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Chapter: Medicine and surgery: Genitourinary system

Benign prostatic hyperplasia - Disorders of the bladder and prostate

Hyperplasia of the prostate is a common cause of bladder outflow obstruction. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Benign prostatic hyperplasia

 

Definition

 

Hyperplasia of the prostate is a common cause of bladder outflow obstruction.

 

Incidence/prevalence

 

Common.

 

Age

 

Affects âˆ¼50% of men age 50–60, >80% of men age >80.

 

Sex

 

Males

 

Aetiology

 

Thought to be due to increased androgen effects (di-hydrotestosterone and its metabolites), or oestrogens. Functioning testes are important: castrati (before puberty) do not get BPH. Castration post-onset gives a 30% reduction in size only.

 

Pathophysiology

 

Androgens appear to act on the periurethral area of the prostate ‘McNeal’s transition zone’ to stimulate hyperplasia. There is compensatory bladder hypertrophy. At 30–40 years there is microscopic evidence, by 50 years it is macroscopically visible, by 60 years the clinical phase begins.

 

The obstruction is due to both direct impingement of the enlarged prostate on the urethra and also the dynamic smooth muscle contraction of the prostate, prostatic capsule and bladder neck.

 

Clinical features

 

Usually a long history of bladder outflow obstruction, but may present as acute urinary retention or a UTI, or with frequency and urgency symptoms. Per rectum examination reveals a smoothly enlarged prostate, with intact median groove.

 

Macroscopy

 

There is hyperplasia of the transition zone. Nodules formed of hyperplastic glandular acini displace and compress the true prostatic glands peripherally forming a false capsule. Weight usually up to 200 g (normal is 15 g).

 

Microscopy

 

Benign epithelial proliferation with large acini, smooth muscle and fibroblast proliferation. Oedema and inflammation are common, as are areas of infarction.

 

Complications

 

Bladder decompensation – due to chronically increased residual volumes (urine retained after voiding), the bladder may become less contractile, lowering flow rates further. Obstruction may lead to dilated ureters and kidney (hydroureter, and hydronephrosis). It may also cause ARF or CRF.

 

Investigations

 

It is important to exclude other causes of bladder outflow obstruction or bladder instability.

 

·        FBC, U&Es, serum prostate specific antigen (PSA) and urine microscopy and culture are routine.

 

·        Urodynamics: Maximal urinary flow rates less than 10 mL/second are almost diagnostic of bladder outflow obstruction. Between 10 and 15 mL/second, combined pressure/flow studies may be done to exclude those with other problems, as resection of the prostate in these patients may not relieve symptoms. The disadvantage of the latter, is that urinary catheterisation is required.

 

·        Bladder scan: This simple scan uses ultrasound to measure the postvoiding residual volume is useful. Patients with a high residual volume are at risk of bladder decompensation and UTIs.

 

·        If there is evidence of renal impairment, renal USS should be performed to look for hydronephrosis.

 

Management

 

In patients with mild symptoms, monitoring may be advised, as symptoms often improve over time. For those with moderate to severe symptoms the choice is between a trial of medical therapy or surgical therapy.

 

Drugs are aimed at relaxing the contractile component and reducing the volume of the prostate.

 

·        Î±-blockers such as doxazosin, terazosin and tamsulosin improve symptoms and bladder outflow rates in 60–90% of patients, but may cause unacceptable hypotension.

 

·        Finasteride is a 5 alpha reductase inhibitor which in-hibits the conversion of testosterone to dihydrotestosterone. It is also useful, but generally less effective for symptoms than Î±-blockers. It seems to be more effective in those with very large prostates and its effects may improve with time.

 

Transurethral resection of the prostate (TURP) has been the standard treatment. The procedure involves removal of prostatic tissue using electrocautery via a resectoscope from within the prostatic urethra, under general or spinal anaethesia. Post-operatively patients require a three-way catheter and continuous bladder irrigation to reduce the risk of clot retention until haematuria is mild.

 

·        Early complications: Post-op (immediate) haemorrhage, urethral blood clot and urinary retention. Antibiotic prophylaxis is usually given to prevent urinary tract infection. Hypervolaemia and hyponatraemia with a metabolic acidosis may occur (TURP syndrome) due to absorption of irrigating fluid (may be > 1 L).

 

·        Later  complications  include:  â‰¤14%  become  impotent, retrograde ejaculation, epididymoorchitis, bladder neck contracture or urethral stricture requiring surgery or dilatation, incontinence. About 20% require further TURP within 10 years.

 

·        Other options (not widely available) include:

 

·        Stent which is costeffective in those with a short life-expectancy or temporarily for patients unfit for surgery, e.g. due to recent MI, and has less operative morbidity.

 

·        Microwave ablation by transurethral catheter (TMT= transurethral microwave thermotherapy) or transrectally.

 

·        Electrovaporisation utilises electrical energy to vaporise prostatic tissue, with the advantage of no further sloughing of tissue and less bleeding post-procedure.

 

·        Endoscopic laser may result in less bleeding and shown to be as effective with similar costs to TURP.

 

·        Radiofrequency ‘needle’ can be used, although further treatment is often required within 5 years.

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Medicine and surgery: Genitourinary system : Benign prostatic hyperplasia - Disorders of the bladder and prostate |


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