Disorders of the prostate

Published on 11/04/2015 by admin

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Last modified 11/04/2015

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Disorders of the prostate


The normal prostate gland is about 3 cm long and 3 cm in diameter and weighs 10–15 g. The gland is situated immediately below the bladder neck so that the first 3 cm of the urethra lies within the gland (Fig. 35.1, p. 452) so the proximal urethral walls (the prostatic urethra) are composed of glandular tissue. The urethra then passes through the pelvic floor muscle that also constitutes the distal sphincteric mechanism. Prostatic hyperplasia or carcinoma may cause local urethral obstruction and carcinoma may invade and disrupt the sphincter mechanism.

The posterior aspect of the gland is palpable rectally (Fig. 35.1, pp. 450, 451) and a median groove can usually be identified. This groove is described as dividing the gland into two lateral lobes and tends to be obliterated in advanced prostatic cancer but is usually exaggerated in benign hypertrophy.

When the prostatic urethra is examined cystoscopically (see Fig. 35.3, p. 450), an important landmark is an elongated mound on the posterior wall known as the veru montanum (urethral crest), which can be variable in size and prominence. At its midpoint is a small depression, sometimes visible, into which the two ejaculatory ducts open. The posterior part of the gland above the ejaculatory ducts is known as the median lobe. If this becomes hypertrophied it may extend into the floor of the bladder (the surgical ‘middle lobe’); this may act as a flap valve and obstruct the bladder outlet.

As seen in Figure 35.1, the bulk of the normal prostate consists of up to 50 peripheral glandular lobules. These converge into about 20 separate ducts opening into the prostatic urethra lateral to the veru montanum. As well as this glandular tissue proper, there is a zone of small para-urethral glands adjacent to the urethra, the transition zone. From middle age onwards, the transition zone tends to enlarge to cause benign prostatic hyperplasia. At the same time, the peripheral glandular tissue is compressed to form a fibrous outer ‘surgical capsule’. In contrast, prostate cancer arises most often in the peripheral glandular tissue, tending to spread outwards into bordering structures more often than obstructing the centrally located urethra. Even after prostatectomy, cancer can arise in the residual peripheral zone.

The normal prostate gland is surrounded by a filmy true capsule of little surgical significance; external to this is a rich venous plexus which, in turn, is invested by a dense fascial sheath. During open or endoscopic prostatectomy, it is important not to disturb this venous plexus as it is a common source of bleeding during and after the operation. There are direct venous connections between the plexus and the vertebral extradural plexus which provide a direct route for blood-borne dissemination of prostate cancer. Posteriorly, the prostatic fascial sheath is fused with the dense fascia of Denonvilliers. This provides a barrier against direct spread of cancer from the prostate to the rectum and vice versa.

Benign prostatic hyperplasia

Benign prostatic hyperplasia (BPH) affects half of all men aged 50, and the proportion increases with advancing age so that BPH is almost universal at 70 years. Approximately half of those with BPH are asymptomatic or have only mild symptoms. In about 50% of men over 60, however, hyperplasia produces enough symptoms for treatment to be considered.

Clinical features of benign prostatic hyperplasia

Symptoms and signs of bladder outflow obstruction (summarised in Box 35.1) are usually gradual in onset. Benign causes are prostatic hyperplasia and the apparently independent disorder of bladder neck hypertrophy and fibrosis. Acute retention of urine may occur suddenly at any time and is commonly precipitated by bladder overfilling after excessive fluid intake. It is also a hazard of many general surgical or orthopaedic operations on older men and also of any pelvic or perineal operations after adolescence. In some patients, the severity of prostatic symptoms fluctuates from month to month (and even perhaps with the season), making it difficult to decide whether an operation is necessary.

Complications of bladder outlet obstruction

Prostatic obstruction can progressively interfere with the patient’s ability to empty his bladder but only 20–30% of patients have progressive symptoms and 50% remain unchanged over 5 years. In progressive cases, the volume of residual urine gradually increases over weeks and months (i.e. chronic retention) and in a minority leads to a rise in intravesical pressure. In the latter, the threshold for the voiding reflex is reached more quickly and calls to void become more frequent. The stagnant residual urine is prone to infection which exacerbates the symptoms. In chronic retention, the bladder becomes vastly distended and atonic, which can lead to overflow incontinence. In other cases, the detrusor muscle undergoes hypertrophy in an attempt to overcome the outflow obstruction. The normally smooth bladder lining then becomes trabeculated. Eventually, muscle fibre bundles are replaced by non-contractile fibrous tissue; this may explain why some patients fail to improve after obstruction is relieved. With a further rise in pressure, the depressions between the muscle bands deepen (sacculation) and eventually form bladder diverticula. Urinary stasis in the diverticula predisposes to stone formation (see Fig. 35.2).

A small proportion of patients with bladder outlet obstruction experience few local symptoms. In these, rising intravesical pressure can be transmitted back into the ureters and kidneys causing hydronephrosis and progressive renal parenchymal damage. Patients often present with systemic illness or symptoms such as anorexia, apparently of non-renal origin. The renal failure may be accompanied by anaemia, dehydration, acidosis and infection. Bladder outflow obstruction in these patients is easily overlooked unless the bladder is examined for distension and plasma urea measured.

Management of benign prostatic hyperplasia

The principles of management of bladder outlet obstruction believed to be due to benign prostatic hyperplasia are outlined in Box 35.2.

Box35.2   Management of chronic bladder outflow obstruction

• Assess the symptoms and the likely need for treatment from the history, particularly how much the symptoms bother the patient

• Estimate the severity of bladder outlet obstruction by ultrasound and by measuring urine flow rate (urodynamics)

• Investigate any disturbance of upper tract function and structure with renal function tests and ultrasound

• Exclude urinary tract infection by urine microscopy and culture

• Exclude prostatic carcinoma clinically, biochemically (prostate specific antigen) and by transrectal diagnostic ultrasound; if necessary, perform guided needle biopsy of abnormal areas

• Treat renal failure and other systemic problems

• Consider whether catheter drainage of the bladder is desirable

• Cystoscope the patient to rule out other pathology and to define the anatomical problem

• Discuss with the patient what can be offered and at what risk, i.e. drug treatment, transurethral resection of prostate (TURP), laser vaporisation or enucleation or, as a last resort, long-term catheterisation

• Implement appropriate non-surgical treatments

    If operation becomes necessary, diagnose the cause and extent of obstruction by cystoscopy, then either:

• Resect benign prostatic hyperplasia, divide bladder neck hypertrophy transurethrally, or obtain biopsy material by TURP if carcinoma seems likely and prior confirmation has been negative


• Consider any other operative measures such as open prostatectomy or excision of diverticula where appropriate


A detailed history is first taken to assess the nature of the symptoms and how much they interfere with the patient’s life. The International Prostate Symptom Score sheet helps in assessing the overall impact of symptoms in a standardised way (Box 35.1). This, and the patient’s general condition, are the principal factors determining whether treatment is needed. The abdomen is examined for an enlarged bladder and the prostate palpated rectally. These clinical examinations, however, reveal only gross abnormalities.

The next step is to investigate the effects of outlet obstruction on the bladder by measuring urinary flow rate and estimating the volume of residual urine using ultrasound. This is reliable, quick, non-invasive, safe and cheap. When urinary symptoms are severe but residual volume is insignificant, the alternative diagnosis of an overactive bladder should be considered. Urodynamic studies are more complex and involve measuring the filling and emptying pressures of the bladder, but may be invaluable if diagnostic doubts remain.

Renal function is assessed by estimating plasma urea, creatinine and electrolytes. If these are abnormal, further metabolic investigations may be necessary and renal tract ultrasound is mandatory.

A midstream specimen of urine should be examined by microscopy and culture as urinary infection alone may be responsible for the symptoms or may have precipitated an episode of urinary retention. In addition, if surgery is intended, it is important that infection is eradicated to minimise risk of perioperative infection and secondary haemorrhage.

If the prostate feels nodular on palpation, cancer should be suspected, particularly if the serum prostate specific antigen (PSA) is elevated. Transrectal ultrasound scanning (TRUS) and needle biopsy should be performed even if prostatectomy is planned because a preoperative diagnosis of cancer is likely to alter the plan of management. Marked elevation of serum PSA is diagnostic of prostatic cancer but a mildly elevated PSA may be due to benign disease or infection. A normal result does not, however, exclude cancer.

Relief of chronic retention and obstructive effects on the kidney

In chronic retention and a large volume of residual urine (750 ml or more), abnormal renal function or upper tract dilatation on renal tract ultrasound, the patient is usually catheterised to allow detrusor tone to recover over a few days. Drainage also allows any reversible component of renal failure to self-correct; it may take 3 weeks of catheter drainage to improve biochemical renal function tests, after which spontaneous improvement is unlikely. Initially, fluid and electrolyte balance is monitored and normalised if necessary by intravenous fluids. In patients with chronic outflow obstruction and obstructive renal failure, catheterisation may produce a massive diuresis and this should be anticipated and treated appropriately.


Despite the above investigations, the anatomical nature of the bladder outlet obstruction can be accurately assessed only by direct cystoscopic examination. At the same time, the bladder can be examined for other problems such as trabeculation, diverticula, tumours and stones. In patients with complications from bladder outlet obstruction or severe symptoms not responding to medical treatment, transurethral resection (TUR) or Holmium laser enucleation of the obstruction is performed under the same anaesthetic (see TURP, below). In elderly or unfit patients, placement of a urethral stent may be considered. However, these devices are prone to displacement, haemorrhage, local irritation and blockage. Only very occasionally are patients too unfit for some form of intervention. It is now rarely necessary to leave a patient with a long-term catheter; in this event a suprapubic catheter is preferable to a urethral catheter because of the ease of changing it and greater patient comfort.