Testicular Tumors and

Tumor-like Lesions:
Radiologic-Pathologic
Correlation

From the Archives of the AFIP. Radiographics. 2002;22:189-216

Testicular Neoplasia
 Testicular carcinoma most common malignancy- 15–34 year.
 Testicular tumors categorized into germ & non–germ cell tumors.
 Non-primary tumors as lymphoma, leukemia & metastases can manifest as
testicular masses.
 Peak prevalence of testicular tumors
 25–35 years.
 71–90 years- lymphoma & metastasis.
 Infants, with rapid decline to nadir for boys 10 years of age.
 Survival rates for patients with testicular carcinoma 95%.
Testicular Neoplasia- Presentations

 Painless scrotal mass.

 Heaviness or fullness in lower abdomen or scrotum.
 Pain in 10%- misdiagnosed as orchitis.
 Tumors may undergo regression, necrosis & scarring “burned-out germ cell
tumors”- normal or small testes at presentation.
 Burned-out germ cell tumors & tumors with aggressive histology may
present with metastases.
 Hormonally active tumors- endocrine abnormalities, commonly
gynecomastia.
Embryologic Development

 No morphologic sexual differentiation until 7th W-

indifferent stage.
 Undifferentiated gonad- 3 cell types: mesenchyme,
mesothelium & germ cells.
 During indifferent stage, genital ridges form on both
sides of midline from mesenchyme condensation & are
covered by mesothelium-Subsequent proliferation forms
primitive sex cords.
 Primordial germ cells form in wall of yolk sac, then
migrate along hindgut to be incorporated into primitive
sex cords.
Embryologic Development
 Y chromosome- undifferentiated gonad into testis.
 Primitive sex cords form seminiferous tubules from
2 cell lines:
 Mesothelium- Sertoli cells.
 Migrated germ cells- spermatogonia.
 Mesenchyme between seminiferous tubules- Leydig
cells.
 Tunica albuginea forms.
 At 8 weeks, Leydig cells secrete testosterone-
mesonephric (wolffian) ducts differentiate into
epididymis, vas deferens, seminal vesicles &
ejaculatory ducts.
 Embryologic Development

 Between 7th & 12th weeks, testes contract and

become more ovoid as they descend into pelvis.
 Until 7th month, near deep inguinal ring, when they
begin descent through inguinal canal into twin
scrotal sacs.
Anatomy & Histologic Characteristics
 Tunica albuginea covered by tunica vaginalis.
 Densely packed seminiferous tubules- tubuli
recti- rete testis at hilum.
 Rete testis converges posteriorly to form 15–20
efferent ductules that penetrate through
tunica albuginea “Mediastinum testis” to form
head of epididymis.
 Efferent ductules converge to form single
convoluted tubule- exits epididymis as vas
deferens.
Anatomy & Histologic Characteristics

 200–300 lobules- each 400–600 seminiferous

tubules.
 Interstitium: between seminiferous tubules-
connective tissue, lymphatics, blood vessels, mast
cells & Leydig cells.
 Seminiferous tubules- two cell types:
 Germ cells: spermatogenic germ cells.
 Sertoli cells:
 Support for maturing germ cells+ phagocytosis of
degenerating germ cells.
 Tight junctions- blood-testis barrier.
 Leydig cells: testosterone production.
 T0 = No evidence of Tumor
 T1s = Intratubular, pre invasive
 T1 = Confined to Testis
 T2 = Invades beyond Tunica Albuginea or into Epididymis
 T3 = Invades Spermatic Cord
 T4 = Invades Scrotum

 N1 = Single < 2 cm
 N2 = Multiple < 5 cm / Single 2-5 cm
 N3 = Any node > 5 cm
 Imaging- Ultrasonography
 100% sensitive  Intra- versus extra-testicular- cystic or solid.
 High frequency transducer with adequate penetration- 5–10 MHz.
 Homogeneous, medium-level, granular echotexture.
 Tunica albuginea not seen separately- echogenic line mediastinum testis.
 Epididymis: iso- or slightly hyperechoic to testis.
Imaging- Ultrasonography
 Solid testicular masses- malignant.
 Most testicular tumors hypoechoic- heterogeneous, with increased
echogenicity, calcifications & cysts.
 Larger tumors more vascular.
 Color Doppler: prepubertal with subtle gray-scale findings.
 MRI: problem solving tool when US inconclusive + cryptorchidism.
 Imaging- MRI
 Surface coil- superior signal-to-noise ratios.
 Patient supine- towel under scrotum- penis on
abdomen- warm towel draped over scrotum with
coil on it.
 Suspected cryptorchidism- abdomen & pelvis.
 Axial & coronal SE T1- WI.
 Axial, coronal & sagittal FSE T2- WI
 Superior & inferior saturation bands  eliminate
ghosting artifacts.
 Gadolinium- indeterminate scrotal masses.
 For staging, axial T1- WI of abdomen 
adenopathy.
Imaging- MRI
 Homogeneous intermediate signal on T1-WI &
high signal “< fluid” on T2-WI.
 Tunica albuginea- thin low-signal band.
 Internal architecture on T2- WI thin low-
signal septa radiating back toward mediastinum
testis which forms band along posterior margin
of testis.
 Epididymis: iso- or slightly hypointense relative
to testis on T1- WI & hypointense on T2- WI.
 Germ Cell Tumors- Pathogenesis
 Intratubular germ cell neoplasia precursor of most germ cell tumors-
equivalent of carcinoma in situ- 50% develop invasive tumor in 5 years.
 Abnormal cells develop either along:
 Unipotential gonadal line- seminoma
 Totipotential cell line- non-seminomatous tumors
 Largely undifferentiated- embryonal carcinoma.
 Extra-embryonic differentiation- yolk sac tumors, choriocarcinoma.
 Embryonic differentiation- teratoma.
 Mixed germ cell tumor.
 Seminomatous & non-seminomatous germ cell tumors.
Germ Cell Tumors- Spread
 Lymphatic- hematogenous- direct.
 Most germ cell tumors spread via lymphatics
except choriocarcinoma.
 Lymphatic involvement in step-wise fashion- basis
for modern surgery-dissections of
retroperitoneal nodes spare sympathetic nerves
involved in antegrade ejaculation.
 Testicular lymphatic drainage follows testicular
veins
Right: interaortocaval chain at L2.
Left: left paraaortic nodes bounded by renal vein,
aorta, ureter, IMA.
Germ Cell Tumors- Spread

 Crossover of lymphatic involvement in right-to-

left fashion.
 Left-to-right crossover rare.
 As tumor volume increases- spread from first-
echelon nodes to common, internal & external
iliac nodes.
 Tumor within epididymis can spread directly to
external iliac nodes.
 Skin involvement may directly spread to inguinal
nodes- transscrotal orchiectomy
contraindicated- inguinal approach.
Germ Cell Tumors- Spread
 Hematogenous spread late for any germ cell tumor- primary mode for
choriocarcinoma.
 Pulmonary metastases most common- liver, brain & bone.
 Brain metastases common with choriocarcinoma.
 Metastases may have histologic characteristics different from
primary tumor- totipotential nature of germ cells.
 TNM classification: local tumor extent, lymph node size, distant
metastases & serum markers.
 Low-stage: tumors confined to testis, epididymis, or spermatic cord
(T1–T3) - mild to moderate adenopathy (N1 & N2).
 Advanced-stage: tumors invading scrotal wall (T4), significant
retroperitoneal adenopathy (N3), or visceral metastases (M1).
Germ Cell Tumors- Tumor Markers
 Alpha-fetoprotein: protein produced early in gestation by liver, GIT, &
yolk sac- elevated in yolk sac tumors & mixed germ cell tumors with yolk
sac elements- rarely teratomas with enteric mucous glands or hepatoid
cells.
 Human chorionic gonadotropin: glycoprotein produced by
syncytiotrophoblasts- level elevated in tumors containing
syncytiotrophoblasts “seminomas or choriocarcinomas”.
Elevated in > 80% non-seminomatous germ cell tumors.
Serial serum levels quantify response to treatment & predict
recurrence.
 Lactate dehydrogenase: produced by multiple organs- < specific.
Germ Cell Tumors- Pathogenesis

 Unipotential gonadal line- seminoma.

 Totipotential cell line- non-seminomatous tumors.

 Largely undifferentiated- embryonal carcinoma.

 Embryonic differentiation- teratoma.

 Extra-embryonic differentiation- yolk sac tumors, choriocarcinoma.

 Mixed germ cell tumor.

Germ Cell Tumors- Seminoma

 35%–50% of all germ cell tumors.

 15% have syncytiotrophoblasts.
 Seminomas
Average 40 Y.
75% limited to testis.
20% retroperitoneal adenopathy.
5% extranodal metastases.
 Small well-defined lesion to large
masses replacing testicle.
 Histology: resembles primitive germ
cells + lymphoid infiltrate.
Germ Cell Tumors- Seminoma- Imaging
 Reflect uniform cellular nature.
 US: uniformly hypoechoic.
 MRI: T2 homogeneous hypointense-
larger tumors heterogeneous.
 Lobulated or multinodular- nodules
commonly in continuity- rarely true
multifocal nodules.
 Bilateral tumors in 2% of patients,
always asynchronous.
Germ Cell Tumors- Seminoma
Germ Cell Tumors- Pathogenesis

 Unipotential gonadal line- seminoma.

 Totipotential cell line- non-seminomatous tumors.

 Largely undifferentiated- embryonal carcinoma.

 Extra-embryonic differentiation- yolk sac tumors, choriocarcinoma.

 Embryonic differentiation- teratoma.

 Mixed germ cell tumor.

Non- Seminomatous Germ Cell Tumors-
Embryonal Carcinoma
 Primitive anaplastic epithelial cells resembling early
embryonic cells.
 Second most common histologic type.
 Pure form 2%–3% of testicular tumors- 87% of mixed
germ cell tumors.
 25–35 years.
 Often smaller than seminoma at presentation but more
aggressive.
Tunica albuginea may be invaded- tumor borders less
distinct, blending into adjacent parenchyma.
 US: > heterogeneous & ill-defined than seminomas.
Non- Seminomatous Germ Cell Tumors-
Embryonal Carcinoma
Germ Cell Tumors- Pathogenesis

 Unipotential gonadal line- seminoma.

 Totipotential cell line- non-seminomatous tumors.

 Largely undifferentiated- embryonal carcinoma.

 Extra-embryonic differentiation- yolk sac tumors,

choriocarcinoma.
 Embryonic differentiation- teratoma.

 Mixed germ cell tumor.

Non- Seminomatous Germ Cell
Tumors- Yolk Sac Tumor
 Endodermal sinus tumors.
 80% of childhood testicular tumors- before 2Y.
 Pure form rare in adults- 44% of adult mixed germ
cell tumor.
 Alpha-fetoprotein elevated in > 90%.
 Imaging non-specific, especially in children-
testicular enlargement with no defined mass.
 Treatment- adults= non-seminomatous tumors.
 Treatment- Pediatric: tumor confined to testis +
alpha-fetoprotein not elevated- orchiectomy +close
monitoring. Relapse, chemotherapy.
Non- Seminomatous Germ Cell
Tumors- Choriocarcinoma
 Rare- pure form < 1% of patients- 8% of mixed
germ cell tumors.
 2nd & 3rd decades.
 Highly malignant- cyto- & syncytiotrophoblasts.
 US: isoechoic +/- invasion of tunica albuginea.
 Early widespread metastasis- lung, liver, GIT &
brain- Primary & metastases hemorrhagic.
 Elevated HCG- gynecomastia in 10%.
 Death within 1 year- Mixed germ cell tumors with
choriocarcinoma of better prognosis.
 Very high HCG-poor prognosis.
Non- Seminomatous Germ Cell Tumors-
Choriocarcinoma
Germ Cell Tumors- Pathogenesis

 Unipotential gonadal line- seminoma.

 Totipotential cell line- non-seminomatous tumors.

 Largely undifferentiated- embryonal carcinoma.

 Extra-embryonic differentiation- yolk sac tumors, choriocarcinoma.

 Embryonic differentiation- teratoma.

 Mixed germ cell tumor.

Non- Seminomatous Germ Cell
Tumors- Teratoma
 2nd after yolk sac tumor in children<4 Y.
 Pure form rare in adults- 50% of adult mixed germ
cell tumor.
 Complex- disorderly arrangement of adult & fetal
tissues, with 3 germ layers “endoderm, mesoderm,
& ectoderm” involved.
 Sub-classified into mature, immature & with
malignant areas.
 Dermoids, most common teratomatous lesion in
ovary- minority of testicular teratomas.
Non- Seminomatous Germ Cell Tumors-
Teratoma
 Complexity reflected in US appearance- complex well-circumscribed
masses; anechoic or complex cysts, cartilage, calcification & fibrosis.
 Biologic behavior depending on pubertal status.
 Pre-pubertal- pure teratomas benign even histologically immature.
 Postpubertal- mature or immature can metastasize- metastases may
contain non-teratomatous germ cell elements.
 Mature teratoma not equated with benignity.
Non- Seminomatous Germ Cell Tumors-
Teratoma
Non- Seminomatous Germ Cell Tumors-
Epidermoid Cysts
 Monodermal development of teratoma, or
squamous metaplasia of surface mesothelium.
 1% of testicular tumors.
 Keratinizing, stratified, squamous epithelium
with defined fibrous wall- benign with no
malignant potential.
 Although pathologically true cysts- filled with
cheesy laminated material that appears solid on
imaging.
Non- Seminomatous Germ Cell Tumors-
Epidermoid Cysts
 Laminated morphology reflected in imaging.
 US:
 Well-circumscribed, round to oval mass
with hyperechoic wall +/- calcified.
 May be hypoechoic.
 Laminations- onion-skin; ringed appearance.
 MRI: "target" appearance, with low-signal
capsule. Layers of keratinized material
within lesion rich in water & lipid- areas of
high signal.
Non- Seminomatous Germ Cell Tumors-
Epidermoid Cysts
 Radiologic appearance characteristic & not pathognomonic- Teratomas
& other malignant tumors.
 Irregular border suggest malignancy.
 As carcinoma cannot be completely excluded, orchiectomy performed.
 If strong likelihood of epidermoid cyst, testis-sparing enucleation.
Germ Cell Tumors- Pathogenesis

 Unipotential gonadal line- seminoma.

 Totipotential cell line- non-seminomatous tumors.

 Largely undifferentiated- embryonal carcinoma.

 Extra-embryonic differentiation- yolk sac tumors, choriocarcinoma.

 Embryonic differentiation- teratoma.

 Mixed germ cell tumor.

Non- Seminomatous Germ Cell Tumors- Mixed
Germ Cell Tumor
 Contain > one germ cell component.
 Of non-seminomatous germ cell tumors, mixed germ cell tumors much
> than any pure histologic forms- 32%–60% of all germ cell tumors.
 Any combination of cell types- embryonal carcinoma most common
component.
 Age of presentation 30 Y.
 Imaging findings variable, reflecting diversity.
 Non-seminomatous tumors not radiosensitive as seminomas-
chemotherapy rather than radiation therapy
 Non- Seminomatous Germ Cell Tumors-
Mixed Germ Cell Tumor
 After treatment, CT often show decrease in
attenuation & size of retroperitoneal masses-
typically interpreted as necrosis-Evolution into
more benign histologic type.
 Resected treated masses- 40% necrosis or
fibrosis- 40% mature teratoma- 20% areas of
residual tumor.
 Mass containing only mature teratoma should be
resected- mature teratoma can grow despite
benign histology “growing teratoma syndrome”, or
transform to more aggressive type.
Non- Seminomatous Germ Cell Tumors-
Regressed Germ Cell Tumors

 = "burned-out" germ cell tumor.

 Metastases though primary involuted.
 Pathogenesis: high metabolic rate of tumor
causes it to rapidly outgrow its blood supply.
 Clinically occult- testis normal to small.
 US: search for primary regressed tumor-
variable appearance; small, can be hypo-,
hyperechoic or focal calcification.
 Histology: minute amounts of residual tumor
or dense deposits of collagen.
 Seminoma Embryonal Carcinoma

Yolk sac tumor Choriocarcinoma Teratoma

Epidermoid cyst Regressed germ cell tumor

Germ Cell Tumors- DDx- Primary Extragonadal
Germ Cell Tumors
 Retroperitoneum, mediastinum, sacrococcygeal area & pineal gland-
differentiate from regressed germ cell tumor with metastasis.
 Pathogenesis:
 Aberrant migration of germ cells from yolk sac.
 Persistent pluripotential cells in primitive rests during somatic
development.
 In retroperitoneal germ cell tumor, consider metastatic disease as
retroperitoneal germ cell tumors are likely of testicular origin rather
than primary- Testes thoroughly evaluated.
Testicular Carcinoma- Risk Factors
 Prior testicular tumor: risk of contralateral tumor > 20 times.
 Positive family history: Testicular carcinoma in first-degree relative
increases risk factor six times.
 Infertility:  
 Cryptorchidism & gonadal dysgenesis implicated in both.
 Biopsies of subfertile men- intratubular germ cell neoplasia.
 Patients with testicular carcinoma- higher serum antisperm antibodies
& 25% have defective spermatogenesis.
 Intersex syndromes: gonadal dysgenesis, true hermaphroditism &
pseudohermaphroditism.
 Cryptorchidism
Testicular Carcinoma- Risk
Factors- Cryptorchidism
 Incomplete descent of testicles to scrotum-
6% term infants- majority distal to external
inguinal ring & palpable- descend into scrotum
by 1 year.
 Non-palpable testicles usually within inguinal
canal- anywhere along path of descent- 15%–
63% agenetic.
 MRI: localizing non-palpable undescended
testes + differentiating from agenesis.
 Gadolinium-enhanced venography: agenesis
from ectopia.
Testicular Carcinoma- Risk
Factors- Cryptorchidism
 Cryptorchidism in 3.5%–14.5% of patients with
testicular carcinoma.
 Pathogenesis: cryptorchidism manifestation of
generalized embryogenesis defect that results in
bilateral dysgenetic gonads.
 Risk for testicular carcinoma in contralateral testis,
even normally descended
 Orchiopexy does not decrease risk of tumor.
 Risk of carcinoma increases with degree of ectopy.
 Seminomas, especially abdominally.
Testicular Microlithiasis

 Relatively uncommon- 0.6% of patients.

 Historically, innocuous incidental finding.
 Associations: cryptorchidism, infertility,
Klinefelter syndrome, Down syndrome,
atrophy, alveolar microlithiasis, and, most
important, testicular carcinoma.
 Sertoli cells: phagocytosis of degenerated
intratubular debris- defective activity.
 Histopathology- laminated concretions
within lumen of seminiferous tubules.
 Prevalence of carcinoma- 40%.
Testicular Microlithiasis

 Microcalcifications result from abnormal

testis- microcalcifications incite damage.
 Rule out mass.
 Compelling questions:
What is risk of developing cancer?
How closely should patients be followed?

Cast JE. Testicular microlithiasis: prevalence and tumor risk in a population referred
for scrotal sonography. AJR; 175:1703-6.
Ganem JP. Testicular microlithiasis is associated with testicular pathology. Urology;
53:209-13.
Furness PD. Multi-institutional study of testicular microlithiasis in childhood: a benign
or premalignant condition?. J Urol; 160:1151-4.
Gooding GA. Detection of testicular microlithiasis by sonography. AJR; 168:281-2.
Non–Germ Cell Tumors- Sex Cord, Stromal &
Sex Cord–Stromal–Germ Cell Tumors

 Leydig cell tumors.

 Sertoli cell tumors.
 Granulose cell tumors.
 Fibroma- thecomas.
 Sex cord– stromal tumors.
 Sex cord– stromal– germ Cell tumors.
Non–Germ Cell Tumors- Sex Cord, Stromal &
Sex Cord–Stromal–Germ Cell Tumors

 4% of testicular tumors from cells forming sex cords “Sertoli cells” &
interstitial stroma “Leydig cells”.
 Higher in pediatric- 10%–30% of testicular neoplasms.
 90% of non–germ cell tumors benign.
 No radiologic criteria differentiating benign from malignant.
 Even histologically, difficult to determine biologic behavior.
 Tumors without aggressive histology may metastasize.
Non–Germ Cell Tumors- Leydig Cell Tumors
 1%–3% of testicular tumors.
 Any age group.
 30% have endocrinopathy secondary to androgens or estrogens-
precocious virilization, gynecomastia, or decreased libido.
 Small solid masses- may show cystic areas, haemorrhage, or necrosis.
 Sonographic appearance variable & indistinguishable from germ cell
tumors.
Non–Germ Cell Tumors- Sertoli
Cell Tumors
 < 1% of testicular tumors.
 Less likely hormonally active.
 Typically well-circumscribed, unilateral, round to
lobulated masses.
 Large-cell calcifying Sertoli cell tumor:
 Pediatric age group.
 Multiple & bilateral masses- large areas of
calcification.
 Association: Peutz-Jeghers & Carney syndromes.
 Testicular Microlithiasis
Epiderrmoid cyst

Sertoli Cell Tumors

Regressed Germ Cell Tumor

Non–Germ Cell Tumors-Gonadoblastoma

 Category containing both sex cord–stromal elements & germ cells.

 Occur with gonadal dysgenesis & intersex syndromes.
 80% phenotypically female.
Lymphoma
 Primary- manifestation of occult disease- site of recurrence.
 5% of testicular tumors- < 1% of lymphoma patients.
 Most common bilateral testicular tumor- synchronous or metachronous.
 Epididymis & spermatic cord involved.
 B-cell lymphomas- diffuse large cell.
 Discrete hypoechoic lesions- may completely infiltrate testicle.
Leukaemia

 Primary leukemia of testis- rare.

 Testis common site of leukemia recurrence in children, with 80% in
bone marrow remission.
 Blood-testis barrier allows leukemic cells to be "hidden" during
chemotherapy.
 Clinical characteristics & sonographic appearance quite varied, as
tumors may be unilateral or bilateral, diffuse or focal, hypo- or
hyperechoic.
Metastases
 Other than from lymphoma & leukaemia- rare.
 Prostate & lung cancer.
 Generally with widespread disease & rarely presenting complaint.
 Tumor-like Lesions

 Orchitis- hemorrhage- ischemia or infarction.

 Ill defined than tumors, with overlap in US appearances.
 Clinical presentation key- acute scrotum.
 Be cautious, since tumors can manifest with pain- dull ache.
 US findings of hemorrhage & orchitis evolve rapidly.
 Granulomatous orchitis
 More indolent course- can manifest as testicular mass
 TB, syphilis, fungi & parasites- granulomatous epididymo-orchitis.
 Epididymis first > testis.
 Isolated testicular mass extremely unusual.
Tumor-like Lesions- Tubular Ectasia of Rete
Testis
 Normal variant- mistaken for neoplasm.
 2ry to obstruction in epididymis or efferent
ductules.
 Posteriorly by mediastinum- composed of series
of dilated tubules.
 US: resemble hypoechoic mass in cross section-
careful scanning shows series of dilated tubules-
often bilateral- frequently spermatocele.
 MRI: hypointense on T1- WI & iso- to
hyperintense on T2- WI.
 Diagnosis prevent orchiectomy.
Tumor-like Lesions- Testicular Cysts

 8%–10% of patients.
 Tunica albuginea or parenchyma.
 Cause of tunica albuginea cysts:
 Fluid within small mesothelial rests.
 Fluid in blind-ending efferent ductules.
 Tunica albuginea cysts peripherally
located & may be single or multiple.
 Classic location & appearance makes
diagnosis straightforward.
Tumor-like Lesions- Testicular Cysts

 Intratesticular cysts problematic- DDx

cystic neoplasms, typically teratomas.
 Cystic lesion with solid components-
consider malignant.
 Benign cysts incidental & not palpable.
 Usually near mediastinum testis-
originate from rete testis.
 Dilated rete testis- not uncommon.
Tumor-like Lesions- Adrenal
Rests
 Rare- with congenital adrenal hyperplasia &
rarely Cushing syndrome.
 Aberrant adrenal rests trapped in developing
gonad.
 Usually < 5 mm- testis & surrounding tissues in
7.5%–15% of newborns & 1.6% of adults.
 Typically multiple, bilateral & eccentric.
 Elevated levels of ACTH- masses.
 Treatment: glucocorticoids- stabilization or
regression of masses.
Tumor-like Lesions- Adrenal
Rests
 US: variable- predominantly hypoechoic masses-
heterogeneously hyperechoic with shadowing.
 MRI: low signal on T1- & T2- WI.
 If there is question about diagnosis  testicular
vein sampling show elevated cortisol levels
compared with peripheral blood levels.
Tumor-like Lesions- Sarcoidosis

 Chronic granulomatous disease- 5% genital

involvement.
 Testicular sarcoidosis more common in
African-Americans.
 Epididymis > testis.
 Testicular lesions can be solitary- typically
multiple, small, bilateral masses.
Fournier Gangrene
 =necrotizing fasciitis- rapidly progressive fasciitis of perineum-
described in 1883 by Jean Alfred Fournier, a French venereologist*.
 Most cases occur in diabetic men 50–70 years old- described in women.
 Often there is point of entry (i.e., urethral, rectal, or subcutaneous
tissue) by polymicroorganisms- rate of fascial necrosis 2–3 cm/h.
 Most commonly isolated organisms: Klebsiella, Proteus, Streptococcus,
Staphylococcus, Peptostreptococcus, and Escherichia coli- soft-tissue
gas comes from by-products of anaerobic metabolism.
 Sudden perineal & and swelling + fever & leukocytosis- examination
reveals pain, redness & swelling of perineal area- sometimes crepitus.
 Treatment: immediate radical débridement of all necrotic areas.

Fournier JA. Gangrène foudroyante de la verge. Semaine Medecine 1883; 3:345-348.

Fournier Gangrene
 Radiography: soft-tissue edema of perineal tissues- subcutaneous
emphysema may be seen tracking along extent of involved tissue planes.
 US: thickened scrotal skin- gas within scrotal skin, seen as hyperechoic
foci with dirty shadowing “ pathognomonic”- hyperechoic foci not within
testicle and should not be confused with calcifications of testicular
microlithiasis, germ cell tumors, teratomas, teratocarcinomas,
sarcoidosis, tuberculosis, or chronic infarct- testicle often normal
because of separate blood supply.
 CT: fascial thickening and fat stranding of involved areas- CT can more
completely depict extent of soft-tissue gas and can often show cause
of Fournier gangrene, such as perianal abscesses, incarcerated inguinal
hernias, or fistulous tracts.
Fournier Gangrene

 Differential diagnosis for acute scrotal pain: testicular trauma,

testicular torsion, acute epididymo-orchitis, and Fournier gangrene.
 Testicular trauma (blunt or penetrating) distinguished from Fournier
gangrene based on history and physical evidence of trauma.
 Although testicular torsion and acute epididymo-orchitis can manifest
with acute scrotal pain without history of trauma and examination can
show swollen, erythematous scrotum, color Doppler flow US can help
distinguish between these diagnoses
 Testicular torsion: Color Doppler US 86% sensitive in showing absent
testicular and epididymal flow.
 Acute epididymo-orchitis: increased epididymal and/or testicular flow.
Fournier Gangrene
THANK YOU