REPRODUCTIVE MODULE

Male
Pathology & Surgery

Academic Circle
MFSU Ragama
 Contents
Prostate Gland
Testis
Penis
Urethra
 1. Prostate Gland
Normal Prostate Gland

• A wedge shaped retroperitoneal organ encircling the bladder neck

• Weighs about 20g in adults
• Lies anterior to the rectum – palpable on rectal examination
• Blood supply – internal iliac artery
• Prostatic veins drain into the prostatic venous plexus

Biological Zones of Prostate

The prostatic parenchyma is divided into 3

zones.

• Transitional
• Central
• Peripheral

The types of proliferative lesions are different in

these zones;

Transitional zone – BPH

Peripheral zone - Carcinoma

Microscopy – Normal Prostate Gland

• Prostate - Parenchymal glands & Fibromuscular stroma

• The glands are branched tubuloacinar and arranged concentrically around urethra
• The stroma is composed of smooth muscle fibers and connective tissue
• Corpora amylacea (formed by condensed prostatic secretions) may be seen within the
acini
 Corpora Amylacea Stroma

Acini

• Glandular acini – convoluted appearance with papillary infoldings

• Lined by cuboidal to pseudostratified columnar epithelium, lying on a
basal/myoepithelial layer
• Surrounded by a fibrous tissue stroma
Prostatic Acinus

Pathologies of Prostate Gland

• Prostatitis
• Benign Prostatic Hyperplasia
• Prostatic Carcinoma

Prostatitis
1. Acute suppurative prostatitis
• Secondary to ascending or descending infection
2. Chronic non specific prostatitis
• Following recurrent episodes of acute prostatitis
• Lymphocyte and plasma cell infiltrate, acinar atrophy and stromal fibrosis
3. Granulomatous prostatitis
• Tuberculosis prostatitis and non specific granulomatous prostatitis
• Can mimic malignancy
Clinically – due to hard enlargement of the gland
Biochemically – due to increased serum PSA level
Benign Prostatic Hyperplasia (BPH) / Nodular Hyperplasia

• A common non-neoplastic condition of prostate gland

• Commonly seen after 50 years of age
• See in 90% of men at the age of 80 years
• Occurs due to proliferation of stromal and glandular elements of the gland
• Mainly involves the periurethral glands
• Not a pre neoplastic condition

BPH – Pathogenesis

• Not fully understood

• Occurs due to hormonal imbalance with advancing age
• Excessive androgen dependent growth of stromal and glandular cells has a central
role
• Prostatic 5 alpha reductase converts testosterone to Dihydrotestosteron (DHT)
• DHT is a potent stimulator for stromal and glandular proliferation

BPH – Morphology

• Enlargement of gland (60-100g)

• Originates in the periurethral region
• Mostly involves the lateral lobes
• Characterized by hyperplasia of both stromal and glandular components resulting in
formation of discrete nodules
• Early nodules – stromal hyperplasia
• Later – glandular hyperplasia

Macroscopy of BPH

• The cut surface- multiple, circumscribed, solid nodules and cysts

• Nodules compress the prostatic urethra
 • Sometimes these nodules can
protrude up into the bladder
neck ‘Median Lobe’

Microscopy of BPH

• There are large hyperplastic nodules composed of variable amount of glands and
stroma
• The glands are lined by 2 layers of cells, hyperplastic columnar epithelium and
basal cells
• The glands are well differentiated and still have some intervening stroma
• Corpora amylacea within the glands

Complications of Prostatic Hyperplasia

• Bilateral hydronephrosis
• Bilateral hydroureter
• Infections and septicaemia
• Renal calculi
• Renal failure
• Bladder diverticuli
• Bladder muscular hypertrophy
• Bladder wall trabeculation
• Compression of urethra
Carcinoma of the Prostate Gland

• One of the most commonest cancer seen in males – however the cancer related
mortality is relatively lower
• A tumour of elderly > 50 years
• Relatively favourable prognosis could be due to
- Early detection by screening
-Indolent clinical course in some
• Only a part of prostate adenocarcinomas behave bad

Aetiology of Prostate Cancer

1. Androgens
-Has a central role
-Provides the ‘soil’ for the development of the cancer
-Androgens do not initiate carcinogenesis

2. Heredity
- A positive family history increases the risk
-Less among Asians
 3. Environment
-The incidence is more in west
-Westernized diet in east also increases the risk

4. Acquired somatic mutations

-Drives the cellular transformation
-Gene rearrangements and fusion of genes

Carcinoma of the Prostate Gland

• BPH is not a pre neoplastic lesion but it is often found coincident with carcinoma
• Prostatic carcinoma is preceded by high grade prostatic intraepithelial neoplasia
(PIN)

Prostatic Intraepithelial Neoplasia (PIN)

• PIN is a precancerous cellular proliferation

• Architecturally normal acini lined by cytologically atypical cells
• PIN could be low or high grade
• The finding of high grade PIN suggests that prostatic adenocarcinoma may also be
present

Prostatic Carcinoma – Clinicopathological Types

1. Clinical (symptomatic) Carcinoma

• Important form
• Arises in the posterior subcapsular area
 • Invades stroma and perineural spaces
• Produces metastasis, mainly to bone

2. ‘Occult’ Carcinoma
• Sometimes small primary in prostate with widespread symptomatic
metastasis

3. Latent (Incidental) Carrcinoma

• Microscopic foci of cancer found incidentally on histological examination of
prostates removed for BPH
• Incidence is high in old age

Morphology – Prostatic Carcinoma

• 70% - posterior subcapsular location – palpable per rectum

• On slicing gritty and firm
• Easy to palpate than seen
Prostatic Hyperplasia versus Carcinoma

Prostatic Hyperplasia Prostatic Carcinoma

Microscopy – Prostatic Carcinoma

• An adenocarcinoma forming acini and tubules

• The neoplastic glands are typically smaller than normal glands, more crowded and
lacks branching pattern
• The glands are lined by a single layer of tumour cells. No basal cell layer
• The cells have pale-clear cytoplasm and central enlarged nuclei with prominent
nucleoli
• Cellular/nuclear pleomorphism is minimal
• Invasion of the stroma and the perineural space is seen
Microscopy of Prostatic Carcinoma

Small crowded glands

Lined by a single layer of cells

Immunostaining with PSA Antigen on Histology Sections

• PSA immunostaining is
important in identifying a
tumour as prostatic origin

• This is very useful in evaluating

metastatic deposits

Prostatic Carcinoma Grading Using Gleason System

• Graded using Gleason’s Grading System

• This is based on architectural pattern of glands
• Low grade tumours – well formed glands
 • With increasing grade – irregular or ragged glandular structures, cribriform glands,
sheets of cells, or infiltrating individual cells
• There are 5 grades according to the differentiation
• Usually tumours have more than one grade
• Most dominant pattern – taken as primary grade
• Next most frequent pattern – secondary grade
• Adding the two numerical grades will give the Gleason Score which correlates with
the prognosis

Grading Using Gleason System

• The most differentiated tumours have a Gleason Score of 2 (1+1)

• The least differentiated tumours have a score of 10 (5+5)
Carcinoma of the Prostate Gland – Spread

1. Direct spread
• Stroma-capsule-urethra-bladder base-seminal vesicles

2. Lymphatic spread
• Sacral, iliac, para aortic nodes

3. Blood spread
• Bone, lung, liver

Bone Metastasis in Prostatic Carcinoma

• Often gives osteosclerotic metastasis

• Sites – lumbar vertebrae and pelvis

• Increased alkaline phosphatase level

in serum

PSA in Prostate Cancer

• PSA is a protease produced from the prostate epithelium – organ specific

• Increase in PSA is not specific for cancer
• PSA is increased in BPH, prostatitis, instrumentation, infarcts, ejaculation etc.
• Slow growing cancers have normal PSA values
• Therefore PSA values need to be interpreted carefully in the diagnosis
• But it has a great value in monitoring progressive or regressive disease
following the treatment for prostate cancer
 Prostate - Surgery
• 10% of male cancer deaths due to prostate ca.
• Slow growing malignancy
• Many go undetected
• Many die from other causes rather than from ca itself
• Occurs de novo (BPH does not lead to CA, but similar symptoms) in the peripheral zone of
prostate
• BPH in central zone – TURP will not help cure a cancer!
• Incidentally found
• TURP specimen may show a cancer
• Nodule felt at DRE

RISK FACTORS
MODIFIABLE NON-MODIFIABLE
Age >40y Family history
Obesity Lynch syndrome : Type of inherited cancer
Diet – high saturated fats syndrome associated with a genetic
predisposition ( autosomal dominant type
inheritance) to different cancer types
(colorectal, uterus, ovarian, stomach CA)
Hereditary breast and ovarian cancer (HBOC)
syndrome (obviously in a sister!)

SPREAD
•LOCAL DISTAL
Seminal vesicles Blood
Bladder base/ trigone/ureters Bone
Rectum (stenosed by tumour Lung
infiltrating around) Lymphatic
Iliac nodes

SYMPTOMS

• Early disease mostly asymptomatic

• Mainly of bladder outflow obstruction
• Pelvic pain
• Haematuria
• Metastatic disease
• Spine/ pelvis (mostly osteosclerotic deposits)
• Sinister backache
• Lower limb neurological deficit
• Pathological fractures – due to bone erosions
EXAMINATION

• DRE
• Hard nodule
• Adhered mucosa
• Obliteration of median sulcus
• Blood on finger

• Spine
• Tender spinous process
• Lower limb neurological deficit

BLOOD INVESTIGATIONS

• Normal in early disease

• Anaemia – due to renal failure/ bone marrow invasion
• Liver function tests
• High ALP – bone deposits, liver secondaries (normal
gammaGT)
• PSA (Prostate Specific Antigen)
• A serine protease which liquefies semen
• Lacks sensitivity or specificity
• Not good as a screening tool
• >10nmol/l – suggestive of cancer
• >35nmol/l – suggestive of advanced cancer
• PSA density (PSA / prostate volume)

TISSUE DIAGNOSIS

• Rectal or perineal biopsy

• Adenocarcinoma
• Gleason score
• Cancer shows heterogeneity
• Two histological areas of cancer are graded 1 to 5
• Overall mark 2 to 10
• Higher the score - higher the complications of disease

IMAGING

• TRUS(Trans Rectal Ultrasound Scan)

• Helps in guided biopsy as well
 • Following confirmed tissue diagnosis;
• CXR
• Lung met HRCT chest
• Pelvic CT
• Best to detect pelvic node involvement
• Multiparametric MRI (mpMRI)
• Best for T staging
• Equally good as pelvic CT
• Bone scan
• For staging
• False + arthritis, healing fracture, osteomyelitis
• PET CT
• When equivalent reports from other
studies

TNM staging

HOW TO DECIDE ON TREATMENT

• Complete History and examination

• Blood tests
• Tissue diagnosis and imaging
• Staging
• Life expectancy
• Patient wishes

• Multi-Disciplinary Team (MDT) meeting to decide best course of action

TREATMENT MODALITIES

• Curative – T1/T2 and MO

• Active surveillance
• Radiotherapy
• Surgery – radical prostatectomy
• Palliative – T3/T4 or M1
• Castration (surgical/ medical)
 • Radiotherapy
• Chemotherapy

ACTIVE SURVEILLANCE

•Rationale

• Statistically – to stop 1 death from prostate CA

• 37 screen detected cancers should be treated
• 100 low grade cancers should be treated
• Slow growing disease with devastating therapy related complication (incontinence/erectile
dysfunction)
•Indications

• Very low risk cancer

• Gleason grade 1, T1 disease, PSA density <0.15ng/ml
• Life expectancy >20y
•Plan

• PSA 6/12
• DRE/mpMRI yearly
•Difficulties

• Patient concerns
• Health costs
• Lost to follow up

SURGERY – CURATIVE INTENT

• Radical prostatectomy
• T1/T2 disease with >10y life expectancy/ M0
• Prostate up to distal sphincter and seminal vesicles removed
• Should be done by high volume surgeon - centers
• Complications - Impotence/urinary incontinence
• +/- pelvic lymph node dissection (PLND) in N1

RADIOTHERAPY

• Curative intent
• EBRT (external beam RT) – more SE (urgency/ frequency)
 • Brachytherapy (radioactive seed implantation under TRUS guidance) – better
• Palliative intent
• For bone mets

CASTRATION – Androgen Deprivation

Therapy (ADT)
• Cancer grows with testosterone
• Surgical ADT (bilateral orchidectomy) for T3/4 or M1
• Medical ADT
• LHRH agonist (Goseraline)
• LHRH antagonist (Degaralix)
• Anti-androgen (flutamide)

CAT Questions

27th Batch

13. Regarding prostate gland

A. Corpora amylacea is an abnormal histological finding
B. Firm enlargement of prostate gland is seen in Granulomatous prostatitis
C. Most of the carcinoma are posterior subcapsular lesion

D. In benign prostatic hyperplasia there is a proliferation of both stromal and glandular

components

E. Grading is done by using Gleason’s score

Answers - FTTTT

56. A 64-year-old male is diagnosed with benign prostatic hyperplasia and had two episodes
of recent

acute urinary retention. He is otherwise healthy. (American society of anaesthalogists (ASA)

category 1 What is the most suitable treatment option for his condition?
A. Increase daily water intake to 3 liters

B. Longterm indwelling urinary catheter

C. Open prostectomy
D. Tamsulosin 0.4mg nocte
E. Transurethral resection of the prostate(TURP)

Answers – E

26th Batch

26. What is true or false regarding BPH

A. Commonly occur in subcapsular region
B. Has both stromal and glandular hyperplasia
C. PSA is elevated
D. Precancerous stage
E. Cause bladder diverticuli

Answers – FTTFT

62. Which of the following method is most appropriate for histologically confirm prostate
gland cancer?

A. Assess the prostate gland shaving of trans urethral resection

B. CT guided prostate gland biopsy

C. Cysto - urethroscopy and biopsy of prostate
D. Trans perineal FNAC of the prostate

E. Trans rectal true cut biopsy of the prostate

Answers – E
 2. Testis

TESTICULAR TUMOUR
that occurs predominantly in young males
• Majority (95%) are derived of germ cells.
• Most germ cell tumours are highly aggressive with wide dissemination; but responds very well to
current therapy
• Others are derived of sex cord-stromal cells, Sertoli cells and interstitial cells
• Sex cord stromal tumours (eg; Sertoli cell tumour, Laydig cell tumour) are generally benign

Testicular tumours-Aetiology

• Maldescended testis
• 3-5 fold increase in risk in undescended/maldescended testis
• Increase risk in contralateral descended testis as well
• Testicular dysgenesis syndromes
• Strong familial predisposition
• 8-10 fold risk among brothers
• Increase in oestragenic substances in the environmentGerm cell neoplasia in-situ (GCNIS)

Germ cell neoplasia in-situ (GCNIS)

• Precursor lesion of most of the postpubertal germ cell tumours

• Carcinoma-in-situ in seminiferous tubules
• Large and pleomorphic cells in tubules
• Also seen in cryptorchid testis

Testicular tumours-classification

Germ cell origin

• Seminomas
• Non seminomatous germcell tumours (NSGCT)
York sac tumour
Embryonal carcinoma
choriocarcinoma
Teratoma
Mixed germ cell tumours

Non germ cell origin

Sex cord stromal
Leydig celltumour
Sertoli cell tumour
Lymphomas

Germ cell tumours-classification

• Seminomas - tumour cells resemble primodial germ cells

• Non seminomatous tumours- undifferentiated cells that differentiate into
various lineages
• Embryonic stem cell- Embryonal carcinoma
• Extra embryonal/York sac – York sac tumour
• Trophoblastic differentiation -Choriocarcinoma
• Somatic differentiation-teratoma
• Some tumours – admixture of seminomatous and non seminomatous
Components

Testicular tumours-presenting features

Painless teticular mass is the

commonest presenting symptom
Testicular biopsy is not recommended in the diagnosis as there can be seeding of tumour cells along
the biopsy tract

Seminoma
• The commonest type of testicular tumour
• Germ cell origin
• Peak incidence occurs in 30-50 years of age
MACROSCOPY
• The testis is enlarged by homogenous firm whitish tumour
• Usually no haemorrhage or necrosis
• “cut-potato “ appearance Seminoma
MICROSCOPY
• The tumour is composed of large polygonal cells with distinct cell borders and
clear cytoplasm
• Round nuclei with distinct nucleoli
• Cytoplasmic clearing is due to glycogen
• Tumour cell islands are separated by lymphocyte rich stroma.
• Histologically identical to ovarian dysgerminoma (ref Ovarian tumours)Seminoma
• Seminomas often remain confined to the testis for long intervals
• Considerably big in size at the time of diagnosis
• Metastasize to lymph nodes -iliac and para aortic
• Hematogenous metastases occur late in the course
IX-
• Extremely radiosensitive
• Has a good prognosis
Embryonal carcinoma
• Pure embryonal carcinomas account for only 2-3% of all testicular germ cell tumors
• Peak age at presentation is 20-30 yrs
• Undifferentiated germ cell tumours
• Macroscopically
ill-defined, invasive masses with hemorrhage and
necrosis
• Microscopically
• large and primitive looking tumour cells with basophilic cytoplasm,
• indistinct cell borders,
• large nuclei with prominent nucleoli “Angry-looking “ cells

York sac tumour

• Most common primary testicular tumour of children less than 3 years
• Good prognosis in this age group
• In adults, yolk sac tumors most often are seen admixed with embryonal carcinoma.
• Αlpha feto protein (AFP) levels are increased in serum in almost all Instances York sac tumour
macroscopy-
large and well demarcated.
MICROSCOPY
• low cuboidal to columnar epithelial cells forming microcysts, lacelike
(reticular) patterns, sheets, glands, and papillae
• A distinctive feature is the presence of structures resembling
primitive glomeruli, the so-called Schiller-Duvall bodies.
• Tumors often have eosinophilic hyaline globules
• α1-antitrypsin and alpha fetoprotein (AFP) can be demonstrated by immunohistochemical
techniques.

Choriocarcinoma
• Pluripotent neoplastic germ cells differentiate along trophoblastic
lines.
• Macroscopy –
haermorrhagic masses.
• Microscopy –
sheets of small cuboidal cells irregularly intermingled
with large, eosinophilic syncytial cells containing multiple dark, pleomorphic nuclei;
• These represent cytotrophoblastic and syncytiotrophoblastic differentiation
• Syncytiotrophoblasts secrete HCG
• Identified by immunohistochemical staining on tissue sections and is elevated in the serum.
 Teratoma
• A tumour representing differentiation of germ cells along somatic cell lines
• Tumour composed of tissue representing endoderm, mesoderm and ectoderm
• Can occur at any age; infancy-adult life
• Peak incidence is 20-30 years
• Pure forms of teratoma are fairly common in infants and children,
• In adults, pure teratomas are rare; most are seen in combination with
other histologic types, embryonal carcinomas and seminomas.
Teratoma
In contrast to seminoma
• heterogenous appearance
• solid tumour with cystic spaces
• haemorrhage and necrosis
Microscopy –teratoma
• Composed of heterogenous collections of differentiated or organoid structures
• Neural tissue, muscle, cartilage, bone, squamous islands thyroid
tissue , bronchial epithelium etc
• These elements may be
• mature-resemble adult tissue
• Immature-resemble fetal tissue
• Malignancy can arise somatic components
• Squamous cell carcinoma
• Mucinous adenocarcinoma
• Sarcomas
Teratoma
• Histologically three major variants
1. Mature teratoma-contain fully mature tissue of one or more germ
cell layer
2. Immature teratoma –contain immature somatic elements
reminiscent of those of developing fetal tissue
3. Teratoma with somatic type malignancy –development of frank
malignancy in preexisting teratomatous component

Teratomas
• Pure differentiated mature teratomas in prepubertal age is
usually benign
• All testicular teratomas in postpubertal age are regarded as
malignant despite the presence of mature or immature tissue
elements

Behaviour of germ cell tumours of testis

• Seminomas are confined to testis for a long duration
• They metastasize to iliac and paraaotic lymph nodes and haematogenous spread is late
• NSGCT metastasize early through lymphatic and blood
• NSGCT presents with advanced clinical disease
• Seminomas are extremely radiosensitive
• NSGCT are less radiosensitive
Tumour markers in testicular tumours
• Certain Germ cell tumours produce tumour markers that appear in serum
• Important in
• Assisting the diagnosis
• Staging the disease
• Assessing tumour burden
• Monitoring the response to therapy
• Early detection of tumour recurrence
Tumour marker
α feto protein (AFP) – yolk sac tumour
β hCG- Choriocarcinoma
Other tumours with a trophoblastic component
PLAP- seminoma
Cryptorchidism
Incomplete descent of the testis into the scrotum from the abdominal cavity.
Normal development

❖ The diagnosis of cryptorchidism is only established with certainty after the age of 1 year
Cryptochoid testis - Morphology
May be normal in size at the beginning , but small size at the puberty
Microscopically,
➢ Atrophy of seminiferous tubules
➢ Peritubular fibrosis and hyalinization
➢ Foci of intratubular germ cell neoplasia

Complications of cryptorchidism
Bilateral cryptorchidism causes sterility due to testicular atrophy.
Even unilateral cryptorchidism may be associated with atrophy of the contralateral descended
gonad and therefore may also lead to sterility.
In addition to infertility, failure of descent is associated with a 3- 5 fold increased risk of testicular
cancer
This arises from Germ cell neoplasia insitu (GCNIS) within the atrophic tubules
Orchiopexy (surgery to move an undescended testicle into the scrotum and permanently fix it
there)typically also reduces the risk of sterility and cancer
Scrotal Swelling
Painful
❖ Orchitis
❖ Epididymo orchitis
Painless
❖ Hydrocele
❖ Haematocele
❖ varicocele
❖ chylocele
❖ tumours

Hydrocele
➢ The commonest cause for intrascrotal swelling
➢ Accumulation of serous fluid (clear fluid)within the tunica vaginalis of the testis
➢ Congenital hydrocele
▪ Appears in first few weeks of life
➢ Secondary hydrocele
▪ Inflammatory
o acute chronic
▪ Neighboring neoplastic lesions

Haematocele
Accumulation of blood within the tunica vaginalis

Chylocele
➢ Accumulation of lymphatic fluid within the tunica vaginalis
➢ # extreme cases of lymphatic obstruction caused by filariasis also cause for hydrocele &
Chylocele (Elephantiasis)

Epididymo-orchitis
➢ Inflammatory lesions usually starts in the epididymis and spread to the testis
➢ 1.Sexually transmitted diseases -Gonorrhoea, Chlamydea
➢ 2. Nonspecific bacterial infections - Spread from the lower urinary tract infections
➢ 3. Mumps
➢ - occurs in 20% of adults infected with the virus
➢ - causes necrosis of testicular tissue with fibrosis
➢ - Sterility is a complication
➢ 4. Tuberculosis causes granulomatous inflammation with caseation
3.Penis

Disorders of the Penis

Are of two types.
A. Inflammatory lesions
B. Penile tumours
• Carcinomas
Carcinoma in situ
Invasive carcinoma
• Condyloma accuminatum(genital warts)
Inflammatory Lesions
Balanitis and balanoposthitis inflammation of the glans penis and overlying prepuce
Common agents are-Candida, anaerobes, Gardnerela and pyogenic bacteria
Related with poor local hygiene
Penile tumours
Tumours of the penis are, on the whole, uncommon.
Most frequent are:
Carcinomas
Carcinoma-in-situ
Two distinct HPV (Type 16/18) related lesions
Bowen disease
Bowenoid papulosis
Both show similar histological features
Epidermal proliferation with numerous mitoses
Atypical mitoses
Markedly dysplastic cells Intact basement membrane (mcq)
Bowen disease Bowenoid papulosis
Over the age of 35 sexually active adults
Solitary, thickened, gray white Multiple reddish papules
plaques on shaft of penis (mcq)

Single / multiple shiny red plaques on

glans

In 10% transform into invasive SCC Never develops into invasive

(mcq) carcinoma

Invasive carcinoma
Invasive squamous cell carcinoma of penis
Relatively common in Asian and African population
Related to
HPV (type 16 and 18)
Poor local hygiene -rare in circumcised males
Smoking
Macroscopically-
Glans penis or inner side of prepuce
Indurated nodule/plaque or ulcer
Microscopically well differentiated squamous cell carcinoma

Condylomata accuminatum(genital warts) (mcq)

Benign and sexually transmitted tumour
Caused by HPV (HPV type 6 and 11) (mcq)

SURGICAL PROBLEMS OF THE PREPUCE (FORESKIN)

PHIMOSIS
PARAPHIMOSIS
BXO
POSTHITIS – BALANOPOSTHITIS

Phimosis
•Prepuce cannot be retracted over the glans penis
•Physiologic in infancy, early childhood
•Generally up to 3 – 4 years
•Prepusal adhesions to gland
•Smegma collection and retraction causes adhesions to break and glans to be free

•Pathologic
•after trauma/ BXO
•Inelastic scar formed at prepuce to block retraction

Symptoms
 •At micturition – ballooning of prepuce, poor flow of urine (dripping rather than in a
trajectory) (mcq)
•Treatment
•Mostly reassurance in early childhood
•Gentle retraction of foreskin
•At bath
•Circumcision
•UTI/ Balanoposthitis/ BXO
•Incomplete preputial separation has been
considered responsible for colonization of the
prepuce by pathogens, which leads to
balanoposthitis or UTI

Paraphimosis
•Prepuce is left retracted because of entrapment of the tight prepuce, proximal to the corona
•The glans engorges and the prepuce becomes edematous because of lymphatic and venous
congestion glans becomes ischaemic if untreated
•Cause – not replacing the foreskin; happens following
•Catheterization
•Masturbation
•Prepusal retraction as treatment for Phimosis

• Treatment (mcq)
1. Manual reduction with lubricant
2. Dundee technique
• Multiple punctures to squeeze out some fluid then reduce

3. Delayed case may need - Dorsal slit

Balanitis Balano – posthitis
•Balanitis
•Inflammation of the glans
•Posthitis
•Inflammation of prepuce
•Common (10%) in uncircumcised boys
•Aetiology
•Trauma, infection, contact irritation, contact allergy
•Treatment
•Gentle handling of prepuce
•Sitz bath
•Cleaning of prepuce
•Suspected bacterial infection?
•Group A beta-haemolytic streptococcal cover – Cephalosporins
•Topical ointment and systemic therapy

Balanitis Xerotica Obliterans (BXO) – Lichen sclerosus

•Acquired phimosis
•Infiltrative skin condition that causes a true phimosis + a clinically recognizable lesion at the tip of
the prepuce
•Late cases – may involve glans, meatus and cause meatal stenosis too
•Causes – unknown ?autoimmune
•? Premalignant lesion
•Diagnosis – biopsy for histology
•Treatment – circumcision

CIRCUMCISION
•Surgical excision of foreskin
•Indications
•Complicated phimosis
 •BXO
•Religious/ cultural
•Neonatal circumcision has proven
to create low incidence of penile cancer
•No evidence in protection against
•STI
•HIV

CONGENITAL PROBLEMS OF THE PENIS

•Hypospadias (mcq)
•Common 1:300 (mild, distal disease in most)
•Combination of 3 defects
•Abnormal ventral meatus
•Lack of ventral foreskin
•Ventral curving of penis (chordee)
•TREATMENT - Surgical correction

•Epispadias
•Rare (1:100,000)
•TREATMENT - Surgical correction

PENILE CANCERS
•Commonly a Squamous cell CA
•Commonest in 60s
•Risk factors
•HPV
•Phimosis (Smegma is not carcinogenic)
•Smoking
•Circumcision at early childhood has shown to be protective
•Premalignant lesions
•Lichen sclerosus (BXO)
•Paget’s disease
•Presentation
•Papule or flat lesion on glans
 •Commonly fungating, smelly lesion with secondary infection
•Early spread to inguinal nodes
•Later into iliac nodes
•Locoregional treatment
•EBRT (external beam radiotherapy)
•Organ sparing surgery
•Partial penectomy
•Inguinal block dissection for lymph nodes
•Metastatic disease
•Chemotherapy

Penile fracture
•Direct blow/ acute angulation of erect penis
rupture of T.albuginea
•Immediate cracking sound
•Detumescence (lost erection)
•Pain and swelling (aurbergine sign)
•If needed – MRI
•Surgical repair of T. albuginea
•If not repaired
•Infection
•Chordee
•Painful erection

4. URETHRAL INJURY
Anterior urethra
• Below the urogenital diaphragm
• Bulbar and penile urethra
Posterior urethra
• Above the urogenital diaphragm
• Membranous, prostatic and pre-prostatic part of urethra
Females
• Only posterior urethra
• Short/ mobile
• Injury – rare – 90% iatrogenic

Injury – Anterior urethra Injury – posterior urethra

 • Common with blunt trauma
• Kick in perineum
• Falling astride
• Common in children
• Mechanism - Relatively fixed bulbar
urethra gets compressed against
inferior surface of the pubic ramus
• Iatrogenic - Urethral
instrumentation and traumatic
catheterization are by far the
commonest at present
• Common with penetrating trauma
• Mostly associated with pelvic
fractures -Straddle fracture,
diastasis
• Common mechanism – rapid
deceleration forces disrupt urethra
at prostate-membranous junction
• Injury patterns – Stretch, Partial
rupture, Complete rupture
• Children - Common in pelvic
fractures (malgaigne’s – vertical
fracture), Associated membranous
urethra and bladder neck injury
• It’s a distracting injury with an
intervening large haematoma
Which gets calcified later on

• Diagnosis
❖ Blood at meatus
• Present in 37 – 93% (maybe absent!)
• Avoid catheterization – suprapubic catheter and RG urethrogram when
stable
• Instrumentation once urethra is imaged
❖ Haematuria
• First voided specimen following trauma is suggestive
• Injury severity doesn’t correlate with haematuria
• Minimal in complete transection
• Copious in partial or mucosal contusion
❖ Pain on micturition
❖ Inability to void
❖ Haematoma or swelling
• If Buck’s fascia intact – swollen penis only
• If ruptured- Can extend up to coracoclavicular fascia superiorly – bruising in
AAW , Fascial lata inferiorly – butterfly bruising in perineum
❖ High riding prostate
• Limited detection with pelvic haematoma – boggy mass
• Blood on finger – rectal injury!
• Not a good clinical sign to elicit
❖ Females – blood at introitus
• Present in 80% with pelvic fracture and urethral injury

• Radiology
❖ Retrograde urethrogram (RGU)
• Gold standard
 • Indicated in suspicion of urethral injury (other Io - stricture)
• Delineates
• CI – unstable patient, contrast allergy, oblique views avoided in pelvic
fractures
• Done after 3/12 if delayed repair is planned

• Other investigations
❖ CT / MRI
• Limited value in urethral injury initial assessment
• Good for associated injuries - Penile crura, Bladder, Kidney
❖ Urethroscopy
• Limited value in initial assessment
• Female – as urethra short – important in classifying the urethral injury

• Complications
✓ Early - Infection , Peri-urethral abscess
✓ Late - Stricures (dense/flimsy), Urethral diverticuli, Urethro-cutaneous fistula

• Management
anterior urethra posterior urethra
Partial tear Acute repair
• Suprapubic • Indications - When BNI(reduce incontinence rates)
cystostomy or rectal injury (reduce impotence rates) id present
• Allow to heal – • Cons - Difficult to delineate anatomy in acute stage
1/12 with haematoma and more injury to pudendal nerve
• Voiding with higher impotence rates
cystourethrogram Early delayed
(VCUG) at 1/12 to • Indication – minor haematoma with less severe
confirm healing initial injury
• Remove • Flex cystoscopy retrograde and anterograde and
suprapubic when pass a wire and a catheter through it  repair
voiding normally • Pros -Ends become closer giving high chance of an
Penetrating injury anastomotic urethroplasty - More chance of a flimsy
• Needs immediate stricture than a dense stricture
exploration and • Cons -Impotence rates higher than delayed repair
Ab cover Management – posterior urethra
Complete tear -Needs Delayed repair
repair • Ideal time of intervention as haematoma is
maximally absorbed
• Pros - Low impotence rates • Anatomy easily
delineated
 • Cons -Higher chance of a substitutional
urethroplasty
Partial tear
• Allow to heal with suprapubic cystostomy • Repeat
RGU at 2/52 intervals
Complete tear
• Commonly managed with a suprapubic cystostomy •
Formal repair in 3/12 via a perineal approach
Stricture
• Flimsy/ short – optical urethrotomy or dilatation •
Dense/ long – excision and anastomosis
(substitutional urethroplasty)

• Iatrogenic injury -Traumatic catheterization

✓ Opt for a suprapubic catheter/ puncture • Urethral injury/ prostatic damage/ false
tract formation may have occurred • Transfer to a GU unit  flexible cystoscopy 
catheter over guidewire • RGU later • suprapubic cystostomy (urinary diversion)
SURGICAL PROBLEMS O