Male Reproductive System

Testes and Scrotum

  • Testis – Ovoid, smooth, ~2x3x4cm. Covered by dense fibrous capsule tunica albuginea. 250 lobules of seminiferous tubules (spermatozoa development) -> tubuli recti -> rete testes -> efferent ductules, exiting at mediastinum (invagination of tinica albuginea on posterior surface containing vessels).
  • Epididymis – Highly convoluted tubule at posterior testis; head (globus major) enlarged (7-8mm) superiory adjacent to superior pole testis; body (1-2mm diameter) along posterolateral testis; tail (globus minor) pointed adjacent to lower pole.
  • Ductus deference – Continuation ascending along posteromedial testis -> spermatic cord.
  • Appendix testis – Mullerian duct remnant, small oval beneath head of epididymis.
  • Appendix epididymis – Small stalked appendage of epididymal head.
  • Scrotal skin – 3-8mm.
  • Tunica vaginalis – Peritoneal membrane, closed sac covering medial anterior and lateral testis and lateral epididymis with ~1-2mL fluid. Bare areas of testis (posterior) anchors against scrotal wall.
  • Midline septum divids scrotum into two.
  • Spermatic cord – Ductus deferens, testicular, deferential and external spermatic aa, pampiniform plexus of veins, lymphatics, covering cremasteric muscle.
  • Testicular aa -> capsular aa beneath tunica albuginea -> centripetal branches towards mediastinum through parenchyma. Vascularity of testes is variable, but should be comparable to other side.

Atrophy is caused by atherosclerosis, end stage orchitis, cryptorchidism, hypopituitarism, malnutrition/cachexia, irradiation, prolonged anti-androgens or exhaustion atrophy (persistent stimulation by FSH).


More common >20yo, gradual onset pain and swelling, pyuria common. From C.trachomatis, Neisseria gonnorrhoeae (posterior urethra -> prostate -> seminal vesicles -> epididymis), E.coli, Pseudomonas, S.aureus, TB. Most affect epididymis (esp gonorrhea and TB) before progressing to testis. Commonly related to UTI, infected via vas deferens or lymphatics. Thickened enlarged epididymis with reduced echogenicity (oedema), diffuse relative incraesed colour Doppler (epididymis and/or testis), variabele MR signal, hydrocoele, inflammatory changes in testis in 20% (hypoechoic from oedema).

Most orchitis is associated with epididymitis. May be primarily involved by mumps, syphilis. Enlarged, oedematous areas may have irregular outline. Heterogeneous T1/T2 indistinguishable from tumour. Fluid-filled lesion suggests abscess which may rupture through tunica albuginea -> pyocoele.

Idiopathic/autoimmune granulomatous orchitis – Middle aged, sudden onset mass (occasionally insidious and painless). Granulomas restricted to spermatic tubules. ?Autoimmune.

Fournier’s gangrene – Necrotizing fasciitis of the scrotal wall.


Testicular torsion – Neonatal torsion (in utero or perinatal) is not associated with any anatomical defect). Adult/adolescent torsion occurs spontaneously, esp 13-16yo, secondary to an anomalous/variant suspension of the testis by long spermatic cord and complete investment of testis and epididymis by tunica vaginalis, usually bilateral (‘bell-clapper’ deformity). Venous obstruction within intact arterial inflow causes marked engorgement then haemorrhagic infarction. Testicular, epidiymis and spermatic cord enlargement, diffuse ± heterogeneous reduced echogenicity (oedema), absent/decreased flow cf contralateral side. Whirlpool sign of twisted spermatic cord. Spontaneous detorsion may -> reactive hyperaemia mimicing orchitis (Hx of decreasing pain prior to US). Tx bilateral orchidopexy within 6hrs usually preserves function, >12hrs salvage rate <20%.

Torsion of the appendix testis or appendix epididymis – Common in children. Enlarged hypoechoic mass medial or posterior to epididymal head with hydrocoele, thickened scrotal wall, normal testis. Tx sympomatic with spontaneous resolution.

Testicular Tumours

95% are germ cell tumours, most 25-35yo, unilateral painles mass. Lymphoma is the most common tumour in older patients. All are low signal cf normal high T2 of testis, disrupted parenchymal septations, high signal areas from haemorrhage. CT and MR not reliable for benign/malignant differentiation, but useful for staging. Lymphatic spread via gonadal vessels -> renal hilar nodes; may -> external iliac, paraaortic nodes; internal iliac and inguinal nodes are rare. May have extensive metastases to lung.

Germ cell tumours (95%) – Most are aggressive. Increased risk with testicular dysgenesis syndromes (TDS) including cryptorchidism, hypospadias, poor sperm quality; ?in utero exposure to pesticides and nonsetroidal oestrogens. Most arise from intratubular germ cell neoplasia (ITGCN, similar to CIS), of which 50% develop into invasive germ cell tumours. Lactate dehydrogenase (LDH) correlates with mass of tumour cells. Marked AFP in yolk sac tumours, HCG in choriocarcinoma elemets; both of these are elevated in >80% of NSGCT.

  • Seminomatous tumours:
    • Seminoma (50% of germ cell tumours) – 20s, identical to ovarian dysgerminoma. Classical/typical seminoma is histologically monotonous with sheets of uniform cells mixed with fibrous strands. US homogeneous, hypoechoic; less aggressive with tunica albuginea usually not penetrated, sensitive to radiotherapy. Anaplastic seminoma has greater irregularity, but has similar prognosis. Minimal elevation of HCG.
    • Spermatocytic seminoma – Uncommon (1-2%), >65yo. Slow-growing, doesn’t metastasize, excellent prognosis.
  • Non-seminomatous germ cell tumours (NSGCT) – More aggressive, resistant to radiotherapy. Heterogeneous masses with haemorrhage and necrosis, cystic areas, calcification, hydroceoele in 15%. CT or MR for tumour staging.
    • Embryonal cell carcinoma – 20s. Generally smaller than seminomas, usually doesn’t replace the entire testis, poorly defined margins.
    • Yolk sac tumour (endodermal sinus tumour) – Most common tumour <3yo with very good prognosis. Histological Schiller-Duval bodies in 50%, pathognomonic. Pure adult form is rare, may occur with embryonal carcinoma. Homogeneous. Characteristic α-fetoprotein (AFP) and α1-antitrypsin.
    • Teratoma – More than one germ layer, pure forms common in infants/children, rare in adults where all are considred malignant and it is commonly mixed with other germ cell tumours. Usually large 50-100mm, heterogeneous with cartilaginous and cystic areas. Haemorrhage and necrosis indicates mixture with embryonal carcinoma and/or choriocarcinoma. Dermoid cysts and epidermoid cyst types are rare in the testis (cf ovary). May have a non-germ cell tumour arising within the teratoma (teratoma with malignant transformation) with SCC, adenocarcinoma or sarcoma.
    • Choriocarcinoma – Rare in its pure form, highly malignant with early haematogenous spread. Usually no testicular enlargement, only small palpable nodules, very common haemorrhage and necrosis. Contains syncytiotrophoblastic and cytotrophoblastic cells. Markedly raised HCG.
    • Mixed cell types – 60% of testicular tumours have more than one pattern.

Gonadal/sex-cord stroma tumours – Most are benign. 3% bilateral.

  • Leydig cell tumour – May produce androgens, occasionally oestrogens, corticosteroids. Most 20-60yo. Usually <50mm circumscribed nodules, golden brown, homogeneous. 10% invasive with metastases.
  • Sertoli cell tumour – Most hormonally silent. Small homogeneous nodules. ~10% malignant.


  • I – Confined to testis, epididymis or spermatic cord.
  • II – Spread to retroperitoneal or paraaortic nodes below diaphragm.
  • III – Spread elsewhere.

Lymphoma, leukaemia and metastases – More common in >50yo, testes have ineffective access for chemothepray. Diffuse or focal, usually hypoechoic. Metastases are most commonly renal cell or prostate carcinoma. Agressive NHL is the most common testicular neoplasms >60yo.

Adenomatoid Tumour

Benign paratesticular mesothelial tumour. Small nodules at upper pole of epididymis, well-circumscribed, may have microscopic invasion into the testis.

Spermatic Granuloma

Solid epididymal lesion. DDx epididymitis, sarcoidosis, adenomatoid tumour.


  • Testicular cysts – Well-defined spherical, uniformly anechoic. Benign intraparanchymal cysts seen in 10% of males.
  • Tunica albuginea cysts – Well-defined, 2-5mm, peripheral.
  • Epididymal cysts – Clear serous fluid collections anywhere along course of epididymis. Loculations and septations are common.
  • Spermatocoele – Cysts of epididymal head containing sperm and cellular debris, contain fat and protein (high T1 ± layering). May be up to several cm.

Dilated Rete Testis

Multiple small spherical or tubular cystic lesions at the mediastinum. Almost all are associated with abnormal epididymis including spermatocoele, epididymal cyst, previous epididymitis, vasectomy.


Dilated serpiginous veins of pampiniform plexus. 15-20% of males, most common correctable cause of infertility. Acute onset >40yo suggests neoplastic obstruction of gonadal/renal vein.

Testicular Microlithiasis

Microcalcifications in seminiferous tubules. Diffuse punctate nonshadowing hyperechoic foci throughout the testicular parenchyma. Associated with testicular carcinoma in 40%, cryptorchidism, infertility, Klinefelter’s syndrome. Almost all are bilateral.

Testicular Trauma

Testicular rupture – 90% of ruptures are salvaged by surgery in the 1st 72hrs. Intratesticular haematoma, haematocoele. Normal shape and definition of testis is lost. Occasional discrete fracture seen. Colour Doppler detects intratesticular vascular disruption.

Infarction may be from torsion or trauma. Focal or diffuse low density -> testicular atrophy and fibrosis.


Serous fluid within the tunica vaginalis, most common cause of painless swelling. Many are idiopathic, may be due to malignant tumour (rarely mesothelioma), torsion, inflammation. Haematocoeles from trauma or surgery; pyocoeles from ruptured abscess; internal septations and loculations. Chylocoeles from widespread lymphatic obstruction eg filariasis.


Volume = width x height x length x 0.52; normal <30mL. Posterior peripheral zone is slightly more echogenic than the more heterogeneous central/inner gland (central and transitional zones). Enlarged prostate elevates the bladder base; may cause bladder outlet obstruction with thickened wall, stasis may -> bladder calculi. Base against bladder base and seminal vesicles, apex rests on urogenital diaphragm. Zonal anatomy best seen on T2.

  • Transitional zone (5%) – Periurethral, heterogeneous with age/BPH.
  • Central zone (25%) – At base, surrounding ejaculatory ducts, and adjacent to vas deferens, seminal vesicles. Heterogeneous with age.
  • Peripheral zone (70%) – Drapes posteriorly around other zones. High T2 from water, looser acinar structure.
  • Fibromuscular stroma – Anterior nonglandular tissue. Low T2, poorly marginated.

Prostatic cysts are common, include mullerian duct cyst (midline), utricle cyst (midline), prostate retention cyst (associated with BPH), seminal vesicle cyst, ejaculatory duct cyst. Lack of testicular androgen stimulation leads to widespread prostatic cell apoptosis and atrophy.

Benign Prostatic Hyperplasia (BPH)

(Nodular prostatic hyperplasia). Benign hypertrophy and hyperplasia of glandular tissue at transitional/peiurethral zone with proliferation of epithelial and supporting smooth muscle and stromal cells. Usually beginning in 40s eventually occuring in all men, 50% of those >50yo. Bladder outflow obstruction causes hesitancy, reduced force and caliber of stream, dribbling, frequency, nocturia, postvoid residual. Focal or diffuse nodular enlagement of prostate, low/high density nodules and heterogeneous TZ, coarse calcifications, cystic degeneration, compression of urethra and central zone, bladder wall thickening/trabeculation, uplifting of trigone, ‘J-hooking’ of distal ureters, may have pseudocapsule, bladder stones. Prostatic urethra is elongated, tortuous and compressed. Transrectal biopsy is not useful as it does not typically sample the TZ and there may be foci of reactive squamous metaplasia mimicking carcinoma. Tx of advanced symptoms with medical therapy (α-blockers), balloon dilatation, stents, transurethral resection (TURP).

Prostate Carcinoma

10% of men develop clinical prostate carcinoma in their lifetime, ~50% >75yo have carcinoma on biopsy/autopsy, uncommon <50yo. Increased risk with african descent, Western culture, age, androgens, FHx. Uncommon in Asians. 70% arises from the peripheral zone, 20% transition zone, 10% central zone. 95% adenocarcinoma (of which 5% are mucinous), others adenosquamous or pure squamous de novo or post-hormone therapy. Prostate-specific antigen (PSA) is a glycoprotein produced only by the prostate, protease for liquefication of seminal coagulum; serum levels elevated (>4ng/mL) in cancer (not raised in 30%), BPH, prostatitis, infarct, instrumentation, ejaculation. Interpretations with improved specificity include PSA-density (PSA/size of prostate), PSA-veolcity (change over time), age-specific reference ranges and ratio of free and bound serum PSA.

Transrectal US sensitivity 60%. Distinct hypoechoic nodule, poorly marginated hypoechoic area in peripheral zone (replacing normal spongy tissue), mass effect on surrounding tissues, asymmetric enlargement of the prostate, deformation of contour, heterogeneous region in otherwise homogeneous gland, focal increased vascularity in peripheral zone; findings are all nonspecific.

Transrectal US-guided biopsy (TRUS) – 6-10 18G core biopsies from different areas, always including all four quadrants; preprocedure ABs required, less painful than transperineal route. 80% also harbour high-grade prostatic intraepithelial neoplasia (PIN), presumptive precursor lesion similar to CIS. Tx surgery, radiotherapy,

Gleason histological grading – Grade 1 well differentiated, grade 5 anaplastic. Gleason score (2-10) adds Gleason grades for the predominant/most common pattern and secondary portions of tumour.

TNM staging:

  • Primary tumour
    • TX – Not assessable.
    • T0 – Not evident.
    • T1 – Not palpable or visible by imaging. T1a incidental </=5% resected tissue, T2b incidental >5% tissue, T1c elevated PSA.
    • T2 – Palpable or visible by imaging. T2a </= 1/2 of one lobe, T2b > 1/2 of one lobe, T2c involves both lobes.
    • T3 – Extracapsular. T3a uni/bi-lateral, T3b invades seminal vesicles.
    • T4 – Invasion of adjacent structures including bladder neck, rectum, external sphincter, levator muscles, pelvic floor.
  • Regional LN – N1 spread to regional nodes. Nodes are abnormal if oval and >10mm, or round and >8mm.
  • Distant metastases
    • M1a – LN beyond regional nodes.
    • M1b – To bone (commonly axial skeleton).
    • M1c – Other sites (late) including lungs, liver, kidneys.


  • Active surveillance
  • Extracopotrsl shock treatment causes haemorrhage then necrosis and scarring.
  • Radical prostatectomy – usually performed if there is extraprostatic extension or involvement of the membranous urethra. Compared to conventional prostatectomy, robotic prostatectomy has less blood loss and reduced hospital stay.
  • Radiotherapy – for extraprostatic or membranous urethra involvement.
  • Hormonal manipulation – orchidectomy, LNRH agonists. Most tumours eventual become resistant with rapid progression.

Prostate MRI

MRI can exclude significant cancer in 95%. Multiparametric MRI includes T2, DWI (with highest b-value at least 1000), dynamic ontrast enhancement (DCE) +/- spectroscopy. Gas in the rectum may cause artifactual distortion of the prostate, in which case the phase encoding gradient should be changed from AP to LR. The higher b-values are better for conspicuity of the tumour, computed DWI values can be done for higher values.


Normal appearances:

  • Peripheral zone (PZ) homogeneous high T2 signal peripheral zone. May have small low T2 foci adjacent to the neurovascular buldles or posterior midline at the apex, with minimal restriction, but no increased perfusion or mass effect.
  • Transition zone (TZ) surrounds prostatic urethra, in BPH has well-circumscribed nodules, which may herniate into the central/peripheral zones. There may be a T2 hypointense (lower signal than Ca) at the anterior aspect of TZ ( = fibromucular stroma).
  • Central zone (CZ) surrounds ejaculatory ducts to the verumontanum, which may have surrounding T2 hypointensity from glands, normal as long as the ducts have normal appearance (no mass effect/invasion).
  • Venous plexus anterior to the gland and surrounding the apex.
  • Membranous urethra (external urethral sphincter) has now T2 inferiorly adjacent to the apex. If <16mm in length, this increases the risk of postsurgical incontinence.
  • Neurovascular bundles (cluster of nerves/vessels rather than a single structure) extend from posterolateral to the gland to the apex. May have small foci of T2 hypointensity and mild restriction at the adjacent peripheral zone. Try to wait at least 8 weeks after biopsy, which causes T1 hyperintense haemorrhage and heterogeneity. The highest grade nodule is the one that metastasizes. Most of the cancers missed on biopsy include the anterior and apical gland.

Features of cancer:

  • T2 – Cancers in the TZ may have have a scimitar/comma-shaped T2 hypointensity anteriorly. May be wedge-shaped if small, but very unusual if large.
  • T1 – Isointense. May have post-biopsy haemorrhagic sparing of the nodule.
  • DWI – Higher signal corresponds to increased cellularity. Not as useful in the TZ.
  • Extracapsular invasion – focal bulge, spiculated contour, obliteration of rectoprostatic angle, >15mm capsular contact. May have neurovascular bundle extension.
  • Seminial vesicle invasion usually after invasion of the ejaculatory duct. Seminal vesicles may be empty in older patients, making it harder to detect invasion. Invasion should have associated diffusion restriction.


  • Granulomatous prostatitis – focal low T2 and mild restriction, but no perfusion (cf Ca).
  • Post-biopsy haemorrhage – high T1 signal.
  • Postatitis – wedge-shaped/ill-defined low T2 signal with mild restriction, extensinvely increased perfusion.


  • Acute bacterial prostatitis – Usually organisms that cause UTIs (E.coli etc), usually intraprostatic reflux of urine from the posterior urethra; occasionally lymphohaematogenous spread or post-isntrumentation. Swelling with small disseminated abscess, large coalescent abscess or diffuse oedema. Prostatic abscess – Focal echogenic fluid within gland ± septations. Biopsy may cause sepsis.
  • Chronic bacterial prostatitis – Incompletely resolved acute prostatitis or insidious infection, recurrent UTIs with the same organisms. Antibiotics have poor penetration of the prostatic parenchyma. Large prostatic calculi are common, serving as a reservoir for persisting/relapsing infection. Calculi may form spontaneously or from chronic inflammation, most periurethral, not associated with malignancy.
  • Chronic abacterial prostitis – Most common prostatitis, indistinguishable from chronic bacterial prostatitis but no recurrent UTIs.
  • Granulomatous prostatitis – Specific (infectious aetiology) or nonspecific. Most from bladder BCG installation for superficial bladder cancer; no clinical significance. Fungal usually only seen in immunocompromised. Nonspecific from reaction to secretions from ruptured prostatic ducts/acini.

Ejaculatory Duct Obstruction

Uncommon, treatable cause of infertility. From congenital obstruction, urethritis or instrumentation. Normal ducts not seen on transrectal US. Obstruction -> cyst posterior to prostatic urethra associated with dilatation of seminal vesicles. Tx aspiration or surgical resection of the obstructing cyst.

Male Urethra

Normal filling of Cowpers ducts and utricle is occasionally seen on urethrography, but is more common with strictures. Visualisation of glands of Littre (anterior urethra) and prostatic ducts are abnormal, associated with prostatitis or distal urethral stricture.


Retrograde/ascending urethrogram – LA gel into penis, 10F ribbed balloon Foley catheter with air/saline in balloon in navicular fossa, XII angled opposite direction to urethra. Oblique fluoroscopy and exposures with constant pressure of 50/50 urograffin. If already catheterised a small 8Fr feeding tube can be inserted alongside. Contast instillation distends anterior urethra fully due to resistance from external sphincter (urogenital diaphragm), but posterior urethra runs freely into bladder.

Voiding/micturiting/antegrade/descending urethragram – Partially fill bladder until feels like voiding then remove catheter. Tilt table/erect ± run tap. Oblique fluoroscopy and exposures while micturiting. Voiding distends both posterior and anterior urethra.

Urethral Stricture

Narrowings from fibrous scar. Abrupt short-segment usually traumatic; long-segment traumatic or inflammatory. Trauma from instrumentation, IDUC, prostatectomy, chemical injury (podophyllin for HPV), straddle injury (bulbous urethra), pelvic fracture. Urethritis is gonococcal (most) or nongonococcal (chlamydia, mycoplasma, E.coli, TB, schistosomiasis; may be associated with Rieter syndrome) with bacteria in glands of Littre inducing granulation tissue and fibrosis. Complications include:

  • False passage – Usually iatrogenic from attempted catheterisation.
  • Periurethral abscess – Usually ventral.
  • Proximal stasis with infection, hydronephrosis, stones.
  • Carcinoma – Most SCC in anterior urethra from chronic urethritis. Filling defect or change in stricture appearance.

Urethral Diverticula

Smooth outpouchings. Congenital or from infection, trauma. Stasis increases risk of stones, recurrent infection.

Urethral Carcinoma

Uncommon. Proximal tumours usually urothelial similar to bladder, distal tumours usually SCC.

Urethral Trauma

Posterior urethral injury in 10% of pelvic fractures esp junction of prostatic and membranous urethra. Stradle injury usually injures the bulbous urethra. Retrograde urethrography should be done prior to catheterisation. Complications are common, including stricture, incontinence, impotence, pelvic and perineal sinus tracts and fistulas. Posterior urethra injury types:

  • Type 1 – Stretch by haematoma.
  • Type 2 – Rupture at apex of prostate with extravasation above the urogenital diaphragm.
  • Type 3 – Rupture of both membranous and bulbous urethra with extravasation above and below the diaphragm.


Peyronie Disease

Fibrous bands in corpus cavernosum, variant of fibromatosis causing penile curvature.

Hypospadias and Epispadias

Malformation fo the urethral groove with a abnormal opening on the ventral (hypospadias) or dorsal (epispadias) surface. Opening is usually small causing a degree of obstruction.


Prepuse orifice too small, inhibiting normal traction. Most from recurrent infection causing scarring. Incresed risk of infection and carcinoma.


  • Condyloma acuminatum – Benign epithelial tumour, sexually transmitted from HPV. Single or multiple, sessile or pedunculated on external genitalia or perineal areas.
  • Bowen disease – SCC in situ, usually >35yo. Associated with HPV. Males usually shaft of penis and scrotum as a plaque. Also occurs in women. Develops into infiltrating SCC in 10%.
  • Bowenoid papulosis – Younger age, multiple lesions, associated with HPV. Most spontaneously regress, almost never develops into carcinoma.
  • Invasive SCC – Uncommon, reduced risk with circumcision ?due to reduced exposure to carcinogens. Increased risk with HPV (16 or 18), smoking, 40-60yo. Usually begins on glans or inner prepuce. Slow growing.