.
  • Posterior surface. Separated from the rectum by Denonvilliers' fascia, a posterior dissection plane in radical prostatectomy and rectourethral-fistula repair.[5][30]
  • Lateral surfaces. Bracketed by the neurovascular bundles running posterolaterally.

The prostatic urethra and its landmarks​

The prostatic urethra runs vertically through the gland (approximately 3–4 cm). The midline verumontanum (colliculus seminalis) is the dominant landmark:

  • Utricle. Midline Müllerian remnant opening at the verumontanum.
  • Ejaculatory ducts. Paired openings on either side of the utricle; formed proximally by the junction of the vas deferens (ampulla) and seminal vesicle duct.
  • Bladder neck and proximal urethra. Smooth-muscle structures involved in emission, which includes bladder-neck closure. α-blockers and outlet operations can cause ejaculatory dysfunction by differing mechanisms; reduced or absent antegrade ejaculation is not automatically retrograde ejaculation.[19]

Fascia and the "surgical capsule"​

Surrounding the prostate are three layers of pelvic fascia, each relevant to dissection:

  • Prostatic capsule. Thin fibromuscular layer, densely adherent to the gland.
  • Prostatic (visceral) fascia. Outer fibrofatty coat carrying the capsular vessels and branches of the pelvic plexus.
  • Denonvilliers' fascia. A posterior fascial structure between the prostate and seminal vesicles and the anterior rectum; cadaveric studies describe both single-layer and multilayer configurations.[38][39]

The surgical capsule is an additional operative "capsule": the compressed peripheral and central zone tissue outside a hypertrophied transition zone. It is not an anatomic layer but the plane exploited in open simple prostatectomy, HoLEP and TURP enucleation. The adenoma shells out along this interface, and the TZ is histologically and biochemically distinct from the PZ/CZ.

Vascular supply and venous drainage​

Prostatic arterial supply arises from internal-iliac branches with substantial side-to-side variation; an inferior-vesical origin is common but not universal. Cadaveric dissections identify superior prostatic arteries and smaller inferior pedicles or plexuses, with variable origins and connections to adjacent pelvic territories.[16][17] A useful operative distinction is between vessels supplying the periurethral/transition-zone tissue and those supplying the capsule.

BranchTerritory
Periurethral branchesSupply the proximal urethra and much of the TZ; prostatic-artery embolization (PAE) requires angiographic identification of the relevant feeding arteries and potentially hazardous collateral supply, not routine targeting of one invariant branch
Capsular branchesRun posterolaterally within the prostatic fascia, accompanying the cavernous nerves, to supply the PZ and CZ

Venous drainage coalesces into the periprostatic venous plexus (Santorini's), which communicates anteriorly with the deep dorsal vein of the penis, drains through inferior vesical veins to the internal iliac system, and communicates with the paravertebral venous plexus (Batson's).[37] Santorini's plexus is the dominant bleeding source at apical prostatectomy dissection, and dorsal-vein-complex hemostasis is planned during apical dissection; the timing of ligation varies by technique.[31]

Lymphatic drainage​

Principally to the obturator, internal iliac, and external iliac basins, with secondary drainage to common iliac and presacral nodes. Lymphadenectomy templates in radical prostatectomy reflect this: limited versus extended dissections are defined by these basins.

Innervation and the neurovascular bundles​

Autonomic innervation arrives from the inferior hypogastric (pelvic) plexus via two anatomically distinct pathways:[5][6][7][8]

  1. Posterior (dorsal) route. Along the ejaculatory-duct / seminal-vesicle axis to the prostate base.
  2. Lateral route. Along the inferior vesical artery, forming the neurovascular bundle (NVB) on each side of the prostatic fascia.

The NVBs run posterolaterally at approximately the 5 and 7 o'clock positions on either side of the prostate, travel with the prostatic capsular arteries and veins, continue past the apex, and become the cavernous nerves supplying the corpora cavernosa (see The Penis). Autonomic fibers distribute in a spray-like pattern along the posterolateral prostatic surface. They form a plexus embedded in the periprostatic fascia and are not a discrete "cord" that can be lifted off.[5]

Nerve-sparing (what the anatomy dictates).

  • Athermal apical dissection. Cautery can damage the nerves; clips or fine dissection are used to avoid thermal injury.
  • Plane of dissection. Intrafascial (between the prostatic capsule and the prostatic fascia) preserves the most nerve tissue; interfascial and extrafascial planes progressively sacrifice innervation.
  • Posterior and lateral fibers both matter. Pelvic autonomic fibers are distributed around the base and posterolateral prostate.[6][8] The nerve-sparing plane is chosen by side-specific cancer risk and baseline function. In a 2025 randomized trial of men with nonmetastatic prostate cancer and unassisted baseline IIEF-5 scores ≥22, intraoperative NeuroSAFE assessment guided nerve sparing; mean IIEF-5 at 12 months was 12.7 versus 9.7 with standard robotic prostatectomy among 344 of 381 operated men assessed.[32] An ICIQ continence-score difference was observed at three months, but no significant difference was detected at six months.[32] AUA/ASTRO recommends nerve sparing when oncologically appropriate ; its discussion includes baseline erectile function and the patient's priority for sexual function in selection, cautions against using MRI alone, and allows partial or unilateral preservation.[20] An RCT summarized in the EAU guideline found no erectile-function or continence benefit from seminal-vesicle-tip sparing during nerve-sparing prostatectomy.[18]
  • Geometry at 5 and 7 o'clock. Cautery or wide resection at these clock positions can injure the nerves bilaterally.

Prostate Physiology — What Matters for the Surgeon​

Androgen dependence​

Testosterone enters prostate cells and is converted to dihydrotestosterone (DHT) by 5α-reductase type 2, the isozyme dominant in the prostate.[10] DHT binds the androgen receptor (AR) with higher affinity than testosterone and drives epithelial survival and proliferation through both direct epithelial AR signaling and through stromal AR-mediated paracrine signaling (via IGF-1).[9]

Clinical translations:

  • 5α-reductase inhibitors (finasteride, dutasteride) reduce DHT and prostate volume, which is the basis of medical BPH therapy. They lower PSA by approximately 50% after 6–12 months of treatment.[17] After six to twelve months of treatment, the approximately 50% PSA reduction is corrected for when deciding on further cancer investigation.[17][29]
  • Androgen-deprivation therapy (ADT): central (LHRH agonists/antagonists) or peripheral (AR antagonists, AR-pathway inhibitors); used in the treatment of advanced prostate cancer.
  • BPH is androgen-dependent. Castration-resistant prostate cancer progresses despite castrate serum testosterone but often remains driven by androgen-receptor signaling.[18]

PSA and the seminal coagulum​

PSA (KLK3) is a kallikrein-family serine protease produced by prostatic luminal epithelial cells. Its physiologic function is to liquefy the seminal coagulum by cleaving semenogelin I/II (the scaffold protein secreted by the seminal vesicles).[11] Clinically:

  • Serum PSA levels reflect prostatic epithelial mass and the integrity of basement membranes; anything that disrupts glandular architecture (cancer, prostatitis, BPH, instrumentation, biopsy) raises PSA.
  • Serum PSA interpretation considers age, race, prostate volume (PSA density), approximately 50% suppression after six to twelve months of 5α-reductase inhibition, and transient elevation after ejaculation; DRE does not affect PSA value.[29]

Other prostatic secretions​

  • Citrate. Uniquely high in prostatic fluid; zinc-regulated pathway that is disrupted in prostate cancer (MR spectroscopic imaging exploits the resulting choline/citrate ratio).
  • Zinc. High concentration; required for seminal function and for the citrate pathway.
  • Prostatic acid phosphatase. Historic prostate-cancer marker; replaced by PSA.

The Seminal Vesicles​

Gross anatomy​

Paired accessory glands (mean length 39.4 mm and width 13.4 mm in a cadaveric series of 31 vesicles; sacculated, resembling a "skein of coral" rather than a single tube)[12] lying on the posterior surface of the bladder, lateral to the ampullae of the vas deferens. Each seminal-vesicle duct joins the ipsilateral vas ampulla to form the ejaculatory duct, which traverses the base of the prostate and opens at the verumontanum.

Operative relations:

  • Superior. Ureter, which lies superior to the seminal vesicle as it enters the trigone. The vas deferens crosses anterior to the ureter here, the male equivalent of "water under the bridge" on the dorsal bladder surface.
  • Posterior. Rectum, separated by Denonvilliers' fascia.
  • Anterior. Bladder trigone.
  • Lateral. Pelvic plexus and autonomic fibers close to the seminal-vesicle tips. Tip-sparing has been studied during radical prostatectomy and did not improve erectile function or continence in a randomized comparison.[18]

Histology and embryologic origin​

The seminal-vesicle mucosa has pseudostratified columnar secretory epithelium, and its secretion is androgen-dependent.[22][13] In a study of nine organ donors, most seminal-vesicle epithelial cells stained for lactoferrin; the prostate central zone shared some histologic and immunohistochemical features, but its Wolffian-duct origin was proposed rather than established.[4] The PZ and TZ arise from the urogenital sinus.[4] In a retrospective review of 2,010 radical prostatectomies, 63 of 2,494 tumors with determined zonal origin arose in the central zone, and the authors reported escape via the ejaculatory ducts and seminal vesicles.[23] Seminal-vesicle invasion is classified as pT3b in pathological prostate-cancer staging.[24]

Secretion and the ejaculatory cascade​

Published reviews estimate that seminal vesicles contribute about 50% to 70% of ejaculate volume.[13][14] Their secretion supplies:

  • Fructose. The dominant energy substrate for sperm metabolism; measurable absence in ejaculate is a marker of ejaculatory-duct obstruction or seminal-vesicle agenesis.
  • Semenogelin. The scaffold protein that forms the seminal coagulum immediately after ejaculation; subsequently liquefied by prostatic PSA over 20–30 minutes.[11]
  • Prostaglandins. Smooth-muscle modulators.
  • Alkaline pH buffer, fibronectin, and various immunomodulatory and antimicrobial factors.

Seminal-vesicle secretion is androgen-dependent; in mice, deletion of androgen receptors from vesicular smooth muscle reduced vesicle size, secretion volume, and seminal protein production.[15] Complete bilateral ejaculatory-duct obstruction (from cysts, stones, or inflammatory stricture) classically produces a low-volume, acidic, azoospermic ejaculate, often with absent fructose; partial obstruction may present with severe oligozoospermia. Fructose testing is relatively unreliable. For infertile men whose semen analysis suggests ejaculatory-duct obstruction, AUA/ASRM says TRUS or pelvic MRI may be recommended ; for infertile men with ejaculatory-duct obstruction, TURED and/or surgical sperm extraction may be considered .[25]

Congenital anomalies​

  • Seminal-vesicle agenesis / hypoplasia. Commonly associated with ipsilateral Wolffian-duct anomalies including ipsilateral renal agenesis and with CBAVD / CFTR mutations.
  • Zinner syndrome. Ipsilateral renal agenesis, ipsilateral seminal-vesicle cyst and ipsilateral ejaculatory-duct obstruction.
  • Müllerian-duct cyst and utricular cyst. Midline, can present with hematospermia, obstructive symptoms, or recurrent epididymitis.

Clinical Correlations for the Reconstructive Urologist​

  • BPH surgery plane. The TZ is histologically and biochemically distinct from the PZ/CZ. The "surgical capsule" between them is the plane of HoLEP, open/robotic simple prostatectomy, and TURP enucleation. Recognizing this plane makes complete adenoma removal possible with any enucleation technology.
  • Ejaculation-preserving BPH surgery. Standard resection can impair antegrade ejaculation, but mechanisms and rates differ across procedures and patients. Tissue-sparing HoLEP/TURP variants, Aquablation, prostatic urethral lift, water-vapor therapy, and iTIND use different approaches and have different effects on antegrade ejaculation. For men with moderate-to-severe LUTS/benign prostatic obstruction and a 30–80 mL prostate, the EAU gives a strong recommendation to offer Aquablation as a TURP alternative, particularly when ejaculation preservation matters; it places iTIND among non-ablative techniques under investigation.[17] Counsel from procedure-specific outcome data.[17] Loss of antegrade ejaculation can occur without retrograde flow into the bladder.[19]
  • Prostatic-artery embolization (PAE). After angiographic mapping, an interventional radiologist embolizes arterial supply to the prostate while avoiding non-target pelvic branches. Arterial origin and feeding pattern vary.[16] The EAU gives a weak recommendation to offer PAE to men with moderate-to-severe LUTS/BPO who accept less symptom and flow improvement and higher retreatment than TURP; it gives a strong recommendation for collaborative urology–interventional radiology workup and follow-up.[17] In a single-center randomized trial of men with refractory LUTS/BPO, 20/48 PAE recipients underwent TURP for unsatisfactory outcomes within five years.[33]
  • Radical prostatectomy and nerve-sparing. Athermal dissection and the choice of fascial plane aim to preserve function where side-specific cancer risk permits.[18] Erectile recovery also depends on baseline function and patient factors.[18]
  • Continence after prostatectomy. Preserved membranous urethral length and rhabdosphincter integrity, including its innervation, are associated with continence recovery. The benefit of posterior musculofascial reconstruction (retrotrigonal plate or Denonvilliers' fascia) for earlier continence remains uncertain because small randomized trials report conflicting results.[18] In a synthesis of nine comparative studies of 1,550 men (including three randomized trials), Retzius-sparing robot-assisted radical prostatectomy was associated with higher zero-pad continence at catheter removal and at one, three and six months than standard robot-assisted surgery, and more positive surgical margins (170/774 versus 115/710), with no clear zero-pad difference at 12 months.[40] See Male Urethra for the sphincter-level anatomy.
  • Transurethral resection of ejaculatory ducts (TURED). For selected men with ejaculatory-duct obstruction causing infertility or pain, preoperative TRUS locates a midline cyst relative to the bladder neck and urethral mucosa; treatment may unroof the cyst or resect near the verumontanum. Paick advises minimal cautery during hemostasis to avoid stricture in the opened ducts. Risks include urinary reflux into the ducts with epididymitis, retrograde ejaculation after bladder-neck injury, rectal or external-sphincter injury, and azoospermia after resection for partial distal obstruction.[26][34]
  • Rectourethral fistula. Occurs after prostate-cancer therapy (surgery, radiation, HIFU/cryoablation) and enters the Denonvilliers'-fascia plane. Repair can use transperineal, transanal, or transabdominal exposure. In a six-patient series, two small, simple fistulas received rectal advancement flaps, and three complex or recurrent fistulas received gracilis or omental interposition.[30] Dartos interposition closed six of eight fistulas in a separate retrospective series, whose authors advised against it after radiation.[35] A 10-study review covering more than 500 patients found more complications and lower healing after irradiation, often requiring further surgery or urinary diversion.[36]
  • Prostate cancer: where it is and where to biopsy. In a radical-prostatectomy series, 68% of 88 cancers with identifiable zonal origin arose in the PZ[21]; Systematic biopsy samples the posterior and lateral peripheral gland; MRI-targeted cores sample suspicious lesions wherever they occur.[29] MpMRI identifies PI-RADS lesions by zone and guides transperineal or transrectal targeting. Seminal-vesicle invasion (pT3b) is an independent adverse feature and influences operative margin strategy and nerve-sparing extent.
  • Pelvic fracture urethral injury (PFUI) and perineal prostatectomy / YV-plasty. Pelvic fracture urethral injury usually involves the bulbomembranous junction distal to the prostatic apex, with variable sphincter involvement.[27][28] Reconstruction requires familiarity with the retropubic fascial planes around the apex.
  • Seminal-vesicle pathology and access. Cysts, stones, and abscesses can be approached transperineally, transrectally, or laparoscopically/robotically. The seminal-vesicle tips lie next to the lateral pelvic plexus, so dissection there is done carefully.

Videos​

Prostate & seminal vesicles — lecture

References​

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