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TESTICULAR
 TUMOURS
      Dr. Abrar Ahmad
Anatomy of the Scrotum
          Scrotum: muscular pouch containing testes
          Testis: a network of tightly coiled

           seminiferous tubules that converge and
           anastamose into efferent tubules
              Encapsulated by tunica albuginea


          Epididymis: a structure formed from merged
           efferent tubules, which attaches along the
           posterior and upper border of the testis
              Described as having head, body & tail

          Vas deferens: tube arising from tail of

           epididymis,
              Passes through inguinal canal and joins

               seminal vesicle duct to form ejaculatory
               duct, which passes into prostate gland
          Spermatic cord: structure formed by vas

           deferens, testicular arteries, and veins
Introduction
• Although rare, is the most common malignancy
  in men in 15-35 yr age group
• Delayed diagnosis
• Has become one of the most curable solid
  tumour
  – Associated with accurate tumour markers
  – Origin in germ cells
  – Capacity to differentiate into histologically more
    benign forms
  – Predictable, systematic pattern of spread
  – Occurrence in young individuals
Etiology/Risk Factors
• Congenital Causes:
               Cryptorchidism
               Klinefelter’s syndrome
• Age: 20-35 years highest risk group
• Hormones
       Maternal hormone ingestion during pregnancy
• History of mumps orchitis, inguinal hernia, hydrocele in childhood -
  Atrophy
• High socioeconomic status
• Testicular cancer contralateral testis
• HIV positive.
CRYPTORCHIDISM & TESTICULAR TUMOUR


    Risk of Carcinoma developing in
         undescended testis is

  14 to 48 times the normal expected
               incidence
CRYPTORCHIDISM & TESTICULAR TUMOUR

The cause for malignancy are as follows:
• Abnormal Germ Cell Morphology
• Elevated temperature in abdomen &
  Inguinal region as opposed to scrotum
• Endocrinal disturbances
CLASSIFICATION
I.    Primary Neoplasma of Testis
      A.Germ Cell Tumour (90-95%)
      B.Non-Germ Cell Tumour
        (5-10%)
II.   Secondary Neoplasms.

III. Paratesticular Tumours.
PRIMARY NEOPLASMS OF TESTIS
Germinal Neoplasms : (90 - 95 %)

      Seminomas - 40%
             (a)   Classic Typical Seminoma
             (b)   Anaplastic Seminoma
             (c)   Spermatocytic Seminoma
      Teratoma - 25 - 35%
             (a)   Mature
             (b)   Immature
      Embryonal Carcinoma - 20 - 25%
      Choriocarcinoma - 1%
      Yolk Sac Tumour
PRIMARY NEOPLASMS OF TESTIS
Nongerminal Neoplasms : ( 5 to 10% )
     Specialized gonadal stromal tumor
           (a) Leydig cell tumor
           (b) Sertoli’s cell tumour
           (c)    Granulosa cell tumour
           (b) Other gonadal stromal tumor
     Gonadoblastoma
     Miscellaneous Neoplasms
           (a) Adenocarcinoma of the rete testis
           (b) Mesenchymal neoplasms
           (c)    Carcinoid
SECONDARY NEOPLASMS OF TESTIS


A.   Reticuloendothelial Neoplasms
B.   Metastases(prostate,lung,colorectal,
     renal cell carcinoma,thyroid,breast)
       PARATESTICULAR NEOPLASMS
A.   Adenomatoid
B.   Cystadenoma of Epididymis
C.   Mesenchymal Neoplasms
D.   Mesothelioma (Benign & malignant)
SEMINOMA
• Typical :         82-85%
                    Thirties
                    Slow growth

• Anaplastic:       5-10%
                    More aggressive, potentially more lethal
                    Greater metastatic potential

• Spermatocytic Seminoma: 2-12 %
                   Cells closely resemble different phases of
                   maturing spermatogonia
                   B/L tumours have been reported
                   Extremely low metastatic potential
                   Favourable prognosis
NON SEMINOMATOUS GERM CELL TUMOURS
• Embryonal carcinoma
   Generally discovered as a small, rounded but
   irregular mass invading the tunica vaginalis
• Choriocarcinoma
     May occur as palpable nodule or normal testis
     Central hemorrhage
     High metastatic potential (blood & lymphatic)
     Most malignant tumor
     Produces HCG
NON SEMINOMATOUS GERM CELL TUMOURS
• Teratoma
   Contains more than one germ cell layers in various
   stages of maturation and differentiation
   Grosssly large, lobulated, nonhomogenous tumours
   Microscopically, cystic & solid componenets
• Yolk cell tumours
   Most common testicular tumour in infants &
   children
   80% confined to testis at time of diagnosis
Pathogenesis & Natural History of Testicular Tumour

   Course of Spread of Germ Cell Tumours are
    predictible once histology of Tumour confirmed
   Local invasion of epidydimis or spermatic cord is
    hindered by tunica albugenia
   Lymphatic Spread has a set pattern depending
    on site of tumour
   Seminoma may have non-seminomatous
    metastasis
   High Grade Tumours spread by both Vascular
    invasion & via Lymphatics
Pattern of Spread of Germ Cell Tumour

   Right sided tumours- intraaortocaval
   Left sided tumours – left paraaortic & preaortic
     nodes
   Then cephalad to cisterna chyli, thoracic duct
    and supraclavicular (usually left)
   Epidydimis- External iliac chain
CLINICAL FEATURES
• Nodule/Painless Swelling of One Gonad
• Dull Ache or Heaviness in Lower Abdomen
• 10% - Acute Scrotal Pain
• 10% - Present with Metatstasis
  - Neck Mass / Cough / Anorexia / Back Ache
• 5% - Gynecomastia
• Infertility
PHYSICAL EXAMINATION
• Bimanual Palpation of testis and paratesticular
  structures


• Abdominal examination


• Lymph nodes


• Chest
WAKE UP

   All patients with a solid, Firm
 Intratesticular Mass that cannot be
Transilluminated should be regarded
as Malignant unless otherwise proved
Differential Diagnosis
• Metastasis from • Spermatocele
  prostate, lung, or • TB, gumma
  melanoma.          • Leukemia
• Epididymitis
• Lymphoma
Clinical Staging of Testicular Tumour

Staging A or I     - Tumour confined to testis.

Staging B or II    - Spread to Regional nodes.

IIA - Nodes <2 cm in size or < 6 Positive Nodes
IIB - 2 to 5 cm in size or > 6 Positive Nodes
IIC - Large, Bulky, abd.mass usually > 5 to 10 cm

Staging C or III - Spread beyond retroperitoneal
Nodes or Above Diaphragm or visceral disease
Requirements for staging

To properly Stage Testicular Tumours following are pre-
requisites:
(a)   Pathology of Tumour Specimen
(b)   History
(c)   Clinical Examination
(d)   Radiological procedure - USG / CT / MRI / Bone Scan
(e)   Tumour Markers -       HCG, AFP
TNM Staging of Testicular Tumour

T0      =       No evidence of Tumour
T1s     =       Intratubular, pre invasive
T1      =       Confined to Testis
T2      =       Limited to testis and epididymis with vascular/ lymphatic
                invasion or tumour extending through Tunica Albuginea with
                involvement of tunica vaginalis
T3      =       Invades Spermatic Cord with/without vascular/ lymphatic
                invasion
T4      =       Invades Scrotum with/without vascular/ lymphatic invasion

N1      =       Single or multiple < 2 cm
N2      =       Multiple < 5 cm / Single 2-5 cm
N3      =       Any node > 5 cm


 Epididymis or Scrotal skin – Lymph drainage to Inguinal Nodes
Investigation
1.   Ultrasound - Hypoechoic area
2.   Chest X-Ray - PA and lateral views
3.   CT Scan
4.   MRI
4.   Tumour Markers
           - AFP
           - HCG
           - LDH
           - PLAP(placental alkaline
             phosphatase)
Left                                                                    Right
Axial CT Section demonstarating - Left Hydronephrosis, due to large Para-Aortic
Nodal Mass from a Germ cell tumour
Tumour Markers

    TWO MAIN CLASSES
•      Onco-fetal Substances : AFP & HCG
•      Cellular Enzymes : LDH & PLAP
       ( AFP - Trophoblastic Cells
       HCG - Syncytiotrophoblastic Cells )
AFP –( Alfafetoprotein )
    NORMAL VALUE: Below 16 ngm / ml
    HALF LIFE OF AFP – 5 and 7 days

    Raised AFP :
    • Pure embryonal carcinoma
    • Teratocarcinoma
    • Yolk sac Tumour
    • Combined Tumour


REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma
HCG – ( Human Chorionic Gonadotropin )
Has   and polypeptide chain

NORMAL VALUE: < 1 ng / ml
HALF LIFE of HCG: 24 to 36 hours

RAISED     HCG -
100 % -   Choriocarcinoma
60% -     Embryonal carcinoma
55% -     Teratocarcinoma
25% -     Yolk Cell Tumour
7%    -   Seminomas
Lactate Dehydrogenase (LDH)
• Nonspecific tumor marker but is a useful prognostic
  indicator
• Indicator of tumor burden
ROLE OF TUMOUR MARKERS

• Helps in Diagnosis - 80 to 85% of Testicular Tumours
  have Positive Markers
• Most of Non-Seminomas have raised markers
• Only 10 to 15% Non-Seminomas have normal marker
  level
• After Orchidectomy if Markers Elevated means
  Residual Disease or Stage II or III Disease
• Elevation of Markers after Lymphadenectomy means
  a STAGE III Disease
ROLE OF TUMOUR MARKERS cont...

• Degree of Marker Elevation Appears to be Directly
  Proportional to Tumour Burden
• Markers indicate Histology of Tumour:
   If AFP elevated in Seminoma - Means Tumour has
  Non-Seminomatous elements
• Negative Tumour Markers becoming positive on
  follow up usually indicates -
  Recurrence of Tumour
• Markers become Positive earlier than X-Ray studies
PRINCIPLES OF TREATMENT

• Treatment should be aimed at one stage above the
  clinical stage
• Seminomas- Radio-Sensitive. Treat with Radiotherapy.
• Non-Seminomas are Radio-Resistant and best treated by
  Surgery
• Advanced Disease or Metastasis - Responds well to
  Chemotherapy
PRINCIPLES OF TREATMENT

• Radical INGUINAL ORCHIDECTOMY is Standard first line of
  therapy
• Lymphatic spread initially goes to RETRO-PERITONEAL
  NODES
• Early hematogenous spread RARE
• Bulky Retroperitoneal Tumours or Metastatic Tumors
  Initially “DOWN-STAGED” with CHEMOTHERAPY
Treatment of Seminomas

Stage I, IIA, IIB –
Radical Inguinal Orichidectomy followed by
radiotherapy to Ipsilateral Retroperitonium &
Ipsilateral Iliac group Lymph nodes


Bulky stage II and III Seminomas -
Radical Inguinal Orchidectomy is followed by
Chemotherapy
Treatment of Non-Seminoma
Stage I and IIA:
RADICAL ORCHIDECTOMY
followed by RETROPERITONEAL LYMPH NODES DISSECTION


Stage IIB:
RPLND with possible ADJUVANT CHEMOTHERAPY



Stage IIC and Stage III Disease:
Initial CHEMOTHERAPY followed by SURGERY for Residual Disease
Radical Orchiectomy
          • Inguinal approach
          • Testicle and spermatic
            cord are excised then
            sent for pathologic
            staging.
Retroperitoneal Lymph Node
              Dissection
• RPLND primary treatment (NSGCTs)

• Remove abdominal lymph nodes
Limits of Lymph Nodes Dissection For Right &
        Left Sided Testicular Tumours
Chemotherapy

BEP: (Bleomycin, Etoposide, Cisplatin)

  2-4 cycles 21d intervals (4 most common)

EP: (Etoposide, Platinol)

  4 cycles 21d intervals
Salvage Thearpy
• No initial complete response
• VIP: (Etoposide, Ifosamide,Mesna, Platinol)
  3-4 cycles 21d intervals

• High-dose chemotherapy with autologous
  bone marrow transplantation in selected
  patients with bulky disease
Complications
• Pulmonary toxicity: Bleomycin keep total dose
  under 400 units.
• Nephrotoxicity: Cisplatin- decreased CrCl:
  Dosed based on CrCl
• Neurologic: Cisplatin- Ototoxicity
• Cardiovascular: HTN, MI, Angina
• Secondary Malignancies: Etoposide
Follow up
– physical examinations, chest radiographs and
  serum tumor markers
– CT scans detect recurrence in the
  retroperitoneum and chest
– Follow-up protocols vary by
  institution, type, stage and treatment
Recommended Exams
•   Every 2-3 months 1st yr.
•   Every 3-6 month 2nd yr.
•   Every 6 month remainder 5 yrs.
•   CTscans: 3-6 months 1st yr. then annually
•   Men at high risk: Annually with self-exam
    monthly
Prognosis
                    Seminoma (at 5 years)
• I: 98%
• IIA: 92-94%
• IIB-III: 33-75%
                     NSGT (at 5 years)
• I: 96-100%
• IIA: >90%
• IIB-III: 55-80%
CONCLUSION

• Improved Overall Survival of Testicular
  Tumour due to Better Understanding of the
  Disease, Tumour Markers and Cis-platinum
  based Chemotherapy
Thanks

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Testicular tumours by dr abrar

  • 1. TESTICULAR TUMOURS Dr. Abrar Ahmad
  • 2. Anatomy of the Scrotum  Scrotum: muscular pouch containing testes  Testis: a network of tightly coiled seminiferous tubules that converge and anastamose into efferent tubules  Encapsulated by tunica albuginea  Epididymis: a structure formed from merged efferent tubules, which attaches along the posterior and upper border of the testis  Described as having head, body & tail  Vas deferens: tube arising from tail of epididymis,  Passes through inguinal canal and joins seminal vesicle duct to form ejaculatory duct, which passes into prostate gland  Spermatic cord: structure formed by vas deferens, testicular arteries, and veins
  • 3. Introduction • Although rare, is the most common malignancy in men in 15-35 yr age group • Delayed diagnosis • Has become one of the most curable solid tumour – Associated with accurate tumour markers – Origin in germ cells – Capacity to differentiate into histologically more benign forms – Predictable, systematic pattern of spread – Occurrence in young individuals
  • 4. Etiology/Risk Factors • Congenital Causes: Cryptorchidism Klinefelter’s syndrome • Age: 20-35 years highest risk group • Hormones Maternal hormone ingestion during pregnancy • History of mumps orchitis, inguinal hernia, hydrocele in childhood - Atrophy • High socioeconomic status • Testicular cancer contralateral testis • HIV positive.
  • 5. CRYPTORCHIDISM & TESTICULAR TUMOUR Risk of Carcinoma developing in undescended testis is 14 to 48 times the normal expected incidence
  • 6. CRYPTORCHIDISM & TESTICULAR TUMOUR The cause for malignancy are as follows: • Abnormal Germ Cell Morphology • Elevated temperature in abdomen & Inguinal region as opposed to scrotum • Endocrinal disturbances
  • 7. CLASSIFICATION I. Primary Neoplasma of Testis A.Germ Cell Tumour (90-95%) B.Non-Germ Cell Tumour (5-10%) II. Secondary Neoplasms. III. Paratesticular Tumours.
  • 8. PRIMARY NEOPLASMS OF TESTIS Germinal Neoplasms : (90 - 95 %) Seminomas - 40% (a) Classic Typical Seminoma (b) Anaplastic Seminoma (c) Spermatocytic Seminoma Teratoma - 25 - 35% (a) Mature (b) Immature Embryonal Carcinoma - 20 - 25% Choriocarcinoma - 1% Yolk Sac Tumour
  • 9. PRIMARY NEOPLASMS OF TESTIS Nongerminal Neoplasms : ( 5 to 10% ) Specialized gonadal stromal tumor (a) Leydig cell tumor (b) Sertoli’s cell tumour (c) Granulosa cell tumour (b) Other gonadal stromal tumor Gonadoblastoma Miscellaneous Neoplasms (a) Adenocarcinoma of the rete testis (b) Mesenchymal neoplasms (c) Carcinoid
  • 10. SECONDARY NEOPLASMS OF TESTIS A. Reticuloendothelial Neoplasms B. Metastases(prostate,lung,colorectal, renal cell carcinoma,thyroid,breast) PARATESTICULAR NEOPLASMS A. Adenomatoid B. Cystadenoma of Epididymis C. Mesenchymal Neoplasms D. Mesothelioma (Benign & malignant)
  • 11. SEMINOMA • Typical : 82-85% Thirties Slow growth • Anaplastic: 5-10% More aggressive, potentially more lethal Greater metastatic potential • Spermatocytic Seminoma: 2-12 % Cells closely resemble different phases of maturing spermatogonia B/L tumours have been reported Extremely low metastatic potential Favourable prognosis
  • 12. NON SEMINOMATOUS GERM CELL TUMOURS • Embryonal carcinoma  Generally discovered as a small, rounded but irregular mass invading the tunica vaginalis • Choriocarcinoma  May occur as palpable nodule or normal testis  Central hemorrhage  High metastatic potential (blood & lymphatic)  Most malignant tumor  Produces HCG
  • 13. NON SEMINOMATOUS GERM CELL TUMOURS • Teratoma  Contains more than one germ cell layers in various stages of maturation and differentiation  Grosssly large, lobulated, nonhomogenous tumours  Microscopically, cystic & solid componenets • Yolk cell tumours  Most common testicular tumour in infants & children  80% confined to testis at time of diagnosis
  • 14. Pathogenesis & Natural History of Testicular Tumour  Course of Spread of Germ Cell Tumours are predictible once histology of Tumour confirmed  Local invasion of epidydimis or spermatic cord is hindered by tunica albugenia  Lymphatic Spread has a set pattern depending on site of tumour  Seminoma may have non-seminomatous metastasis  High Grade Tumours spread by both Vascular invasion & via Lymphatics
  • 15. Pattern of Spread of Germ Cell Tumour  Right sided tumours- intraaortocaval  Left sided tumours – left paraaortic & preaortic nodes  Then cephalad to cisterna chyli, thoracic duct and supraclavicular (usually left)  Epidydimis- External iliac chain
  • 16. CLINICAL FEATURES • Nodule/Painless Swelling of One Gonad • Dull Ache or Heaviness in Lower Abdomen • 10% - Acute Scrotal Pain • 10% - Present with Metatstasis - Neck Mass / Cough / Anorexia / Back Ache • 5% - Gynecomastia • Infertility
  • 17. PHYSICAL EXAMINATION • Bimanual Palpation of testis and paratesticular structures • Abdominal examination • Lymph nodes • Chest
  • 18. WAKE UP All patients with a solid, Firm Intratesticular Mass that cannot be Transilluminated should be regarded as Malignant unless otherwise proved
  • 19. Differential Diagnosis • Metastasis from • Spermatocele prostate, lung, or • TB, gumma melanoma. • Leukemia • Epididymitis • Lymphoma
  • 20. Clinical Staging of Testicular Tumour Staging A or I - Tumour confined to testis. Staging B or II - Spread to Regional nodes. IIA - Nodes <2 cm in size or < 6 Positive Nodes IIB - 2 to 5 cm in size or > 6 Positive Nodes IIC - Large, Bulky, abd.mass usually > 5 to 10 cm Staging C or III - Spread beyond retroperitoneal Nodes or Above Diaphragm or visceral disease
  • 21. Requirements for staging To properly Stage Testicular Tumours following are pre- requisites: (a) Pathology of Tumour Specimen (b) History (c) Clinical Examination (d) Radiological procedure - USG / CT / MRI / Bone Scan (e) Tumour Markers - HCG, AFP
  • 22. TNM Staging of Testicular Tumour T0 = No evidence of Tumour T1s = Intratubular, pre invasive T1 = Confined to Testis T2 = Limited to testis and epididymis with vascular/ lymphatic invasion or tumour extending through Tunica Albuginea with involvement of tunica vaginalis T3 = Invades Spermatic Cord with/without vascular/ lymphatic invasion T4 = Invades Scrotum with/without vascular/ lymphatic invasion N1 = Single or multiple < 2 cm N2 = Multiple < 5 cm / Single 2-5 cm N3 = Any node > 5 cm Epididymis or Scrotal skin – Lymph drainage to Inguinal Nodes
  • 23. Investigation 1. Ultrasound - Hypoechoic area 2. Chest X-Ray - PA and lateral views 3. CT Scan 4. MRI 4. Tumour Markers - AFP - HCG - LDH - PLAP(placental alkaline phosphatase)
  • 24.
  • 25. Left Right Axial CT Section demonstarating - Left Hydronephrosis, due to large Para-Aortic Nodal Mass from a Germ cell tumour
  • 26. Tumour Markers TWO MAIN CLASSES • Onco-fetal Substances : AFP & HCG • Cellular Enzymes : LDH & PLAP ( AFP - Trophoblastic Cells HCG - Syncytiotrophoblastic Cells )
  • 27. AFP –( Alfafetoprotein ) NORMAL VALUE: Below 16 ngm / ml HALF LIFE OF AFP – 5 and 7 days Raised AFP : • Pure embryonal carcinoma • Teratocarcinoma • Yolk sac Tumour • Combined Tumour REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma
  • 28. HCG – ( Human Chorionic Gonadotropin ) Has and polypeptide chain NORMAL VALUE: < 1 ng / ml HALF LIFE of HCG: 24 to 36 hours RAISED HCG - 100 % - Choriocarcinoma 60% - Embryonal carcinoma 55% - Teratocarcinoma 25% - Yolk Cell Tumour 7% - Seminomas
  • 29. Lactate Dehydrogenase (LDH) • Nonspecific tumor marker but is a useful prognostic indicator • Indicator of tumor burden
  • 30. ROLE OF TUMOUR MARKERS • Helps in Diagnosis - 80 to 85% of Testicular Tumours have Positive Markers • Most of Non-Seminomas have raised markers • Only 10 to 15% Non-Seminomas have normal marker level • After Orchidectomy if Markers Elevated means Residual Disease or Stage II or III Disease • Elevation of Markers after Lymphadenectomy means a STAGE III Disease
  • 31. ROLE OF TUMOUR MARKERS cont... • Degree of Marker Elevation Appears to be Directly Proportional to Tumour Burden • Markers indicate Histology of Tumour: If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elements • Negative Tumour Markers becoming positive on follow up usually indicates - Recurrence of Tumour • Markers become Positive earlier than X-Ray studies
  • 32. PRINCIPLES OF TREATMENT • Treatment should be aimed at one stage above the clinical stage • Seminomas- Radio-Sensitive. Treat with Radiotherapy. • Non-Seminomas are Radio-Resistant and best treated by Surgery • Advanced Disease or Metastasis - Responds well to Chemotherapy
  • 33. PRINCIPLES OF TREATMENT • Radical INGUINAL ORCHIDECTOMY is Standard first line of therapy • Lymphatic spread initially goes to RETRO-PERITONEAL NODES • Early hematogenous spread RARE • Bulky Retroperitoneal Tumours or Metastatic Tumors Initially “DOWN-STAGED” with CHEMOTHERAPY
  • 34. Treatment of Seminomas Stage I, IIA, IIB – Radical Inguinal Orichidectomy followed by radiotherapy to Ipsilateral Retroperitonium & Ipsilateral Iliac group Lymph nodes Bulky stage II and III Seminomas - Radical Inguinal Orchidectomy is followed by Chemotherapy
  • 35. Treatment of Non-Seminoma Stage I and IIA: RADICAL ORCHIDECTOMY followed by RETROPERITONEAL LYMPH NODES DISSECTION Stage IIB: RPLND with possible ADJUVANT CHEMOTHERAPY Stage IIC and Stage III Disease: Initial CHEMOTHERAPY followed by SURGERY for Residual Disease
  • 36. Radical Orchiectomy • Inguinal approach • Testicle and spermatic cord are excised then sent for pathologic staging.
  • 37. Retroperitoneal Lymph Node Dissection • RPLND primary treatment (NSGCTs) • Remove abdominal lymph nodes
  • 38. Limits of Lymph Nodes Dissection For Right & Left Sided Testicular Tumours
  • 39. Chemotherapy BEP: (Bleomycin, Etoposide, Cisplatin) 2-4 cycles 21d intervals (4 most common) EP: (Etoposide, Platinol) 4 cycles 21d intervals
  • 40. Salvage Thearpy • No initial complete response • VIP: (Etoposide, Ifosamide,Mesna, Platinol) 3-4 cycles 21d intervals • High-dose chemotherapy with autologous bone marrow transplantation in selected patients with bulky disease
  • 41. Complications • Pulmonary toxicity: Bleomycin keep total dose under 400 units. • Nephrotoxicity: Cisplatin- decreased CrCl: Dosed based on CrCl • Neurologic: Cisplatin- Ototoxicity • Cardiovascular: HTN, MI, Angina • Secondary Malignancies: Etoposide
  • 42. Follow up – physical examinations, chest radiographs and serum tumor markers – CT scans detect recurrence in the retroperitoneum and chest – Follow-up protocols vary by institution, type, stage and treatment
  • 43. Recommended Exams • Every 2-3 months 1st yr. • Every 3-6 month 2nd yr. • Every 6 month remainder 5 yrs. • CTscans: 3-6 months 1st yr. then annually • Men at high risk: Annually with self-exam monthly
  • 44. Prognosis Seminoma (at 5 years) • I: 98% • IIA: 92-94% • IIB-III: 33-75% NSGT (at 5 years) • I: 96-100% • IIA: >90% • IIB-III: 55-80%
  • 45. CONCLUSION • Improved Overall Survival of Testicular Tumour due to Better Understanding of the Disease, Tumour Markers and Cis-platinum based Chemotherapy