EMBRYOLOGY

 ★ Origin: From the primitive urethra, solid epithelial buds develop and later
canalise.
 Surrounding mesenchyme forms muscular and connective tissue; stromal–
epithelial interactions are critical for differentiation.
 Female homologue: Skene’s tubules, opening on either side of the female
urethra, are the embryological counterpart of the prostate.

SURGICAL ANATOMY – McNEAL ZONAL CLASSIFICATION

 ★ Peripheral Zone (PZ)

o Lies mainly posteriorly;

o Most prostate carcinomas arise here.

o Ducts are long, branched, opening into posterolateral grooves of the

verumontanum.

 ★ Central Zone (CZ)

o Located posterior to the urethral lumen and above the ejaculatory

ducts

o Glands shorter, unbranched.

 ★ Transitional Zone (TZ)

o Periurethral location.

o Most benign prostatic hyperplasia (BPH) originates here.

o As BPH enlarges, it compresses the outer PZ → forms the false capsule.

 Capsular & fascial layers

o True anatomical capsule: outer fibrous layer.

o Periprostatic sheath: condensation of endopelvic fascia external to the

capsule.

o Between them lies the prostatic venous plexus.

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 Sphincters & clinical significance

o Preprostatic sphincter (upper prostate/bladder neck): smooth

muscle, sexual function, closes during ejaculation; Resection
→ retrograde ejaculation.

o Distal striated urethral sphincter: at junction of prostate and

membranous urethra, horseshoe-shaped, bulk anteriorly; distinct from
pelvic floor muscle.

 Neurovascular bundles (NVB)

o In very close relationship to the posterolateral prostatic capsule.

o At risk during radical prostatectomy/cystoprostatectomy → erectile

dysfunction.

o Inadvertent diathermy near NVB during TURP can cause uncommon erectile
impotence.

 ○ All ducts, ejaculatory ducts, and prostatic utricle open into the prostatic
urethra.

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 PHYSIOLOGY

SYSTEMIC HORMONAL INFLUENCES (ENDOCRINE) & LOCAL GROWTH

FACTORS (PARACRINE/AUTOCRINE)

 ★ Hypothalamic–pituitary–gonadal axis

o Hypothalamus → pulsatile LHRH → anterior pituitary → LH → Leydig cells

→ testosterone (90% of total).

o Pulsatile LHRH release is crucial; continuous occupation → receptor

desensitisation.

o This principle underlies LHRH analogue therapy in advanced prostate

cancer (continuous non-pulsatile administration → castrate levels).

 ★ Peripheral androgen conversion

o Testosterone → 5α-dihydrotestosterone (DHT) by 5α-reductase type

II (high concentration in prostate and perigenital skin).

o DHT is 5× more potent than testosterone.

 Adrenal androgens: account for 5–10% of total testosterone, minimal effect in

normal males.

 Oestrogens in the aging male

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 o Adrenal cortex secretes oestrogenic steroids.

o ↑ Oestrogen may disrupt DHT–growth factor balance → ↑ BPH risk.

o Pharmacological oestrogens → ↓ LHRH (via hypothalamic feedback) →

↓ LH → ↓ testosterone → atrophy of testes and prostate.

 Local growth factors (EGF, IGFs, bFGF, TGF-α, TGF-β) are secreted by epithelium
and stroma in response to steroids; their exact roles in normal/abnormal growth are
still unclear.

ELABORATION AND SECRETION OF PROSTATE-SPECIFIC ANTIGEN (PSA)

 ★ PSA is a glycoprotein serine protease, likely facilitating semen liquefaction.

 No true “normal” upper limit; levels ↑ with age, BPH, and prostate cancer.

 Clinical PSA thresholds

o Men 50–69 years: PSA ~3–4 ng/mL → discuss prostate biopsy.

o Metastatic prostate cancer: PSA usually >30 ng/mL, ↓ dramatically after

successful androgen ablation.

o Localised prostate cancer: PSA typically <10–15 ng/mL.

 Sensitivity and specificity pitfalls

o In the 3–15 ng/mL range, PSA cannot reliably distinguish early prostate
cancer from BPH.

o ~25% of men with PSA 4–10 ng/mL have prostate cancer (low
specificity).

o ~15–20% of men with PSA 1–4 ng/mL have prostate cancer (cancer does
exist at low PSA levels).

o Hence, for men 50–69, biopsy often advised when PSA >~3 ng/mL;
threshold lowered for younger men with a strong family history.

 ★ Post-treatment utility

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o Supersensitive PSA assay (detection limit 0.02 ng/mL) allows early
detection of biochemical recurrence after radical prostatectomy.

BENIGN PROSTATIC HYPERPLASIA (BPH)

ETIOLOGY
 ★ Hormonal imbalance theory: Serum testosterone slowly ↓ with age, but
oestrogenic steroids do not decrease proportionally → ↑ oestrogenic effects
may drive prostate enlargement.
 ✓ Local growth factors: Intermediate peptide growth factors likely
contribute to BPH development (exact roles still under investigation).
 ○ Epidemiology: BPH occurs in men >50 years; by age 60, 50% have
histological evidence. It is the most common cause of bladder outflow
obstruction (BOO) in men >70 years.

PATHOLOGY
 ★ Tissue involvement: Affects both glandular
epithelium and connective tissue stroma to variable degrees,
resembling breast dysplasia (adenosis, epitheliosis, stromal proliferation).
 ★ Zonal origin & gross appearance
 Transitional zone (TZ): Submucous glands → nodular
enlargement → compresses peripheral zone (PZ) into a false
capsule → typical “lateral” lobes.
 Central zone (CZ): Subcervical glands → “middle” lobe that projects
into the bladder within the internal sphincter.
 Both lateral and middle lobes may project intravesically, forming
an intravesical prostatic collar around the internal urinary meatus.

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 EFFECTS OF BPH
 Complex relationship: Anatomical prostatic enlargement, lower urinary
tract symptoms (LUTS), and urodynamic BOO do not always correlate.
 ★ Pathophysiology of obstruction: BOO is partly caused by increased
smooth muscle tone mediated by α-adrenergic receptors.
 Anatomical consequences
 Urethra: Lengthened (up to 2× normal), not anatomically
narrowed; posterior curve may become exaggerated → may require
a curved catheter; unilateral lobe enlargement distorts urethra.
 Bladder: If BOO develops, detrusor hypertrophies → trabeculation;
increased blood flow → prominent veins at bladder base → tendency
to haematuria.

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 LOWER URINARY TRACT SYMPTOMS (LUTS)
 Non-specific nature: Bladder dysfunction symptoms become more
common with age due to smooth muscle and neurovesical coordination
decline → not all voiding symptoms in ageing men are due to
BPH/BOO (avoid term “prostatism”).
 ★ Coexisting conditions causing diagnostic confusion:
 Idiopathic detrusor overactivity
 Neuropathic bladder (diabetes, stroke, Alzheimer’s disease,
Parkinson’s disease)
 Bladder smooth muscle degeneration → impaired voiding, detrusor
instability

 Symptom classification
 Voiding (obstructive):
○ Hesitancy (worse with very full bladder)
○ Poor flow (unimproved by straining)
○ Intermittent stream
○ Postmicturition dribbling (⚠️not due to BOO and usually not
improved by prostatectomy)
○ Sensation of incomplete emptying
○ Episodes of near-retention
 Storage (irritative):
○ Frequency
○ Nocturia
○ Urgency

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 ○ Urge incontinence
○ Nocturnal enuresis
 Pitfalls in symptom interpretation
 Low voided volumes (<100 mL) give a false sensation of poor flow.
 Severe irritative symptoms = typically associated with detrusor
instability, not purely BOO.
 Symptom scores offer semi-objective severity, but underlying
pathophysiology may differ.

BLADDER OUTFLOW OBSTRUCTION (BOO) – URODYNAMIC

CONCEPT
 Definition: Low flow rate + high voiding detrusor pressure.
 Definitive diagnosis only by pressure–flow urodynamic
studies (symptoms and flow rate alone are insufficient).
 Causes of urodynamic BOO:
 BPH
 Bladder neck stenosis or hypertrophy
 Prostate cancer
 Urethral strictures
 Functional obstruction from neuropathic conditions
 Primary urodynamic effects on bladder
o ↓ Peak flow rate (Qmax) (voided volume >200 mL):
○ Normal: >15 mL/s
○ Equivocal: 10–15 mL/s
○ Low: <10 mL/s
o ↑ Voiding detrusor pressure (Pdet@Qmax):
○ High: >80 cmH₂O
○ Equivocal: 60–80 cmH₂O
○ Normal: <60 cmH₂O
 ⚠️Diagnostic caveat: Low peak flow (<10–12 mL/s) can also result
from weak detrusor contraction or low voided volumes (e.g., due to
detrusor overactivity), not just BOO.

LONG-TERM EFFECTS AND COMPLICATIONS OF BOO

 Bladder decompensation: Progressively inefficient detrusor contractions
→ residual urine.
 Bladder irritability: ↓ functional capacity due to detrusor
overactivity (may be obstruction-induced, neuropathic, age-related or
idiopathic).

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 ★ Acute urinary retention
 May be the first symptom of BOO.
 Common precipitants: postponed micturition, excessive alcohol (beer),
bed rest from illness/surgery.
 ★ High-pressure chronic retention (HPCR)
 Residual volume >250 mL → ↑ bladder wall tension (combination of
large volume + high resting/filling pressures).
 Leads to functional upper tract obstruction → bilateral
hydronephrosis → renal impairment.
 Presentation: overflow incontinence, nocturnal enuresis, uraemic
symptoms (must be recognized promptly).
 Other complications
 Impaired bladder emptying (large residual) → urinary tract
infection, bladder calculi.
 Haematuria: may arise from BPH, but must exclude other causes
(IVU, cystoscopy, urine culture/cytology).
 Pain is not a symptom of uncomplicated BOO; its presence demands
exclusion of retention, infection, stones, prostate cancer, or carcinoma
in situ of the bladder.

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10 | P a g e
 ASSESSMENT OF THE PATIENT WITH LUTS

HISTORY & SYMPTOM QUANTIFICATION

 ★ International Prostate Symptom Score (IPSS)

o Assigns a semi-objective severity score, trackable over time and after

intervention.

o Must include a quality-of-life (bother) assessment.

 Frequency–volume diary (completed before clinic)

o Reveals fluid intake habits, diurnal output variation, and low-volume,

frequent voiding patterns.

ESSENTIAL & ADDITIONAL INVESTIGATIONS

 Essential investigations (routine for all men with LUTS)

o Urine dipstick: blood, glucose, protein.

o Mid-stream urine (MSU) for culture (infection).

o Serum creatinine.

o Urinary flow rate + ultrasound postvoid residual volume.

 Additional investigations

o Serum PSA if indicated (age, family history, treatment preference).

o Pressure–flow urodynamic studies in selected cases.

PHYSICAL EXAMINATION

ABDOMINAL EXAMINATION

 Chronic retention: Distended bladder visible (loss of transverse suprapubic

skin crease), palpable, and dull to percussion.

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 Look for signs of chronic renal impairment: anaemia, dehydration.

 External meatus: examine for stenosis.

 Epididymides: palpate for inflammation.

DIGITAL RECTAL EXAMINATION (DRE)

 ★ Characteristics of benign enlargement:

o Posterior surface: smooth, convex, typically elastic (firm if fibrous

element dominant).

o Rectal mucosa moves freely over the gland.

o Residual urine may be felt as a fluctuant swelling above the prostate.

 Pitfall: Large residual volume pushes the prostate downward, making it feel
larger than it truly is.

 ★ Volume estimation: Inability to reach the cranial extreme (base) suggests a

volume ≥ 50 mL.

NEUROLOGICAL EXAMINATION

 ★ Purpose: Exclude neurological lesions that can mimic BOO.

o Diabetes mellitus, tabes dorsalis, multiple sclerosis, cervical spondylosis,

Parkinson’s disease, etc.

o If neuropathy is suspected → pressure–flow urodynamics are mandatory

to diagnose true BOO.

 ✓ S2–S4 integrity: Check perianal sensation and anal tone to rule out cauda
equina pathology.

SERUM PROSTATE-SPECIFIC ANTIGEN (PSA)

 Informed decision-making: Men must be counselled about the uncertain
benefit of early detection, the risks of biopsy, and the potential detection of
cancers with unclear optimal management, as well as the advantages of finding a
small, treatable cancer.

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 When to offer PSA:

 Men <70 years or with a positive family history in whom a diagnosis of early
cancer would change management (i.e., radical treatment offered).

 Threshold: PSA > 2.5–4 ng/mL → consider transrectal ultrasound (TRUS)

+ 12-core transrectal biopsies (from six areas).

 ★ When PSA is NOT routinely indicated:

 DRE completely normal, no suspicion of cancer.

 No change in treatment plan would result from early cancer diagnosis (e.g.,
elderly, comorbidities).

 In practice, many clinicians offer PSA due to medicolegal concerns.

FLOW RATE MEASUREMENT

 ★ Technique and requirements

 Use a calibrated flow meter; record 2–3 voids, each with voided volume >150–
200 mL.

 Flow rate is interpreted together with ultrasound postvoid residual.

 Clinical decision threshold: A typical history + peak flow <10 mL/s (for volume
>200 mL) is sufficient for most urologists to recommend treatment.

 Causes of reduced flow rates (not always BOO):

 BOO (bladder outlet obstruction).

 Low voided volumes (<150 mL), commonly due to detrusor overactivity.

 Weak detrusor contractions (low pressure–low flow voiding).

 Improperly calibrated equipment.

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 PRESSURE–FLOW URODYNAMIC STUDIES
(=GOLD STANDARD FOR BOO)
 ★ Indications (patients in whom flow rate and symptoms are insufficient to diagnose
BOO)

 Suspected neuropathic bladder: Parkinson’s, dementia, long-standing

diabetes, stroke, multiple sclerosis.

 Dominant storage (irritative) symptoms, or lifelong urgency/frequency.

 Doubtful history with flow rates in the near-normal range (≥15 mL/s).

 Invalid flow rate due to low voided volumes.

LABORATORY & URINE TESTS

 Blood tests: Serum creatinine, electrolytes, haemoglobin.

 Urine examination:

 Dipstick for glucose and blood.

 MSU for bacteriological culture.

 Cytology if carcinoma in situ (CIS) is suspected (e.g., irritative symptoms,

haematuria).

UPPER TRACT IMAGING

 Not routine in men with straightforward LUTS.

 Mandatory if:

 Urinary tract infection is present.

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  Haematuria is present.

 Modalities: intravenous urogram (IVU) or renal ultrasound.

CYSTOURETHROSCOPY
(IMMEDIATELY BEFORE PROSTATECTOMY)
 ★ Purpose: Exclusion of other pathology, not to decide on surgery.

 Urethral stricture.

 Bladder carcinoma.

 Non-opaque vesical calculus.

 Crucial rule: The decision to operate must be made pre-cystoscopy, based on

symptoms, signs, and non-invasive tests. Direct inspection of the prostate is a
poor indicator of BOO and the need for surgery.

TRANSRECTAL ULTRASOUND SCANNING (TRUS)

 Not a routine investigation.

 Use: Accurate estimation of prostatic volume when a very large prostate is

suspected, via transrectal or transabdominal ultrasound.

MANAGEMENT OF MEN WITH BPH OR BOO

STRONG INDICATIONS FOR TREATMENT (USUALLY

PROSTATECTOMY)
 Acute urinary retention (accounts for 25% of prostatectomies) – in fit men
with no other cause (drugs, constipation, recent surgery).

 Chronic retention with renal impairment (15% of prostatectomies):

 Residual urine ≥ 200 mL

 ↑ Blood urea, hydroureter/hydronephrosis on imaging

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  Uraemic manifestations

 Complications of BOO: bladder stone, recurrent infection, diverticulum

formation.

 Haemorrhage: occasionally venous bleeding from a ruptured prostatic vein

necessitates prostatectomy.

 Elective prostatectomy for severe symptoms (60% of prostatectomies):

 Severe symptoms (hesitancy, poor stream, frequency day and night) +

low maximum flow rate <10 mL/s + increased residual volume 100–250
mL.

 Frequency alone is not a strong indication.

 The natural progression is variable and rarely worsens after 10 years.

 For very large prostates, consider HOLEP or open prostatectomy.

MANAGEMENT OF ACUTE RETENTION

 Immediate: Bladder drainage via catheter; then assess fitness.

 If no reversible cause (drugs, constipation) → prostatectomy is the definitive

management.

 Unfit men or dementia: indwelling prostatic stent or long-term catheter.

 Trial without catheter: α-blockers → trial of void; may succeed in short history, low
residual, but recurrence rate cumulatively high.

 ✓ 5α-reductase inhibitors (finasteride/dutasteride) are given to prevent symptom

progression in men with prostates >35 mL.

SPECIAL PROBLEMS IN CHRONIC RETENTION

 Low-pressure chronic retention (low residual, good renal function, no infection):
may proceed to prostatectomy without prior catheterisation.

 Uraemic, dehydrated patients: urgent catheterisation mandatory to allow renal

recovery.

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o Haematuria often follows decompression (bladder/upper tract collapse) – settles
within days.

 ★ Post-obstructive diuresis:

 Chronic back-pressure → loss of distal tubular salt/water reabsorption

→ massive salt and water loss after relief.

 Monitor: strict fluid chart, daily weight, serial creatinine/electrolytes.

 IV fluid replacement if oral intake insufficient.

 Anaemia common; transfuse if Hb <9 g/dL after fluid stabilisation.

INDICATIONS FOR ELECTIVE TREATMENT IN LUTS/BPH

– KEY QUESTIONS
1. Failed medical therapy? Many men are referred after failing α-blockers or
5α-reductase inhibitors.

2. Is BOO present?

o Working diagnosis: significant symptoms + benign prostate + Qmax <10–12

mL/s (volume >200 mL).

o Pressure–flow studies needed if: irritative symptoms dominate, suspected

neurological disease, or technically imperfect flow rates.

3. Symptom severity and risk of doing nothing?

o Severe symptoms + large residual → usually treat.

o Mild symptoms, flow >15 mL/s, residual <100 mL → safe to reassure and
review; rarely progress to retention.

4. Is the man fit for surgery?

5. Available treatments, outcomes, and side-effect trade-off?

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 TREATMENT MODALITIES

CONSERVATIVE (WATCHFUL WAITING)

 For men with mild symptoms, Qmax >10 mL/s, residual <100 mL.

 Re-assess after 6 months (symptoms, flow rate, ultrasound). Many remain

stable.

 ○ Adjuncts: evening fluid restriction, propantheline for irritative symptoms.

DRUG THERAPY

 α-Adrenergic blockers (e.g., tamsulosin, alfuzosin)

 Inhibit smooth muscle contraction in prostate → rapid symptom relief.

 5α-Reductase inhibitors (finasteride, dutasteride)

 Block conversion of testosterone to DHT → ~25% prostate volume

reduction after 1 year, best in glands >50 g.

 Require ≥6 months for maximal effect; fewer side effects but slower
onset.

 ★ Comparative efficacy:

 Drugs: Qmax improvement ~2 mL/s over placebo, symptom score ↓ ~20%.

 TURP: Qmax improvement from 9 → 18 mL/s, symptom score ↓ 75%.

 Drugs are expensive relative to effectiveness; a significant proportion later

undergo TURP.

 Best role: men who fail watchful waiting and wish to postpone surgery.

OPERATIVE TREATMENT – PRE-OPERATIVE COUNSELLING

 Retrograde ejaculation: occurs in ~65% of men.

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 Erectile impotence: ~5%, mostly in men with pre-existing waning potency.

 Success rates:

 Acute/chronic retention → excellent symptom relief.

 90% success in severe symptoms + urodynamically proven BOO.

 Only ~65% success if mild symptoms or weak detrusor contraction.

 Unobstructed detrusor instability responds poorly to TURP.

 Reoperation risk: ~15% at 8–10 years after TURP.

 Morbidity/mortality:

 Death <0.5%; severe sepsis ~6%; transfusion >2 units ~3%.

 Post-discharge antibiotics for UTI symptoms: 15–20%.

 Risk factors: retention, prostate cancer, renal impairment, advanced age.

SURGICAL TECHNIQUES

TRANSURETHRAL RESECTION OF THE PROSTATE (TURP)

 It is the GOLD STANDARD

 Technique: Loop diathermy cuts strips from bladder neck

to verumontanum (proximal border of external sphincter). Chips evacuated with
Ellik evacuator.

 Monopolar TURP: 1-hour limit due to risk of water absorption (irrigant: 1.5%
glycine).

 Bipolar TURP: uses normal saline → allows longer resection for larger prostates.

 ○ Small prostate/bladder neck stenosis → Collings knife incision.

 ○ Post-op: 3-way catheter irrigation until effluent pale pink; catheter removed day 2–
3.

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 LASER PROCEDURES

 Holmium Laser Enucleation of the Prostate (HOLEP)

o Laser seals small vessels along the avascular plane between PZ and
TZ (Millin’s plane).

o Enucleation with cystoscope beak (like surgeon’s finger in open Millin’s) →

adenoma pushed into bladder → morcellation.

o Landmark: verumontanum = distal limit to protect external sphincter.

o ○ Low morbidity, sustained long-term results.

 ★ Green Light (KTP) Laser Vaporisation

o Vaporises prostate tissue; deeper penetration than holmium.

o Highly haemostatic → can be used in anticoagulated patients.

o Less durable than HOLEP/TURP (less tissue removed).

OPEN PROSTATECTOMY (FOR VERY LARGE GLANDS OR CONCOMITANT

PATHOLOGY)

 Retropubic (Millin):

o Low transverse Pfannenstiel incision; anterior capsule incised, finger

enucleation along avascular plane.

o Wedge resected from posterior bladder neck to prevent secondary

stricture.

o Capsule closed over Foley catheter.

 Transvesical (Freyer/Harris) – rarely used:

o Bladder opened, enucleation via urethra.

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 o Freyer left bladder widely open with large suprapubic tube; Harris added
lateral prostatic artery stitches and closed bladder.

COMPLICATIONS OF PROSTATECTOMY

LOCAL

 Primary haemorrhage: check catheter drainage; wash out clots

aseptically; change catheter by surgeon; return to OR if needed.

 Secondary haemorrhage (post-discharge): warn all patients; rest and high

fluid intake; clot retention → readmit, catheter, washout.

 Perforation: bladder/prostatic capsule – if vision obscured by bleeding,

stop, achieve haemostasis, plan second-look; large extravasation may need
suprapubic drain. Rectal perforation extremely rare.

 Urethral stricture: meatal or bulbar; due to catheter size, prolonged

instrumentation. Early → bouginage; later → optical urethrotomy.
Routine Otis urethrotomy prior to TURP ↓ incidence.

 Bladder neck contracture: over-resection of small prostate or excessive

diathermy → transurethral incision.

SEPSIS

 ★ Bacteraemia in >50% with infected urine, prolonged catheter, chronic

retention.

 Prophylactic antibiotics based on local sensitivity profiles.

 ⚠️Postoperative rigor → may progress to septic shock; take blood cultures,

IV antibiotics (e.g., amoxicillin + cefuroxime, or gentamicin).

INCONTINENCE

 External sphincter damage → incontinence; bladder neck is rendered

incompetent by any prostatectomy → intact distal sphincter is essential.

 Verumontanum marks proximal limit of external sphincter.

 Treatment: physiotherapy; if fails → artificial urinary sphincter or sling.

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  Detrusor instability may contribute: anticholinergics (imipramine, duloxetine)
may help.

RETROGRADE EJACULATION & IMPOTENCE

 Retrograde ejaculation >50% (bladder neck disruption).

 Impotence uncommon in men with good preoperative function.

SYSTEMIC

 Water intoxication (TUR syndrome): absorption of hypotonic irrigant →

confusion, hyponatraemia, haemolysis, pulmonary oedema, cardiovascular
collapse. Incidence ↓ with isotonic glycine, further ↓ with bipolar TURP
(saline). Treatment: fluid restriction.

 Cardiovascular: atelectasis, pneumonia, myocardial infarction, cardiac

failure, DVT.

 Mortality: 0.2–0.3% elective; up to 1% in elderly, cancer, emergency

retention, very large prostates.

 Reoperation: 15–18% after 8 years (TURP); ~5% after open prostatectomy.

OTHER MODALITIES
 Intraurethral stents: reserved for men in retention who are grossly
unfit (ASA grade IV) – very rare indication.

BOO CAUSED BY THE BLADDER NECK

AETIOLOGY
 ★ Primary condition: Usually occurs in men, but can rarely affect children (both
sexes) and women.

 Causes

 ★ Marion’s disease: – muscular hypertrophy of the internal sphincter in a

young person leading to vesical diverticulum or hydronephrosis.

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  Bladder neck dyssynergia (functional obstruction): dyssynergic smooth
muscle contraction during voiding → BOO.

 Fibrosis of the bladder neck tissues, typically following TURP or radical

prostatectomy (especially if compounded by external beam radiotherapy –
EBRT).

TREATMENT

DIAGNOSIS

 ★ Urodynamic confirmation is essential: demonstrates ↑ voiding

pressures and ↓ flow rate (pressure-flow pattern of BOO).

PHARMACOLOGICAL MANAGEMENT

 ★ α-Adrenergic blockers (relax smooth muscle at bladder neck/prostatic urethra)

 Alfuzosin 10 mg once daily

 Tamsulosin 0.4 mg once daily

 Doxazosin 1 mg at night (max 8 mg/day)

 Indoramin 20 mg twice daily (max 100 mg/day)

 Prazosin 2.5 mg twice daily (maintenance up to 2 mg/day)

 Terazosin 1 mg at night (max 10 mg/day)

 Silodosin 4–8 mg once daily

 Side effect warning: Postural hypotension, usually limited to the first few doses
(drugs are not target-specific to bladder neck).

 SURGICAL MANAGEMENT – TRANSURETHRAL INCISION

 Transurethral incision of the bladder neck is the operation of choice.

 Symptom recurrence is usually due to inadequate division of the bladder

neck fibres.

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 PROSTATIC CALCULI

CLASSIFICATION OF PROSTATIC CALCULI

 ★ Endogenous calculi (common): formed within the prostate, composed of calcium
phosphate with ~20% organic material.

 ○ Exogenous calculi (rare): a urinary calculus (often ureteric) that becomes

arrested in the prostatic urethra.

CLINICAL FEATURES
 Usually asymptomatic – incidental findings on:

 Transrectal ultrasound (TRUS), Pelvic radiography, During prostatectomy, and

 Associated with carcinoma of the prostate or chronic prostatitis

 Diagnostic pitfall: In severe chronic prostatitis, the fibrosis and

nodularity caused by calculi and inflammation can be difficult to differentiate
from carcinoma on DRE.

 Radiographic hallmark: On X-ray or ultrasound, calculi often appear as

a horseshoe or circle distribution.

 Postulated association with bladder outflow obstruction (BOO).

TREATMENT OF PROSTATIC CALCULI

GENERAL PRINCIPLE: Most prostatic calculi require no treatment.

CONSERVATIVE MEASURES: If associated with chronic prostatic infection, give

Antibiotics – ciprofloxacin or trimethoprim.

TRANSURETHRAL RESECTION (TURP)

 TURP performed for concurrent BPH will often release small calculi as tissue strips
are excised; residual calculi may pass spontaneously later.

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 Associated benign prostatic enlargement is treated at the same sitting with
TURP.

CORPORA AMYLACEAE
 Definition: Tiny calcified, lamellated bodies found in the glandular alveoli of the
prostate in elderly men.

 Significance: Considered the forerunners of endogenous prostatic calculi.

 Distinct from true calculi but represent an early stage of calcification.

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 CARCINOMA OF THE PROSTATE

EPIDEMIOLOGY
 ★ Most common malignant tumor in men >65 years.

 ★ Autopsy incidence:

 25% of men 50–65 years have microscopic foci.

 ~70% in men >80 years.

 Most are tiny and latent; men often die with, not because of, prostate
cancer.

 Family history: 10–15% of younger men have a positive family history;

aetiology unclear.

 Geographic variation: Autopsy micro-cancers are equally prevalent

worldwide, but clinically evident disease is much lower in Japan, China and
India.

 Origin: Almost always in the peripheral zone (PZ) → BPH surgery

(TURP/open) does not protect against subsequent carcinoma.

PATHOLOGY & TUMOR TYPES

 ★ Classification (clinical context is everything)

 Microscopic latent cancer: found at autopsy or cystoprostatectomy; never

caused symptoms.

 Incidentally found:
○ T1a/T1b – during TURP for presumed BPH.
○ T1c – after PSA screening, no palpable abnormality.

 Early, localised disease (T2): organ-confined, palpable but curable.

 Locally advanced/high-risk (T3–T4): beyond capsule, may involve seminal

vesicles/bladder neck/sphincter.

 Metastatic disease (M1): may arise from clinically obvious primary or from an
occult primary (T0/T1) — i.e. occult prostate cancer.

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 Symptomatic disease = incurable: Only T3/T4 and metastatic tumours cause
symptoms; they are not curable.

 Cure is only possible with early detection (T1–T2) via screening or incidental
discovery — but many such tumors would never have progressed during the
patient’s lifetime. This is the fundamental dilemma of prostate cancer.

SCREENING FOR PROSTATE CANCER

 PSA screening is controversial and does not fulfil WHO criteria for a population
screening program.

 Key trial findings (4 largest RCTs, ~700,000 men)

 No improvement in overall mortality.

 Small improvement in prostate cancer-specific mortality.

 Screening increased prostate cancer detection by 18 per 1000 men

screened.

 Leads to overdiagnosis and complications from biopsies (infection,

bleeding, pain).

 ★ Summary: Screening the entire population with PSA is not cost-

effective because too many men must be screened, biopsied and treated to
prevent each death.

 High-risk groups (family history, African ancestry) are often underrepresented in

trials.

PATTERNS OF SPREAD

LOCAL SPREAD

 Upward extension:

 Seminal vesicles → bladder neck → trigone.

 Later → distal sphincter mechanism.

 Ureteral obstruction: Bilateral involvement → anuria.

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 Rectum: may be encircled and stenosed, but direct mucosal invasion is
rare.

BLOODSTREAM (HAEMATOGENOUS)

 ★ Prostate is the most common primary site for skeletal

metastases (followed by breast, kidney, bronchus, thyroid).

 ★ Bones most frequently involved:

 Pelvic bones and lower lumbar vertebrae (most common).

 Femoral head, ribcage, skull.

 Bone metastases are typically osteoblastic (sclerotic) on radiographs.

LYMPHATIC SPREAD

 ★ Primary routes:

 (i) Lymphatics to obturator fossa → along the sides of rectum → internal iliac
and sacral nodes.

 (ii) Lymphatics over seminal vesicles and along vas deferens → external iliac
nodes.

 Sequential progression: Retroperitoneal nodes → mediastinal → occasionally

supraclavicular (Virchow’s node).

TNM STAGING SYSTEM FOR PROSTATE CANCER

★ T1 – Clinically inapparent tumor, not palpable or visible by imaging

 T1a: Incidental finding at TURP; ≤5% of resected tissue involved; usually

well/moderately differentiated.
 T1b: Incidental finding at TURP; >5% of resected tissue.
 T1c: Tumor identified by needle biopsy performed because of elevated PSA; no
palpable abnormality.

★ T2 – Palpable tumour confined within the prostate capsule

 T2a: Suspicious nodule involving ≤ half of one lobe.

 T2b: Involves > half of one lobe but not both sides.
 T2c: Involves both lobes (bilateral) but still organ-confined.

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★ T3 – Extraprostatic extension

 T3a: Extracapsular extension (unilateral or bilateral).

 T3b: Seminal vesicle invasion.

★ T4 – Invasion of adjacent structures

 Fixation or invasion of levator ani muscles, external sphincter, rectum,

bladder neck (beyond trigone), or pelvic side wall (excluding seminal
vesicles).

NATURAL HISTORY & PROGRESSION RISK

★ Prognosis is highly dependent on stage and grade.

 T1 and T2 (localised)

 Well-differentiated T1a: progression rate very low — 10–14% at 8 years.

 Moderately differentiated T1a: progression ~20% at 8 years.
 T1b and T2 tumours: progression risk >35% (higher potential for metastasis).

 T3 and T4, M0 (locally advanced): ~50% progress to bony metastases within

3–5 years.
 M1 (metastatic disease)
 Median survival ~3 years.
 Many men with metastatic disease die with prostate cancer rather than
from other causes; advanced disease is ultimately fatal.

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 CLINICAL FEATURES & PRESENTATION
 Only advanced disease typically causes symptoms, but even extensive
metastases can be asymptomatic initially.
 Symptoms of advanced disease:

 BOO (hesitancy, poor stream, retention).

 Pelvic pain and haematuria.

 Bone pain (often back, pelvis), malaise, ‘arthritis’, anaemia

or pancytopenia (marrow infiltration).

 Renal failure (bilateral ureteral obstruction).

 Locally advanced pelvic mass, or asymptomatic metastases found

incidentally.

★ Early prostate cancer (T1–T2) is ASYMPTOMATIC and detected only by:

 Incidental TURP for clinically benign disease (→ T1a/T1b).

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  Serum PSA screening (→ T1c).

 Nodule on digital rectal examination (DRE) (→ T2).

DIGITAL RECTAL EXAMINATION (DRE) IN PROSTATE

CANCER
★ Classic DRE findings suggestive of carcinoma:

 Irregular induration, characteristically stony hard in part or whole gland.

 Obliteration of the median sulcus.

 Extension beyond the capsule: palpable involvement of the bladder base and
seminal vesicles is diagnostic of T3b.

 Local extension through the capsule → loss of tissue plane, fixation (T3a/T4).

TRUS may show a hypoechoic nodule (Fig. 84.15), normal seminal vesicles (Fig.
84.16), or extraprostatic extension (Fig. 84.17).

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 MULTIPARAMETRIC MAGNETIC RESONANCE IMAGING
(mpMRI)
 Purpose: Diagnose early prostate cancer and reduce overdiagnosis of insignificant
disease.

 Required sequences (4 core components):

 T1-weighted imaging

 T2-weighted imaging

 Diffusion-weighted imaging (DWI)

 Dynamic contrast-enhanced (DCE) imaging

 Spectroscopic imaging (often included)

 ★ Standardised reporting: Use PI-RADS v.2 scoring system.

 PI-RADS ≥3 is indicative of malignancy.

 Accuracy varies between reporting radiologists.

 Low-grade, insignificant tumours are frequently not visible on MRI.

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 PROSTATIC BIOPSY
 Indication: Suspicious DRE, elevated PSA, or evidence of metastatic disease.

 Guidance: TRUS (transrectal ultrasound) with an automated biopsy gun.

 Routes:

 Transrectal: can be done under local anaesthesia; higher sepsis risk → requires
broad-spectrum antibiotic cover.

 Transperineal: gaining popularity, often requires sedation or general

anaesthetic; lower sepsis risk; better access to anterior prostate.

 ★ Advanced targeting:

 Areas suspicious on mpMRI can be targeted to increase diagnostic yield.

 Fusion biopsy: software fuses mpMRI and real-time TRUS images to accurately
sample the index lesion.

HISTOLOGICAL APPEARANCES & GLEASON GRADING

 Prostate cancer is an adenocarcinoma (glandular structure of ducts and acini).

 Early change: loss of the basement membrane, glands become confluent.

With dedifferentiation, solid sheets of cells appear.

 ★ Gleason grading system:

 Two most prevalent patterns on biopsy each scored 3–5 (Grades 1 and 2
no longer reported; behave like Grade 3).

 Grade 3 cancers almost never metastasise.

 Summed to Gleason score 6–10. Score and tumour volume correlate

with spread and prognosis.

 ★ ISUP/WHO Grade Groups (prognostic classification):

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 o Group 1: Gleason 6 (3+3)

o Group 2: Gleason 7 (3+4)

o Group 3: Gleason 7 (4+3)

o Group 4: Gleason 8 (4+4, 3+5, 5+3)

o Group 5: Gleason 9–10 (4+5, 5+4, 5+5)

o Higher grade group = poorer prognosis.

BLOOD TESTS & TUMOUR MARKERS

 Early disease: Blood tests normal.

 Metastatic disease:

o Leukoerythroblastic anaemia due to marrow infiltration.

o Anaemia of renal failure.

o Thrombocytopenia, disseminated intravascular coagulopathy (DIC) with ↑

fibrinogen degradation products.

 Liver function: Abnormal if extensive liver metastases.

o ↑ Alkaline phosphatase (ALP) – distinguish bone vs liver source

by isoenzymes or GGT.

 ★ PSA pearls:

 PSA >10 ng/mL suggestive of cancer; >35 ng/mL almost diagnostic

of advanced prostate cancer (in absence of UTI).

 After hormonal ablation, PSA fall to normal range = good prognosis.

 Post-radical prostatectomy PSA should become undetectable (<0.03 ng/mL

with supersensitive assay).

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 RADIOLOGICAL EXAMINATION (PLAIN FILMS)
 Chest X-ray: May show lung or rib metastases.

 ★ Abdominal X-ray: Characteristic sclerotic (osteoblastic) bone

metastases in lumbar spine and pelvis (appear dense, coarse).

o May resemble Paget’s disease of bone.

o Osteolytic metastases are also common and often coexist with sclerotic
lesions.

CROSS-SECTIONAL IMAGING FOR STAGING

MRI (HIGH-TESLA 1.5–3 T)

 ★ Most accurate method for local staging.

 mpMRI roles:

o Preoperative assessment of pelvic lymph nodes and local extent.

o ⚠️Sensitivity limited for small capsular penetration.

o Key in active surveillance and detecting local recurrence post-treatment.

 ○ Low-grade tumours often invisible on MRI and are frequently clinically

insignificant.

TRANSRECTAL ULTRASOUND (TRUS)

 More sensitive than DRE for locally extensive (≥T2) disease.

 Many tumours still missed.

 ★ In screening, TRUS + DRE + PSA detects only 30–50% of autopsy-proven

cancers (though likely identifies the larger, clinically significant ones).

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 BONE SCAN (TC-99M)
 ★ Indications:

o PSA >10 ng/mL

o Locally advanced disease (≥T3)

o Gleason score ≥7

 If PSA <10 ng/mL, perform bone scan only on clinical indication (e.g.,
bone pain, ↑ ALP).

More sensitive than skeletal survey.

 ⚠️False positives in arthritis, osteomyelitis, healing fractures.

PSMA-PET SCAN (GALLIUM-68 PSMA)

 ★ Increasingly used in prostate cancer staging.

 ✓ High sensitivity for detecting lymph node and distant metastases; may
be superior to MRI.

 ⚠️Small lymph node metastases can be missed.

 ○ Applications:

o Initial staging prior to definitive treatment.

o Restaging after biochemical recurrence (rising PSA post-treatment).

GENERAL PRINCIPLES OF TREATMENT

DECISION-MAKING

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 ★ Risk stratification is based on PSA level, Gleason grade, and clinical
stage – the strongest predictors of metastasis.

 ✓ Nomograms/tables use these three parameters to predict lymph node

involvement and metastatic risk.

 ⚠️Treatment choice also depends on life expectancy and comorbidities,

not just tumour factors.

 ○ Curative treatment is possible only in early (organ-confined)

disease.

 ★ Advanced disease (T4, N1, M1) → treatment is palliative only.

EARLY DISEASE – ACTIVE SURVEILLANCE & CURATIVE

OPTIONS
 ★ Low-risk disease (low PSA, small foci of Gleason 6) is suitable for active
surveillance:

o Protocol:
○ 3–6-monthly DRE + PSA
○ mpMRI yearly or every 2 years
○ Repeat prostate biopsy

o ⚠️~1/3 of patients will require definitive radical treatment within a few

years.

o ✓ Avoids toxicity of immediate radical therapy (impotence, incontinence).

 ○ Options for T1, T2, and some T3 disease: radical prostatectomy,

radical radiotherapy, or active monitoring, tailored to patient age,
performance status, and lifestyle preferences.

SUMMARY OF TREATMENT BY RISK GROUP

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 LOW-RISK DISEASE

 ★ Men in their 70s: conservative management (active surveillance) is

usually correct.

 ✓ Younger men (<70 years) and/or positive family history: radical

surgical treatment may be considered, but many still opt for active
surveillance after counselling about the risks of impotence and
incontinence.

 ○ Even in this group, conservative approach is an acceptable option when

risks versus benefits are discussed.

INTERMEDIATE-RISK DISEASE

 ★ Younger, fitter men (<70 years): radical prostatectomy or radical

radiotherapy.

 ✓ Active monitoring remains an option, especially for elderly patients at

the lower end of the risk spectrum.

 ○ Elderly with outflow obstruction: TURP ± hormone therapy.

 ★ The absolute benefit of radical over conservative treatment is

about 25% at 10 years (reflecting the ~35% progression risk of T2 disease,
much of which is curtailed by treatment).

HIGH-RISK DISEASE (INCLUDING T3)

 ★ Significant risk of progression → multimodal therapy is mandatory.

 ✓ Early androgen ablation is favoured if close follow-up is impossible.

 ○ Sexually active men: a careful conservative approach with androgen

ablation at symptom onset is reasonable.

 ★ Standard for younger men with T3 disease: androgen ablation +

radiotherapy, with surgery (radical prostatectomy + salvage radiotherapy)
as part of a multimodal strategy.

METASTATIC DISEASE (M1)

 ★ Prognosis is poor once metastases develop.

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 ✓ Symptomatic patients: androgen ablation provides relief in >2/3 –
no dilemma.

 ⚠️Asymptomatic metastases: timing of treatment is less clear (immediate

vs deferred androgen deprivation).

 ✓ Systemic chemotherapy with docetaxel should be considered

in younger, fitter men.

 ○ After failure of first-line androgen ablation, chemotherapy offers

short-term success.

PRINCIPLES OF TREATMENT MODALITIES (TEXT

REFERENCE)
 ★ Summary Box 84.8 key takeaways:

o Treatment depends on stage, life expectancy, patient preference.

o PSA, DRE, biopsy Gleason grade predict pathological stage.

o Localised cancers: radical prostatectomy, radiation therapy, active

surveillance.

o Advanced disease: hormone ablation is first-line; upon

failure, chemotherapy provides temporary benefit.

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