Bladder outlet obstruction

Regulation of prostate growth and development of benign prostatic hyperplasia (BPH)

The REAWAKENING OF THE PROSTATE

BPH is characterized by an increase in epithelial and stromal cell numbers (hyperplasia) in the periurethral area of the prostate. New epithelial gland formation is normally only seen during fetal development. The development of new glands in the adult prostate has given rise to the concept of  reawakening of the inductive effect of the prostatic stroma on the prostatic epithelium.

The increase in prostate cell number could reflect proliferation of epithelial and stromal cells, impairment of programmed cell death, or a combination of both. During the early phases of development of BPH, cell proliferation occurs rapidly. In established BPH, cell proliferation slows down and there is impairment of programmed cell death (androgens and oestrogens actively inhibit cell death).

The role of androgens in BPH 

Testosterone can bind directly to the androgen receptor, or may be converted to a more potent form, dihydrotestosterone (DHT), by the enzyme 5(-reductase (5AR). There are two isoforms of 5AR, type I or  extra-prostatic 5AR (which is absent in prostatic tissue and present in, for example, skin and liver) and type II or prostatic 5AR (which is found exclusively on the nuclear membrane of stromal cells, but not within prostatic epithelial cells). Type I 5AR is not inhibited by finasteride, whereas type II 5AR is. 

Testosterone diffuses into prostate and stromal epithelial cells. Within epithelial cells it binds directly to the androgen receptor. In prostate stromal cells a small proportion binds directly to the androgen receptor, but the majority binds to 5AR (type II) on the nuclear membrane, is converted to DHT, and then binds (with greater affinity and therefore greater potency than testosterone) to the androgen receptor in the stromal cell. Some of the DHT formed in the stromal cells diffuses out of these cells and into nearby epithelial cells (a paracrine action). The androgen receptor/testosterone or androgen receptor/DHT complex then binds to specific binding sites in the nucleus, thereby inducing transcription of androgen-dependent genes and subsequent protein synthesis.

It is thought that stromal/epithelial interactions may be mediated by soluble growth factors small peptides that stimulate or inhibit cell division and differentiation. Growth stimulating factors include basic fibroblastic growth factor (bFGF), epidermal growth factor (EGF), keratinocyte growth factor (KGF), and insulin-like growth factor (IGF). Transforming growth factors (e.g. TGFb) normally inhibit epithelial cell proliferation, and it is possible that in BPH, TGFb is downregulated. 

Pathophysiology and causes of bladder outlet obstruction (BOO) and BPH

The principle cause of BOO in men is BPH. Less common causes are urethral stricture and malignant enlargement of the prostate. BOO in women is altogether less common, the causes including pelvic prolapse (cystocoele, rectocoele, uterine), the prolapsing organ directly compressing the urethra; urethral stricture; urethral diverticulum; post-surgery for stress incontinence; Fowler's syndrome (impaired relaxation of external sphincter occuring in premenopausal women, often in association with polycystic ovaries); and pelvic masses (e.g. ovarian masses). In either sex, neurological disease (spinal cord injury, spina bifida, MS) can cause failure of relaxation of the external sphincter during voiding (detrusor sphincter dysynergia, DSD).

The pathophysiological basis of BOO due to benign prostatic enlargement (BPE) secondary to BPH (benign prostatic obstruction, BPO) has been studied more than any other type of obstruction. BPO has dynamic and static components:

• 
  
  
  Dynamic component of BPO: α1-adrenoceptor mediated prostatic smooth muscle contraction. Smooth muscle accounts for approximately 40% of the area density of the hyperplastic prostate and human prostate contracts following administration of alpha adrenergic agonists. This effect is the rationale for α-adrenoceptor blocker treatment for symptomatic BPO.
• 
  
  
  Static component of BPO: mediated by the volume effect of BPE.

Pathophysiological consequences of BOO

John Hunter (1786), who founded the Royal College of Surgeons of England, noted that The disease of the bladder arising from obstruction alone is increased irritability and its consequences, by which it admits of little distension, becomes quick in its action and thick and strong in its coats. BOO causes thickening of the wall of the bladder. Microscopically smooth muscle cells enlarge and there is an increase in connective tissue (collagen and elastin) between the smooth muscle bundles. In some cases this may lead to poor compliance, with development of high bladder and intrarenal pressures. Progressive hydronephrosis can develop, with impairment of renal function and even renal failure (high pressure chronic urinary retention).

Experimentally created BOO causes development of bladder overactivity (unstable bladder contractions during bladder filling). This may be due to prolonged increased intravesical pressure during voiding causing ischaemia and leading to ischaemic damage to neurons within the bladder (i.e. denervation). Symptomatically, many patients with BOO develop frequency, urgency, and urge incontinence.

Benign prostatic obstruction (BPO): symptoms and signs

Clinical practice guidelines

Developed to standardize the approach to diagnosis (and treatment) of men presenting with symptoms suggestive of BPH. Every guideline agrees that a history should be taken, an examination performed, and that the severity of urinary symptoms should be formally assessed using the IPSS (the International Prostate Symptom Score). This includes a measure of the bother caused by the patient's symptoms (i.e. the degree to which the symptoms are troubling).

Urinary symptoms what do they mean?

During the 1990s, the classic prostatic symptoms of frequency, urgency, nocturia, hesitancy, poor flow, an intermittent flow, and terminal dribbling traditionally said to indicate the presence of BOO due to benign prostatic enlargement were shown to bear little relationship to prostate size, flow rate, residual urine volume, or indeed urodynamic evidence of BOO. Age-matched elderly men and women have similar symptom scores (IPSS), despite the fact that women have no prostate and rarely have BOO.

Prostatism v. lower urinary tract symptoms (LUTS) v. LUTS/BPH

Prostatism has therefore been replaced by the expression LUTS which avoids any implication about the cause of these symptoms. More recently, the expression LUTS/BPH has been used to describe the symptoms of BPH. It doesn't really matter whether you use prostatism, LUTS or LUTS/BPH as long as you remember that urinary symptoms may have non-prostatic causes. Try to avoid treating the prostate when the problem may lie elsewhere.

Ask specifically about the presence of:

• Bedwetting: suggests the presence of high pressure chronic retention (look for distension of the abdomen due to a grossly enlarged bladder which is tense on palpation and dull to percussion).
• Marked frequency and urgency, particularly when also combined with bladder pain: look for carcinoma in situ of the bladder (urine cytology, flexible cystoscopy, and bladder biopsy)
• Macroscopic haematuria: sometimes due to a large vascular prostate, but exclude other causes (bladder and kidney cancer and stones) by flexible cystoscopy and upper tract imaging.
• Back pain and neurological symptoms (sciatica, lower limb weakness or tingling). Rarely, LUTS can be due to neurological disease.

Diagnostic tests in men with LUTS thought to be due to BPH

Clinical practice guidelines

Developed as an attempt to standardize the approach to diagnosis and treatment of men presenting with symptoms suggestive of BPH. All agree that a history should be taken and an examination performed and all recommend assessment of symptom severity using the IPSS (International Prostate Symptom Score). This includes a measure of the bother caused by the patient's symptoms. There is considerable variation between guidelines in terms of recommended diagnostic tests. High-quality guidelines (e.g. based on results of randomized trials) recommend few diagnostic tests urine analysis, completion of a voiding diary (frequency volume chart) to detect the presence of polyuria and nocturnal polyuria (which may be the cause of a patient's increased frequency or nocturia), measurement of serum creatinine. They regard flow rate measurement and assessment of residual urine volume as optional tests.

Digital rectal examination (DRE) and PSA

Done to detect nodules which may indicate an underlying prostate cancer and to provide a rough indication of prostate size. Size alone is not an indication for treatment, but if surgical treatment is contemplated, marked prostatic enlargement can be confirmed by transrectal ultrasound scan (prostate volume in the order of 100ml or more increases the likelihood of an open prostatectomy). Discuss the pros and cons of PSA testing with the patient.

Serum creatinine

Baseline measure of renal function and to detect renal failure secondary to high pressure urinary retention.

Post-void residual urine volume (PVR)

Varies considerably (by as much as 600ml between repeat measurements) on the same or on different days. It cannot predict sympto-matic outcome from TURP. Along with serum creatinine it indicates whether watchful waiting is safe. It is safe not to operate where the PVR volume is <350ml, since the majority of men show no worsening of creatinine, no increase in PVR, no worsening of symptoms, and do not require TURP.

Flow rate measurement

This is variously regarded as optional, recommended, and obligatory prior to undertaking surgical treatment for BPH. Like PVR, measurement flow rate varies substantially on a given day,⁸ cannot distinguish between BOO and a poorly contractile bladder, and is not good at predicting the likelihood of a good symptomatic outcome after TURP.

Pressure flow studies

Reasonably good at predicting symptomatic outcome after TURP. However, most patients without obstruction have a good outcome and the time, cost, and invasiveness of pressure flow studies is perceived by most urologists as not justifying their routine use.

Renal ultrasonography

To detect hydronephrosis if serum creatinine is elevated. The percentage of patients having upper tract dilatation on ultrasound according to serum creatinine is: creatinine <115mmol/l: 0.8%, creatinine 115 to 130mmol/l: 9%, and creatinine >130mmol/l: 33%.

Why do men seek treatment for their symptoms?

Men seek treatment for their LUTS for several reasons:

• the symptoms may be bothersome
• they may fear that the symptoms are a warning that acute urinary retention will develop
• they may be concerned that their symptoms indicate that they have prostate cancer.

Establish what the patient wants from his consultation with you. Once reassured that the likelihood of urinary retention and prostate cancer is low, he may not want treatment for symptoms which on the surface may appear quite bad and he may be happy to adopt a policy of watchful waiting.

Bothersome symptoms

Bothersomeness does not necessarily equate with symptom severity as assessed by symptom scores. Thus, a man with a low symptom score may find his symptoms very bothersome and may want treatment, whereas another man with a high symptom score may not be bothered and may want no treatment. If one symptom is particularly bad, but the other 6 symptoms in the 7-symptom score are minimal, overall symptom score will obviously be relatively low, but the patient may find that one symptom very bothersome (e.g. urgency and nocturia tend to be more bothersome than hesitancy or poor flow).

Are my symptoms due to prostate cancer?

No particular LUTS are specific for prostate cancer. Even if it later turns out that he does have prostate cancer, a patient's symptoms might be due to coexistent BPH or some other LUT pathology. If he is concerned about the possibility of prostate cancer, counsel him with regard to PSA testing and prostate biopsy.

Am I likely to develop retention of urine?

Watchful waiting for uncomplicated BPH

A number of studies have shown that in a substantial proportion of men, symptoms do not progress, even for those with severe symptoms:

• Ball:¹² 107 men followed with watchful waiting over 5 years. In none was there an absolute indication for surgery. Half of the patients were obstructed on urodynamic testing. A third of the patients got better, just under a half stayed the same, a quarter got worse (of whom 8 underwent TURP). 2% went into retention.
• PLESS study (Proscar long-term efficacy and safety study):¹³ 1500 men with moderate to severe symptoms were randomized to placebo (and a similar number to active drug). Those on placebo had an average fall in symptom score of 1 point at 4 years.
• 
  
  
  Wasson study of watchful waiting versus TURP:¹⁴ for men with moderate symptoms, the risk of progression to retention, worsening symptoms, or need for TURP was relatively low in those who chose watchful waiting. 40% noticed an improvement in their symptoms, 30% got worse, and TURP was required in about a quarter.
• Five centres’ study:¹⁵ 500 men referred by their family doctors for consideration for TURP were managed non-operatively after viewing an educational programme. Over the following 4-year period a proportion of the men chose drug treatment or surgery. For men with mild, moderate, or severe symptoms, 10%, 24%, and 39% respectively had undergone surgery at the end of 4 years. For the same symptom categories, 63%, 45%, and 33% were still not receiving any treatment at the end of 4 years. Almost a quarter of men who initially presented with severe symptoms noted an improvement in their symptoms, to mild or moderate.

On the basis of these studies we can say that symptoms, even if severe, do not necessarily get worse even over fairly long periods of time. This forms the foundation of watchful waiting as an option for many patients, even if the symptoms at baseline are severe. The IPSS (International Prostate Symptom Score) measures both symptom ‘severity’, but more importantly the bother that the symptoms cause the patient. Thus, if a patient has a high symptom score (severe symptoms), but is not bothered by these symptoms, there is no indication for treatment. Some patients on the other hand have a low symptom score but may find even this degree of symptoms very bothersome. Treatment is indicated in such cases (usually starting with medical therapy such as an alpha blocker or 5 alpha reductase inhibitor).

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Medical management of BPH: alpha blockers

The rationale for α blocker therapy in BPH

As described earlier, BPO is caused partly by α1-adrenoceptor mediated prostatic smooth muscle contraction, and this is the rationale for α-adrenoceptor blocker treatment for symptomatic BPO.

There are two broad subtypes of α-adrenoceptor (AR)—α1 and α2. Molecular cloning studies have identified three α1-AR subtypes—α1a (predominant in human stroma and therefore mediates prostate smooth muscle contraction), α1b (predominant in human prostate epithelium), and α1L (believed to be a conformational state of the α1a-AR). The AR subtypes mediating efficacy and side-effects of α-adrenoceptor blocking drugs are unknown.

Alpha blocker classification

Alpha blockers are categorized by their selectivity for the AR, and by their elimination half-life.

• 
  
  
  Non-selective: phenoxybenzamine—effective symptom control, but high side-effect profile
• 
  
  
  α1: prazosin, alfuzosin, indoramin
• 
  
  
  Long-acting α1: terazosin, doxazosin, alfuzosin SR
• 
  
  
  Subtype selective: tamsulosin—relatively selective for (1a-AR subtype compared to the α1b subtype.

No study has directly compared one alpha blocker with another in terms of efficacy or side-effects.

Indications for treatment

Bothersome lower urinary tract symptoms where watchful waiting has failed or the patient wishes to have treatment.

Efficacy

Percentage of patients who respond to alpha blockers

If ‘response’ is defined as >25% improvement in symptoms relative to placebo, most studies describe response rates of 30–40%.¹⁶ The mean probability for improvement in symptom score after TURP is in the order of 80% (i.e. 8 out of 10 men will notice an improvement in their symptoms after TURP).

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Improvements in symptom score in men who ‘respond’ to alpha blockers

The average improvement in symptom score after TURP is about 85%.¹⁷ While some of this may represent a placebo response, this improvement is considerably better than that seen with the alpha blockers which result in a 10–30% improvement in symptom score relative to placebo.¹⁸ This equates to a 4–5 points’ improvement in symptom score over placebo.

Side-effects

A substantial proportion of men stop taking their medication either because of side-effects (15–30% report some constellation of side-effects) or because of a perceived lack of effectiveness. Side-effects: asthenia (weakness, in 5%), dizziness (6%), headache (2%) and postural hypotension (1%), and retrograde ejaculation (8%).

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Medical management of BPH: 5α-reductase inhibitors

5α-reductase inhibitors inhibit the conversion of testosterone to dihydrotestosterone, the more potent androgen in the prostate. This causes shrinkage of the prostatic epithelium and therefore a reduction in prostate volume, thereby reducing the ‘static’ component of benign prostatic enlargement. This takes some months to occur, so urinary symptoms will not improve initially. Finasteride is a competitive inhibitor of the enzyme 5α-reductase (type II isoenzyme) which converts testosterone to DHT. Finasteride therefore lowers serum and intraprostatic DHT levels. Epristeride is a dual inhibitor of 5α-reductase. Whether it has any clinically significant advantages over finasteride remains to be established.

Efficacy

A number of large studies have shown symptom improvement over placebo in the order of 2–3 points on the IPSS and improvements in flow rate in the order of 1–2ml/s (SCARP¹⁹ (Scandinavian BPH Study Group), PROSPECT²⁰ (Proscar safety plus efficacy Canadian two-year study), PROWESS Study Group,²¹ and more recently, PLESS²² (Proscar long-term efficacy and safety study)). The PLESS data also shows a small reduction in the risk of urinary retention.

Side-effects

Generally speaking, fairly mild. Principally centre around sexual problems (e.g. loss of libido, 5%; impotence, 5%; reduced volume of ejaculate in a few percent).

5α-reductase inhibitors and the risk of urinary retention

The PLESS data²² have been widely publicized as showing a substantial reduction in the risk of urinary retention. In this 4-year follow-up study, 42 of 1471 men on finasteride went into urinary retention (3%), while 99 of 1404 on placebo experienced an episode of retention (7%). This represents an impressive 43% relative reduction in risk in those taking finasteride. However, the absolute risk reduction over a 4-year period is a less impressive 4%. So, finasteride does reduce the risk of retention, but it is reducing the risk of an event which is actually quite rare as suggested by the fact that 93% of men on placebo in this study did not experience retention over a 4-year period. Put another way, to prevent 1 episode of retention, 25 men would have to continue treatment with finasteride for 4 years.

5α-reductase inhibitors for haematuria due to BPH

Shrinking large vascular prostates probably helps reduce the frequency of haematuria in men with BPH.²³

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Medical management of BPH: combination therapy

A combination of an alpha blocker and a 5(-reductase inhibitor. The studies:

• 
  
  
  MTOPS study³⁰ (Medical Therapy of Prostatic Symptoms): this combination prevented progression of BPH (progression being defined as a worsening of symptom score by 4 or more, or the development of complications such as UTI or acute urinary retention).
• 
  
  
  Veterans Affairs Combination Therapy Study:³¹ 1200 men randomized to placebo, finasteride, terazosin, or a combination of terazosin and finasteride. At 1-year follow-up, relative to placebo, finasteride had reduced the symptom score by an average of 3 points, whereas terazosin alone or in combination with finasteride had reduced the symptom score by an average of 6 points.
• 
  
  
  PREDICT study³² (Prospective European Doxazosin and Combination Therapy): randomized over 1000 men to placebo, finasteride, doxazosin, or a combination of finasteride and doxazosin. The difference in symptom score at baseline and at 1-year follow-up were -5.7 and -6.6 for placebo and finasteride, and -8.3 and -8.5 for doxazosin and combination therapy.
• 
  
  
  ALFIN study³³ (Alfuzosin, Finasteride, and combination in the treatment of BPH): 1000 men were randomized to alfuzosin, finasteride, or a combination. At 6 months, the improvement in the IPSS was not significantly different in the alfuzosin versus the combination group.

Thus most studies, except for the MTOPS, suggest that combination therapy is NO more useful than an alpha blocker alone. Enthusiasm for dual therapy has been dampened somewhat by the Prostate Cancer Prevention Trial.³⁴ Over 18,000 men were randomized to finasteride or placebo over a 7-year period. Those in the finasteride group had a lower prevalence of prostate cancer detected on prostate biopsy. However, higher-grade tumours, which are biologically more aggressive than low-grade cancers were more common in the finasteride group. The jury is out on whether finasteride causes higher-grade cancers or not.

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Medical management of BPH: alternative drug therapy

Anticholinergics

For a man with frequency, urgency, and urge incontinence—symptoms suggestive of an overactive bladder—consider prescribing an anticholinergic (e.g. oxybutynin, tolterodine, trospium chloride, or flavoxate). There is the concern that these drugs could precipitate urinary retention in men with BOO (because they block parasympathetic/cholinergic mediated contraction of the detrusor), but the risk of this occurring is probably very low, even in men with urodynamically proven BOO.³⁵

Phytotherapy

An alternative drug treatment for BPH symptoms, and one which is widely used in Europe and increasingly in North America, is phytotherapy. 50% of all medications consumed for BPH symptoms are phytotherapeutic ones.³⁶ These agents are derived from plants and include the African plum (Pygeum africanum), purple cone flower (Echinacea purpurea), South African star grass (Hipoxis rooperi), and saw palmetto berry (Seronoa Repens, Permixon).

Saw palmetto contains an anti-inflammatory, antiproliferative, oestrogenic drug with 5α-reductase inhibitory activity, derived from the American dwarf palm. It has been compared with finasteride in a large double-blind, randomized trial, and equivalent (40%) reductions in symptom score were found with both agents over a 6-month period. A meta-analysis of 18 randomized controlled trials of almost 3000 men suggests that Seronoa repens produces similar improvements in symptoms and flow rates to those produced by finasteride.³⁷

South African star grass (Hipoxis rooperi, marketed as Harzol) contains beta-sitosterol, which may induce apoptosis in prostate stromal cells, by causing elevated levels of TGF-β₁. In a double-blind, RCT symptom improvement was 5 points over that with placebo.

For other agents (e.g. Urtica dioica—stinging nettle; the African plum) the studies have not been placebo controlled and lack sufficient statistical power to prove conclusively that they work.³⁶

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Minimally invasive management of BPH: surgical alternatives to TURP

In 1989, Roos reported a seemingly higher mortality and re-operation rate after TURP when compared with open prostatectomy.³⁸ This, combined with other studies suggesting that symptomatic outcome after TURP was poor in a substantial proportion of patients and that TURP was associated with substantial morbidity, prompted the search for less invasive treatments.

The two broad categories of alternative surgical techniques are minimally invasive and invasive. All are essentially heat treatments, delivered at variable temperature and power and producing variable degrees of coagulative necrosis of the prostate or vaporization of prostatic tissue.

Transurethral radiofrequency needle ablation (TUNA) of the prostate

Low-level radiofrequency is transmitted to the prostate via a transurethral needle delivery system; the needles which transmit the energy being deployed in the prostatic urethra once the instrument has been advanced into the prostatic urethra. It is done under local anaesthetic, with or without intravenous sedation. The resultant heat causes localized necrosis of the prostate.

Improvements in symptom score and flow rate are modest. Side-effects include bleeding (one third of patients), UTI (10%), and urethral stricture (2%). No adverse effects on sexual function have been reported.³⁹ The UK National Institute for Clinical Excellence⁴⁰ has endorsed TUNA as a minimally invasive treatment option for symptoms associated with prostatic enlargement. Concerns remain with regard to long-term effectiveness.

Transurethral microwave thermotherapy (TUMT)

Microwave energy can be delivered to the prostate via an intraurethral catheter (with a cooling system to prevent damage to the adjacent urethra), producing prostatic heating and coagulative necrosis. Sub-sequent shrinkage of the prostate and thermal damage to adrenergic neurons (i.e. heat-induced adrenergic nerve block) relieves obstruction and symptoms.

Many reports of TUMT treatment are open studies, all patients receiving treatment (no ‘sham’ treatment group where the microwave catheter is inserted, but no microwave energy is given—this results in 10-point symptom improvements in approximately 75% of men). Compared with TURP, TUMT results in symptom improvement in 55% of men and TURP in 75%. Sexual side-effects after TUMT (e.g. impotence, retrograde ejaculation) are less frequent than after TURP, but catheterization period is longer and UTI and irritative urinary symptoms are more common.⁴¹ European Association of Urology Guidelines state that TUMT ‘should be reserved for patients who prefer to avoid surgery or who no longer respond favourably to medication’.

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High-intensity focused ultrasound (HIFU)

A focused ultrasound beam can be used to induce a rise in temperature in the prostate, or indeed in any other tissue to which it is applied. For HIFU treatment of the prostate a transrectal probe is used. A general anaesthetic or heavy intravenous sedation is required during the treatment. It is regarded as an investigational therapy.

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Invasive surgical alternatives to TURP

Transurethral electrovaporization of the prostate (TUVP)

Vaporizes and dessicates the prostate. TUVP seems to be as effective as TURP for symptom control and relief of BOO, with durable (5-year) results. Operating time and in-patient hospital stay are equivalent. Requirement for blood transfusion may be slightly less after TUVP. TUVP does not provide tissue for histological examination so prostate cancers cannot be detected. The National Institute for Clinical Excellence in the UK has endorsed TUVP as a surgical treatment option for prostatic symptoms.⁴²

Laser prostatectomy

Several different techniques of ‘laser prostatectomy’ evolved during the 1990s.

Transurethral ultrasound-guided laser-induced prostatectomy (TULIP)

Performed using a probe consisting of a Nd:YAG laser adjacent to an ultrasound transducer.

Visual laser ablation of the prostate (VLAP)

This side-firing system used a mirror to reflect or a prism to refract the laser energy at various angles (usually 90°) from a laser fibre located in the prostatic urethra onto the surface of the prostate. The principle tissue effect was one of coagulation with subsequent necrosis.

Contact laser prostatectomy

Produces a greater degree of vaporization than VLAP, allowing the immediate removal of tissue.

Interstitial laser prostatectomy (ILP)

Performed by transurethral placement of a laser fibre directly into the prostate which produces a zone of coagulative necrosis some distance from the prostatic urethra.

TULIP, VLAP, contact laser prostatectomy, and ILP have been succeeded by holmium laser prostatectomy.

Holmium laser prostatectomy

The wavelength of the holmium: YAG laser is such that it is strongly absorbed by water within prostatic tissue. It produces vaporization at the tip of the laser fibre. Its depth of penetration is <0.5mm and thus it can be used to produce precise incisions in tissue. When the beam is ‘de-focused’, it provides excellent haemostasis. It can be used with normal saline, so avoiding the possibility of TURP syndrome.

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Three techniques Holmium laser prostatectomy developed in progression:

• 
  
  
  Vaporization (holmium-only laser ablation of the prostate, HoLAP); time consuming, suitable only for small prostates.
• 
  
  
  Resection (holmium laser resection of the prostate, HoLRP); similar symptomatic outcome to TURP.
• 
  
  
  Enucleation (holmium laser enucleation of the prostate, HoLEP); lobes of the prostate are dissected off the capsule of the prostate and then pushed back into the bladder. A transurethral tissue morcellator is introduced into the bladder and used to slice the freed lobes into pieces that can then be removed. Improvement in symptom scores and flow rates are equivalent, and though the operation time with HoLEP is longer, catheter times and in-hospital stays are less with HoLEP.⁴³

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TURP and open prostatectomy

TURP

Removal of the obstructing tissue of BPH or obstructing prostate cancer from within the prostatic urethra, leaving the compressed outer zone intact (the ‘surgical capsule’). An electrically heated wire loop is used, through a resectoscope, to cut the tissue and diathermy bleeding vessels. The cut ‘chips’ of prostate are pushed back into the bladder by the flow of irrigating fluid, and at the end of resection are evacuated using specially designed ‘evacuators’—a plastic or glass chamber attached to a rubber bulb which allows fluid to be flushed in and out of the bladder.

Indications for TURP

• 
  
  
  Bothersome lower urinary tract symptoms which fail to respond to changes in life style or medical therapy
• 
  
  
  Recurrent acute urinary retention
• 
  
  
  Renal impairment due to BOO (high pressure chronic urinary retention)
• 
  
  
  Recurrent haematuria due to benign prostatic enlargement
• 
  
  
  Bladder stones due to prostatic obstruction

Open prostatectomy

Indications

• 
  
  
  Large prostate (>100g)
• 
  
  
  TURP not technically possible (e.g. limited hip abduction)
• 
  
  
  Failed TURP (e.g. because of bleeding)
• 
  
  
  Urethra too long for the resectoscope to gain access to the prostate
• 
  
  
  Presence of bladder stones which are too large for endoscopic cystolitholapaxy, combined with marked enlargement of the prostate

Contraindications

• 
  
  
  Small fibrous prostate
• 
  
  
  Prior prostatectomy in which most of the gland has been resected or removed; this obliterates the tissue planes
• 
  
  
  Carcinoma of the prostate

Techniques

Suprapubic (transvesical)

The preferred operation if enlargement of the prostate involves mainly the middle lobe. The bladder is opened, the mucosa around the protruding adenoma is incised and the plane between the adenoma and capsule is developed to enucleate the adenoma. A 22Ch urethral and a suprapubic catheter are left, together with a retropubic drain. Remove the urethral catheter in 3 days and clamp the suprapubic at 6 days, removing it 24h later. The drain can be removed 24h after this (day 8).

Simple retropubic

Popularized by Terence Millin (Ireland 1947). Compared with the supra-pubic (transvesical) approach it allows more precise anatomic exposure of the prostate, thus giving better visualization of the prostatic cavity which allows more accurate removal of the adenoma, better control of

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bleeding points, and more accurate division of the urethra, so reducing the risk of incontinence.

As well as the contraindications noted above, the retropubic approach should not be employed when the middle lobe is very large because it is difficult to get behind the middle lobe and so to incise the mucosa (safely) distal to the ureters.

The prostate is exposed by a Pfannenstiel or lower midline incision. Haemostasis is achieved before enucleating the prostate, by ligating the dorsal vein complex with sutures placed deeply through the prostate. The prostatic capsule and adenoma are incised transversely with the diathermy just distal to the bladder neck. The plane between the capsule and adenoma is found with scissors and developed with a finger. Sutures are used for haemostasis. A wedge of bladder neck is resected. A catheter is inserted and left for 5 days and the transverse capsular incision is closed. A large tube drain (30Ch Robinson's) is left for 1–2 days.

Complications

Haemorrhage; urinary infection; rectal perforation (close and cover with a colostomy).

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Acute urinary retention: definition, pathophysiology, and causes

Definition

Painful inability to void, with relief of pain following drainage of the bladder by catheterization.

The combination of reduced or absent urine output with lower abdominal pain is not in itself enough to make a diagnosis of acute retention. Many acute surgical conditions cause abdominal pain and fluid depletion, the latter leading to reduced urine output, and this reduced urine output can give the erroneous impression that the patient is in retention, when in fact they are not. Thus, central to the diagnosis is the presence of a large volume of urine, which when drained by catheterization, leads to resolution of the pain. What represents ‘large’ has not been strictly defined, but volumes of 500–800ml are typical. Volumes <500ml should lead one to question the diagnosis. Volumes >800ml may be defined as acute-on-chronic retention.

Pathophysiology

Normal micturition requires:

• 
  
  
  afferent input to the brainstem and cerebral cortex
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  coordinated relaxation of the external sphincter
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  sustained detrusor contraction
• 
  
  
  the absence of an anatomic obstruction in the outlet of the bladder

Four broad mechanisms can lead to urinary retention:

• 
  
  
  increased urethral resistance (i.e. bladder outlet obstruction (BOO))
• 
  
  
  low bladder pressure (i.e. impaired bladder contractility)
• 
  
  
  interruption of sensory or motor innervation of bladder
• 
  
  
  central failure of coordination of bladder contraction with external sphincter relaxation

Causes in men

Benign prostatic enlargement; malignant enlargement of prostate; urethral stricture; prostatic abscess.

Urinary retention in men is either spontaneous or precipitated by an event. Precipitated retention is less likely to recur once the event which caused it has been removed. Spontaneous retention is more likely to recur after trial of catheter removal, and therefore to require definitive treatment (e.g. TURP). Precipitating events include anaesthetic and other drugs (anticholinergics, sympathomimetic agents such as ephedrine in nasal decongestants); non-prostatic abdominal or perineal surgery; immobility following surgical procedures.

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Causes of acute urinary retention in either sex

• 
  
  
  Haematuria leading to clot retention
• 
  
  
  Drugs (as above)
• 
  
  
  Pain (adrenergic stimulation of the bladder neck)
• 
  
  
  Post-operative retention (see below)
• 
  
  
  Sacral cord (S2–4) injury
• 
  
  
  Sacral (S2–4) nerve or compression or damage, resulting in detrusor areflexia—cauda equina compression (due to prolapsed L2–L3 disc or L3–L4 intervertebral disc pressing on sacral nerve roots of the cauda equina, trauma to vertebrae, benign or metastatic tumours)
• 
  
  
  Suprasacral spinal cord injury (results in loss of coordination of external sphincter relaxation with detrusor contraction—so-called detrusor-sphincter dyssynergia (DSD)—so external sphincter contracts when bladder contracts)
• 
  
  
  Radical pelvic surgery damaging pelvic parasympathetic plexus (radical hysterectomy, abdomino-perineal resection): unilateral injury to pelvic plexus (preganglionic parasympathetic and postganglionic sympathetic neurons) denervates motor innervation of detrusor muscle
• 
  
  
  Pelvic fracture rupturing urethra (more likely in men than women)
• 
  
  
  Neurotropic viruses involving sensory dorsal root ganglia of S2–4 (herpes simplex or zoster)
• 
  
  
  Multiple sclerosis (can affect any part of CNS—Fig. 4.2); retention caused by detrusor areflexia or DSD
• 
  
  
  Transverse myelitis
• 
  
  
  Diabetic cystopathy (causes sensory and motor dysfunction)
• 
  
  
  Damage to dorsal columns of spinal cord causing loss of bladder sensation (tabes dorsalis, pernicious anaemia)

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Causes in women

Pelvic prolapse (cystocoele, rectocoele, uterine); urethral stricture; urethral diverticulum; post-surgery for ‘stress’ incontinence; pelvic masses (e.g. ovarian masses); Fowler's syndrome.

Fowler's syndrome: increased electromyographic activity can be recorded in the external urethral sphincters of these women (which on ultrasound are of increased volume) and is hypothesized to cause impaired relaxation of external sphincter. Occurs in premenopausal women, often in association with polycystic ovaries.

Risk factors for post-operative retention

Instrumentation of lower urinary tract; surgery to perineum or anorectum; gynaecological surgery; bladder overdistension; reduced sensation of bladder fullness; pre-existing prostatic obstruction; epidural anaesthesia. Post-partum retention is not uncommon, particularly with epidural anaesthesia and instrumental delivery.

Fig. 4.2 MRI of cervical and sacral cord in a young patient presenting with urinary retention. The patient had undiagnosed MS. Signal changes are seen in the cervical, thoracic, and lumbosacral cord

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Acute urinary retention: initial and definitive management

Initial management

Urethral catheterization to relieve pain (suprapubic catheterization if urethral route not possible). Record the volume drained—this confirms the diagnosis, determines subsequent management, and provides prognostic information with regard to outcome from this treatment.

Definitive management in men

Discuss trial without catheter (TWOC) with the patient. Precipitated retention often does not recur; spontaneous retention often does. 50% with spontaneous retention will experience a second episode of retention within the next week or so, and 70% within the next year. A maximum flow rate (Qmax) <5ml/s and low voiding detrusor pressure predict subsequent retention. Thus, while most will require definitive treatment (e.g. TURP), a substantial minority will get away without needing surgery.

Options to avoid TURP

• 
  
  
  Prostate shrinking drugs followed by a TWOC several months later (5(-reductase inhibitors in those with benign feeling prostates, LHRH agonists in those with malignant feeling prostates on DRE, confirmed by TRUS guided prostate biospy)
• 
  
  
  Prostatic stents
• 
  
  
  Long-term urethral or suprapubic catheter
• 
  
  
  Clean, intermittent self-catheterization (CISC)—not a realistic option for most men, but some will be able and happy to do this.

Definitive management in women

CISC either until normal voiding function recovers, or permanently if it does not. Fowler's syndrome—sacral neuromodulation (e.g. Medtronic Interstim).

Risks and outcomes of TURP for retention

Relative risks of TURP for retention v. TURP for lower urinary tract symptoms (LUTS): post-operative complications 26:1; blood transfusion 2.5:1; in-hospital death 3:1.⁴⁶

Failure to void after initial catheter removal: high retention volume, greater age, and low maximum detrusor pressure are predictive for failure to void after TURP. 10% in those with acute retention of urine and 40% in those with acute-on-chronic retention fail to void after initial post-TURP TWOC. Overall, 1% of men will fail to void after subsequent TWOCs and will require long-term catheterization.⁴⁷

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Indications for and technique of urethral catheterization

Indications

Relief of urinary retention; prevention of urinary retention—a period of post-operative catheterization is commonly employed after many operations where limited mobility makes normal voiding difficult; monitoring of urine output (e.g. post-operatively); prevention of damage to the bladder during caesarian section; bladder drainage following surgery to the bladder, prostate, or urethra (e.g. TURP, TURBT, open bladder stone removal, radical prostatectomy); bladder drainage following injuries to the bladder.

Technique

Explain the need for and method of catheterization to the patient. Use the smallest catheter—in practical terms usually a 12Ch, with a 10ml balloon. For longer catheterization periods (weeks) use a silastic catheter to limit tissue ‘reaction’, thereby reducing risk of a catheter-induced urethral stricture. If clot retention, use a 3 way catheter (20Ch or greater) to allow evacuation of clots and bladder irrigation to prevent subsequent catheter blockage.

Technique is aseptic. One gloved hand is sterile, the other is ‘dirty’. Dirty hand holds penis or separates labia to allow cleansing of urethral meatus; this hand should not touch catheter. Use sterile water or sterile cleaning solution to ‘prep’ skin around meatus.

Apply lubricant jelly to urethra. Traditionally this contains local anaesthetic (e.g. 2% lignocaine) which takes between 3–5 min to work. However, a randomized, placebo controlled trial showed that 2% lignocaine was no more effective for pain relief than anaesthetic-free lubricant,⁴⁸ suggesting that it is lubricant action which prevents urethral pain. If using local anaesthetic lubricant, warn patient that it may ‘sting’. Local anaesthetic lubricant is contraindicated in patients with allergies to local anaesthetics and in those with urethral trauma, where there is a (theoretical) risk of complications arising from systemic absorption of lignocaine. When instilling jelly, do so gently—a sudden, forceful depression of the plunger of the syringe can rupture the urethra! In male, ‘milk’ gel towards posterior urethra, while squeezing meatus to prevent it from coming back out of meatus.

Insert the catheter using sterile hand, until flow of urine to confirm it is in bladder. Failure of urine flow may indicate that the catheter balloon is in the urethra. Intra-urethral inflation of balloon can rupture urethra. If no urine flows attempt aspiration of urine using a 50ml bladder syringe (lubricant gel can occlude eye-holes of catheter). Absence of urine flow indicates either catheter is not in the bladder or, if indication for catheterization is retention, that the diagnosis is wrong (there will usually be

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a few ml of urine in the bladder even in cases where the absence of micturition is due to oliguria or anuria, so complete absence of urine flow usually indicates the catheter is not in the bladder). If the catheter will not pass into the bladder, and you are sure that the patient is in retention, proceed with suprapubic catheterization.

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Indications for and technique of suprapubic catheterization

Indications

Failed urethral catheterization in urinary retention; preferred site for long-term catheters.

Long-term urethral catheters commonly lead to acquired hypospadias in males (ventral splitting of glans penis) and patulous urethra in females (leading to frequent balloon expulsion and bypassing of urine around the catheter). Hence, suprapubic site is preferred for long-term catheters.

Contraindications

Suprapubic catheterization is best avoided in:

• 
  
  
  patients with clot retention, the cause of which may be an underlying bladder cancer (the cancer could be ‘spread’ along the catheter track to involve the skin)
• 
  
  
  patients with lower midline incisions (bowel may be ‘stuck’ to the deep aspect of the scar, leading to the potential for bowel perforation)
• 
  
  
  pelvic fractures, where the catheter may inadvertently enter the large pelvic haematoma which always accompanies severe pelvic fracture. This can lead to infection of the haematoma, and the resulting sepsis can be fatal. Failure to pass a urethral catheter in a patient with a pelvic fracture usually indicates a urethral rupture (confirmed by urethrography) and is an indication for formal open, suprapubic cystotomy.

Technique

Prior to insertion of trocar, be sure to confirm the diagnosis by:

• 
  
  
  abdominal examination (palpate and percuss lower abdomen to confirm bladder is distended)
• 
  
  
  ultrasound (in practice, usually not available) and
• 
  
  
  aspiration of urine (using a green needle).

Patients with lower abdominal scars may have bowel interposed between the abdominal wall and bladder and this can be perforated if the trocar is inserted near the scar and without prior aspiration of urine. In such cases, ultrasound guided catheterization may be sensible.

Use a wide-bore trocar if you anticipate that the catheter will be in place for more than 24h (small-bore catheters will block within a few days). Aim to place the catheter about 2–3 finger-breadths above the pubis symphysis. Placement too close to the symphysis will result in difficult trocar insertion (the trocar will hit the symphysis). Instil a few ml of local anaesthetic into skin of intended puncture site and down to rectus sheath. Confirm location of bladder by drawing back on needle to aspirate urine from bladder. This helps guide the angle of trocar insertion. Make a 1cm incision with a sharp blade through the skin. Hold trocar handle in your right hand, and steady needle end with your left hand (this hand helps prevent insertion too deeply). Push the trocar in the same direction in which you previously aspirated urine. As soon as urine issues from the trocar, withdraw the latter, holding the attached sheath in place. Push the catheter in as far as it will go. Inflate the balloon. Peel away the side of the sheath and remove it.

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Management of nocturia and nocturnal polyuria

Nocturia can be particularly resistant to treatment.

Firstly, establish whether the patient is polyuric (>3L or urine/24h) by getting them to complete a frequency volume chart. If they are polyuric, this may account for their daytime and night-time voiding frequency. Establish whether they have a solute or water diuresis and the causes thereof (see box).

If non-polyuric (<3L urine output/24h), determine the distribution of urine output over the 24-h period. If >1/3 of urine output is between the hours of midnight and 8a.m. then the patient has nocturnal polyuria (NP).

Non-polyuric nocturia

BPH medical therapy

The impact of alpha blockers, 5α-reductase inhibitors, and anticholinergics on nocturia is modest.

TURP

Nocturia persists in 20–40% of men after TURP.

Medtronic Interstim therapy for nocturia

Patients pre-selected on the basis of a favourable symptomatic response to a test stimulation can experience a reduction in nocturia,⁴⁹ but not all patients respond to the test stimulation and the treatment is expensive and not yet widely available in all countries.

Treatment for nocturnal polyuria (NP)

The evidence base for NP treatments is limited (very few randomized, placebo controlled trials).

Fluid restriction

Many patients have reduced their afternoon and evening fluid intake in an attempt to reduce their night-time diuresis.

Diuretics

Diuretics, taken several hours before bedtime, reduce nocturnal voiding frequency in some patients.⁵⁰

DDAVP

A synthetic analogue of arginine vasopressin (endogenous ADH), which if taken at night can reduce urine flow by its antidiuretic action. It has been suggested that NP may be caused by a lack of endogenous production of ADH in elderly people. However, adults both with and without NP have no rise in ADH at night (i.e. ADH secretion remains remarkably constant throughout the day in adults with and without NP). Furthermore, the diuresis in adults with NP is a solute diuresis due to a nocturnal natriuresis.⁵¹ Thus, lack of ADH secretion at night is not the cause of the diuresis in nocturnal polyuric adults and, therefore, from a theoretical perspective there is no logical basis for using DDAVP in NP.⁵² There is limited

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evidence that it reduces night-time voiding frequency (at least in res-ponder enrichment studies) and increases sleep duration in a proportion of patients with NP.⁵³

Side effects: hyponatraemia (Na < 130mmol/l) in 5% of patients. Measure serum Na 3 days after starting DDAVP and stop if hyponatraemia develops.

Nocturia and sleep apnoea

Obstructive sleep apnoea (OSA) is highly prevalent in those over 65 years of age. It is often manifested by snoring. There is a strong associa-tion between OSA symptoms and nocturia.⁵⁴ Large negative intrathoracic pressure swings may trigger a cardiac mediated natriuresis and hence cause NP.

Investigation of the polyruic patient (= urine output of >3L per 24h)

Urine osmolality?

>250mosm/kg = solute diuresis

<250mosm/kg = water diuresis

Solute diuresis—poorly controlled diabetes mellitus; saline loading (e.g. post-operative diuresis); the diuresis following relief of high pressure chronic retention

Water diuresis—primary polydipsia; diabetes insipidus (nephrogenic—e.g. lithium therapy, central—ADH deficiency)

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High pressure chronic retention (HPCR)

This is maintenance of voiding, with a bladder volume of >800ml and an intravesical pressure above 30cmH₂O, accompanied by hydronephrosis.^55,56 Over time this leads to renal failure. When the patient is suddenly unable to pass urine, acute-on-chronic high pressure retention of urine has occurred.

A man with high pressure retention who continues to void spontaneously may be unaware that there is anything wrong. He will often have no sensation of incomplete emptying and his bladder seems to be insensitive to the gross distension. Often the first presenting symptom is that of bedwetting. This is such an unpleasant and disruptive symptom that it will cause most people to visit their doctor. Visual inspection of the patient's abdomen may show marked distension due to a grossly enlarged bladder. The diagnosis of chronic retention can be confirmed by palpation of the enlarged, tense bladder, which is dull to percussion.

Acute treatment

Catheterization relieves the pressure on the kidneys and allows normalization of renal function. A large volume of urine is drained from the bladder (often in the order of 1–2L, and sometimes much greater). The serum creatinine is elevated and an ultrasound will show hydronephrosis with a grossly distended bladder if the scan is done before relief of retention.

Anticipate a profound diuresis following drainage of the bladder. This is due to:

• 
  
  
  Excretion of salt and water that has accumulated during the period of renal failure
• 
  
  
  Loss of the corticomedullary concentration gradient, due to continued perfusion of the kidneys with diminished flow of urine through the nephron (this washes out the concentration gradient between the cortex and medulla)
• 
  
  
  An osmotic diuresis caused by elevated serum urea concentration

A small percentage of patients have a postural drop in blood pressure. It is wise to admit patients with HPCR for a short period of observa-tion, until the diuresis has settled. A few will require intravenous fluid replacement if they experience a symptomatic fall in blood pressure when standing.

Definitive treatment

TURP or a long-term catheter. In those unable to void who have been catheterized, a trial without catheter is clearly not appropriate in cases where there is back pressure on the kidneys. Very rarely a patient who wants to avoid a TURP and does not want an indwelling catheter will be able to empty their bladder by intermittent self-catheterization, but such cases are exceptional.

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Bladder outlet obstruction and retention in women

Relatively rare (~5% of women undergoing pressure flow studies have BOO, compared with 60% of unselected men with LUTS).⁵⁷

It may be symptom-free, and present with LUTS or as acute urinary retention. In broad terms, the causes are related to obstruction of the urethra (e.g. urethral stricture, compression by a prolapsing pelvic organ such as the uterus, post-surgery for stress incontinence) or have a neurological basis (e.g. injury to sacral cord or parasympathetic plexus, degenerative neurological disease e.g. MS, diabetic cystopathy).

Voiding studies in women

Women have a higher Qmax, for a given voided volume, than do men. Women with BOO have lower Qmax than those without BOO. There are no universally accepted urodynamic criteria for diagnosing BOO in women.

Treatment of BOO in women

Treat the cause (e.g. dilatation of a urethral stricture; repair of a pelvic prolapse). Where this it is not possible (because of a neurological cause such as MS or spinal cord injury), the options are:

• 
  
  
  Intermittent self-catheterization (ISC) or intermittent catheterization by a carer
• 
  
  
  Indwelling catheter (preferably suprapubic rather than urethral)
• 
  
  
  Mitrofanoff catheterizable stoma

Where urethral intermittent self-catheterization is technically difficult, a catheterizable stoma can be constructed between the anterior abdominal wall and the bladder, using the appendix, Fallopian tube, or a narrowed section of small intestine. This is the Mitrofanoff procedure. It is simply a new urethra which has an abdominal location, rather than a perineal one, and is therefore easier to access for ISC.

For women with a suprasacral spinal cord injury with preserved detrusor contraction and urinary retention due to detrusor-sphincter dyssynergia (DSD), sacral deafferentation combined with a Brindley stimulator can be used to manage the resulting urinary retention.

Fowler's syndrome

A primary disorder of sphincter relaxation (as opposed to secondary to, for example, SCI). Increased electromyographic activity (repetitive discharges on external sphincter EMG) can be recorded in the external urethral sphincters of these women (which on ultrasound are of increased volume) and is hypothesized to cause impaired relaxation of external sphincter. Occurs in premenopausal women, typically aged 15–30, often in association with polycystic ovaries (50% of patients), acne, hirsutism, and menstrual irregularities. May also be precipitated by childbirth or gynaecological or other surgical procedures. They report no

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urgency with bladder volumes >1000ml, but when attempts are made to manage their retention by ISC, they experience pain, especially on withdrawing the catheter.

Pathophysiology

May be due to a channelopathy of the striated urethral sphincter muscle leading to involuntary ES contraction.

Treatment

ISC, sacral neuromodulation with Medtronic Interstim (90% void post implantation and 75% are still voiding at 3-years’ follow-up). The mechanism of action of sacral neuromodulation in urinary retention is unknown.*

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Urethral stricture disease

A urethral stricture is an area of narrowing in the calibre of the urethra due to formation of scar tissue in the tissues surrounding the urethra. The disease process of anterior urethral stricture disease is different to that in the posterior urethra.

Anterior urethra

The process of scar formation occurs in the spongy erectile tissue (corpus spongiosum) of the penis that surrounds the urethra—spongiofibrosis.

• 
  
  
  Inflammation (e.g. balanitis xerotica obliterans—BXO), gonococcal infection leading to gonococcal urethritis (less common nowadays because of prompt treatment of gonorrhea)
• 
  
  
  Trauma
  • 
    
    
    Straddle injuries—blow to bulbar urethra (e.g. cross-bar injury)
  • 
    
    
    Iatrogenic—instrumentation (e.g. traumatic catheterization, traumatic cystoscopy, TURP, bladder neck incision)

The role of non-specific urethritis (e.g. Chlamydia) in the development of anterior urethral strictures has not been established.

Posterior urethra

Fibrosis of the tissues around the urethra results from trauma—pelvic fracture or surgical (radical prostatectomy, TURP, urethral instrumentation). These are essentially distraction injuries, where the posterior urethra has been pulled apart, and the subsequent healing process results in the formation of a scar, which contracts and thereby narrows the urethral lumen.

Symptoms and signs of urethral stricture

• 
  
  
  Voiding symptoms—hesitancy, poor flow, post-micturition dribbling
• 
  
  
  Urinary retention—acute, or high pressure acute-on-chronic
• 
  
  
  Urinary tract infection—prostatitis, epididymitis

Management of urethral strictures

Where the patient presents with urinary retention, the diagnosis is usually made following a failed attempt at urethral catheterization. In such cases, avoid the temptation to ‘blindly’ dilate the urethra. Dilatation may be the wrong treatment option for this type of stricture—it may convert a short stricture, which could have been cured by urethrotomy or urethroplasty, into a longer and more dense stricture, thus committing the patient to more complex surgery and a higher risk of recurrent stricturing. Place a suprapubic catheter instead, and image the urethra with retrograde and antegrade urethrography to establish the precise position and the length of the stricture.

Similarly, avoid the temptation to inappropriately dilate a urethral stricture diagnosed at flexible cystocopy (urethroscopy). Arrange retrograde urethrography so appropriate treatment can be planned.

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Treatment options

Urethral dilatation: designed to stretch the stricture without causing more scarring; bleeding post dilatation indicates tearing of the stricture (i.e. further injury has been caused) and restricturing is likely.

Internal (optical) urethrotomy: stricture incision, with an endoscopic knife or laser. Divides the stricture, followed by epithelialization of the incision. If deep spongiofibrosis is present, the stricture will recur. Best suited for short (<1.5cm) bulbar urethral strictures with minimal spongiofibrosis.⁵⁹ Leave a catheter for 3–5 days (longer catheterization does not reduce long-term restricturing). Consider ISC for 3–6 months, starting several times daily, reducing to once or twice a week towards the end of this period.

Excision and reanastomosis or tissue transfer: excises the area of spongiofibrosis with primary reanastomosis or closure of defect with buccal mucosa or pedicled skin flap; best chance of cure.

A stepwise progression up this ‘reconstructive ladder’ (the process of starting with a simple procedure and moving onto the next level of complexity when this fails) is not appropriate for every patient. For the patient who wants the best chance of long-term cure, offer excision and reanastomosis or tissue transfer up front. For the patient who is happy with lifelong ‘management’ of his stricture (with repeat dilatation or optical urethrotomy), offer dilatation or optical urethrotomy.

Balanitis xerotica obliterans (BXO)

Genital lichen sclerosis and atrophicus in the male. Hyperkeratosis is seen histologically. Appears as a white plaque on the foreskin, glans of the penis, or within the urethral meatus. Most common cause of stenosis of the meatus. Foreskin becomes thickened and adheres to the glans, leading to phimosis (a thickened, non-retractile foreskin). Patients with long-standing BXO and meatal stenosis often have more proximal urethral strictures.

References

1 Walsh PC, Retik AB, Vaughan D, et al. (eds.) (2002) Campbell's Urology, 8th Edition, p. 1299. Philadelphia: WB Saunders/Elsevier.

2 Irani J, Brown CT, van der Meulen J, Emberton M (2003) A review of guidelines on benign prostatic hyperplasia and lower urinary tract symptoms: are all guidelines the same? Br J Urol Int 92:937–42.

3 Roehrborn CG, Bartsch G, Kirby R, et al. (2001) Guidelines for the diagnosis and treatment of benign prostatic hyperplasia: a comparative international overview. Urology 58:642–50.

4 Irani J, Brown CT, van der Meulen J, Emberton M (2003) A review of guidelines on benign prostatic hyperplasia and lower urinary tract symptoms: are all guidelines the same? Br J Urol Int 92:937–42.

5 Dunsmuir WD, Feneley M, Corry DA, et al. (1996) The day-to-day variation (test-retest reliability) of residual urine measurement. Br J Urol 77:192–93.

6 Bates TS, Sugiono M, James ED, et al. (2003) Is the conservative management of chronic retention in men ever justified? Br J Urol Int 92:581–83.

7 Wasson JH, Reda DJ, Bruskewitz RC, et al. (1995) A comparison of transurethral surgery with watchful waiting for moderate symptom of benign prostatic hyperplasia. The Veterans Administration Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 332:75–79.

8 Reynard JM, Peters TJ, Lim C, Abrams P (1996) The value of multiple free-flow studies in men with lower urinary tract symptoms. Br J Urol 77:813–18.

9 Koch WF, Ezz el Din KE, De Wildt MJ, et al. (1996) The outcome of renal ultrasound in the assessment of 556 consecutive patients with benign prostatic hyperplasia. J Urol 155:186–89.

10 Jacobsen SJ, Jacobson DJ, Girman CJ, et al. (1997) Natural history of prostatism: risk factors for acute urinary retention. J Urol 158:481–87.

11 McConnell JD, Bruskewitz R, Walsh PC, et al. (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyper-plasia (PLESS). N Engl J Med 338:557–63.

12 Ball AJ, Feneley RC, Abrams PH (1981) Natural history of untreated ‘prostatism’. Br J Urol 53:613–16.

13 McConnell JD, Bruskewitz R, Walsh PC, et al. (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia (PLESS). N Engl J Med 338:557–63.

14 Wasson JH, Reda DJ, Bruskewitz RC, et al. (1995) A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 332:75–79.

15 Barry MJ, Fowler FJJ, Bin L, et al. (1997) The natural history of patients with benign prostatic hyperplasia as diagnosed by North American urologists. J Urol 157:10–14.

16 Lowe F (1999) Alpha-1-adrenoceptor blockade in the treatment of benign prostatic hyperplasia. Prostate Cancer and Prostatic Diseases 2:110–19.

17 McConnell JD, Barry MD, Bruskewitz RC, et al. (1994) The BPH Guideline Panel. Benign prostatic hyperplasia: diagnosis and treatment. Clinical practice guideline. Agency for Health Care Policy and Research, publication No.94–0582, 1994, Rockville, Maryland. Public Health Service, US Department of Health and Human Sciences.

18 Boyle P, Robertson C, Manski R, et al. (2001) Meta-analysis of randomized trials of terazosin in the treatment of benign prostatic hyperplasia. Urology 58:717–22.

19 Andersen JT, Ekman P, Wolf H, et al. (1995) Can finasteride reverse the progress of benign prostatic hyperplasia? A two-year placebo-controlled study. The Scandinavian BPH Study Group. Urology 46:631–37.

20 Nickel J, Fradet Y, Boake RC, et al. (1996) Efficacy and safety of finasteride therapy for benign prostatic hyperplasia: results of a 2-year randomised controlled trial (the PROSPECT study). PROscar Safety Plus Efficacy Canadian Two Year Study. Can Med Assoc J 155:1251–59.

21 Marberger MJ (1998) Long-term effects of finasteride in patients with benign prostatic hyperplasia: a double-blind, placebo-controlled, multicenter study. PROWESS Study Group. Urology 51:677–86.

22 McConnell JD, Bruskewitz R, Walsh PC, et al. (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia (PLESS). N Engl J Med 338:557–63.

23 Foley SJ, Soloman LZ, Wedderburn AW, et al. (2000) Finasteride for haematuria due to BPH. A prospective study of the natural history of hematuria associated with BPH and the effect of finasteride. J Urol 163:496–98.

24 Debruyne FM, Jardin A, Colloi D, et al. (1998) Sustained-release alfuzosin, finasteride and the combination of both in the treatment of benign prostatic hyperplasia. Eur Urol 34:169–75.

25 Kirby RS, Roerborn C, Boyle P, et al. (2003) Efficacy and tolerability of doxazosin and finasteride, alone or in combination, in treatment of symptomatic benign prostatic hyperplasia: the Prospective European Doxazosin and Combination Therapy (PREDICT) trial. Urology 61:119–26.

26 Lepor H, Williford WO, Barry MJ, et al. (1996) The efficacy of terazosin, finasteride, or both in benign prostatic hypertrophy. N Engl J Med 335:533–39.

27 McConnell JD, Roehrborn CG, Bautista OM, et al. (2003) The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. New Engl J Med 349:2387–98.

28 Reynard J (2004) Does anticholinergic medication have a role for men with lower urinary tract symptoms/benign prostatic hyperplasia either alone or in combination with other agents? Current Opinions in Urology 14:13–16.

29Thompson IM, Goodman PJ, Tangen CM, et al. (2003) The influence of finasteride on the development of prostate cancer. N Engl J Med 349:215–24.

30 McConnell JD, Roehrborn CG, Bautista OM, et al. (2003) The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. New Engl J Med 349:2387–98.

31 Lepor H, Williford WO, Barry MJ, et al. (1996) The efficacy of terazosin, finasteride, or both in benign prostatic hypertrophy. N Engl J Med 335:533–39.

32 Kirby RS, Roerborn C, Boyle P, et al. (2003) Efficacy and tolerability of doxazosin and finasteride, alone or in combination, in treatment of symptomatic benign prostatic hyperplasia: the Prospective European Doxazosin and Combination Therapy (PREDICT) trial. Urology 61:119–26.

33 Debruyne FM, Jardin A, Colloi D, et al. (1998) Sustained-release alfuzosin, finasteride and the combination of both in the treatment of benign prostatic hyperplasia. Eur Urol 34:169–75.

34 Thompson IM, Goodman PJ, Tangen CM, et al. (2003) The influence of finasteride on the development of prostate cancer. N Engl J Med 349:215–24.

35 Reynard J (2004) Does anticholinergic medication have a role for men with lower urinary tract symptoms/benign prostatic hyperplasia either alone or in combination with other agents? Current Opinions in Urology 14:13–16.

36 Lowe FC, Fagelman E (1999) Phytotherapy in the treatment of benign prostatic hyperplasia: an update. Urology 53:671–78.

37 Wilt JW, Ishani A, Stark G, et al. (1998) Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review. JAMA 280:1604–8.

38 Roos NP, Wennberg J, Malenka DJ, et al. (1989) Mortality and reoperation after open and transurethral resection of the prostate for benign prostatic hyperplasia. New Engl J Med 320:1120–24.

39 Fitzpatrick JM, Mebust WK (2002) Minimally invasive and endoscopic management of benign prostatic hyperplasia. In Campbell's Urology, 8th Edition. Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds.). Philadelphia: Saunders.

40 Transurethral radiofrequency needle ablation of the prostate. National Institute for Clinical Excellence Interventional Procedure Guidance, October 2003.

41 D'Ancona FCH, Francisca EAE, Witjes WPJ, et al. (1998) Transurethral resection of the prostate vs high-energy thermotherapy of the prostate in patients with benign prostatic hyperplasia: long-term results. Br J Urol 81:259–64.

42 National Institute for Clinical Excellence Interventional Procedure Guidance 14, London, October 2003.

43 Gilling PJ, Kennett KM, Westenberg AM, et al. (2003) Holmium laser enucleation of the prostate (HoLEP) is superior to TURP for the relief of bladder outflow obstruction (BOO): a randomised trial with 2-year follow-up. J Urol 169:1465.

44 Hammadeh MY, Madaan S, Hines J, Philp T (2000) Transurethral electrovaporization of the prostate after 5 years: is it effective and durable. Br J Urol Int 86:648–51.

45 McAllister WJ, Karim O, Plail RO, et al. (2003) Transurethral electrovaporization of the prostate: is it any better than conventional transurethral resection of the prostate? Br J Urol Int 91:211–14.

46 Pickard R, Emberton M, Neal D (1998) The management of men with acute urinary retention. Br J Urol 81:712–20.

47 Reynard JM (1999) Failure to void after transuretural resection of the prostate and mode of presentation. Urology 53:336–39.

48 Birch BR (1994) Flexible cystoscopy in men: is topical anaesthesia with lignocaine gel worthwhile? Brit J Urol 73:155.

49 Spinelli M (2003) New sacral neuromodulation lead for percutaneous implantation using local anesthesia: description and first experience. J Urol 170:1905–7.

50 Reynard JM, Cannon A, Yang Q, Abrams P (1998) A novel therapy for nocturnal polyuria: a double-blind randomized trial of frusemide against placebo. Br J Urol 81:215–18.

51 Matthiesen TB, Rittig S, Norgaard JP, Pedersen EB, Djurhuus JC (1996) Nocturnal polyuria and natriuresis in male patients with nocturia and lower urinary tract symptoms. J Urol 156:1292–99.

52 McKeigue P, Reynard J (2000) Relation of nocturnal polyuria of the elderly to essential hypertension. Lancet 355:486–88.

53 Mattiasson A (2002) Efficacy of desmopressin in the treatment of nocturia: a double-blind placebo-controlled study in men. Br J Urol 89:855–62.

54 Umlauf M (1999) Nocturia and sleep apnea symptoms in older patients: clinical interview. Sleep 22:S127.

55 Mitchell JP (1984) Management of chronic urinary retention. BMJ 289:515–16.

56 Abrams P, Dunn M, George N (1978) Urodynamic findings in chronic retention of urine and their relevance to results of surgery. BMJ 2:1258–60.

57 Madersbascher S, Pycha A, Klingler CH, et al. (1998) The aging lower urinary tract: a comparative urodynamic study of men and women. Urology 51:206–12.

58 Swinn MJ, Fowler C, et al. (2002) The cause and treatment of urinary retension in young women. J Urol 167:151–56.

59 Pansadoro V, Emiliozzi P (1996) Internal urethrotomy in the management of anterior urethral strictures: long term follow-up. J Urol 156:73–75.