TESTICULAR TUMOURS PREVALANCE 99% of testicular tumours are malignant. Life time prevalence of getting testicular tumour is 0.2%. Very common in Scandinavia; least common inAfrica andAsia. 4 times common in whites than blacks.

1. en love da Homoeopathy
TESTICULAR
TUMOURS

2. TESTICULAR
TUMOURS

3. TESTICULAR TUMOURS
PREVALANCE
• 99%of testicular tumours
are malignant.
• Life time prevalence of
getting testicular tumour is
0.2%.
• Verycommonin
Scandinavia; least common
inAfricaandAsia.
• 4 times common in whites
than blacks.

4. PRE-DISPOSINGFACTORS
• Undescendedtestis and
testicular atrophy
• Cryptorchidism—it is
probably due to abnormal
germcell agenesis, gonadal
dysgenesis, rise in
temperature, change in
blood supply and endocrine
dysfunction.
• Klinefelter’s syndrome—
testicular atrophy, absence
of spermatogenesis, eunuch,
gynaecomastia—features.
• Thesepatients are prone to
seminoma testis.
• Testicular atrophy.
CLASSIFICATION
Classification
• Seminoma—40%
• Teratoma—32%3.
• Seminoma + teratoma—
14%4.
• Interstitial tumours—1.5%
[Leydig cell tumour
(musculinises), Sertoli cell
tumour (feminises)]
• Lymphomas—7%6.

5. Histological Classification
Germcell tumour
• Seminomatous—classic
• spermatocytic
• anaplastic.
Nonseminomatous type—
embryonal carcinoma
• teratomas
• choriocarcinoma
• yolk sac tumour
(endodermal sinus tumour
contains Schiller-Duval
bodies).
Nongermcell tumour
• Sex cordstromal
tumours—Leydig cell
tumour
• Sertoli cell tumour
• granulosa cell tumour.

6. Combined germcell and
gonadal stromal tumour—
gonadoblastoma.
• Miscellaneous tumours:
• Adenocarcinomaof rete
testis
• mesenchymal neoplasm.
• Adnexal and paratesticular
tumours—mesothelioma;
sarcomas.
• Others—carcinoids;
lymphomas.
• Secondaries.
SEMINOMA
• Seminoma Testis
• Starts in the mediastinum
of testis and lower pole.
GROSSAPPEARANCE
• Grosslyit is lobulated,
fleshy, homogeneous,
creamy or pinkishin
colour and it compresses
adjacenttesticular tissue.
HISTOLOGICAL
APPEARANCE
• Histologically, malignant
cells resemble
spermatocytes

7. • whichare cellscontaining
clear cytoplasmwith large
nucleus
• and are arranged in sheets
with fibrous stroma
• in between which is in turn
infiltratedby lymphocytes.
SPREAD
• It spreads throughtesticular
lymphatics into the para-
aortic lymphnodes and then
to left supraclavicular lymph
node.
• Throughblood, it spreads to
lungs, bone, brain, liver.
TYPES
• Typical/classic form—it is
most common type; occurs
in middle age;
syncytiotrophoblastic type
(15%) occurs and produces
highlevels of betaHCG.
• Spermatocyticseminoma—
occurs in older people with
different phases of
spermatogonia. Spreadin
this type is very rare.

8. • Anaplastic typehas got high
mitoticindex/nuclear
pleomorphism/ anaplasia
with highpotentiality to
spread.
• Atypical formof seminoma
shows cytoplasmic
expression of low molecular
weight keratin type 1
precursor to blood group
antigen where typical
seminoma stains negative.
TERATOMA
• It arises fromtotipotent
cells, i.e. ecto, meso,
endoderms.
GROSSAPPEARANCE
• Grosslytumour surfaceis
irregular, cut section shows
solid and cysticspaces with
areas of haemorrhage. It
often contains gelatinous
fluid and cartilaginous
nodules.

9. SPREAD
• Teratoma spreads mainly
through blood, less
commonly through
lymphatics.
TYPES
• Mature
• Immature
• choriocarcinoma or
• mixedgermcell tumour.
TYPES– Histologically
4 Types
1. Teratoma differentiated(1%)
2. Teratoma intermediate (30%)
common–
• Type A contains
matured cells
• but type B is
more malignant
consisting of less
proper
differentiated
tissues.

10. 3. Teratoma anaplastic (15%)
– Secretes alpha-fetoprotein
(AFP)
4. Teratoma trophoblastic
(1%) It shows highlevelsof
beta-HCG(normal level is100
IU)
INTERSTITIALTUMOUR
1. Leydig cell tumour (2%):
• Masculinises.
• Prepubertal tumour shows
excessive output of
androgens
• causing sexual precocity,
extrememuscular
development often
mimicking infant hercules.
• They are relativelybenign,
spread occurs to lymph
nodes and lungs.

11. • It is treatedby surgery.
• It is radioresistant and
chemoresistant.
2. Sertoli cell tumour (1%):
• Feminises.
• Postpubertal tumour
commonly arising from
sertoli cells
• causes feminising effect with
gynaecomastia, loss of libido
and aspermia.
• It may be classic/large cell
type; calcifying/sclerosing.
• Surgeryis the treatment
SPREAD
Local
• To epididymis, cord,
tunica albuginea,
scrotumand so inguinal
nodes. Lymphaticspread
↓
Lymphatics drainage of testis
is through its mediastinum
↓
along the gonadal vessels to
para-aorticand
retroperitoneal nodes.

12. ↓
Throughthe lymphatics along
the medial side of testis
↓
may runwiththe arteryof vas
draining
↓
intothecommoniliacnodes at
the bifurcationof common
iliac artery.
↓
Spreadmainlyoccurs to para-
aortic; oftento retroperitoneal
and common iliac nodes.
↓
Malignancy spreads to inguinal
nodes, only if scrotal skinis
involved.
• Right testicular tumour
spreads to interaortocaval
nodes
↓
immediately below the renal
vessels as primary landing zone
(L2 level)

13. ↓
thento para-aorticnodes.
Paracaval, preaortic, common
iliac nodes are also can be
involved.
• Left testicular tumour
↓
spreads to true para-aortic
nodes
↓
to beginwith just belowthe
renal vessels
↓
thento preaorticand common
iliac nodes.
• Fromretroperitoneal and
para-aorticnodes spread
occurs to left supraclavicular
nodes and posterior
mediastinal nodes.
• Seminoma mainlyspreads
through lymphatics than
teratoma. Extranodal
spread
• To lungs, liver, brain, bone,
kidney, adrenals in
frequencyorder.

14. CLINICALFEATURES
• Enlargement of testis.
• Fullness and heaviness in
the scrotum.
• Painin the testis
• Testis is enlarged, firm,
heavy, with loss of testicular
sensation (in early stage
only).
• Secondaryhydrocele is
common.
• Cremaster is hypertrophied
and thickened.
• Vas, prostate and seminal
vesicles are normal.
• Oftenin epigastric region
para-aorticlymph nodes
may be palpable as hard,
nodular, nontender,
nonmobile, vertically placed,
resonantmass (not moving
with respiration
• Haemoptysis
• alteredbreathsounds
and pleural effusion.
• Bone pain and
tenderness due to
secondaries in bone.

15. • Nodular secondaries in the
liver.
• Occasionally, it may mimic
acuteepididymo-orchitis or
acutehaematocele.
• Gynaecomastia may be
present in few teratomas—
5%. It is due to raisedβ-
HCG.
• Hemiscrotumwith absence
of rugae
• with cuspicious mass in the
groin withsuspicious mass
• in the groinsuggests
undescended testis with
testicular tumour.
• 3% of testicular tumours are
bilateral
• Inguinal nodes are involved
if tumour breaches the
tunica albuginea to spread
to scrotum
• previous surgeries like
testicular fixation, hernia
surgery can also predispose
inguinal node spread.

16. • CNS/spinal cord may be
involved by secondaries.
• In 10% of cases it present
as asymptomatic,
identifiedincidentally.
• Hurricane type is very
aggressive, highly
malignant testicular
tumour whichis more
oftenfatal in few weeks.
• Rarely, if tumour comes
out of the tunica
albuginea (tunica
albuginea is resistant for
malignant cell
infiltration), thenscrotum
gets infiltrated and
spread canoccur to
inguinal lymph nodes.

17. • Sign of vas:
• To differentiate tumour
frominfection—in
testicular tumours vas is
normal, cord structures
may become bulky
becauseof cremasteric
hypertrophy whereasin
infectionvas is
thickened, beaded,
tender.
STAGINGTNMstaging
• T0 – No evidence of
tumour
• Tis – Carcinoma in situ
• T1 – Tumour limited to
testis and epididymis.
Vascular/lymphatic
invasion not present.
Tumour may invade
tunica albuginea but not
tunica vaginalis
• T2 – Tumour limited to
testis and epididymis with
vascular/lymphatic
invasion.

18. • Or tumour extends through
the tunica albuginea with
involvement of tunica
vaginalis
• T3 – Tumour invades to
spermaticcord withor
without vascular/ lymphatic
invasion
• T4 – Tumour invades to
scrotumwithor without
vascular/lymphatic invasion
• N- Nodal spread
• N0 – Regional Nodes not
involved
• N1 – Single/multiple
nodes—not more than 2
cm in size
• N2 – Regional nodes—
between2–5 cm
• N3 – Regional nodes >5
cm

19. • M- Metastasis
• M0 – Distant spread not
present
• M1 – Distant spread present
• M1a – Distant spreadto
nonregional nodes or to
lungs
• M1b – Distant spread to
other thannonregional
nodes or lungs
• DIFFERENTIAL
DIAGNOSIS
• Acute and chronic
haematocele
• Acute epididymo-orchitis
• Syphiliticorchitis
• Lepra orchitis
INVESTIGATION
• No FNAC
• No scrotal approach
• No incision biopsy.
• Chest X-ray to look for
lung secondaries
• HRCTscanis ideal.

20. • Ultrasoundabdomento see
nodal status like para-aortic
nodes and liversecondaries.
• CT abdomen is better.
• Ultrasoundscrotumto see
echogenicity of testis and
tumour within.
• CT scanabdomenand pelvis
to look for secondaries, iliac
and para-aortic nodes.
• CT chest is neededto
confirmlungsecondaries
TREATMENT
• Seminomas are
radiosensitive.
• So after highorchidectomy,
• radiotherapy is given to
increasethe cure rateand
also to reduce relapse.
• It is the treatment of choice
in stage I seminomas.
• Opposite testis shouldbe
shieldedduring
radiotherapy.

21. • Seminomaswith high levels
of tumour marker are
treated as nonseminomatous
tumours.
• Chemotherapyis also
effective.
• Cisplatinis veryuseful drug
in seminoma.
• In teratoma, Retroperitoneal
Radical LymphNode
Dissection
COMPLICATION
• Haemorrhage
• injuryto main structures
likemajor
vessels/ureter/bowel
• chylous ascites
• Lymphocele
• retrogradeejaculation.
• Radiotherapy is not
beneficial in teratoma.
• Chemotherapeutic drugs for
teratoma are cisplatin,
bleomycin, vinblastine,
etoposide, ifosfamide, mesna,
paclitaxel.

22. • BEP regimenis commonly
used.
PROGNOSIS
• Measurement of tumour
markers at regular intervals
for 5 years and yearlyafter5
years.
• CT abdomen and chest once
a year. Factors Affecting the
Prognosis
• Histological appearance of
tumour.
• Staging of the tumour: II—
90%; III—70%5-year
survival.
• Age of the patient, younger
theage grouppoorer the
prognosis.
• Seminoma has got better
prognosis thanteratomas.
• Spermatocyticseminoma
has got good prognosis.
• Hurricane type has got
worst prognosis.
• Seminoma responds well to
RT (melts-like snow).
• Teratoma is less sensitive
RT.

23. REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

24. A
Special Thanks
To A Very
Special Doctor