Scrotal Masses

Contents
1. List the common causes of scrotal masses, and where possible distinguish
between these causes on clinical grounds.............................................................3
Hydrocele........................................................................................................... 3
Clinical presentation........................................................................................ 3
Diagnosis......................................................................................................... 3
Management................................................................................................... 3
Inguinal hernias.................................................................................................. 4
Direct Hernias.................................................................................................. 4
Indirect Hernia................................................................................................. 4
Anatomy of the inguinal canal.........................................................................4
Anatomy of Spermatic Cord............................................................................. 4
Varicocele........................................................................................................... 4
Clinical Presentation........................................................................................ 4
Surgical Anatomy............................................................................................ 5
Treatment........................................................................................................ 5
Spermatocele..................................................................................................... 5
Localised oedema form insect bites...................................................................5
Nephrotic syndrome (bilateral swelling).............................................................5
Testicular cancer................................................................................................. 5
Clincial Presentation........................................................................................ 6
Diagnosis......................................................................................................... 6
2. Discuss the pathophysiology of disorders of the tunica vaginalis, undescended
testis, indirect inguinal hernia, hydrocoele, haematocoele and spermatocoele.. . .7
Tunica Vaginalis.................................................................................................. 7
Undescended testes (cryptorchidism)................................................................8
Pathophysiology.............................................................................................. 8
Clinical Features.............................................................................................. 9
Complications.................................................................................................. 9
Considerations................................................................................................. 9
Incompletely descended testis...........................................................................9
Haematocele.................................................................................................... 10
3. Explain the pathogenesis and consequences of torsion of the testis...............11
4. Distinguish between the causes of acute and chronic epididymo-orchitis and
relate these causes to the clinical manifestations...............................................12

Acute............................................................................................................. 12
Chronic Tuberculous Disease.........................................................................12
5. List the factors that predispose to testicular neoplasms.................................13
Germ Cell Tumours........................................................................................... 13
Environmental factors and genetic predisposition.........................................13
Classification and Pathogenesis....................................................................13
Clinical features of Germ cell testicular tumours...........................................14
Biologic Markers............................................................................................ 15
6. Compare and contrast the epidemiology, morphology, biological behaviour
and prognosis of seminomas and non-seminomatous germ cell tumours of the
testis.................................................................................................................... 16
7. Discuss the role of biochemical tumour markers in the diagnosis and
management of testicular tumours.....................................................................16

1. List the common causes of scrotal masses, and

where possible distinguish between these causes
on clinical grounds.
Hydrocele

Tunica Vaginalis

Mesothelial lined surface exterior to testis

Lined by mesothelial cells

A collection of peritoneal fluid between parietal and visceral layers of tunica
vaginalis.
Two types:

Communicating:
Result of failure of processus vaginalis to close during development
Fluid around testis is peritoneal fluid
Most common in newborns

Usually resolves within the first birthday

Non-communicating
May be idiopathic or secondary to epididymitis, orchitis, testicular
torsion, torsion of appendix testis, trauma or tumour.

Clinical presentation
Communicating:

Presents with a cystic scrotal masses

May increase in size during the day or with Valsalva manoeuvre
Usually present with risk of incarceration of inguinal hernia

Non-communicating:
Not reducible
Does not change in size or shape
Examination:
Palpation of entire testicular surface:

Findings of epididymitis, orchitis, testicular torsion, etc.

Diagnosis
Physical Examination
Transillumination of scrotum
Communicating hydroceles reducible, non-communicating hydroceles are not.
Management
Surgical repair indicated for newborns that persist beyond one year of age, for
communicating hydroceles, and for symptomatic hydroceles.
Management of child under one year is usually supportive

Inguinal hernias

Direct and indirect hernias

Direct Hernias
Direct hernias: pass directly through Hasselbachs triangle

Hasselbachs triangle
Medial border: Lateral margin of rectus abdominus muscle
Superolateral border: Inferior epigastric artery
Inferior border: Inguinal ligament

Passes through inguinal canal and exits via the superficial ring

Direct hernias pass medial to inferior epigastric artery

Indirect Hernia
Passes from deep inguinal ring through inguinal canal through to superficial
ring.
Enters laterally to the inferior epigastric arteries.
Usually occurs due to non fully obliterated processus vaginalis during
development

Connection between peritoneal cavity and scrotal cavity.

Anatomy of the inguinal canal
Deep inguinal ring

Located 2cm superior to midpoint between ASIS and pubic tubercle

Spermatic cord passes through inguinal canal in men, and round ligament of
uterus in women.
Ilioinguinal nerve passes through this canal
Walls:

Superior wall: Aponeurosis of external oblique + transversalis fascia

Inferior wall: Inguinal ligament

Anterior wall: Aponeurosis of external oblique, superficial inguinal

ring and internal oblique

Posterior wall: Transversalis Fascia, conjoint tendon (aponeurosis of

internal oblique and transversalis abdominis)
Anatomy of Spermatic Cord
3 arteries: Testicular artery, cremaster artery, artery to vas deferens
3 fascial layers: external spermatic, cremasteric, and internal spermatic fascia
3 other features: pampiniform plexus, vas deferens, testicular lymphatics
3 nerves: genital branch of genitofemoral nerve, sympathetic and visceral
afferent nerves, illioinguinal nerve (NB outside spermatic cord but only leaves
superficial ring and not run through canal)

Varicocele

A collection of dilated and tortuous veins in pampiniform plexus surrounding

spermatic cord in the scrotum.
Result from increased venous pressure and incompetent valves.
Occur more commonly on left side (85-95%) because left spermatic vein
enters left renal vein at 90 degree angle, while the right side is more obtuse
and directly into the vena cava.

Clinical Presentation
Patients can complain of full scrotum or heaviness when standing.
Examination

Initially done with patient standing

Scrotum inspected for any visible distention

Scrotum, testes and cord structures palpated

Grade 1: palpable only with Valasalva manoeuvre

Grade 2: palpable but not visible

Grade 3: visible distention

Examine supine patient

Idiopathic: changes when patient lies down
Secondary: does not get smaller in size when patient lies down

Processes that cause IVC obstruction (IVC thrombosis, right renal

vein thrombosis or abdo mass including retroperitoneal tumours, kidney
tumours, or lymphadenopathy) should be ruled out via Doppler ultrasound
if:
Acute
Right sided
Does not get smaller when supine
Surgical Anatomy
Pampiniform plexus drains epididymis and testis
Left testicular vein empties into left renal vein
Right testicular vein empties into vena cava below right renal vein.
Treatment
Not indicated for asymptomatic varicocele
Laparoscopic ligation of testicular vein above inguinal ligament
Embolisation of testicular veins under radiographic treatment of choice

Spermatocele

Painless fluid filled cyst of the head of the epididymis that may contain nonviable sperm
Can be distinctly palpated from testis and transilluminates as a cystic mass
Lies in epididymal head above and behind upper pole of testis
Ultrasound can also be used
Does not affect fertility
Treatment (surgical excision) is done for comfort or aspiration

Localised oedema form insect bites

Swelling can be accompanied by erythema/ pruritus

Nephrotic syndrome (bilateral swelling)

Lack of albumin causes oedema and hyperlipidaemia

The oedema is gravity dependent

Testicular cancer

Accounts for 20% of cancers in 15-35 year olds

Clincial Presentation
Painless mass
Testicular enlargement and swelling
Aching feeling in lower abdo or scrotum
Examination:

Firm, nontender masses

Do not transilluminate and are palpated within the testis

May be accompanied by hydrocele

Some patients may have gynaecomastia

Diagnosis
Scrotal ultrasound initial diagnostic test
Pathology definitive diagnostic test
Several conditions may mimic testicular cancer:

Inflammation

Haematoma

Infarct

Fibrosis

2. Discuss the pathophysiology of disorders of the

tunica vaginalis, undescended testis, indirect inguinal
hernia, hydrocoele, haematocoele and spermatocoele.
Tunica Vaginalis

Serous covering of the testis

Derived from processus vaginalis
After decent of testes from abdomen via gubernaculum, processus vaginalis
obliterates.
Lower portion of processus vaginalis remains as a shut sac, and is reflected
on the internal surface of the scrotum.

Tunica Vaginalis hence consists of parietal and visceral layer

Visceral layer

Covers testis and epididymis

Connects epididymis to testes by a fold

Parietal layer

Extends upward in front and on medial side of cord, and reaches

below testes

Inner layer is smooth, covered by simple squamous mesothelial

cells

An unobliterated processus vaginalis would cause:

Peritoneal fluid can travel down a patent processus vaginalis leading

to formation of hydrocele

Accumulation of blood can lead to haematocele

Potential for indirect inguinal hernia to form

Leading cause of testicular torsion

Lack of attachment of testicles to inner lining of scrotum leaves the
testicles free to twist.
Persistent patent processus vaginalis more common on the right than the left.

Undescended testes (cryptorchidism)

Most cryptorchidism is due to undecended testes, but some are absent

(agenesis or atrophy).
Testes not yet descended in 3 months unlikely to descend
Undescended testes:

May remain in abdo cavity

May be palpable in inguinal canal or just outside the superficial ring

(suprascrotal)

Pathophysiology
Intraabdominal descent is thought to be androgen independent
Unsure pathophys:

Changes in abdo pressure

Patency of processus vaginalis

Gubernacular regression

Gonadotrophins

Gonadotrophin deficiency in utero

Decreased Mullerian inhibiting substance (inhibits the development

of paramesonephric ducts)
Usually an isolated finding

Clinical Features
Empty and hypoplastic or poorly rugated scrotum
Inguinal fullness may be present
10% of cases is bilaterally
For unilateral cases, most are left sided
Most common location is just outside the superficial ring, followed by inguinal
canal, and then abdomen.
Most undescended testicles are left until 6 months, if after that they are
unlikely to descend and require surgical manipulation.
Complications
Inguinal hernia
Testicular torsion
Testicular trauma (if intracanulicular then can be damaged from pubic
symphysis)
Subfertility
Malignant transformation
Considerations
Identify from rectracile testes, or ectopic testes

True undescended testes: palpable in inguinal canal or just outside

superficial ring and been in this position since birth

Retractile testes: Can be brought into testes by manipulation.

Can overcome cremasteric reflex by holding it in the testes for
>1minute.

Ectopic testes
Located in areas distinct from undescended testes

E.g. abdomen, femoral etc.

Incompletely descended testis

4%
Pathology:

Macroscopically normal at birth but poor compared to rest of scrotal

components at puberty

Epithelium histologically immature

By late puberty, decreased spermatogenesis and decreased

androgen production
Clincial features:

More common right and bilateral 20%

Testes may be :

Intra abdominal above superficial ring

Inguinal (not palpable)
Superficial inguinal pouch

Scrotum generally underdeveloped (scrotum developed in

rectractile testes)

Hazards:
Sterility in bilateral cases
Pain due to trauma
Associated indirect inguinal hernia generally present
Torsion
Increased liabilities to malignancies
Surgical Treatment:

Orchidopexy
Testis and spermatic cord mobilised and testis repositioned in the
scrotum.
Operation performed through incision over deep inguinal ring
Testes placed in pouch between dartos muscle and skin

Haematocele

Presence of blood in tunica vaginalis

Uncommon

Usually occurs due to direct trauma to testis or torsion of testis with

haemorrhage into surroundings, or with haemorrhagic diseases associated
with widespread bleeding.

3. Explain the pathogenesis and consequences of

torsion of the testis.

Typically cuts off venous drainage of testis.

Arteries remain patent

Vascular engorgement may be followed by haemorrhagic infarction.

Two types of testicular torsion

Neonatal torsion
Occurs in utero or immediately after birth until first 30 days of life.
Occurs because tunica vaginalis is not well fixed to scrotal wall, and
torsion involves the whole testicle, including tunica vaginalis, leading to
extravaginal torsion.
Attachment of tunica vaginalis thought to occur at several weeks of
life.
Theory: increased intrauterine pressure during 3 rd trimester causes
brisk cremaster response in setting of loose tunic-scrotal attachment.

Adult torsion
Seen in adolescence
Sudden onset of testicular pain
Urologic emergency
Pathology:

Separation of epididymis from body of testis

Testicular inversion
If surgery within 6 hours, testis will likely remain viable.
Results from anatomic defect where testes has increased mobility,
referred to as bell clapper abnormality.

Occurs due to unobliterated processus vaginalis, so there are

no adhesions of testicles to any walls.
To prevent future recurrence, testis surgically fixed to scrotum.
Clinical features

Most common between 10 and 25 years

Sudden agonising pain in groin and lower abdomen

Patient becomes nauseated and may vomit

Testes seems high and twisted cord can be palpated

Elevation of testes makes pain worse

Treatment

First hour or so untwist testes by gentle manipulation, then

arrangement for surgery to prevent recurrent torsion.

Other testes should also be tethered between tunica albuginea and

tunica vaginalis.

Infarcted testes should be removed, other testis is tethered

Complications

Testicular ischaemia
Twisting of spermatic cord compromises testicular vasculature
Dependent on duration

If ischaemia lasts between 4-6 hours

Increasing rotation of spermatic cord

Degree of rotation affects potential for testicular damage

Complete vs partial torsion (complete is 360)

4. Distinguish between the causes of acute and chronic

epididymo-orchitis and relate these causes to the
clinical manifestations.

Inflammation confined to the epididymis is epididymitis

Inflammation spreading to testis is epididymoorchitis

Acute
Mode of infection

Infection reaches epididymis via vas deferens from urethral,

prostate, or seminal vesicles infection.

Can be secondary from UTI from outflow obstruction (old men) or

from STI in young men

Blood borne infections of epididymis is less common unless E.Coli

Develops in 18% of males with mumps

May be involved by infection with other enteroviruses and in

brucellosis
Clinical features

Initially symptoms of UTI

Later ache in groin and fever

Epididymis and testes swell

Scrotal wall can become adherent to epididymis

Sometimes abscess and may form with pus discharge

6-8 weeks before resolution

Occurs most commonly with catheter and infection of prostate

Reduced incidence in those with prostatectomy
Treatment

Doxycycline (100mg daily) for chlamydia infection

Otherwise broad spectrum antibiotics e.g ceftriaxone and

metronidazole

Patient drink a lot of fluids

Abx for 2 weeks

Chronic Tuberculous Disease
Aetiology

Lower pole when attacked first indicates that infection is retrograde

from tuberculous (tuberculosis) foci in seminal vesicles.
Clinical features

Firm discrete swelling of lower pole of testis, slightly tender

Disease progresses until whole epididymis is firm behind normal

feeling testis

Body of testis may be uninvolved for years

Urine and semen should be examined for tubercle bacilli in all

patients, and IV urogram and chest X-ray should be performed
Treatment

Treat primary focus


If resolution does not occur within 2 months, epididymectomy or
orchidectomy

Course of anti-tuberculous chemo should be commenced even if no

sign of tb anywhere else.

5. List the factors that predispose to testicular

neoplasms.
Testicular neoplasms divided into two major categories:
Germ cell tumours and sex cord-stromal

Germ Cell Tumours

Environmental factors and genetic predisposition
Testicular germ cell tumours associated with testicular dysgenesis syndrome
(TDS)

TDS:
Cryptorchidism (10% association with testicular germ cell tumours)
Hypospadias
Poor sperm quality
Strong family predisposition

x4 for fathers

x8-10 for brothers

Classification and Pathogenesis
Generally there is a mix of seminomatous and non-seminomatous
components
Most testicular germ cell tumours originate from lesions called intratubular
germ cell neoplasia
ITGCN thought to occur in utero and develop into seminomas or nonseminomatous tumours.
Seminomatous tumours

Composed of cells that resemble primordial germ cells

Most common type of germ cell tumour, makes up to 50%

Almost never occur in infants, usually occur in 3 rd decade

Identical tumour in the ovary referred to dysgerminoma

25% of tumours have c-KIT activating mutations

Morphology
Produces bulky masses
Generally tunica albuginea is not penetrated, but occasionally
extension to epididymis, spermatic cord, or scrotal sac occurs.

Microscopically, seminoma composed of sheets of uniform cells

divided into poorly demarcated lobules by fibrous tissue, containing
moderate amount of lymphocytes.
15% of seminomas contain syncytiotrophoblasts, accounting for
increased bHCG levels, and granulomas can be formed
Do not confuse with spermatocytic seminoma
Uncommon tumour (1% to 2% of all testicular germ cell neoplasms)
Slow growing tumour which does not metastasise
In contrast to seminomas, these lack syncytiotrophoblasts,
lymphocytes, ITGCN and extratesticular origin sites.

Non-seminomatous tumours

Composed of undifferentiated cells that resemble embryonic stem

cells

Malignant cells can differentiate into different lineages e.g.

teratoma, yolk sac tumours

Embryonal Carcinoma
These tumours are more aggressive than seminomas
Generally smaller than seminoma and does not replace the entire testis.
Extension through tunica albuginea into the epididymis or cord frequently
occurs
Lack well-formed glands with basally situated nuclei and apical cytoplasms
seen in teratomas.
In contrast to seminoma, the cell borders are usually indistinct, and there is
considerable variation in cell and size and shape.
Yolk Sac Tumour
AKA Endodermal sinus tumour
Most common testicular tumour in infants and children up to 3 years of age.
Good prognosis
In adults, usually occurs in combination with embryonal carcinoma
Choriocarcinoma
Highly malignant form of testicular tumour
In its pure form choriocarcinoma is rare, but less than 1% of all germ cell
tumours
Often causes no testicular enlargement and are detected only as a small
palpable nodule. Typically these tumours are small, rarely larger than 5cm.
HCG usually demonstrated in cytoplasm.
Teratoma
Complex testicular tumours having various cellular or organic components
from more than one germ layer
Can occur at any age
Pure forms of teratoma are fairly common in infants and children, second in
frequency to yolk sac tumours

Haemorrhage and necrosis usually indicate mixture of embryonal carcinoma,

choriocarcinoma or both.
Composed of collection of differentiated cells, such as neural tissue, muscle
bundles, islands of cartilage, clusters of squamous epithelium, etc. embedded
in fibrous or cartilaginous stroma
Rarely are malignant non germ-cell tumours arise

If there is malignancy, referred to as teratoma with malignant

transformation

Non germ cell malignancies does not respond to chemo when it

spreads outside the testes.
In child, differentiated mature teratoma usually benign
In postpubertal male all teratomas are regarded as malignant.

Clinical features of Germ cell testicular tumours

Painless enlargement of testis is characteristic
Any solid testicular mass should be considered as neoplastic.
Biopsy of testicular neoplasm is associated with tumour spillage

If tumour spillage, excision of scrotal skin/ orchidectomy is required.

Lymphatic spread is common
General retroperitoneal lymph nodes are first to be involved.
Subsequent spread can occur o mediastinal or supraclavicular
nodes
Haematogenous spread

Primarily to lung, but can also go to liver, brain and bones.

Seminomas tend to remain localised to testis for a long time
Non seminomatous germ cell tumours not only metastasise earlier but more
frequently via haematogenous route
Choriocarcinoma is most aggressive NSGCT, may not cause any testicular
enlargement and spread mostly by bloodstream, with very common lung and
liver involvement.
In general, NSGCT more aggressive than SGCT, and seminomas are
radiosensitive, while NSGCT are not.
Three stages:

Stage 1: tumour confined to testis, epididymis or spermatic cord

Stage 2: distant spread confined to retroperitoneal nodes below the

diaphragm

Stage 3: mets outside retroperitoneal nodes or above the

diaphragm

Stage 4: nonlymphatic met spread

Biologic Markers
HCG, AFP, lactate dehydrogenase correlates with mass of tumour cells
Marked elevation of HCG or AFP levels by yolk sac tumours and
choriocarcinoma elements
Approximately 15% of seminomas have syncytiotrophoblast giant cells and
minimal elevation of HCG levels, which does not affect prognosis.

6. Compare and contrast the epidemiology,

morphology, biological behaviour and prognosis of
seminomas and non-seminomatous germ cell tumours
of the testis.
7. Discuss the role of biochemical tumour markers in
the diagnosis and management of testicular tumours.