Testicular tumors - ramu

IT INCLUDES BASIC SCIENCES AND MANAGEMENT

1. Testicular tumors

2. •Testicular tumors are rare.
•1 – 2 % of all malignant tumors.
•Most common solid malignancy in men in the
15 to 35 year age group.
•The incidence of Testicular Cancer for men
from India is less than 1 man per 1,00,000
•Seventeen percent of all Genito-urinary cancers
among men in the year 2006 at the T.M.H.
were attributable to Testicular cancer.

4. •Germcell tumour
–Seminoma
–Non Seminomatous germ cell tumor
•Embryonal carcinoma
•Teratoma
•Choriocarcinoma
–Tumours of more than one histologic
type (mixed forms)

5. •Non-germ cell tumors
1.Specialized gonadal stromal tumor
(a) Leydig cell tumor
(b) Other gonadal stromal tumor
2. Gonadoblastoma
3. Miscellaneous Neoplasms
(a) Adenocarcinoma of the rete testis
(b) Mesenchymal neoplasms
(c) Carcinoid
(d) Adrenal rest “tumor”
4. secondary neoplasams
(a)Lymphoma
(b)metastasis

6. Risk factors
•Cryptorchidism – 4-6 times more riskCryptorchidism – 4-6 times more risk
–Abnormal Germ Cell MorphologyAbnormal Germ Cell Morphology
–Elevated temperature in abdomen & Elevated temperature in abdomen &
Inguinal region as opposed to scrotumInguinal region as opposed to scrotum
–Endocrinal disturbancesEndocrinal disturbances
–Gonadal dysgenesisGonadal dysgenesis
–Interference with blood suplyInterference with blood suply

7. •Rule of ten
–Pt with cryptorchidism relative risk for
testicular tumor 10%
–If one testis involved, chances of other
testis involved is 10%
– 10% testicular tumor patients have
cryptorchidism retrospectively

8. •Family history of testicular cancer
–If brother is affected R.R is 8- 12
–If father is affected R.R is 2- 4
•H/O testicular cancer
–12 folds increasing risk to contra lateral testis
•ITGCN
–50% risk of GTC in 5 years
–70% risk of GTC in 7 years
•Acquired causes
–Trauma
–Hormones – estrogen, diethyl stillbestrol
–infections

9. PATHOGENESIS & BIOLOGY
•Arrested primordial germ cells or gonocytes
that failed to differentiate into
prespermatogonia
•After puberty stimulated by increased
testosterone levels
•70% of GCT have extra copy of short arm of
chrmosome 12 in form of isochromosome

10. •Chemo sensitive
–Low threshold for apoptosis – high intrinsic
levels of wild type TP53
–Anti-apoptotic expression is low – low BCL-2
–Lack of transporter to export cisplatin
•Extragonadal GCT – 10%
–Mis-integration along genital ridge
–Reverse migration from testis to extragonadal
location

11. Histologic classification

13. •ITGCN
–Undifferentiated germcells located with
in the seminiferous tubules
–Except spermatocytic seminoma all
GCT arises from it

14. •Seminoma
–M.C type of GCT
–4
th
to 5
th
decade
–Gross
•Soft tan to white
diffuse or
multinodular
mass
•Necrosis may
present – focal
not diffuse

15. •Histologic types

–Classical seminoma
–Atypical seminoma
–Spermatocytis seminoma

16. •Microscopy
–Sheet like
arrangement of
cells
–Polygonal nucleoli
and clear
cytoplasm
–Fibro-vascular
septa containing
lymphocytes
–Syncytiotrophoblast
15% of pure
seminoma

17. •Immuno histochemistry
–Negetiv e for CD 30
–Positive for CD
117(negetive
indicates poorly
differentiated
malignancy)
–Stong positive for
placental alkaline
phosphatase

18. •Spermatocytic seminoma
–<1% of GCT
–Peak in 60s
–Not arises from ITGCN
–Not arises from cryptorchid testis
–Do`s not express PLAP or i(12p)
–Histology
•Nuclei are round, minimal lymphocytes
•Three distinct cells
–Small lymphocyte like cell
–Medium sized cells
–Large mono/multi nucleated cells
–It is benign tumor almost always cured with
orchidectomy

19. •Embyonal carcinoma
–Most undifferentiated malignancy
–M.C tumor in orchidopexy testis
–Cells resembles primitive epithelial
cells of early stage embryo
–Cells have totipotential to
differentiated to other NSGCT in
primary or at metastasis site
–Gross
•Tan to yellow neoplasam
•Large ares of heamorrhage
and necrosis

20. •Microscopy
–Alveolar, tubular or
solid sheet like
growth pateren
–Syncytiotrophoblasts
are seen in some
•IHC
–Positive for low
mollicular Wt.
keratin(AE1/AE3),
PLAP, CD30
–Doesn`t stain for C-
KIT

21. •Choriocarcinoma
–Rare and aggressive carcinoma
–Commonly spread by hematogenus route to
lungs and brain
–Disseminated disease
–Hemorrhage is common
–Elevated hCG
–Microscopy
–Both cytotrophoblast and syncytiotrophoblasts
are seen

22. •Yolk sac tumours / endodermal sinus
tumor
–Significant % of primary mediastinal
NSGCT
–Most common testicular tumor in
infancy and childhood
–In adults mostly presents as mixed
tumor
–Almost always produce AFP but not
hCG
–Microscopy
•Reticular network of medium sized
cuboidal cells
•Cytoplasmic and extracytoplasim
esinophilic hyaline globules
•Schiller-Duval bodies

23. •Teratoma
–Well differentiated, incomplete differentiated elements
of two or more germ layers
–Mature teratoma
–Immature teratoma- partial somatic differentiation
–Growing teratoma syndrome
–Teratoma with somatic malignancy
–Normal serum markers
–Produces AFP

25. •Mixed germ cell tumors
–common form is teratoma with endodermal
sinus tumor.
–Teratocarcinoma refers to a germ cell tumor
that is a mixture of teratoma with embryonal
carcinoma, or with choriocarcinoma, or with
both.
–Ignoring the teratoma component and
referring only to its malignant component

26. SIGNS AND SYMPTOMS
•10% are asymptomatic
•Painless testicular mass
•Vague scrotal discomfort and heaviness
•Acute testicular pain-heamorrage and rapid
tumour growth
•Symptoms related to metastatic disease-10-
20%
–Abdominal pain
–Palpable abdominal mass
–Lower extremity edema
–Low back ache
–Anorexia, nausea, vomting
–Pulmonary metastasis-dyspnea,chest pain,cough
and hemoptysis

27. •Gynacomastia 2% in tumor producing
hCG
•Diminished fertility 2\3
rd
of patient but
uncommon in initial presentation
•Hydrocoele - secondary
•Loss of testicular sensation
•sign of vas

28. Bilaterality of tumors
•Synchronous and metachronous testicular tumors
account for 1%–5% of all testicular cancer
•Synchronous testicular tumors are much less common,
account for approximately 10% of bilateral tumors.
•Most synchronous tumors have an identical histologic
diagnosis
•malignant lymphoma is the most common bilateral tumor
of the testis
•Seminoma is the most common germ cell tumor in
bilateral primary testicular tumors

29. All patients with a solid, Firm
Intratesticular Mass that cannot
be Transilluminated should be
regarded as Malignant unless
otherwise proved

30. DIFFERENTIAL DIAGNOSIS
•Epididymoorchitis
•Torsion
•Hematoma
•Para-testicular neoplasm
•Patient with presumptive diagnosis of
epididymo-orchitis should be re evaluated
with in 2 years of completion of an
appropriate course of oral antibiotics

31. DIAGNOSTIC TESTING AND
INITIAL MANAGEMENT
•SCROTAL ULTRASONOGRAPHY
–High frequency probe 5-10m Hz
–Few millimeter lesion can be identified
–Differentiated from extra testicular pathology
–Hypo echoic and two or more discrete lesion
may be identified
–Heterogeneous echo texture with in lesion-
NSGCT
–Homogenous echo texture with in lesion-
seminoma mostly

33. –Increased flow with in the lesion in color
Doppler
–Both testis should be evaluated
–Burned out primary in advance GCT-
normal testicular examination
•Scrotal USG shows small impalpable
scar or calcifications

34. SERUM TUMOUR MARKER
•DIAGNOSIS,PROGNOSIS,TREATMENT
MONITORING
•AFP:
–50-70% low stage NSGCT,
–60-80% advance NSGCT
–E.C and yolk sac tumours secrete AFP
–Choriocarcinoma and seminomas do not
produce
–Half life is 5-7 days
–NORMAL VALUE: Below 16 ngm / ml

35. –Other conditions:
•HCC
•cancer of stomach,pancreas,biliary tract
and lung
•Ataxia telangiectasia and
•hereditary tyrosinone

36. •HCG:
–20-40% low stage NSGCT
–40-60% advanced NSGCT
–15% of seminomas secrete HCG
–Choriocarcinoma and E.C secrete HCG
–Half life of HCG is 24 -36 hrs
–NORMAL VALUE: < 1 ng / ml
–Also elevated in cancers of liver biliary tract,
pancreas, stomach, lung, breast, kidney and
bladder

37. •LDH:
–20%low stage GCT
–20 -60% of advance GCT
–LDH-1 iso-enzyme most frequently elevated
–Magnitude of LDH correlates with bulk of
disease
–Nonspecific marker used in prognostic
assesment {tumour burden ,cellular
proliferation}
–Half life is 24 hrs

38. FNAC in testicular tumor

39. RADICAL INGUINAL
ORCHIDECTOMY
•Transcrotal orchidectomy/biospy
contraindicated
–Leaves inguinal portion of sperm cord
–Alter lymphatic drainage of testis-pelvic
and inguinal node metastasis
–Increases risk of local recurrence
•Histological diagnosis
•Primary-T stage

40. Radical Orchiectomy
•A radical orchiectomy with high
ligation of the spermatic cord at the
level of the internal ring is the first step
in the treatment of patients suspected
of harboring a testicular neoplasm.

41. Radical Orchiectomy - Steps
•General, spinal, or local anesthesia; outpatient
•A 5- to 7-cm oblique incision 2 cm above the
pubic tubercle.
•Camper's and Scarpa's fascia are incised to the
level of the external oblique aponeurosis
•The ilioinguinal nerve is preserved. The
spermatic cord is isolated and occluded
•If a diagnostic biopsy or subtotal orchiectomy is
planned, meticulous draping off is necessary
before opening the tunica vaginalis and incising
testicular parenchyma.

43. •Chevassu maneuver
–In 1906 Chevassu suggested this technique
–Its use during inguinal explorations for
suspicious intrascrotal masses
–Inguinal exploration and occlusion of the
testicular vessels before biopsy of suspicious
lesions.
–We have added scrotal hypothermia, double
ligation of the gubernaculum before its
division and irrigation with distilled water to
provide a procedure that adheres to the
principles of good cancer surgery.
–Testis is bisected and see for any growth

44. •Radical orchiectomy is completed by mobilizing the cord 1 to 2 cm
inside the internal ring
•Individually ligating the vas deferens and the cord vessels between
separate clamps
•The cord vessels are secured with silk ligatures, which can then be
used to identify the stump if a retroperitoenal lymph node dissection
(RPLND) is performed.
•The wound and scrotum are thoroughly irrigated, and hemostasis is
secured.
•A testicular prosthesis can be placed at this time.
•The external oblique aponeurosis is closed.
•Rest of wound is closed

45. Figure 30-2 After the cord has been controlled with a tightened Penrose drain or rubber-shod clamp, the testis is mobilized out of the scrotum using blunt dissection.
(Adapted from Gottesman JE: Radical inguinal orchiectomy. In Crawford ED [ed]: Current Genitourinary Cancer Surgery. Philadelphia, Lea & Febiger, 1990, p 319.)
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46. Scrotal Violation
•Patient who have undergone previous inguinal or
scrotal surgery have altered lympatic drainage
•low-stage seminoma -- radiation portals should be
extended to include the ipsilateral groin and
scrotum.
•low-stage nonseminomatous GCT (NSGCT)-- the
scrotal scar should be widely excised with the
spermatic cord remnant at the time of RPLND.
•Patients treated with full-dose platinum-based
regimens should have the cord stump removed at
the time of RPLND; however, given the relative
absence of local relapse after systemic treatment,
extensive groin dissection or hemiscrotectomy is
not required

47. •HPE include
–Histological type
–Tumor size
–Multi-focality
–Local tumor invasion
–Primary T stage
–Presence of
–Lymph vascular invasion
–Surgical margin status

48. •Immunohistochemistry-
–PLAP,
–CD117,
–OCT 3\4,
–CD30 and
–Low molecular Wt keratin

49. TESTIS SPARING SURGERY/ PARTIAL
ORCHIDECTOMY
•Indications
–Organ confined tumor
–Less than 2 cms
–Synchronous bilateral tumor or
–Tumor in solitary testis with sufficient
testicular androgen production
•Biopsy of adjacent testicular parenchyma should
not be done
•Adjuvant chemotherapy using dose of 20 gy
•Biopsy of contra lateral testis

50. •Metastatic spread
–Except for choriocarcinoma M.C route of
disease dissemination is via lymphatic
to retroperitoneum.
–Chorio carcinoma -- heamatogenous
dissemination
–Right testicular tumour-primary drainage
right interaortocaval lymphnode inferior
to renal vessel followed by paracaval
and paraaortic node.

51. •Left testicular tumour
–Para-aortic node
–interaortocaval node lymphatic
•spread from right to left.
•More caudal deposition reflex retrograde
spread
•Retrocrural lymph node to posterior
mediastinal and left supra-clavicular fossa

53. •Inguinal lymphadenopathy
–Scrotal violations
–Tumou invade into layers of tunica
albugenia and scrotal layers

54. •CT abdomen and pelvis with oral and
IVcontrast-
–R.P lymph node >5mm in primary
landing zone suspicion of region lymph
node metastasis
•MRI-vascular anatomy.
•No role of FDG-PET in routine evaluation

55. •Extranodal involvement
–Lungs
–Liver
–brain

56. CHEST IMAGING
•Initial chest x ray.
•CT scan chest-
–Elevated post orchidectomy levels of serum
marker.
–Abnormal or equivocal findings in chest X-ray
–Evidence of metastasis in clinical
examination.
•Brain CT
–Patient with high levels of hCG >10,000

57. •Post orchidectomy serum tumour marker
levels

59. •M0 no metastasis
•M1 distantmetastasis
–M1a non regional nodes and pulmonary
metastasis
–M1b distant metastasis other than non
regional nodes and pulmonary
metastasis

61. •Stage I:
–Cancer is found only in the testicle
•Stage II:
– Cancer has spread to the lymph nodes in the
abdomen
•Stage III:
–Cancer has spread to areas above the
diaphragm such as the lungs, bone, neck or
brain

63. Treatment
Chemotherapy
Surgery
Radiation therapy

64. seminoma
•Clinical stage 1
–Radiation therapy
–Surveillance
–chemotherapy

66. •Many clinical practice guidelines now
recommend surveillance as preferred
approach
•Dog field radiotherapy – non complaint
patient or those unwilling to accept
surveillance

67. Clinical stage IIa & IIb seminoma
•15-20%
•Induction chemotherapy:
–BEP x 3 or EPx 4
–Preferentially given in patient bulky
disease(>3 cm) & multiple retroperitoneal
masses because risk of relapse is low
•Radiotheray:
–For rest of cases
–Dog leg radiotherapy- 25-30Gy –
–Including 5-10g% boost to involved areas

68. Clinical stage IIc &III seminoma :
•Chemotherapy :
•95% patient are good risk .
–Rx is BEP x 3 or EP x 4
–Complete radiographic response 70-
90%
•Intermediate risk –seminoma –
–BEP x 4 chemotherapy

69. Post chemotherapy residual mass
•Patient with discrete residual mass greater
than 3cm evaluated with FDG PET : those
who have PET +ve ,PCS

70. Relapse seminoma
•Patients not used chemotherapy
–CS – I-- Dog leg radiotherapy
–CS – II & IIb -- first line cisplastin based
chemotherapy
•Post chemotherapy seminoma relapse
–VeIP x 4 – second line treatment

71. NSGCT
Clinical stage I
•33 %
•Surveillance for CS1 with low risk patient
•RPLND or primary chemotherapy to those
to high risk

72. •Clinical stage I s :
–Elevated post orchidectomy serum
tumour marker without clinical or
radiographic evidence of metastatic
disease
– Rx similar to those with cs-IIc , cs-III

73. Clinical stage IIa & IIb treatment
•Induction chemotherapy
–Elevated AFP or HCG or
–Bulky lymphnode >3cm should receive
•RPLND
–Patient with risk of teratoma ,
–low risk for systemic disease ,
–normal serum tumour marker ,
– lymphadenopathy <3cms

74. Clinical stage IIIc & III :
•Induction chemotherapy with cisplastin
based multiagent regimen
•Good risk NSGCT :
–BEP x 3 has become standard regimen
& EP x 4 both accept regimen
–Over all survival 91 – 94%
•Intermediate and poor risk NSGCT
–BEP x 4
–VIP- 4 – preferred in patient with
compromised pulmonary function

75. Management of post chemotherapy residual
mass
•Second line – salvage chemotherapy
•Residual masses larger than 1cm should
undergo PCS
•small residual masses at other site is
reasonable option of histology of RPLND
is necrosis

76. Relapse of NSGCT:
•Chemotherapy naïve NSGCT relapse :
–Retroperitoneum with non bulky disease & normal
serum tumour marker RPLND
–Rest of patient induction chemotherapy
•Post chemotherapy NSGCT relapse early ,
occur < 2 yrs
–Salvage / second line chemotherapy
–GTIP x 4 , VIP x 4 , VEIP-4
•Declining or normalized serum tumour marker
during first line chemotherapy with enlarging
mass – growing teratoma syndrome – patient
are taken for surgical resection

77. •Post salvage chemotherapy residual
mass:
•Patient with serological complete
response- PSCS
•Desperation surgery – patient with raising
serum tumour markers who have
resectable disease limited to single site

78. •Post chemotherapy NSGCT relapse –
–Occuring > 2years after treatment
–Three histopathological categories
–1. viable malignancy
–2. teratoma
–3. malignant
–Late relapses have-- worst prognosis ,
resistant to chemotherapy
–Rx – surgical resection of all site of disease

79. •ITGCN :
–Rx –50% risk of developig an invasive GCT
with in 5 yrs
–Orchidectomy ,
–low dose radiotherapy &
–close observation

82. •Treatment related sequele:
•Early toxicity :
–cisplastin – fatigue , myelosuppresion ,
infection , peripheral neuropathy , hearing
loss , decreased RFT &death
–Radiotherapy : fatigue , nausea & vomiting ,
leucopenia , dyspnea
•Late toxicity :
–peripheral neuropathy , reynauds
phenomemon , hearing loss , hypogonadism ,
10-20% infertility , second malignant
neoplasms & cardiovascular diseases

83. RPLND

84. RETROPERITONEAL LYMPH
NODE DISSECTION
•Bilateral infrahilar RPLND is new current standard
•suprahilar dissections are usually performed for residual
hilar or suprahilar masses after cytoreductive
chemotherapy for advanced stage
•Loss of antegrade ejaculation most common morbidity
–advised to complete sperm banking before surgery
–Preservation R > L
–paravertebral sympathetic ganglia, postganglionic
sympathetic fibers T2-L4, and their convergence at the
hypogastric plexus are most crucial in the preservation of
antegrade ejaculation.

85. RETROPERITONEAL LYMPH
NODE DISSECTION - Technique
•Transabdominal or a thoracoabdominal
approach
• Thoracoabdominal
–Easier visualization and dissection of the
suprahilar lymphatic tissues and less risk of
postoperative small bowel obstruction

86. Figure 30-4 Surgical template for bilateral RPLND. IVC, inferior vena cava; SMA, superior mesenteric artery; IMA, inferior mesenteric artery.
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87. Figure 30-5 Surgical template for modified left-sided RPLND.
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88. Figure 30-6 Surgical template for modified right-sided RPLND.
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89. Thoraco-Abdominal Approach -
Steps
•Torqued position
• The operating table is hyperextended
•The incision starts obliquely over the eighth or
ninth rib and curves downward toward the pubic
ramus
•A subperiosteal rib resection is performed, and
the ipsilateral rectus muscle is divided.
•The peritoneum and contents are mobilized from
the undersurface of the rectus sheath, and the
diaphragm is divided and the pleura is entered

90. •The retroperitoneum is exposed to the level of
the contralateral ureter. Full bilateral RPLND can
be carried out as described for the
transabdominal approach.
•The most common site of residual suprahilar
disease is in the retrocrural space
•The wound is closed by reapproximation of the
diaphragm with silk sutures and of the costal
cartilage with Prolene. Chest tube drainage is
established, and the flank is closed
•COMPLICATIONS - Atelectasis, prolonged
chest tube drainage, and increased need for
postoperative analgesia

91. Trans – Abdominal - Steps
•The falciform ligament is either divided between silk ligatures or
excised en bloc with the preperitoneal fat.
•The small bowel is reflected to the right, and an incision is made in
the posterior peritoneum medial to the inferior mesenteric vein
•This incision is continued cephalad to the ligament of Treitz and is
extended superiorly and medially to the duodenojejunal flexure,
allowing for superior mobilization of the fourth portion of the
duodenum and pancreas.
•The proper plane of dissection is the avascular plane between the
inferior mesenteric vein and the left gonadal vein. This maneuver
further defines a thick condensation of fibrovascular tissue (ligament
of Treitz) and several large lymphatic trunks, which should be
divided between silk sutures

92. •Alternatively, to gain adequate exposure in the
area of the left renal hilum, particularly with large
postchemotherapy masses, the inferior
mesenteric vein can be doubly ligated and
divided
•The incision is continued lateral to the right
gonadal vein
•The duodenum is then kocherized.
•It is important to ligate or clip the numerous
lymphatic vessels in this area to minimize
postoperative lymphatic complications

93. Figure 30-7 Incision of the posterior parietal peritoneum. The incision extends from the ligament of Treitz along the left side of the root of the small bowel mesentery to
the ileocecal region (1). It may be extended superiorly and medially to the duodenojejunal flexure and inferolaterally around the cecum and ascending colon. The left leaf
of the incised posterior peritoneum is defined (2).
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94. Figure 30-8 Development of the left leaf of the incised posterior peritoneum in the avascular plane between the inferior mesenteric vein (IMV) and the left gonadal vein.
The colonic mesentery lies anteriorly and the para-aortic space and Gerota's fascia lie posteriorly. LRV, left renal vein; SMA, superior mesenteric artery.
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95. Figure 30-9 The retroperitoneal space has been exposed. The duodenum has been kocherized; its second, third, and fourth portions have been reflected superiorly along
with the pancreas and superior mesenteric artery (SMA). The entire right colon has been mobilized and exteriorized. LRV, left renal vein; IMV, inferior mesenteric vein;
IVC, inferior vena cava; IMA, inferior mesenteric artery.
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96. Figure 30-10 Division of attachments between the undersurface of the duodenum and pancreas and the anterior surface of the left renal vein (LRV). It is important to clip
or ligate the numerous lymphatic channels in this area. Prominent lacteals in the vicinity of superior mesenteric artery (SMA) are often seen. IMV, inferior mesenteric
artery; IVC, inferior vena cava.
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97. •20% of patients will have accessory renal
arteries
•2% to 3% of patients will have a retroaortic
left renal vein
•Important to recognize a retroaortic left
renal vein because it may be inadvertently
mistaken for a lumbar vein and ligated or
the pancreas and SMA may be injured
CAUTION!!

98. Lymphadenectomy
•Attention is initially directed to the left renal vein, and the renal
perivascular lymphatic tissue is mobilized inferiorly.
•Aadrenal, spermatic, and lumbar branches are tied.
• The dissection along the anterior surface of the left renal vein
continues to the right until the anterior surface of the IVC is
encountered, and the first anterior "split" is then performed. The split
and roll technique is illustrated in Figure 30-11.
•The right gonadal vein is ligated at the vena cava. Lymphatic tissue
can then be rolled off the IVC laterally and medially as the dissection
proceeds inferiorly. Lumbar veins are dissected, doubly ligated with
3-0 silk, and divided.
•At this point, nerve-sparing techniques can be performed if clinically
indicated
•The anterior split on the surface of the aorta should then be carried
inferiorly to the bifurcation of the common iliac arteries.

99. •The origin of the IMA is identified. If necessary,
this artery can be sacrificed
•The gonadal arteries should be ligated early to
prevent the subadventitial hematoma that may
result if they are avulsed.
•Following the anterior aortic split, lymphatic
tissue is retracted medially and laterally and
lumbar arteries are dissected
•The right and left renal arteries are skeletonized,
and the lymphatic tissue is separated from the
psoas fascia and anterior spinous ligament,
which are the posterior limits of dissection.

100. •Great care should be taken to control lumbar
vessels as they pass into the posterior body wall
near the sympathetic chains to avoid possible
injury to sympathetic innervation in attempting to
control problematic bleeding.
•Throughout the procedure it is important to ligate
or clip the cut ends of lymphatic vessels,
particularly in the region of the right renal artery,
where large tributaries to the cisternae chyli are
located.
•Postoperative tachycardia is common due to
sympathetic discharge.

101. Figure 30-11 A to G, Sequentially, this diagram shows the "split and roll" technique that allows for en bloc removal of the nodal package. The lumbar vessels must be
divided twice, first at the wall of the great vessels and again as they enter the foramina alongside the vertebral bodies.
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102. Figure 30-12 Nerve-sparing technique with soft vascular tapes around the right postganglionic branches of the sympathetic chains as they course in an oblique fashion
toward the hypogastric plexus. Their relationship to the great vessels, lumbar veins, and root of the inferior mesenteric artery (IMA) is shown. SMA, superior mesenteric
artery.
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103. Nerve Sparing
•Candidates include patients with clinical stage I and low-
volume stage II NSGCT undergoing primary RPLND, as
well as a carefully selected subset of patients undergoing
post-chemotherapy lymphadenectomy
•The most important aspect in performing nerve-sparing
RPLND is the prospective identification and preservation
of relevant sympathetic nerves
–(1) the sympathetic chains bilaterally
–(2) the postganglionic sympathetic nerves arising from the
sympathetic chains
–(3) the hypogastric plexus, which is the anastomosing
network of nerve fibers anterior to the lower aorta

104. Figure 30-12 Nerve-sparing technique with soft vascular tapes around the right postganglionic branches of the sympathetic chains as they course in an oblique fashion
toward the hypogastric plexus. Their relationship to the great vessels, lumbar veins, and root of the inferior mesenteric artery (IMA) is shown. SMA, superior mesenteric
artery.
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105. Figure 30-5 Surgical template for modified left-sided RPLND.
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106. Figure 30-6 Surgical template for modified right-sided RPLND.
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© 2007 Elsevier

107. Prognosis in testicular tumors
•Seminoma
–Stage 1 – 98%
–Stage 2a – 92% - 95%
–Stage 2b &3 – 35% -75%
•NSGCT
–Stage 1 – 96% - 100%
–Stage 2a & 2b – 90%
–Stage 3 – 55% – 80%

108. Non germ cell tumours
•Sex cord/ stromal tumours
–4%
–Neoplasms
•leydig cells ,
•sertoli cells ,
•granulosa cells or
•thecal cells .

109. •Leydig cell tumours-
–Most common
–No association with cryptorchidism
–20-60 years ;1/4
th
occurs in children
–Painless testicular mass.frequently with
feminism
–Characters-
•Androgen excess & peripheral conversion
to estrogen.
•Gynecomastic , impotence &decreased
libido
•Children-testicular mass ;isosexual
precocious puberty

110. –90% are benign ,10% are malignant
–Gross- small ,yellow to brown, well circumscribed
without areas of necrosis & hemorrhage
–Histology-
•uniform , polygonal cells with round nuclei
•Reinke crystals , 20-40% - densely esinophilic
,needle like & rhomboid structures within
cytoplasm
–Presence of metastatic disease is only reliable criteria
for malignancy
–Radical inguinal orchidectectomy
–Chemoresistant &radio resistant. So RPLND for
metastasis
–Mitotan-potent inhibitor of steroidogenesis has
sympomatical improvement

111. •Sertoli cell tumour :
–< 1% of
–occurs in any age including infants
–Microscopic- epithelial elements ,
resembling sertoli cells with varying
amount of stroma organised into tubules
–Treatment-similar to leydig cell tumour

112. •Granulosa cell tumour :
–Rare & resemble adult type of granulosa
cell tumour of ovary
–Radical inguinal orchidectomy

113. •Gonadoblastoma :
–Mixed germ cell & sex cord cells showing
sertoli differentiation
–Occurs in dysgenic gonads & intersex
syndrome
–1/3
rd
of cases are bilateral
–Considered insitu form of malignant GCT
–Bilateral orchidectomy required
–80% of affected individuals are phenotypic
female

114. Miscellaneous testicular neoplasms
•Epidermoid cysts:
–Benign neoplasm
–Thought to be monodermally differentiated
mature teratoma
–Adjuvant ITGCN
–Association with crytorchidism
–Bilaterally have been reported
–Enucleation / partial archidectomy

115. •Adenicarcinoma of rete testis :
–Rare but highly malignant neoplasm
–Arises from collecting system of testis
–Painless testicular mass with hydrocele
–Median survival rate 1year
–Chemo &radio therapies ineffective

116. Secondary tumours of testis
•Lymphoma:
–Primary – 1-2%
–Secondary
•85%-men older than 60
•Non-hodgkins lymphoma most common
•35% - bilatera testicular involvement
•Painless testicular mass
•Radical inguinal orchidectomy
•Leukemia
–Testis is considered a barometer of
extramedullary involvement in ALL.
–In majority of the children with isolated
testicular relapses

117. •Metastasis:
–Prostate,
–lung
–melanoma ,
–Colon&
–kidney

118. Tumours of testicular adnexa
•Adenomatoid tumour:
–Most common para testicular tumour
–Most common involving epididymis
–Most common presentation-painless
paratesticular tumour
–Microscopy-epithelial like cells contain
vacuoles & fibrous stroma
–Rx – inguinal exploration & surgical excision

119. •Sarcoma:
–Sarcomas of spermatic cord,epididymis &
testis are most common genitourinary
sarcomas in adults
–Liposarcoma-most common histological type
in adults
–Embryonal rhabdomyosarcoma-most
common histological type in children
–Rx-wide excision of spermatic cord & testis
with high ligation
–In presence of normal metastatic evaluation
patient with sarcoma other than liposarcoma
should undergo RPLND & post-operative
chemotherapy ,should be given to patient with
retro peritoneal lymphnode metastasis

120. Sperm banking
•Treatments have a high likelihood of destroying
fertility
•Sperm is frozen or "cryopreserved“
•The sperm cells enter a state of suspended
animation
•Sperm activity is essentially halted until thawing
•Sample collection
–Through masturbation in a private room
–Directly from testis during orchidectomy