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SU29.{7,9-10} | Urinary Retention and Prostate Disorders — SDL Guide (Part 2)

Management: Relieving Retention and Treating Prostate Disease

Management follows directly from the diagnosis, and the first principle is to relieve the obstructed bladder. Acute retention is treated by immediate bladder drainage: pass a urethral catheter without delay, and if the urethra cannot be catheterised or is contraindicated (for example after pelvic trauma or impassable stricture) place a suprapubic catheter instead. Record the drained volume, treat the precipitant, and in men with presumed BPH start an alpha-blocker before a planned trial without catheter to improve the chance of voiding. Chronic retention is relieved more cautiously — decompress the bladder and then watch closely for post-obstructive diuresis, replacing fluids and electrolytes and monitoring renal recovery, because high-pressure chronic retention with renal impairment needs the kidneys protected, not the patient sent home. For benign prostatic hyperplasia the ladder of treatment runs from lifestyle measures and watchful waiting for mild symptoms, through medical therapy — alpha-blockers such as tamsulosin that relax prostatic smooth muscle to relieve symptoms quickly, and 5-alpha-reductase inhibitors such as finasteride that shrink a large gland over months — to surgery, of which transurethral resection of the prostate (TURP) is the gold-standard operation, indicated for failed medical therapy, recurrent retention, recurrent infection or stones, refractory haematuria or renal impairment; very large glands may need open or laser enucleation. For carcinoma of the prostate management is dictated by stage and risk: active surveillance for low-risk localised disease; radical prostatectomy or radical radiotherapy for localised disease in fit men; and androgen deprivation therapy (ADT) — using LHRH agonists or antagonists and anti-androgens — for locally advanced or metastatic disease, often with additional agents, because prostate adenocarcinoma is androgen-driven. Always pair treatment with appropriate counselling and consent, especially around the urinary and sexual side-effects of prostate surgery.

Provided image

Feature	Benign prostatic hyperplasia	Carcinoma of the prostate
Zone of origin	Transition (periurethral) zone	Peripheral zone (adenocarcinoma)
DRE finding	Smooth, firm, rubbery, sulcus preserved	Hard, irregular, nodular, sulcus lost
PSA	Normal or mildly raised	Often raised (organ-specific, not cancer-specific)
Key investigation	IPSS, post-void residual USG, uroflowmetry	Multiparametric MRI → targeted biopsy (Gleason/ISUP), bone scan
Metastasis	None	Bone — typically osteoblastic (sclerotic)
Principles of management	Lifestyle, alpha-blocker (tamsulosin), 5ARI (finasteride), TURP (gold standard)	Surveillance; radical prostatectomy/radiotherapy; androgen deprivation therapy for advanced disease

Check Your Understanding

Bring the threads together by reasoning back through the two men from the hook. The first, in agony at 2 a.m. with a sudden tender palpable bladder, has acute retention — an emergency demanding immediate urethral catheterisation (or suprapubic drainage if the urethra fails), recording of the drained volume, treatment of any precipitant, and an alpha-blocker before a trial without catheter; the likely culprit behind it is benign prostatic hyperplasia of the transition zone. The second, comfortable but with nocturia, terminal dribbling, weight loss and a raised PSA, sits at the worrying end: his story and biochemistry mandate a digital rectal examination and, if the gland is hard and nodular with a lost sulcus, multiparametric MRI, targeted biopsy and a bone scan to look for the osteoblastic metastases that prostate adenocarcinoma of the peripheral zone classically produces. Use these to self-test the three competencies this module covers. First, can you state the principles of managing acute retention (immediate catheterisation; suprapubic if urethral fails) and chronic retention (controlled decompression; watch for post-obstructive diuresis; protect the kidneys in high-pressure disease)? Second, can you distinguish benign prostatic hyperplasia (transition zone, smooth sulcus-preserved gland, LUTS scored by IPSS, alpha-blocker/5ARI/TURP) from carcinoma (peripheral zone, hard nodular sulcus-lost gland, raised PSA, Gleason/ISUP, MRI-targeted biopsy, ADT for advanced disease, osteoblastic bone metastases)? Third, can you describe and demonstrate a digital rectal examination — consent, chaperone, left-lateral positioning, inspection, lubricated gloved finger, assessment of anal tone and then the prostate's size, surface, consistency, sulcus, nodules and tenderness, glove inspection and documentation — and name the findings that separate a benign from a malignant gland? The questions that follow check exactly these links.