Testicular tumours

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  • 1. Changes start to develop at the age of 2 yrs
  • 1.
  • dichlorodiphenyltrichloroethane
  • 1. Exception: spermatocytiv seminoma with sarcoma
  • 1. Post chemothearpy of embryonal cell they are found at metastatic sites.
  • 1. Post chemothearpy of embryonal cell they are found at metastatic sites.
  • Testicular tumours

    1. 1. Dr. Minhajuddin Khurram Moderator: Dr Sajid A. Mudhol (Prof . And HOD Dept. Of Surgery) Al-Ameen Medical College, Bijapur, India. TESTICULAR TUMOURS
    2. 2. IntroductionIntroduction Comprise a morphologically and clinically diverse group of tumors +1-2% of all malignancies 95% are Germ Cell Tumours (GCTs) Predominantly affects young males
    3. 3. EpidemiologyEpidemiology 1 -2 % of all cancers in USA 5 per 1 lac cases 90% GCT are in testes 2-5% in extra gonadal (eg retropreitoneum) Cure rate increased with introduction of platinum based chemotherapy from 10 to 80%
    4. 4. Predisposing FactorsPredisposing Factors 1. Cryptochordism 2. Positive family history 3. Positive personal history 4. Intratubular germ cell neoplasia 5. Trauma 6. Hormonal factors 7. Exposure to environmental oestrogen and contaminations
    5. 5. Predisposing FactorsPredisposing Factors 1. Cryptochordism  Most important risk factor  6 times higher risk1  Risk reduces to 2-3 times if orchidopexy done before puberty  One in five will have tumors in the normally descended testis  Probable pathogenesis: Increased gonadotrophins/ abnormal reaction to gonatrophins
    6. 6. Predisposing FactorsPredisposing Factors 2. Positive family history Men with first degree relative with testicular cancer Median age being less by 2-3 yrs Affected brother: 8-10 times more Affected father: 2-4 times
    7. 7. Predisposing FactorsPredisposing Factors 3. Positive personal history 12 folds increased risk of developing GCT in the contralateral testis Higher risk for contralateral tumor if  Younger age  Seminoma
    8. 8. Predisposing FactorsPredisposing Factors 4. Intratubular Germ Cell Neoplasia (ITGCN)  A precursor lesion  ITGCN consists of undifferentiated germ cells having appearance of seminoma located basally within seminiferous tubules.  No spermatogenesis  Present in adjascent testicular parenchyma in 80%  50% risk of GCT in 5 yrs, 70% in 7yrs  5-9% in unaffected contralateral testis; increases to 36% in atrophy or cryptochordism
    9. 9. Predisposing FactorsPredisposing Factors 5. Trauma  No link proved yet between trauma and testicular tumor  May simply draw the patient’s attention to the site  Or may possibly hasten the growth of the tumor
    10. 10. Predisposing FactorsPredisposing Factors 6. Hormonal Factors  Thought to be a contributing factor  Peak incidence after puberty  Tumors are more common in dizygous twin pregnancies than monozygous : More maternal oestrogen in dizygous pregnancy!!
    11. 11. Predisposing FactorsPredisposing Factors 7. Exposure to environmental oestrogen and contaminations Testicular tumors on a rise in the past 30yrs Synthetic oestrogen in plastics and detergents Exposure to DDT (dichlorodiphenyltrichloroethane): It is a potent androgen receptor antagonist Half life 60-100 yrs: trapped in food chain
    12. 12. ClassificationClassification Classified according to predominant cell type: 1. Germ Cell tumors (95%) a) Seminoma b) Embyonal cell carcinoma c) Choriocarcinoma d) Yolk sac tumor e) Teratoma
    13. 13. ClassificationClassification Classified according to predominant cell type: 2. Non Germ Cell tomors a) Interstitial Cell Tumors / Sex Cord / Stromal Tumors  Leydig cell tumors  Sertoli Cell Tumors  Gonadoblastoma  Granulosa Cell tumors a) Miscellaneous Testicular Neoplasms  Epidermoid cyst  Adenocarcinoma of rete testis a) Secondary Tumors  Lymphoma  Leukemic Infiltration  Metastases
    14. 14. ClassificationClassification Classified according to predominant cell type: 3. Tumors of the testicular adnexa a) Adenamatoid Tumor b) Cystadenoma c) Mesothelioma
    15. 15. WHOClassificationWHOClassification
    16. 16. SeminomaSeminoma The commonest variety of testicular tumour Adults are the usual target (4th and 5th decade); never seen in infancy Right > Left Testis Starts in the mediastinum: compresses the surrounding structure. Patients present with painless testicular mass 30 % have metastases at presentation, but only 3% have symptoms related to metastases
    17. 17. SeminomaSeminoma Serum alpha fetoprotein is normal Beta HCG is elevated in 30% of patients with Seminoma Classification (of no clinical significance) a) Typical b) Anaplastic c) Spermatocytic
    18. 18. SeminomaSeminoma Macroscopically: Characterized by a circumscribed lobular gray white fleshy tumor that have areas of necrosis & hemorrhage Cut surface in homogenous and greyish white or pinkish in colour
    19. 19. SeminomaSeminoma Microscopically: Typical seminoma Cells have round to oval nuclei with one to several nucleoli & clear to eosinophillic cytoplasm. Cell borders are well defined arranged in solid nests separated by fibrous septa. Active lymphocytic infiltration in 80% cases. Strongly positive for placental Alkaline phosphatase (PLAP)
    20. 20. SeminomaSeminoma Microscopically:
    21. 21. Spermatocytic SeminomaSpermatocytic Seminoma A rare GCT and accounts for less than 1% It represents a distinct clinicopathological entity from other GCT Does not arise from ITGCN Not associated with crytochordism Benign tumour; complete cure by orchidectomy1 Not positive to PLAP
    22. 22. Spermatocytic SeminomaSpermatocytic Seminoma Microscopically: Three types of cells: a) Small cells with narrow rim of cytoplasm resembling secondary spermatocytes b) Medium sized cells with eosonophilic cytoplasm c) Scattered Giant cells No lymphocytic infiltration
    23. 23. Embryonal CarcinomaEmbryonal Carcinoma 2nd most common germ cell tumor Present in majority of mixed germ cell tumors Most men present in their 20s to 30s with a testicular mass Highly malignant tumours; may invade the cord stuctures High degree of metastasis Serum AFP is normal , & beta HCG is elevated in 60 % of cases
    24. 24. Embryonal CarcinomaEmbryonal Carcinoma Macroscopically: Tan to yellow neoplasms (fleshy tumor) that exhibit large areas of hemorrhage and necrosis. Microscopically: Undifferentiated malignant cells with crowded pleomorphic nuclei Solid sheets, Papillary Glandular Tubular arrangement of cells • Most undifferentiated; capacity to differentiate to other NSGCT within primary or mets
    25. 25. Embryonal CarcinomaEmbryonal Carcinoma
    26. 26. Embryonal CarcinomaEmbryonal Carcinoma
    27. 27. ChoriocarcinomaChoriocarcinoma A rare and aggressive tumour (5yrs survival is 5%) Typically elevated hCG Presents with disseminated disease Metastasis to lungs and brain Primary is very small and often exhibit NO TESTICULAR ENLARGEMENT Small palpable nodule may be present. Prone to hemorrhage, sometimes spontaneous (lungs and brain) Catastrophic hemorrhage immediately after chemotherapy;
    28. 28. ChoriocarcinomaChoriocarcinoma Macroscopically: Primary lesion may be a hemorrhagic or a clotted mass in which bits of grey tumor can be seen Presents as nodules • Microscopically: Consists of both syncitiotrophoblast and cytotrophoblast Prominent areas of hemorrhage and necrosis.
    29. 29. ChoriocarcinomaChoriocarcinoma
    30. 30. Yolk Sac TumourYolk Sac Tumour Most common germ cell tumor ( & most common testicular tumor ) in children, where it occurs in its pure form. In adults, it is unusual in pure form, but is found approx. 50 % of mixed germ cell tumors. Testicular mass the most usual presentation. Always produce AFP, never hCG Easily detectable, lower relapse
    31. 31. Yolk Sac TumourYolk Sac Tumour Macroscopically: White to tan masses, with myxoid & cystic changes • Microscopically: Reticular network of medium sized cuboidal cellswith cytoplasmic and extracytoplasmic eosinophil, hyaline like goblets (84%) Glandular, papillary or microcystic pattern Schiller-Duval bodies are characteristic
    32. 32. TeratomaTeratoma Teratoma in greek means “monster tumor” Occurs in its pure form with a mean age of diagnosis at 20 months In adults, occur as a component of mixed germ cell tumor & is identified in > 47 % of mixed tumors. Pure teratomas are uncommon. Normal serum markers. ◦ Mildly elevated AFP levels
    33. 33. TeratomaTeratoma Histologically benign, but found at metastatic sites in NSGCT Perhaps metastatised as Embryonal cell ca They are resistant to chemotherapy1 Surgical resection required post chemotherapy in 40-50% cases
    34. 34. TeratomaTeratoma Growing Teratoma Syndrome: May grow uncontrollably, invade the surrunding tissueand become unresectable Teratoma with malignant transformation Rarely teratoma may transform into a somatic malignancy such as rhabdomyosarcoma, adenocarnoma or primitive neuroectodermal tumour
    35. 35. TeratomaTeratoma Macroscopically: Largely depends on elements within it with solid & cystic areas Microscopically: Contain more than one germ cell layers(ectoderm, endodermand mesoderm). Range from “mature” with well differentiated tissue to “immature” with undifferentiated primitive tisuue. Composed of somatic type of tissues that include enteric type glands, respiratory epithelium, cartilage, muscles, hair etc. Immature Teratomas contain immature neuroepithelium, blastema or cellular stroma. Can give rise to carcinoma, such as adenocarcinoma , or sarcoma, such as rhabdomyosarcoma.
    36. 36. TeratomaTeratoma
    37. 37. SpreadSpread 1. Direct Spread:  This spread occurs by invasion.  Whole of testis in involved and restricted  Tunica albuginea is rarely penetrated  May be crossed by “blunder biopsy”  Scrotal skin involvement  Fungation on the anterior aspect  Spread to spermatic cord and epidedymis may occur : points towards bad prognosis
    38. 38. SpreadSpread 1. Direct Spread:
    39. 39. SpreadSpread 2. Lyphatic spread: Seminoma metastasize exclusively through lymphatics They drain primarily to para-aortic lymph nodes in the region of origin of tetsticular arteries Left supraclavicular fossa through the thoracic duct Lymph from medial side of testes run along the artery to the vas to drain to nodes at the bifurcation of common iliac No inguinal nodes until scrotal skin involvement
    40. 40. SpreadSpread 2. Lyphatic spread:
    41. 41. SpreadSpread 3. Blood Spread  NSGCT spread through blood route  Lungs, liver, bones and brain are the usual sites usually involved
    42. 42. Clinical Features / PresentaionClinical Features / Presentaion 1. Due to primary tumor a) Painless testicular lump b) Sensation of heaviness if size > than 2-3 times c) Rarely dragging pain is complained of (1/3rd cases) d) May mimic epidedymo-orchitis e) Sudden pain and enlargement due to hemorrhage mimicking torsion f) History of trauma (co-incidental)
    43. 43. Clinical Features / PresentaionClinical Features / Presentaion 2. Due to metastasis  Abdominal or lumbar pain (lymphatic spread)  Mass in epigastrium  Dyspnoea, hemoptysis and chest pain with lung mets  Jaundice with liver mets  Hydronephrosis by para-aortic lymph nodes enlargement  Pedal oedema by IVC obstruction  Troiser’s sign
    44. 44. Clinical Features / PresentaionClinical Features / Presentaion 3. Clinical examination: a) Enlarged testis (except choriocarcinoma) b) Nodular testis c) Firm to hard in consistency d) Loss of testicular sensation (be gentle) e) Secondary hydrocele f) Flat and difficult to feel epidedymis g) Sign of Vas negetive h) General examination for mets
    45. 45. Clinical Features / PresentaionClinical Features / Presentaion 3. Clinical examination: a) Enlarged testis (except choriocarcinoma) b) Nodular testis c) Firm to hard in consistency d) Loss of testicular sensation (be gentle) e) Secondary hydrocele f) Flat and difficult to feel epidedymis g) Sign of Vas negetive h) General examination for mets
    46. 46. InvestigationsInvestigations 1. USG testes: gold standard 2. Tumor markers/ hormones a) AFP b) Beta hCG 3. Chest radiography 4. USG abdomen 5. CT abdomen 6. MRI: intra-abdominal and intra-thoracic secondaries 7. IVP and RFT : obstruction on ureters
    47. 47. Clinical StagingClinical Staging Stage I – Tumor confined to the testis Stage II – Nodal disease present but confined to below the diaphragm Stage III – Nodal disease above the diaphragm Stage IV – Nonlymphatic metastatic disease
    48. 48. AJCC Staging (TNM)AJCC Staging (TNM) Primary Tumor (pT) pTx: Primary tumor cannot be assessed pT0: No evidence of primary tumor pTis: ITGCN pT1: Tumor confined to testicle; may invade into the albuginea but not the tunica vaginalis pT2: Tumor extending thru tunica albuginea with involvement of tunica vaginalis or the presence of angiolymphatic invasion. pT3: Spermatic cord involvement. pT4: Scortal involvement
    49. 49. AJCC Staging (TNM)AJCC Staging (TNM) Regional Lymph nodes (by non-invasive assessment) Nx: nodal status unknown. N0: No regional lymph node metastasis. N1:single or multiple lymph node involved, < 2 cm N2: single node, 2-5 cm or multiple nodes < 5 cm N3:any nodes > 5 cm
    50. 50. AJCC Staging (TNM)AJCC Staging (TNM) Distant metastasis (M) Mx: status of metastases unknown M0: no distant metastasis M1: Distant metastasis
    51. 51. TreatmentTreatment 1. Inguinal orchidectomy as soon as the diagnosis is confirmed 2. Then the treatment differs as per the histological type: seminoma or NSGCT
    52. 52. TreatmentTreatment 1. Scrotal exploration and orchidectomy for suspected testicular tumor  Orchidectomy undertaken by the inguinal incision  Spermatic cords are displayed  A soft clamp applied across the cord  Mobilise testis to the wound  If neseccary, bisect the testes along the anterior convexity to examine  Take biopsy, send for frozen section  In case of tumor, double transfix and divide at the level of the deep ring  Some advice hemi-scrotectomy along with orchidectomy
    53. 53. TreatmentTreatment 2. Radio/Chemotherapy A. Stage I tumor:  Seminomas:  Radio-sensitive and chemo sensitive (platinum based regimen)  Current protocol: radiotherapy is the mainstay of treatment with CT and tumor marker based surveillance  In men who demonstrate relapse, chemotherapy to be applied  NSGCT  Not radio-sensitive  Subjected to BEP (Bleomycin, etoposide and cis-platinum)
    54. 54. TreatmentTreatment 2. Radio/Chemotherapy A. Stage II- IV  Combination chemotherapy for seminoma and NSGCT  RPLND needed in some cases for post chemotherapy masses in the retroperitoneum
    55. 55. TreatmentTreatment  Radiotherapy:  Given to para-aortic and ipsilateral lymph nodes, field extending from D10-11interspace to the lower border of the obturator foramen  Anterior and posterior fields are given alternatively  Laterally to the hila of the kidneys  Contralateral testis being protected by thick lead cups  High enery Xrays- 6-8MeV with linear accilerator  3000 rads delivered in 3-4 wks
    56. 56. TreatmentTreatment  Chemotherapy Chemotherapy Toxicity BEP - Bleomycin Pulmonary fibrosis Etoposide (VP-16) Myelosuppression Alopecia Renal insufficiency(mild) Secondary leukemia Cis-platin Renal insufficiency Nausea, vomiting Neuropathy
    57. 57. TreatmentTreatment Retroperitoneal lymph node dissection: Rationale for RPLND: The retroperitoneum is the most common site of occult metastasis 15-25% of retroperitoneal teratoma, resistant to cheotherapy Low risk of Abdomino-pelvic recurrence no need for long term surveillance after bilateral RPLND Offers high cure rates The long term survival approaches 100% with RPLND + adjuvant chemotherapy Disadvantage: Experienced surgeon Major surgical procedure
    58. 58. TreatmentTreatment Lymph node dissection:
    59. 59. SurveillanceSurveillance Rationale for surveillance: 70-80% patients of stage I are cured by orchidectomy alone No need of chemotherapy in majority of the patients The disadvantages being: Higher risk of relapse Need for long term surveillance (>5yrs) Potential for secondary malignancies by surveillance CT More intensive therapy required in cases of relapse than primary chemotherapy
    60. 60. SurveillanceSurveillance No fixed surveillance protocol Surveillance imaging and testing intense in first 2 yrs Less frequent in 3-5 yrs Surveillance after 5 yrs for late relapse Different studies had surveillance CT scans 2-13 times in 5 yrs
    61. 61. Interstitial cell tumorsInterstitial cell tumors 1. Leydig cell tumors Considered a pre-ubertal tumor May affect 20-60yrs of age A masculinising tumor, produces androgens No association with crytochordism Presents with painless testicular mass Precocious puberty  Prominent external genitalia  Deep masculinised voice  Pubic hair Gynacomastia and decreased libodo due to oestrogen production by perpheral conversion
    62. 62. Interstitial cell tumorsInterstitial cell tumors 1. Leydig cell tumors 10% are malignant Orchidectomy is te treatment of choice Regression of symptoms after orchidectomy may not be complete Metastasize by blood to lungs and retroperitoneum Abdominopelvic CT, chest Xray, RPLND Insensitive to radiotherapy and chemtherapy
    63. 63. Interstitial cell tumorsInterstitial cell tumors 2. Sertoli Cell Tumor  Considered a post pubertal tumor  But can occur in any age group including infants  No association with crytochordism  Gynacomastia in 1/3rd of cases  10 % are malignant  Inguinal orchidectomy is the treatment  RPLND  Radiotherapy and chemotherapy are ineffective
    64. 64. Interstitial cell tumorsInterstitial cell tumors 3. Gonadoblastoma  Mixed germ cell/sex cord/stromal tumor  Composed of seminoma like germ cells and Sertoli differentiation  Exclusively in patients with dysgenic gonads and intersex syndromes  80% are phenotype females with primary amenorrhoea  20% are males with crytochordism and dysgenic gonads and hypospadias
    65. 65. Interstitial cell tumorsInterstitial cell tumors 3. Gonadoblastoma  Considered in-situ malignant form of GCT  Bilateral orchidectomy because of risk of bilateral tumours
    66. 66. Miscellaneous Testicular NeoplasmsMiscellaneous Testicular Neoplasms 1. Epidermoid Cyst  A rare benign neoplasm  Mondermally differentiated teratoam  Resemmbles Dermoid cyst  Enucleation or orchidectomy  HPR is must
    67. 67. Miscellaneous Testicular NeoplasmsMiscellaneous Testicular Neoplasms 2. Adeno-carcinoma of rete testis  A rare but highly malignant neoplasm  Arises from collecting system of testis  Usual presentation: painless swellinng with hydrocoele  More than 50% present with mets  Mean survival period is 1 yr  Radiotherapy and chemotherapy are ineffective  RPLND in cases of limited retroperitoneal mets
    68. 68. Secondary tumorsSecondary tumors 1. Lymphoma  Primary testicular Non-Hodgekin’s lymphoma is rare  Mostly involvement of testes by dissemination from other sites  Bilateral involvement in 35 % cases  Presents as painless testicular mass  25% have systemic symptoms (fever, night sweats and weight loss)  10% CNS involvement  Radical inguinal orchidectomy  Refer to heamto-oncologist for staging and subsequent therapy
    69. 69. Secondary tumorsSecondary tumors 2. Leukemic Infiltration  Relapse of ALL in testes  Diagnosis by biopsy  No orchidectomy  Local control with low dose radiotherapy (20Gy)  Should include the contralateral testis: Bilateral involvement
    70. 70. Secondary tumorsSecondary tumors 3. Metastases  Metastases from prostate cancer  Lung cancer  Melanoma  Colon cancer  Kidney malignancy  Presents as diffuse metastatic disease
    71. 71. Tumours of the Testicular AdnexaTumours of the Testicular Adnexa 1. Adenomatoid  Most cmmon paratesticular tumour  Involving the epidedymis mostly  May arise from spermatic cord  Presents as small (0.5 to 5cm) painless paratesticular mass detected on routine examination  3rd to 4th decade of life  Benign  Excision by inguinal route
    72. 72. Tumours of the Testicular AdnexaTumours of the Testicular Adnexa 2. Cystadenoma  Cystadenoma is benign epithelial hyperplasia of epidedymis  Multicystic  Glandular or pappillary configuration 3. Mesothelioma  Arises from tunica vaginalis  Painless scrotal mass with hydrocele  Older adults  Both Benign and malignant varieties have been identified  Malignant cases ralted to asbestos exposure  Radical orchidectomy  RPLND in malignant cases
    73. 73. ReferencesReferences 1. Textbook of Urology 10th Ed. By Cambell and Walsh 2. Short practice of surgery, Bailey and Love 3. A concise textbook of surgery by Dr S. Das
    74. 74. THANK YOU

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