Tumours
of the testes
The lymphatic drainage of the testes follows
the spermatic cord to end in the para-aortic lymph nodes near the origin of the
gonadal vessel. Lymphatics from the medial side of the testis may run with the
artery to the vas and drain into a node at the bifurcation of the common iliac
artery. The contra-lateral para-aortic lymph nodes are sometimes involved by
tumour spread but the inguinal lymph nodes are only affected if the scrotal skin
is involved.
Malignant
About 99 per cent of testicular neoplasms are
malignant, and although they make up only about 12 per cent of malignant
tumours in men, they are one of the commonest forms of cancer
in the young male adult.
Maldescent undoubtedly predisposes to malignancy. It is curious that despite the
fact that the
testis is usually easily palpable, a testicular tumour often escapes detection
until after it has
metastasised. There is a campaign to encourage men to perform regular testicular
self-examination in the hope that tumours will be detected earlier but as yet
this has not been as successful as a similar drive to get women to screen their
own breasts for lumps.
Tumours
of the testis are classified according to the predominant cellular type:
seminoma (40 per cent);
teratoma (32 per cent);
combined seminoma and teratoma (14 per cent);
interstitial tumours (1.5 per cent);
lymphoma (7 per cent);
other tumours (5.5
per cent).
Teratomas
tend to occur in a younger age group, the peak incidence being between 20
and 35 while that
of seminoma is between 35 and 45. Seminoma
is extremely rare before
puberty.
Seminoma
Seminoma compresses neighbouring testicular
tissue as it grows
(Fig. 68.13). The enlarged testis is smooth and firm. The cut surface is
homogeneous and pinkish cream in colour. Occasionally fibrous septa give a
lobulated appearance. In rapidly growing tumours there may be areas of necrosis
of variable consistency.
Histologically, a seminoma is made of slightly oval cells with clear cytoplasm and large rounded nuclei with prominent acidophilic nucleoli. The cells are arranged in sheets separated by a fine fibrous stroma. Derived from seminiferous tubules, the cells resemble spermatocytes. Active infiltration of the tumour with lymphocytes suggests a good host response and a better prognosis.
Seminomas
spread via the lymphatics (Fig. 68.14) and metastasis via the bloodstream is
uncommon.
Teratoma
Teratoma arises from totipotent cells in the
rete testis and often contains a variety of cell types of which one or more
predominate. The tumour may be as small as a peanut or as large as a coconut.
Even when large, the tumour is moulded by the tunica albuginea so the overall
outline of the testis is maintained although the surface may be slightly
irregular.
The usual variety is yellowish in colour with cystic spaces containing gelatinous fluid (Fig. 68.15). Nodules of cartilage are often present.
Histology. The Testicular Tumour Panel has
classified teratomas as follows:
Teratoma differentiated
(TD) (uncommon)
has no histologically recognisable malignant components but cannot be considered
benign because such growth has metastasised. The best known variety is a dermoid
cyst which may contain cartilage and muscle as well as glandular elements.
Malignant
teratoma intermediate, teratocarcinoma (MTI A and B)
(most
common) contains definitely malignant and incompletely differentiated
components. There is some mature tissue in type A but not in type B.
Malignant
teratoma anaplastic (MTA), embryonal carcinoma is composed of anaplastic cells of embryonal origin in
parts. Cells presumed to be derived from yolk sac are often responsible for
elevated ct-fetoprotein levels. MTA is not always radiosensitive.
Malignant
teratoma trophoblastic (MTT) (uncommon)
contains within other cell types a syncytial cell mass with malignant villous or
papillary cytotrophoblast (chroriocarcinoma). It often produces human chorionic
gonadotrophin (HCG). Spread by bloodstream and lymphatics is early. It is one of
the most malignant tumours known.
Interstitial
cell tumours
Interstitial cell
tumours arise from Leydig or
Sertoli cells. A Leydig cell tumour masculinises; a Sertoli cell tumour
feminises.
Prepubertal
interstitial cell tumours excrete .androgens which cause sexual precocity and
extreme muscular development. Regression of the symptoms after orchidectomy may
be incomplete because of hypertrophy of the contralateral testis.
Postpubertal
interstitial cell
tumours usually arise from Sertoli cells with output of feminizing
hormones leading to gynaecomastia, loss of libido and a-spermia. As a
rule the tumour is benign and orchidectomy cures.
Clinical
features
The patient may not seek advice for several
months after first noticing that he has a testicular lump. A sensation of
heaviness
occurs when the testis is two or three times its normal size
but there is pain
in only 30 per cent or so. There is a history of trauma to the affected side in over
10 per cent. It
is generally conceded that this merely calls attention to the testicular
enlargement and in no way initiates the neoplasm.
On
examination, the testis is enlarged, smooth, firm and heavy. Later
one or more softer protruberances may be palpable. In no other disease is
testicular sensation lost so early or
so completely but the sign should be elicited with care for fear of
disseminating the disease. Ten per cent have a lax secondary hydrocele which
does not usually obscure the underlying tumour. The epididymis is normal at
first but becomes more difficult to feel as it is flattened or incorporated in the growth. Thickening of the spermatic
cord occurs later due to cremasteric hypertrophy and enlargement of the
testicular vessels. The vas is never thickened and rectal examination shows the
prostate and seminal vesicles to be normal.
Secondary
retroperitoneal deposits may be palpable especially just above the umbilicus
on the side of the tumour.
There may be hepatic enlargement. Occasionally, an enlarged supraclavicular
node is the presenting sign of a testicular tumour
(Fig. 68.16). A chest radiograph is most likely to show pulmonary metastases when the primary tumour is a teratoma (Fig. 68.17).
Occasionally,
the predominant symptoms are those of metastatic disease. Intra-abdominal
disease may cause abdominal or lumbar pain and the mass may be discovered in the
epigastrium. Lung metastases are usually silent but they can cause chest pain,
dyspnoea and haemoptysis in the later stages of the disease. The primary tumour
may not have been noticed by the patient and may indeed be so tiny that it
can only be
detected by sophisticated ultrasound imaging or operative exploration.
The hurricane tumour is a ferocious malignancy
which kills in a matter of weeks. A few teratomas grow slowly with increasing
enlargement of the testis over 2 or 3 years.
Treatment
of testicular tumours
Staging is an essential first step in planning
treatment.
Blood is collected for radioimmunoassay of tumour markers (human
chorionic gonadotrophin, alpha-foetoprotein and lactate dehydrogenase. Their level
in the blood can be used to monitor the response to treatment.
A chest radiograph will show whether there are pulmonary
deposits.
Orchidectomy is essential to remove the primary tumour and to obtain
information about the histological type of the tumour.
Computerised tomography and magnetic resonance imaging are the most
useful means of detecting intraabdominal and intrathoracic secondaries and for
detecting their response to therapy.
Scrotal
exploration and orchidectomy for suspected testicular tumour. The spermatic
cord is displayed by dividing the external oblique aponeurosis through a groin
incision. A soft clamp is placed across the cord to stop dissemination of
malignant cells as the testis is mobilised into the wound. If there is doubt about the diagnosis at this stage, the testis
should be bisected along its anterior convexity so that its internal structure
can be examined. If there is a tumour or doubts still remain even after
frozen section,
the cord should be double ligated at the level of the inguinal ring and divided
so that the testis can
be removed.
Staging
of testicular tumours
The stages are:
stage 1: testis lesion only
no spread;
stage 2: nodes below the diaphragm only;
stage 3: nodes above the diaphragm;
stage 4: pulmonary or
hepatic metastases.
Management
by staging and histological diagnosis (after orchidectomy)
Seminomas are radiosensitive and excellent
results have been obtained by irradiating stage 1 and stage 2
tumours. More
recently, the tumour has been shown to be highly sensitive to cisplatin, which
is already being used for patients with metastatic disease. The experts are
divided as to whether patients with stage 1 disease should have adjuvant
chemotherapy.
Teratomas
are less sensitive to radiation. Stage 1 tumours can be managed by watching the
level of serum markers and by repeated computerised tomography. Teratomas at
stages 24 are
managed by chemotherapy. Cisplatin, methotrexate, bleomycin and vincristine have
been used in
combination with great success. There are those who advocate adjuvant
chemotherapy for stage 1 teratoma arguing that effective prophylaxis is less troublesome to the patient than prolonged
surveillance.
Retroperitoneal
lymph node dissection is sometimes needed when retroperitoneal masses remain
after chemotherapy
Prognosis of testicular tumours depends on the
histological type and the stage of the growth.
Seminoma.
If there are
no metastases 95 per cent will be alive 5 years after orchidectomy and
radiotherapy or chemotherapy. If there are metastases survival drops to 75 per
cent.
Teratoma.
More than
85 per cent 5-year survival is achievable in stages 1 and 2 teratoma. In stages
3 and 4, the survival is about 60 per cent and getting better with improvements
in chemotherapy.
Testicular
tumours in children are
usually anaplastic teratomas. They occur before the age of 3 years and are often
rapidly fatal.
Tumours
of the epididymis may
be benign mesothelioma or malignant sarcoma or secondary carcinoma. They are
extremely rare but should not be forgotten when the patient presents with a
noncystic lump in the epididymis.