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Testicular cancer
&
Wilms tumor
Dr. RUTAYISIRE François Xavier
PGY1
Common surgical conditions module
University of Rwanda
Lecturer: Dr. Alexandre NYIRIMODOKA
Definition
• Testicular cancer is cancer that develops in the testicles, a part of the
male reproductive system
Epidemiology
• Account for 1% of all solid tumors in male.
• Age – most common solid tumor of men between 15-35 years
• Side – Right > Left
• Socio-economic status – high : low = 2:1
• Geographical
• Highest in Scandinavia, Germany, Switzerland
• Intermediate – USA & UK
• Low – Africa and Asia
Anatomy
• The testis is the male gonad.
• It is homologous with the ovary
in female.
• It lies obliquely within the
scrotum suspended by the
spermatic cord
• The left testis is slightly lower
than the right
• Shape: Oval
• Weight: about 10-15 gm.
Arterial supply
• The testicular artery branch of
abdominal aorta .
• The testis has collateral blood supply from
1. the cremasteric artery
2. artery to the ductus deferens
Venous drainage
• The veins emerge from the back of the
testis, and receive tributaries from the
epididymis; they unite and form convoluted
plexus, called the
pampiniform plexus.
• plexus to form a single vein, which opens,
on the right side, into the inferior vena
cava ,on the left side into the left renal
vein
Lymphatic Drainage
• Drain into the retroperitoneal lymph nodes
between the levels of T11 and L4, but they are
concentrated at the level of the L1 and L3
vertebrae
• Lymph nodes located lateral or anterior to the
inferior vena cava are called paracaval or precaval
nodes, respectively.
Interaortocaval nodes are located between the
inferior vena cava and the aorta.
• Nodes anterior or lateral to the aorta are preaortic
or paraaortic nodes, respectively
Lymphatic Drainage
• On the right:
Interaortocaval region, followed by the
paracaval, preaortic, and paraaortic lymph nodes.
On the left:
Preaortic and para-aortic nodes and thence to
the interaortocaval.
Metastatic nodal disease to the common
iliac, external iliac, or inguinal lymph nodes is
usually secondary to a large volume of disease
with retrograde spread.
If the patient has undergone a
herniorrhaphy, vasectomy, or other transscrotal
procedure, metastasis to the pelvic and
inguinal lymph nodes is more likely
Through the thoracic duct to lymph nodes in
the posterior mediastinum and supraclavicular
fossae and occasionally to the axillary nodes.
Contralateral spread is mainly seen with
right-sided tumors.
In 15% to 20%, bilateral nodes are involved
Predisposing Factors
•1. Cryptorchidism
2. Positive family history
4. Positive personal history
5. Intratubular germ cell neoplasia
6. Trauma
7. Viral infection
8. Hormonal factors
9. Exposure to environmental oestrogen
Seminoma
• 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
• Serum alpha fetoprotein is normal
• Beta HCG is elevated in 30% of patients with Seminoma
• Classification
a) classical
b) Anaplastic
c) Spermatocytic
Spread
1. Lymphatic spread:
Seminoma metastasize exclusively
through lymphatics
They drain primarily to para-aortic
lymph nodes
From RPLN drain into cysterna chili,
thoracic duct ,posterior mediastinum &
left supraclavicular 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
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 epididymis may
occur : points towards bad prognosis
blunder
/ˈblʌndə/
noun
noun: blunder; plural noun: blunders
1.a stupid or careless mistake.
verb
2.make a stupid or careless mistake; act or speak
clumsily.
Definitions
• 3. Blood Spread
NSGCT spread through blood route
Lungs, liver, bones and brain are the usual sites usually involved
Clinical Features
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) History of trauma (co-
incidental)
e)History of cryptorchidism or
previous testicular cancer
• 2. Due to metastasis
Abdominal or lumbar pain
(lymphatic spread)
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
Clinical examination:
a) Enlarged testis (except choriocarcinoma)
b) Nodular irregular testis
c) Firm to hard in consistency
d) Loss of testicular sensation
e) Secondary hydrocele
f) Flat and difficult to feel epididymis
g) General examination for metastasis
WAG 2002 UBC Phase IV Urology
Self - Examination
Self – examination should
be taught to young men
They need to be shown
the difference between the
testicle and the epididymis
They need to report any
hard or suspicious lesions
immediately
Diagnostic modalities
• General
History (document cryptorchidism
and previous inguinal or scrotal
surgery)
Physical examination
• Laboratory Studies
CBC, LFT, RFT, LDH
• Serum assays
Alpha fetoprotein (AFP)
Beta human chorionic
gonadotropin
• Diagnostic Radiology
– Chest x-ray films, PA and lateral
views
– Computed tomography (CT) scan of
abdomen and pelvis
– CT scan of chest for non seminomas
and stage II seminomas
–Ultrasound of the ipsilateral testes
and of contralateral testis
Clinical Staging
(Boden and Gibbs – 1971)
• Stage I (A) – confined to testis with no spread
through capsule or spermatic cord
• Stage II (B) – Clinical or radiological evidence of
spread beyond testis but with in regional L.N.
• B1 -<2cm
• B2 -2-5cm
• B3 - >5cm
• Stage III (C) - Disseminated above diaphragm /
visceral disease
Management
• Multimodal approach
Surgery
Chemotherapy
Radiotherapy
• NB: On clinical assessment: any painless solid mass in the testis is
malignant until proven otherwise
• Biopsy is contraindicated
Management
• Inguinal Exploration & radical orchiectomy:
all patients done via an inguinal incision, with
cross clamping of spermatic cord vasculature
and delivery of testis into the surgical field.
Scrotal violation, increased local/regional
recurrence, but no difference in distant
recurrence rate or overall survival.
Wilms Tumor
• Wilms' tumor or nephroblastoma is malignant tumor of the kidneys that
typically occurs in children.
• Dr. Max Wilms, the German surgeon (1867–1918) first described this kind of tumor.
Epidemiology
• Wilms tumor is the fifth most common pediatric malignancy (7% of all
childhood tumors).
• Incidence is 1 in 10,000,
• Girls are slightly more affected
• 70% of cases occur before the child is 5 years of age.
• Most commonly unilateral, but in 5% - 10% both kidneys are involved.
• The tumor involves left kidney more than right kidney.
• The majority (75%) occurs in otherwise normal children; a minority
(25%) is associated with other developmental abnormalities.
• It is highly responsive to treatment, with about 90% of patients
surviving at least five years.
Etiology
• Unknown,
• But it has been identified that tumor
suppressor gene acts to promote normal
kidney development.
• This gene may be absent or missing in
wilm’s tumor.
• Genetic abnormalities WT1 gene;
dominant oncogene (at chromosome
11p13), WT2 gene (at chromosome
11p15)
• It is believe that tumor begins to grow as a
fetus develops in the womb, with some
cells that are destined to form into the
kidneys malfunctioning and forming a
tumor.
• Wilms tumor has capacity for rapid
growth, usually grows to a large size.
Clinical features
• Wilms tumor is diagnosed at a mean age of 3.5 years.
• The most common feature is an upper quadrant abdominal mass (firm,
nontender)
• Abdominal pain occurs in 30%-40% of cases, related to rapid growth of
tumor.
• Urethral obstruction due to compression
• Constipation, vomiting, abdominal ditress, anorexia, weight loss and
dyspnea due to enlargement of tumor.
• Other signs and symptoms of Wilms tumor include hypertension, fever
caused by tumor necrosis, hematuria, and anemia.
• The neoplasm metastasize either by direct extension or by bloodstream.
• They may invade perirenal tissues, lymph nodes, the liver, the diaphragm,
abdominal muscles and the lungs.
• Invasion of bone and brain are less common.
Diagnostic evaluation
• Laboratory studies:
• FBC for baseline data
• Platelet count: Coagulation
abnormalities
• Urinalysis for hematuria and urine
culture
• Liver function tests
• Renal function tests
• Blood chemistry; sr. electrolytes,
uric acid
• Imaging Studies
• Ultrasonography
– Initial diagnosis of a renal or abdominal
mass,
– Possible renal vein or inferior vena cava
(IVC)
thrombus (Doppler flow study may be helpful
in the setting of vascular invasion.)
– Information regarding liver and other kidney
CT scanning of the chest and abdomen
– Differential diagnosis of a kidney tumor
versus
adrenal tumor (neuroblastoma)
– Liver metastases
– Status of opposite kidney
– Lymph node assessment
– Status of chest with respect to metastases
• Chest radiography - As a baseline for
pulmonary metastases
• Magnetic resonance imaging
MANAGEMENT
• The management of children with
wilm’s tumor include:
• Radiation therapy
• Chemothrapy
• Surgical management
Radiation Therapy
Wilm’s tumor may be bilateral or
large in size , may be inoperable, for
such cases radiation therapy may be
used to reduce the size of tumor, so
that surgery can be performed.
• CHEMOTHERAPY
• The objective of chemotherapy is
to treat any metastatic lesions that
may exist and destroy any cells in
blood stream, before they get
implanted.
• The drugs used for chemotherapy
are •Actinomycin D; 0.06 - 0.12
mg/kg, IV, Doxorubicin (
adriamycin); 1.25 – 1.9 mg/ kg,
Vincristine; 0.125 – 0.05 mg/kg
• SURGICAL MANAGEMENT
Staging and treatment
• Staging is determined by
combination of imaging studies
and pathology findings.
• Treatment strategy is
determined by the stage.
• Stage I (43% of patients)-
Tumor limited to kidney and
completely resectable.
• Treatment:
• Nephrectomy +/- 18 weeks of
chemotherapy depending on
age of patient and weight of
tumor.
• EG: less than 2 years old and
less than 550g only requires
Nephrectomy with observation.
• Outcome: 98% 4-year survival
Stage II
• Stage II (23% of
patients)- Tumor extend
beyond kidney , into
nearby fatty tissue, but it
is resectable.
Treatment:
• Nephrectomy + abdominal
radiation + 24 weeks of
chemotherapy
• Outcome: 96% 4-year
survival.
Stage III
• Stage III (23% of patients) –
Non hematogenous spread in
abdomen, like spread to
lymph nodes in abdomen or
pelvis, but this stage tumor is
not completely resectable.
• Treatment:
• Abdominal radiation + 24 weeks
of chemotherapy + nephrectomy
after tumor shrinkage
• Outcome: 95% 4-year survival
• Stage IV (10% of patients)
• Stage IV Wilms' tumor is defined
as the presence of hematogenous
metastases (lung, liver, bone, or
brain), or lymph node metastases
outside the abdominopelvic region.
• Treatment:
• Nephrectomy + abdominal
radiation + 24 weeks of
chemotherapy + radiation of
metastatic site as appropriate.
• Outcome: 90% 4-year survival
• Stage V (5% of patients)
• Stage V Wilms’ tumor is defined
as bilateral renal involvement at
the time of initial diagnosis.
• The 4-year survival in 94%
patients with stage I or stage II;
76% for with stage III.
• Treatment: Individualized
therapy based on tumor
burden
Thank you

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Testicular cancer.pptx

  • 1. Testicular cancer & Wilms tumor Dr. RUTAYISIRE François Xavier PGY1 Common surgical conditions module University of Rwanda Lecturer: Dr. Alexandre NYIRIMODOKA
  • 2. Definition • Testicular cancer is cancer that develops in the testicles, a part of the male reproductive system
  • 3. Epidemiology • Account for 1% of all solid tumors in male. • Age – most common solid tumor of men between 15-35 years • Side – Right > Left • Socio-economic status – high : low = 2:1 • Geographical • Highest in Scandinavia, Germany, Switzerland • Intermediate – USA & UK • Low – Africa and Asia
  • 4. Anatomy • The testis is the male gonad. • It is homologous with the ovary in female. • It lies obliquely within the scrotum suspended by the spermatic cord • The left testis is slightly lower than the right • Shape: Oval • Weight: about 10-15 gm.
  • 5. Arterial supply • The testicular artery branch of abdominal aorta . • The testis has collateral blood supply from 1. the cremasteric artery 2. artery to the ductus deferens Venous drainage • The veins emerge from the back of the testis, and receive tributaries from the epididymis; they unite and form convoluted plexus, called the pampiniform plexus. • plexus to form a single vein, which opens, on the right side, into the inferior vena cava ,on the left side into the left renal vein
  • 6. Lymphatic Drainage • Drain into the retroperitoneal lymph nodes between the levels of T11 and L4, but they are concentrated at the level of the L1 and L3 vertebrae • Lymph nodes located lateral or anterior to the inferior vena cava are called paracaval or precaval nodes, respectively. Interaortocaval nodes are located between the inferior vena cava and the aorta. • Nodes anterior or lateral to the aorta are preaortic or paraaortic nodes, respectively
  • 7. Lymphatic Drainage • On the right: Interaortocaval region, followed by the paracaval, preaortic, and paraaortic lymph nodes. On the left: Preaortic and para-aortic nodes and thence to the interaortocaval. Metastatic nodal disease to the common iliac, external iliac, or inguinal lymph nodes is usually secondary to a large volume of disease with retrograde spread. If the patient has undergone a herniorrhaphy, vasectomy, or other transscrotal procedure, metastasis to the pelvic and inguinal lymph nodes is more likely Through the thoracic duct to lymph nodes in the posterior mediastinum and supraclavicular fossae and occasionally to the axillary nodes. Contralateral spread is mainly seen with right-sided tumors. In 15% to 20%, bilateral nodes are involved
  • 8. Predisposing Factors •1. Cryptorchidism 2. Positive family history 4. Positive personal history 5. Intratubular germ cell neoplasia 6. Trauma 7. Viral infection 8. Hormonal factors 9. Exposure to environmental oestrogen
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  • 10. Seminoma • 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 • Serum alpha fetoprotein is normal • Beta HCG is elevated in 30% of patients with Seminoma • Classification a) classical b) Anaplastic c) Spermatocytic
  • 11. Spread 1. Lymphatic spread: Seminoma metastasize exclusively through lymphatics They drain primarily to para-aortic lymph nodes From RPLN drain into cysterna chili, thoracic duct ,posterior mediastinum & left supraclavicular 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
  • 12. 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 epididymis may occur : points towards bad prognosis blunder /ˈblʌndə/ noun noun: blunder; plural noun: blunders 1.a stupid or careless mistake. verb 2.make a stupid or careless mistake; act or speak clumsily. Definitions
  • 13. • 3. Blood Spread NSGCT spread through blood route Lungs, liver, bones and brain are the usual sites usually involved
  • 14. Clinical Features 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) History of trauma (co- incidental) e)History of cryptorchidism or previous testicular cancer • 2. Due to metastasis Abdominal or lumbar pain (lymphatic spread) 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
  • 15. Clinical examination: a) Enlarged testis (except choriocarcinoma) b) Nodular irregular testis c) Firm to hard in consistency d) Loss of testicular sensation e) Secondary hydrocele f) Flat and difficult to feel epididymis g) General examination for metastasis
  • 16. WAG 2002 UBC Phase IV Urology Self - Examination Self – examination should be taught to young men They need to be shown the difference between the testicle and the epididymis They need to report any hard or suspicious lesions immediately
  • 17. Diagnostic modalities • General History (document cryptorchidism and previous inguinal or scrotal surgery) Physical examination • Laboratory Studies CBC, LFT, RFT, LDH • Serum assays Alpha fetoprotein (AFP) Beta human chorionic gonadotropin • Diagnostic Radiology – Chest x-ray films, PA and lateral views – Computed tomography (CT) scan of abdomen and pelvis – CT scan of chest for non seminomas and stage II seminomas –Ultrasound of the ipsilateral testes and of contralateral testis
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  • 19. Clinical Staging (Boden and Gibbs – 1971) • Stage I (A) – confined to testis with no spread through capsule or spermatic cord • Stage II (B) – Clinical or radiological evidence of spread beyond testis but with in regional L.N. • B1 -<2cm • B2 -2-5cm • B3 - >5cm • Stage III (C) - Disseminated above diaphragm / visceral disease
  • 20. Management • Multimodal approach Surgery Chemotherapy Radiotherapy • NB: On clinical assessment: any painless solid mass in the testis is malignant until proven otherwise • Biopsy is contraindicated
  • 21. Management • Inguinal Exploration & radical orchiectomy: all patients done via an inguinal incision, with cross clamping of spermatic cord vasculature and delivery of testis into the surgical field. Scrotal violation, increased local/regional recurrence, but no difference in distant recurrence rate or overall survival.
  • 22. Wilms Tumor • Wilms' tumor or nephroblastoma is malignant tumor of the kidneys that typically occurs in children. • Dr. Max Wilms, the German surgeon (1867–1918) first described this kind of tumor.
  • 23. Epidemiology • Wilms tumor is the fifth most common pediatric malignancy (7% of all childhood tumors). • Incidence is 1 in 10,000, • Girls are slightly more affected • 70% of cases occur before the child is 5 years of age. • Most commonly unilateral, but in 5% - 10% both kidneys are involved. • The tumor involves left kidney more than right kidney. • The majority (75%) occurs in otherwise normal children; a minority (25%) is associated with other developmental abnormalities. • It is highly responsive to treatment, with about 90% of patients surviving at least five years.
  • 24. Etiology • Unknown, • But it has been identified that tumor suppressor gene acts to promote normal kidney development. • This gene may be absent or missing in wilm’s tumor. • Genetic abnormalities WT1 gene; dominant oncogene (at chromosome 11p13), WT2 gene (at chromosome 11p15) • It is believe that tumor begins to grow as a fetus develops in the womb, with some cells that are destined to form into the kidneys malfunctioning and forming a tumor. • Wilms tumor has capacity for rapid growth, usually grows to a large size.
  • 25. Clinical features • Wilms tumor is diagnosed at a mean age of 3.5 years. • The most common feature is an upper quadrant abdominal mass (firm, nontender) • Abdominal pain occurs in 30%-40% of cases, related to rapid growth of tumor. • Urethral obstruction due to compression • Constipation, vomiting, abdominal ditress, anorexia, weight loss and dyspnea due to enlargement of tumor. • Other signs and symptoms of Wilms tumor include hypertension, fever caused by tumor necrosis, hematuria, and anemia. • The neoplasm metastasize either by direct extension or by bloodstream. • They may invade perirenal tissues, lymph nodes, the liver, the diaphragm, abdominal muscles and the lungs. • Invasion of bone and brain are less common.
  • 26. Diagnostic evaluation • Laboratory studies: • FBC for baseline data • Platelet count: Coagulation abnormalities • Urinalysis for hematuria and urine culture • Liver function tests • Renal function tests • Blood chemistry; sr. electrolytes, uric acid • Imaging Studies • Ultrasonography – Initial diagnosis of a renal or abdominal mass, – Possible renal vein or inferior vena cava (IVC) thrombus (Doppler flow study may be helpful in the setting of vascular invasion.) – Information regarding liver and other kidney CT scanning of the chest and abdomen – Differential diagnosis of a kidney tumor versus adrenal tumor (neuroblastoma) – Liver metastases – Status of opposite kidney – Lymph node assessment – Status of chest with respect to metastases • Chest radiography - As a baseline for pulmonary metastases • Magnetic resonance imaging
  • 27. MANAGEMENT • The management of children with wilm’s tumor include: • Radiation therapy • Chemothrapy • Surgical management Radiation Therapy Wilm’s tumor may be bilateral or large in size , may be inoperable, for such cases radiation therapy may be used to reduce the size of tumor, so that surgery can be performed. • CHEMOTHERAPY • The objective of chemotherapy is to treat any metastatic lesions that may exist and destroy any cells in blood stream, before they get implanted. • The drugs used for chemotherapy are •Actinomycin D; 0.06 - 0.12 mg/kg, IV, Doxorubicin ( adriamycin); 1.25 – 1.9 mg/ kg, Vincristine; 0.125 – 0.05 mg/kg • SURGICAL MANAGEMENT
  • 28. Staging and treatment • Staging is determined by combination of imaging studies and pathology findings. • Treatment strategy is determined by the stage. • Stage I (43% of patients)- Tumor limited to kidney and completely resectable. • Treatment: • Nephrectomy +/- 18 weeks of chemotherapy depending on age of patient and weight of tumor. • EG: less than 2 years old and less than 550g only requires Nephrectomy with observation. • Outcome: 98% 4-year survival
  • 29. Stage II • Stage II (23% of patients)- Tumor extend beyond kidney , into nearby fatty tissue, but it is resectable. Treatment: • Nephrectomy + abdominal radiation + 24 weeks of chemotherapy • Outcome: 96% 4-year survival.
  • 30. Stage III • Stage III (23% of patients) – Non hematogenous spread in abdomen, like spread to lymph nodes in abdomen or pelvis, but this stage tumor is not completely resectable. • Treatment: • Abdominal radiation + 24 weeks of chemotherapy + nephrectomy after tumor shrinkage • Outcome: 95% 4-year survival
  • 31. • Stage IV (10% of patients) • Stage IV Wilms' tumor is defined as the presence of hematogenous metastases (lung, liver, bone, or brain), or lymph node metastases outside the abdominopelvic region. • Treatment: • Nephrectomy + abdominal radiation + 24 weeks of chemotherapy + radiation of metastatic site as appropriate. • Outcome: 90% 4-year survival
  • 32. • Stage V (5% of patients) • Stage V Wilms’ tumor is defined as bilateral renal involvement at the time of initial diagnosis. • The 4-year survival in 94% patients with stage I or stage II; 76% for with stage III. • Treatment: Individualized therapy based on tumor burden