With the patient relaxed, the kidney can be balloted; lifted with one hand placed behind the loin and compressed by the other hand pressing downwards (Fig. 23.1). The ureter cannot be palpated. An enlarged bladder rises centrally out of the pelvis, is dull to percussion and may even be visible. In men, the hernial orifices, cords, testes and epididymes are examined with the patient standing and lying. If the foreskin is uncircumcised, it must be confirmed that it retracts and that the glans and meatus are normal. In women, the vulva, urethra and vagina must also be examined. A speculum examination should be carried out if there is any suspicion of vaginal or cervical abnormality. A full pelvic bimanual examination, whether in males or females, is best carried out under general anaesthesia with a muscle relaxant. A rectal examination is mandatory, not only to examine the prostate but also to detect abnormalities of the anal margin (haemorrhoids, fissures) and lower rectum (carcinoma).

Fig. 23.1 Bimanual palpation of the right kidney.

Investigations

Ultrasonography

This is another means of first-line imaging (Fig. 23.3), tending to give superior information about the renal parenchyma but less about the collecting system. It also allows visualization of other related organs, such as the liver, spleen and gynaecological organs.

Fig. 23.3 Renal ultrasound.

A Normal kidney. B A simple cyst occupies the upper pole of an otherwise normal kidney. C The renal pelvis and calyces are dilated by a chronic obstruction to urinary outflow. The thinness of the remaining renal cortex indicates chronicity. D, E and F The diagrams beneath show the anatomical features.

CT Urogram

The IVU is largely becoming superceded by the ‘plain’ CT KUB, a non contrast enhanced CT, which has a higher specificity and sensitivity for the detection of renal and ureteric calculi. Furthermore, CT urography allows the ureters to be delineated by contrast, as in an IVU, but also allows other structures within the abdomen to be assessed.

Special radiological investigations

In certain circumstances a retrograde ureteropyelogram may be necessary. This involves retrograde injection of contrast material through a catheter placed in the lower ureter (Fig. 23.4). Abnormalities of the renal vessels can be demonstrated by renal angiography. Computed tomography (CT) is now the preferred method for imaging renal tumours. A micturating cystourethrogram (MCU) will outline the bladder, detect ureterovesical reflux and examine the bladder neck and urethra. The bladder is filled with contrast material (via a catheter) and emptying is then studied by X-ray screening. An ascending urethrogram, in which contrast medium is injected into the urethra, can be used to define strictures. When used in conjunction with a MCU, a descending urethrogram can also be obtained.

Fig. 23.4 Retrograde ureteropyelography.

A Cystoscope and ureteric catheterization. B The best views of the normal collecting system are shown by pyelography. A catheter has been passed into the left renal pelvis at cystoscopy. The anemone-like calyces are sharp-edged and normal.

Nuclear imaging

Radio-labelled substances are used for two main purposes:

1. Detecting bony metastases from carcinoma of the prostate (bone scan). ^99mTc-labelled methylene diphosphonate (MDP) is the most reliable method.

2. Measurement of renal function (scintigraphic renography). Occasionally ‘how a kidney looks’ does not correlate with ‘how it behaves’, e.g. hydronephrosis does not always mean the presence of obstruction. Renography allows assessment of obstruction to a kidney (e.g. from a pelviureteric obstruction), differential kidney function (i.e. how much each kidney is contributing to overall function), assess non-functioning areas of renal parenchyma (e.g. scarring) and allow accurate assessment of GFR. Radio-labelled mercaptuacetyltriglycine (MAG-3) has largely superseded technetium labeled diethylenetriamine pentaacetic acid (Tc-DTPA) for dynamic scanning. It is secreted from the renal tubules and is used in the identification of obstructed kidneys and to assess differential function. Dimercaptosuccinic acid (DMSA) is concentrated in the renal tubules and static imaging can be carried out some 2–3 hours after injection. Parenchymal defects such as scars, haematomas, lacerations or ischaemia may be demonstrated. Differential renal function can be quantified from measuring the DMSA concentration/density in each kidney.

Urodynamic studies

The maximum urinary flow rate during micturition can be measured using a flow meter when the voided volume is at least 150 ml or the values may be misleadingly low. The norm in males is 15–30 ml/s and in females 20–40 ml/s and a flow rate of less than 10 ml/s is abnormal. The flow rate pattern can help to determine the cause of obstruction (Fig. 23.5). Measurements of flow rate can be combined with cystometry to provide a measure of residual urine, bladder capacity, the capacity at which a desire to void occurs, and the detrusor pressures when the bladder is full and during maximum flow. Spontaneous detrusor contractions during bladder filling may indicate an unstable bladder, a cause of urgency and urge incontinence.

Fig. 23.5 Urinary flow rates.

The normal flow rate shows a rapid rise to maximum high-peak flow. In a typical bladder outflow obstruction due to benign prostatic hyperplasia, there is a slow rise to poor maximum flow rate and prolonged variable flow. In a typical urethral stricture, there is prolonged flow with little variability, giving a plateau- or box-shaped curve.

Semen analysis

Microscopic examination of the semen is a basic investigation in infertile males. The specimen is collected following a period of abstinence of at least 3 days and is examined within 2 hours. Normal semen has a volume of > 2 ml and a sperm concentration of > 20 × 10⁶/ml. More than 50% of the sperm should be motile at 2 hours. The morphology, biochemistry and viability of the sperm may also be studied. In selected cases, immunological tests may help to determine the cause of infertility.

Biochemical screening for stones

Recurrent urinary tract calculi should raise the suspicion of hyperparathyroidism, idiopathic hypercalciuria, hyperoxaluria or cystinuria. Serum calcium, phosphate, oxalate and uric acid should be measured. If more detailed investigation is required a 24-hour collection of urine for determination of calcium, phosphate, oxalate and uric acid excretion can be obtained. The composition of passed or removed stones should be analysed to determine their metabolic type.

Upper urinary tract (kidney and ureter)

Anatomy

The two kidneys lie retroperitoneally on the posterior abdominal wall. Each is approximately 12 cm long, 6 cm wide and 3 cm thick. The upper pole of the kidney lies on the diaphragm, which separates it from the pleura and the 11th and 12th ribs. Below this, it lies on the psoas, quadratus lumborum and transversus abdominis muscles from medial to lateral (Fig. 23.6). Anteriorly, the right kidney is covered by the liver, the second part of the duodenum and the ascending colon. The spleen, stomach, tail of pancreas, left colon and small bowel overlie the left kidney. The renal hilum lies medially and transmits from front to back the renal vein, renal artery and renal pelvis. The ureter begins at the renal pelvis and runs for 25 cm to the bladder. The abdominal ureter lies on the medial edge of the psoas muscle, which separates it from the tips of the transverse processes. It then crosses the bifurcation of the common iliac artery, which separates it from the sacroiliac joint, to enter the pelvis. The pelvic ureter runs on the lateral pelvic wall to just in front of the ischial spine, when it then turns medially and forward to enter the bladder. In the male, it is crossed by the vas deferens. In the female, it lies close to the lateral fornix of the vagina and is crossed by the uterine vessels, where it is vulnerable to damage during hysterectomy. The section of ureter that lies within the bladder wall functions as a flap valve to prevent reflux. Stones tend to impact at the three points where the ureter narrows: namely, the pelviureteric junction, the pelvic brim and the ureteric orifice.

Fig. 23.6 Anatomy of kidneys and ureters.

Physiology

The healthy kidney can produce between 0.3 and 17 ml of urine per minute, depending on the state of hydration, but on average produces 1 ml of urine per minute. This is transported down the ureter by 4–5 peristaltic waves per minute to reach the bladder, where it is stored without refluxing up the ureters.

Renal cysts

Simple cysts

These are usually single, almost always asymptomatic, and often found incidentally on ultrasound where they can usually be differentiated from carcinoma. Complex cysts containing multiple septa raise the suspicion of malignant change

Polycystic kidney disease

An autosomal dominant congenital anomaly affecting both kidneys that often leads to chronic renal failure in middle life. Despite their very large size, the cystic kidneys cause few symptoms. Infection or bleeding may occur in a cyst causing pain or haematuria.

Benign tumours

Renal adenomas are small and are usually an incidental finding. Haemangiomas are a rare cause of dramatic haematuria.

Nephroblastomas

Epidemiology

This tumour usually occurs in children under 4 years of age, and is the most common childhood urological malignancy, with an incidence of 7 per million children per year. Growth is rapid and there is early local spread, including invasion of the renal vein. Invasion of the renal pelvis occurs late, and so haematuria is seen in only 15% of cases. Distant metastases most commonly appear in the lungs, liver and bones. Tumours presenting in the first year of life have a better prognosis.

Clinical features

The cardinal sign is a large abdominal mass. Some of the unusual clinical features associated with a renal carcinoma in adults, such as fever or hypertension, may be present.

Investigations

CT of the abdomen and chest is essential for diagnosis and staging. The main differential diagnosis to consider is adrenal neuroblastoma, but other causes of a large kidney, such as hydronephrosis and cystic disease, must also be considered. The tumour is bilateral in 5–10% of cases.

Management

The diagnosis is confirmed by biopsy. Chemotherapy is followed by transabdominal nephrectomy with wide excision of the mass. Further chemotherapy ± radiotherapy is performed dependent upon the histopathological features of the removed tumour; the 5-year survival rate is in the region of 70–90%.

Renal adenocarcinoma

Epidemiology

This tumour arises from the renal tubules and is the most common malignant tumour of the kidney. The incidence is 16 cases per 100 000, being twice as common in males. It is uncommon before the age of 40 years and has a peak incidence between 65 and 75 years of age. There can be spread into the renal pelvis, causing haematuria. Invasion of the renal vein, often extending into the inferior vena cava, can also occur. Direct spread into perinephric tissues is common, so that the whole fascial envelope and kidney should be removed en bloc. Lymphatic spread occurs to para-aortic nodes, but blood-borne metastases (which may be solitary) may develop almost anywhere. In the lungs, these characteristically give the appearance of ‘cannon ball’ metastases.

Clinical features

The triad of pain, haematuria and a mass is an important, albeit late, feature occurring in only 15% of cases. Historically, 60% present with haematuria, 40% with loin pain and only 25% with a mass, but increasing access to ultrasonagraphy and CT has increased incidental diagnosis. Patients may present with pyrexia of unknown origin, raised ESR, polycythaemia, disorders of coagulation, and abnormalities of plasma proteins and liver function tests, or with neuromyopathy due to secretion of renin, erythropoietin, parathormone and gonadotrophins.

Investigations

The initial investigation is ultrasound, followed by a staging contrast CT of the abdomen and chest (Fig. 23.7).

Fig. 23.7 Contrast-enhanced CT of renal cancer.

The right kidney is expanded by a low-density cancer that fails to take up the contrast. Tumour is seen extending into the renal vein and inferior vena cava (arrow).

Management

Organ confined renal adenocarcinoma should be treated with curative intent, either by laparoscopic or open nephrectomy. Metastatic renal adenocarcinoma is relatively radio and chemoresistant. Immunotherapy, in the form of interferon, gives a modest survival benefit (3–5 months) but angiogenesis inhibiting drugs, such as tyrosine kinase inhibitors, are showing more promising results. A further modest survival benefit may be seen in metastatic disease by reducing the tumour burden if nephrectomy is performed prior to starting immunotherapy.

Summary Box 23.1 Renal carcinoma

• Renal adenocarcinoma is the most common malignant renal tumour and is twice as common in males

• The carcinoma arises in the renal tubules and spreads early to the renal pelvis, producing haematuria. Later spread involves the renal vein (with bloodstream dissemination), perinephric invasion and lymphatic spread

• The clinical presentation is very varied. The triad of pain, haematuria and a mass may be late features, and early systemic effects include fever, polycythaemia, disordered coagulation and pyrexia of unknown origin

• The key investigations are ultrasonography, chest X-ray and contrast CT

• Treatment consists of radical nephrectomy; the tumour is not radiosensitive. The natural history of renal carcinoma is very variable and excision of solitary metastases may be worthwhile.

Renal and ureteric calculi

Mechanism of stone formation

A solute dissolves in a solvent to form a solution but when the concentration of solute in solution reaches a certain level, termed the solubility product, the compound precipitates out to form crystals. This initial crystal formation (nucleation) may progress such that crystals clump together (aggregation) to form calculi. There are substances in urine that act to keep compounds in solution by inhibiting nucleation (inhibitors) but, above a certain concentration of solute, nucleation will occur despite their presence (formation product). Where the concentration of a compound lies between the solubility product and the formation product, being kept in solution solely by the action of inhibitors, it is described as being metastable. A solution with a concentration above the formation product is described as being supersaturated. The ability of urine to keep compounds in solution, and prevent calculus formation is a balance between forces keeping the solute in solution and those that promote nucleation. Therefore, stones form when the amount of solute increases (e.g. hypercalcuria), the amount of solvent decreases (e.g. dehydration) or the concentration of inhibitors falls (e.g. decreased citrate excretion). Foreign bodies, anatomical abnormalities, and calculi can all act as a nidus for nucleation and promote further stone formation.

Types and causes of stone formation

The commonest stone types are; calcium oxalate (85%), uric acid (10%), mixed calcium phosphate/calcium oxalate (10%), magnesium ammonium phosphate (5–15%) and cystine (1%). Calcium oxalate stones are commonly caused by hypercalciuria, hypercalcaemia, hyperoxaluria or hypocitraturia. Uric acid stones are formed due to increases in uric acid formation either through gout or myeloproliferative disorders. Approximately 50% of patients with urate stones have gout but only 20% of patients with gout develop urate stones. Calcium phosphate stones are generally secondary to renal tubular acidosis. Magnesium ammonium phosphate (struvite) stones are usually due to urinary tract infection by pathogens that can break urea down into CO₂ and ammonia, thereby alkalinizing the urine.

Clinical features

Renal pain, renal colic and ureteric colic are characteristically unilateral. Renal pain is dull and aching, whereas ureteric colic is acute and severe, occurring in waves. A stone may cause bleeding or there may be symptoms of urinary tract infection. However, a stone in the kidney may remain silent, even one large enough to fill the pelvis and calyces (‘staghorn’ calculus).

Investigations

IVU or CT KUB provides all the necessary information on the position of the stone (Fig. 23.8). Routine hematological and biochemical tests are needed to assess renal function and to exclude metabolic causes. A urine sample is cultured to determine whether there is infection. If obstruction is acute, its relief is the prime clinical need; if it is chronic and has caused renal damage, the surgical approach depends on the function of the affected kidney. This is best determined by radioisotope methods (renography).

Fig. 23.8 IVU showing ureteric stone.

A Eighty percent of stones are visible on a plain X-ray (arrow). B The contrast excreted by the kidney in an IVU clearly shows the obstruction caused by the stone in the ureter (arrow).

Management

Symptomatic treatment should be instituted as soon as the diagnosis is confirmed. Intramuscular diclofenac, a non-steroidal anti-inflammatory, is the most effective analgesic; pethidine is an alternative. The likelihood of spontaneous passage depends on the size of the stone and on its smoothness. A stone less than 0.5 cm in diameter should pass. Immediate treatment should be considered in cases of ongoing pain, renal obstruction or, more importantly, where there are signs of sepsis (infected obstructed kidney). Extracorporeal shock-wave lithotripsy (ESWL), the technique of focusing external shock waves to break up stones, has revolutionized the treatment of renal and ureteric stones. If a stone can be visualized on X-ray or ultrasound, then it can be treated by ESWL. Other stones can be visualized directly by passing a fine telescope up the ureter (ureteroscope) and the stones may be either broken up or removed intact. Some stones in the kidney that are unlikely to pass even if broken up are best treated by direct puncture of the kidney, insertion of a sheath and removal under vision with a nephroscope (percutaneous nephrolithotomy, PCNL). It is now very rare to remove stones from the renal tract at open operation. In cases of acute obstruction leading to sepsis (infected obstructed kidney) or renal impairment, decompression of the kidney either via insertion of a ureteric stent or percutaneous nephrostomy is required. Stones and infection within a kidney can be the cause of renal destruction and if the kidney contributes less than 10% of total renal function, then a nephrectomy is recommended.

Upper tract obstruction

Obstruction may be due to extrinsic, intrinsic or intraluminal causes (Table 23.1). In the kidney, stones within the pelvicalyceal system and a congenital abnormality of the pelviureteric junction (see below) are the main causes of obstruction leading to hydronephrosis. More rarely, a sloughed renal papilla, blood clot or tumour may be the cause.

Table 23.1 Causes of urinary tract obstruction

Extrinsic

• Retroperitoneal fibrosis

• External pressure (e.g. carcinoma of the cervix, prostate)

Intrinsic

• Transitional cell tumours

• Tuberculosis / schistosomiasis

• Ureterocoele

• Ectopic ureter

Intraluminal

• Calculi

Pelviureteric junction obstruction (idiopathic hydronephrosis)

Narrowing of the junction between the renal pelvis and the ureter is a common cause of hydronephrosis. As the aetiology is obscure, the term ‘idiopathic’ hydronephrosis is appropriate. This condition is seen in very young children. It is likely to be congenital and can be bilateral, but gross hydronephrosis may present at any age.

Clinical features

Idiopathic hydronephrosis may produce a large painless mass in the loin; in its grossest form, the volume of urine in the hydronephrotic sac may simulate free fluid in the peritoneal cavity. The more usual moderate hydronephrosis causes ill-defined renal pain or ache that may be exacerbated by drinking large volumes of liquid (Dietls’ Crisis). The patient may regard these symptoms as ‘indigestion’. Rarely, there may be no symptoms.

Investigations

IVU or a CT urogram (CTU) provides sufficient information in many cases. The calibre of the ureter is normal. There are a few patients in whom there is doubt as to whether the dilatation of the pelvis and calyces is truly obstructive in nature. In these cases a MAG-3 renogram is performed.

Management

Either laparoscopic or open pyeloplasty is performed to remove the obstructing tissue and refashion the pelviureteric junction (PUJ) so that the lower part of the renal pelvis drains freely into the ureter (Fig. 23.9). It is not possible to predict the degree of recovery of renal function after the relief of obstruction, but a kidney contributing less than 10% of total renal function should be removed.

Fig. 23.9 Anderson–Hynes pyeloplasty.

Retroperitoneal fibrosis

Pathology

Fibrosis of the retroperitoneal connective tissues may encircle and compress the ureter(s), causing hydroureter and hydronephrosis. Fibrosis occurs in three groups of conditions:

• Idiopathic. The aetiology is unknown, although it may be associated with methysergide or analgesic abuse Mediastinal fibrosis and Dupuytren’s contracture may coexist

• Malignant infiltration. The fibrosis contains malignant cells that have metastasized from primary sites such as the breast, stomach, pancreas and colon

• Reactive fibrosis. Radiotherapy, resolving blood clot, or extravasation of sclerosants can lead to fibrotic change in the retroperitoneum.

As the gross appearance of fibrosis in all three groups may be similar, biopsy of the tissue is essential for diagnosis.

Clinical features

Ureteric obstruction may cause symptoms similar to idiopathic hydronephrosis: namely, ill-defined renal pain or ache, and low backache.

Investigations

IVU or CTU shows hydronephrosis and usually hydroureter down to the level of the obstruction. The ureter is often difficult to define, but it is usually pulled medially. A markedly raised ESR is found in more than 50% of cases with idiopathic fibrosis.

Management

Relief of obstruction may be difficult. Where ureteric stenting fails to give adequate drainage uretrolysis can be performed; the ureter is dissected out of the fibrous sheet of tissue (ureterolysis) and wrapped in omentum to prevent further involvement.

Summary Box 23.2 Urinary tract obstruction

Common causes of obstruction of the lower outflow tract

• Benign prostatic hyperplasia

• Prostatic cancer

• Bladder cancer involving the bladder neck

• Bladder-neck obstruction (dyssynergia, infection, neurological disorders)

• Urethral obstruction (congenital posterior urethral valves, blocked urinary catheter, trauma, infection, stricture).

Common causes of obstruction of the upper urinary tract

• Renal and ureteric calculi (80% are calcium oxalate/phosphate stones)

• Pelviureteric junction obstruction (idiopathic hydronephrosis)

• Retroperitoneal fibrosis (idiopathic/malignant infiltration/radiotherapy)

• Transitional cell carcinoma (with or without bleeding and clot)

• Congenital abnormalities (e.g. ectopic ureter, ureterocoele)

• Infections (notably schistosomiasis and tuberculosis).

Lower urinary tract (bladder, prostate and urethra)

Anatomy

The bladder is a muscular reservoir that receives urine via the ureters and expels it via the urethra. In children up to 4 years of age, it lies predominantly in the abdomen; in the adult it is a pelvic organ, well protected in the bony pelvis. Superiorly, the bladder is covered with peritoneum, which separates it from coils of small bowel, the sigmoid colon and, in the female, the body of the uterus. Posteriorly lie the rectum, the vas deferens and seminal vesicles in the male, and the vagina and supravaginal cervix in the female. Inferiorly, the neck of the bladder transmits the urethra and fuses with the prostate in the male and with the pelvic fascia in the female.

The bladder is composed of whorls of detrusor muscle, which in the male become circular at the bladder neck. They are richly supplied with sympathetic nerves that cause contraction during ejaculation, thereby preventing semen from entering the bladder (retrograde ejaculation). There is no such sphincter in the female. The bladder is lined with specialized waterproof epithelium, the urothelium. This is thrown into folds over most of the bladder, except the trigone where it is smooth.

The male urethra is 20 cm long; the prostatic urethra descends for 3 cm through the prostate gland, and the membranous urethra is 1–2 cm long and intimately associated with the main urethral sphincter, the rhabdosphincter. The spongy urethra is 15 cm long and is surrounded by the corpus spongiosus throughout its complete length, opening on the tip of the glans penis as the external meatus. The spongy urethra is further subdivided into the proximal bulbar urethra and the distal penile urethra. The female urethra is 3–4 cm long, descending through the pelvic floor surrounded by the urethral sphincter and embedded in the anterior vaginal wall to open between the clitoris and the vagina.

In the male, the prostate is pyramidal, with its base uppermost. It resembles the size and shape of a chestnut and surrounds the prostatic urethra. Traditionally described as having a median and two lateral lobes, it is better considered as being composed of a small central and a larger peripheral zone (Fig. 23.10).

Fig. 23.10 Anatomy of the lower urinary tracts.

A Female. B Male.

Physiology

Neurological control of micturition

Detrusor contraction is mediated through cholinergic parasympathetic nerves arising from the nerve roots S2–S4, and relaying through ganglia lying predominantly within the detrusor. Sympathetic nerves arise from T10 to L2 and relay via the pelvic ganglia. Their exact role in the control of micturition is unclear. It is known that α-adrenergic receptors and their nerve terminals are found mainly in the smooth muscle of the bladder neck and proximal urethra. The α-receptors respond to noradrenaline (norepinephrine) by stimulating contraction, thereby maintaining closure of the bladder neck.

The distal sphincter mechanism is innervated from the sacral segments S2–S4 by somatic motor fibres that reach the sphincter either by the pelvic plexus or via the pudendal nerves. Afferent nerves are carried in both the parasympathetic and pudendal pathways and transmit sensory impulses from the bladder, urethra and pelvic floor. These sensory impulses pass to the cerebral cortex and the micturition centre, where they produce reflex bladder relaxation and increased tone in the distal sphincter, so helping maintain continence. Cortical control is a basic part of the micturition cycle described below. The higher centres suppress detrusor contractions and their main function is to inhibit micturition until an appropriate time.

The micturition cycle

The micturition cycle has two phases.

Storage (or filling) phase

Due to the high compliance (elasticity) of the detrusor muscle, the bladder fills steadily without a rise in intravesical pressure. As urine volume increases, stretch receptors in the bladder wall are stimulated, resulting in reflex bladder relaxation and reflex increased sphincter tone. At three-quarters of bladder capacity, sensation produces a desire to void. Voluntary control is now exerted over the desire to void, which temporarily disappears. Compliance of the detrusor allows further increase in capacity until the next desire to void. Just how often this desire needs to be inhibited depends on many factors, not the least of which is finding a suitable place in which to void.

Emptying (or micturition) phase

The act of micturition is initiated first by voluntary and then by reflex relaxation of the pelvic floor and distal sphincter mechanisms, followed by reflex detrusor contraction. These actions are coordinated by the pontine micturition centre. Intravesical pressure remains greater than urethral pressure until the bladder is empty.

The normal control of micturition requires coordinated reflex activity of autonomic and somatic nerves, as described above. These responses depend on normal anatomical structures and normal innervation. There are thus two main types of disorders of micturition: structural and neurogenic. Examples are extensive carcinoma of the prostate that has damaged the sphincter mechanism (structural), and spinal cord injury that has damaged the innervation (neurogenic).

Trauma

Bladder

Open injuries

The bladder may be damaged as a result of a penetrating injury to the lower abdomen, or through the course of pelvic surgery; during which damage to the urethra, rectum, vagina or uterus may also occur. Unrecognized damage during surgical procedures may lead to a wound fistula, a vesicovaginal fistula or a vesicocolic fistula.

Closed injuries

Intraperitoneal rupture typically occurs in a patient who has been drinking alcohol, has a full bladder and is assaulted and kicked in the abdomen. The dome of the bladder ruptures and urine extravasates into the peritoneum, causing intestinal ileus and abdominal distension. Extraperitoneal rupture is usually due to a major road traffic accident in which the pelvis has also been fractured when the bladder is not full, but may follow endoscopic resection of the prostate or a bladder tumour (Fig. 23.11).

Fig. 23.11 Rupture of the bladder.

A Intraperitoneal. B Extraperitoneal.

Clinical features

The ileus and distension that occur with intraperitoneal rupture of the bladder are often detected late because of the circumstances surrounding the injury. However, the patient will be aware of the inability to pass urine and seek advice. Extraperitoneal extravasation of urine, if part of a major accident, adds to what already are severe pelvic injuries. When the leak occurs during an endoscopic procedure, the patient later complains of suprapubic pain with varying degrees of lower abdominal tenderness.

Investigations

Generally, the circumstances of the bladder injury establish the diagnosis. If confirmation of injury is required, water-soluble contrast is injected via a urethral catheter and the bladder examined on the X-ray screen (cystogram).

Management

Intraperitoneal rupture demands laparotomy and repair. Extraperitoneal rupture in the absence of other injuries tends to be managed conservatively through drainage of the bladder with a urethral catheter left in situ for 6–10 days. Occasionally, surgical exploration is required.

Urethra

Open injuries

Penetrating injuries resulting in damage to the anterior or posterior urethra are rare.

Closed injuries

Damage to the anterior urethra is typically due to falling astride a hard object, although a kick can cause a similar injury. The mechanism of injury to the posterior urethra is similar to that of extraperitoneal rupture of the bladder. In the majority of cases, posterior urethral injuries are associated with a fracture of the pubis or fracture-dislocation of the pelvis. Both the posterior urethra and bladder are damaged in 10% of cases.

Clinical features

Anterior urethral injuries are usually located at the bulb, so that the patient presents with a perineal haematoma. If this becomes infected, there may be sloughing of the skin, urethra and even the scrotal tissues. Because of the mechanism of injury, patients with posterior urethral tears are usually shocked and require resuscitation before a detailed assessment can be made. If the patient has passed clear urine, the bladder and urethra are probably intact. If there is blood at the external meatus, urethral injury must be suspected. A distended bladder can occur because of spasm of the urethral sphincter or because of a torn posterior urethra.

Investigations

If the physical signs suggest an anterior urethral injury, and the patient has passed clear urine, no further steps need be taken. If there is blood at the external meatus or the urine is blood-stained, a urethrogram using water-soluble contrast material may demonstrate the extravasation (Fig. 23.12). A catheter should never be passed in the emergency room. If urine is blood-stained, retrograde urethrography may be carried out but the radiological distinction between a rupture of the membranous urethra and an extraperitoneal bladder rupture may be difficult.

Fig. 23.12 Ascending ureterogram in urethral rupture.

Contrast is seen extravasating at the site of the disrupted urethra (arrow).

Management

All patients with an injury to the bulb of the urethra have a perineal haematoma. If the injury is only a contusion, this will resolve, but prophylactic antibiotics are indicated. A large haematoma may require drainage if the urethra has been lacerated. The extent of injury should be defined and the urethra repaired if possible. A urethral or suprapubic catheter drains the bladder. Treatment of a posterior urethral injury depends on the expertise available. It is quite acceptable to perform a suprapubic cystostomy and deal with the injury to the urethra at a later date. If laparotomy is necessary for other reasons, this may give an opportunity to pass a catheter. If the rupture is incomplete, the catheter will act as a splint. If the rupture is complete, the ends of the urethra can be approximated and splinted by the catheter. The late complications of these injuries are stricture and impotence.

Bladder tumours

Pathology

The vast majority of bladder tumours arise from the urothelium or transitional cell lining, which it shares in continuum with the renal pelvis and the proximal urethra. The urothelium is exposed to chemical carcinogens excreted in the urine, such as naphthylamines and benzidine, which were extensively used in the chemical and dye industries in the past. The bladder is more susceptible to urinary carcinogens, as urine is stored in the bladder for relatively long periods of time.

Almost all tumours are transitional cell carcinomas. Squamous carcinoma may occur in urothelium that has undergone metaplasia, usually due to chronic inflammation or irritation caused by a stone or schistosomiasis. An adenocarcinoma is a rarity but may occur in an urachal remnant in the dome of the bladder, or from local infiltration, e.g. bowel cancer. The prevalence of transitional cell carcinoma in the bladder is 45 cases per 100 000, and it is three times more common in men than women. The appearance of a transitional cell tumour ranges from a delicate papillary structure to a solid ulcerating mass. Papillary tumours are less aggressive superficial cancers, whereas those that ulcerate are much more aggressive.

Staging

Biopsy is essential to confirm the diagnosis (cell type), determine the degree of cell differentiation (grade), and assess the depth to which the tumour has penetrated the bladder wall (stage). The TNM system of tumour classification is applicable to bladder tumours. Assessment of the primary tumour (T) is of prime clinical importance and requires bimanual examination under anaesthesia to judge the degree of penetration through the bladder wall. This is especially important for T₂ and T₃ tumours (Fig. 23.13). Clinical examination, urography and CT are used to assess the involvement of regional and juxtaregional lymph nodes (N). Assessment of distant metastases (M) requires clinical examination and CT. Histopathological examination guides the choice of treatment. Biopsy gives accurate information on superficial tumours, but depth of invasion of invasive tumours cannot be assessed precisely as the biopsy does not examine the full thickness of the bladder wall.

Fig. 23.13 T categories of bladder tumour.

(Cis = carcinoma in situ)

Clinical features

More than 80% of patients have haematuria, which is usually painless (Fig. 23.14). It should be assumed that such bleeding is from a tumour until proved otherwise. In women, symptoms of cystitis are so common that occasional bleeding may be thought to be part of an infective problem. Therefore, in cases of haematuria, MSSU is mandatory with further investigation required if no growth is found. In men, symptoms of bladder outflow obstruction are common and may include bleeding. Bleeding at initiation of micturition suggests a prostatic, or urethral, origin. Haematuria throughout micturition suggests either a bladder or upper tract cause. A tumour at the lower end of a ureter or a bladder tumour involving the ureteric orifice may cause obstructive symptoms. However, frank haematuria may be the only presenting symptom. Examination is usually unhelpful. Rectal examination detects only advanced tumours.

Fig. 23.14 Haematuria.

A Microscopic. B Macroscopic.

Investigations

Because upper tract tumours are much less common, they may be overlooked in the presence of an obvious bladder tumour. Both may occur together, and the whole of the urothelium must be examined on the IVU or CTU (Fig. 23.15). If there is any suspicious filling defect in the ureter, a retrograde ureteropyelogram is necessary. In cases of frank haematuria, investigations consist of flexible cystoscopy, peformed under local anaesthesia, and either an ultrasound of the kidneys with an IVU or a CTU. Where a lesion is found within the bladder, cystourethroscopy and examination under anaesthesia are performed (Fig. 23.16). With the patient relaxed under general anaesthesia, the bladder and tumour are examined bimanually to determine the depth of spread. The physical features of the tumour(s) are noted, the normal bladder mucosa is inspected and the tumour is fully resected if possible. If not, biopsies are taken from the tumour and any other suspicious areas.

Fig. 23.15 Filling defect on IVU due to bladder tumour.

Fig. 23.16 Common pathologies of the urinary tract.

Management

Superficial bladder tumours (T_a, T₁)

Ideally these are treated by formal transurethral resection of the blabber tumour (TURBT) down to and including detrusor muscle; however, they can also be treated solely by endoscopic diathermy if required. Intravesical chemotherapy (mitomycin C) is useful to treat multiple low-grade bladder tumours and to reduce recurrence (EBM 23.1). Regular check cystoscopies are required. Recurrences are mostly treated by repeat diathermy or resection but, if they become very frequent and excessive, cystectomy may be advisable. Carcinoma in situ (Cis) may be present in mucosa that appears normal or in association with a proliferative tumour. Cis can also exist as a separate entity, when there may be only a generalized redness (malignant cystitis). Cis should be considered in patients with ongoing irritative urinary symptoms associated with pain or symptoms suggestive of ongoing urinary tract infection, both in the absence of urinary tract infection upon MSSU culture. Untreated patients with Cis have a high risk of progression to invasive cancer. Cis responds well to intravesical bacille Calmette-Guérin (BCG) treatment. However, if there is any doubt about the response, and especially if there is any pathological evidence of progression, more aggressive treatment is warranted.

23.1 Role of intravesical chemotherapy in superficial bladder cancer

‘A single dose of intravesical mitomycin C following transurethral resection of a bladder tumour reduces the risk of subsequent recurrence.’

Tolley DA, et al. J Urol 1996; 155(4):1233–1237.

Invasive bladder tumour (T₂–T_3s)

Management is controversial. For patients under 70 years of age, radical cystectomy is recommended. In older patients, radiotherapy may be a better option. Unfortunately, this may not always cure the tumour and ‘salvage’ cystectomy may be needed. Cystectomy always necessitates urinary diversion. Where the urethra can be retained, it may be possible to construct a new bladder from colon or small bowel (orthotopic bladder replacement), so achieving continence. Alternatively, the urine is collected in an internal reservoir that is connected to the body surface via a continent conduit (ileum or appendix), through which the patient drains the urine at regular intervals with a catheter. In less favourable circumstances, an ileal conduit should be performed (Fig. 23.17). In some countries where an ‘ostomy’ is not acceptable, the ureters can be implanted into the sigmoid colon (ureterosigmoidostomy). However, renal infection and metabolic disturbances are potentially serious complications of this procedure. An invasive T₄ tumour, fixed to the pelvis or surrounding organs, is inoperable and only palliative treatment can be given.

Fig. 23.17 Ileal conduit urinary diversion.

A and B Isolation of segment of terminal ileum. C Fashioning of uretero-ileal anastomosis. The stoma is made to protrude from the skin to minimize skin contact with urine and so reduce irritation.

Prognosis

Outlook depends on tumour stage and grade. Superficial disease carries a much better prognosis with a 5-year survival of 70–90%. Muscle invasive disease has a 5-year survival of 10–60%.

Carcinoma of the prostate

Epidemiology

In the UK, this is the fourth most common malignancy in males, with a prevalence of 50 cases per 100 000 population, and is increasing in frequency. It is the second most common cause of cancer death in men in the UK. The tumour is common in northern Europe and the USA (particularly in the black population), but rare in China and Japan. It rarely occurs before the age of 50 and is uncommon before the age of 60. The mean age at presentation is approximately 70 years. The aetiology is unknown, but genetic, hormonal and possibly viral factors are implicated.

Pathology

Almost all malignant tumours of the prostate are carcinomas with the most common being adenocarcinoma (> 95%). If a prostate is examined by serial section, a small malignant focus is detected in almost all men over the age of 80. Thus, there is a very high prevalence of histological prostate cancer and many men will die with a cancer of the prostate – but not from that cancer. It is estimated that the prevalence of focal histological cancer in men aged 50–75 is approximately 40%, whereas the prevalence of clinical prostate cancer is approximately 8%, one-quarter of whom will die from that cancer. The TNM system is used in classification

Summary Box 23.3 Urothelial tumours

• The urothelium or transitional cell epithelial lining of the urinary tract extends from the renal papilla to the distal urethra

• The incidence of urothelial cancer is increasing, possibly because of increasing exposure to occupational carcinogens, smoking and analgesic abuse

• Almost all urothelial cancers are transitional cell tumours and the vast majority occur in the bladder. Squamous cancers are rarer and are associated with chronic irritation or inflammation (e.g. calculi and schistosomiasis). Adenocarcinomas are extremely rare

• Frank haematuria is present in 80% of cases

• Transitional cell cancers of the bladder are treated as follows:

° Carcinoma in situ (Cis) may respond to intravesical BCG but is unpredictable and may require more aggressive treatment

° Superficial tumours (T_a, T₁) are usually treated by transurethral resection ± intravesical chemotherapy

° Invasive tumours (T₂, T₃) may be best dealt with by radical cystectomy (or by radical radiotherapy)

° Invasive T₄ tumours with fixation to the pelvis or surrounding organs are dealt with by palliative radiotherapy.

(Table 23.2). Metastatic spread to pelvic lymph nodes occurs early. One-third of clinically localized tumours at the time of presentation will have spread to regional nodes. Metastases to bone, mainly the lumbar spine and pelvis, occur in some 10–15% of cases.

Table 23.2 TNM classification of prostate cancer *

T (Tumour)
• T₀

No evidence of primary tumour

• T_X

Primary tumour cannot be assessed

• T₁

Tumour clinically inapparent and not palpable

• T_1a

Incidental finding following TURP in < 5% prostate chips

• T_1b

Incidental finding following TURP in > 5% prostate chips

• T_1c

Prostate cancer detected by prostate biopsy

• T_2a

Palpable nodule involving half of one lobe

• T_2b

Palpable nodule involving one lobe

• T_2c

Palpable nodule involving both lobes

• T_3a

Extracapsular extension of prostate cancer

• T_3b

Prostate cancer involving the seminal vesicles

• T_4a

Prostate cancer involving the bladder neck and/or external sphincter and/or rectum

• T_4b

Prostate cancer involving the lateral pelvic wall N (Nodes)

• N₀

No regional lymph node metastasis

• N_X

Regional lymph nodes cannot be assessed

• N₁

Regional lymph node metastasis M (Metastases)

• M₀

No distant metastasis detected

• M_X

Distant metastasis cannot be assessed

• M_1a

Metastasis to non-regional lymph nodes

• M_1b

Skeletal metastasis present

• M_1c

Metastasis to other sites

(TURP = transurethral resection of the prostate)

* Sobin LH, Wittekind C, eds. TNM classification of malignant tumours, 6th edn. Chichester: John Wiley; 2002.

The Gleeson score is also used to grade prostate adenocarcinoma. Cells are graded 1–5 depending upon their level of differentiation (grade 1 = most differentiated, grade 5 = least or most anaplastic). The pathologist uses the two most common malignant cell types to determine a ‘Gleeson score’; (most common type + second most common type = Gleeson score). Therefore, Gleeson scores range from 2–10 and are always expressed as an equation (e.g. 4 + 3 = 7).

Clinical features

The presentation of patients with prostatic carcinoma is similar to benign prostatic hyperplasia (BPH); one-quarter present with acute retention (Fig. 23.18). Occasionally, the tumour extends posteriorly around the rectum and causes alteration in bowel habit. Presenting symptoms and signs due to metastases are much less common, but include back pain, weight loss, anaemia and renal failure secondary to ureteric obstruction. On rectal examination, the prostate feels nodular and stony hard but many irregular prostates, even those with nodules, are not malignant. Conversely, 50–60% of malignant prostates are not palpably abnormal on rectal examination.

Fig. 23.18 Endoscopic view of prostate.

A Normal. B Obstructed.

Investigations

As most patients present with outflow tract obstruction, ultrasound and serum creatinine determinations are performed to assess the urinary tract. An X-ray of the pelvis or lumbar spine (to investigate backache) may show osteosclerotic metastases as the first evidence of prostatic malignancy. Whenever possible, the diagnosis is confirmed by needle biopsy, usually performed under transrectal ultrasound (TRUS) guidance, or by histological examination of tissue removed at endoscopic resection if this is needed to relieve outflow obstruction. The patient is assessed for distant metastases by a radioisotope scan. Prostate-specific antigen (PSA) is the main serum marker for the detection of prostate cancer. A PSA of < 4.5 is generally regarded as normal although there has been a move to regard < 3.5 as being normal if less than 65 years of age. Metastatic disease is exceptional when the PSA level is < 15, but levels > 100 ng/ml almost always indicate distant bone metastases. PSA is the main test for monitoring response to treatment and disease progression. A bone scan may be carried out at follow-up to localize and define the extent of metastases, whereas CT is useful to assess pelvic lymphadenopathy.

Management

Prostatic cancer is sensitive to endocrine influences (EBM 23.2) as testoterone is a trigger for moving prostate cells through the cell cycle thereby stimulating mitosis. Management is best considered in three clinical groups, as follows.

23.2 Hormone manipulation in prostate cancer

‘Reducing circulating testosterone levels (either by castration or by medication) results in a 70% initial response rate. Additional androgen blockade produces a small increase in survival but with poorer quality of life.’

Huggins C, et al. Cancer Res 1941; 1:293–297. Schmitt B, et al. Cochrane Library, issue 3, 2005. Oxford: Update Software.

Organ confined / localized disease

With increasing use of PSA, a raised value may be the only abnormality that leads to the diagnosis of cancer confirmed by a needle biopsy. A patient with a small focus of well-differentiated carcinoma may be managed by an active surveillance policy, as usually these patients remain unaffected by their prostate cancer for between 10–15 years. In younger patients with a longer life expectancy (i.e. > 10 years), or in patients with a large tumour with a less well-differentiated cell pattern (Gleeson score 7 or more) there is an increased risk of progression. In these cases, treatment with curative intent by either surgery or radiotherapy is suggested. The prostate can be removed laparoscopically, robotically or by the traditional open route. Radiotherapy can be performed by external beam radiotherapy (EBRT) or by the insertion of radioactive seeds in the prostate (brachytherapy). There are no data to support one treatment over the other in terms of overall survival. However, each treatment modality has a different side effect and complication profile. Therefore, the choice of treatment tends to be based upon patient preference. In active surveillance, patients tend to have regular PSA measurements and only undergo treatment if the level rises.

Locally advanced disease; no evidence of bone metastases

This term refers to cases where the prostate cancer has invaded directly outside the prostate but has not metastasized. Surgery does not confer a cure in this situation. However, EBRT along with hormonal therapy has shown some survival benefit. In patients not able to tolerate EBRT, hormone therapy alone or palliative treatment can be considered.

Metastatic prostate cancer

Approximately half of the men diagnosed with prostate cancer will have metastatic disease. The basis of treatment in these cases is castration either physically by androgen depletion (orchiectomy) or chemically, by androgen suppression (gonadotrophin-releasing hormone analogues) and/or androgen receptor antagonists. A small number of patients fail to respond to endocrine treatment; a larger number respond for a year or two, but then suffer disease progression. PSA levels are a useful marker of response, ideally falling to < 0.01 in well controlled cases. Oestrogens are useful but are limited by their thromboembolic effects. Chemotherapy with taxanes has shown a marginal improvement in both symptoms and survival. Radiotherapy is an effective treatment for localized bone pain. For severe generalized bone pain, intravenous ⁸⁹Strontium may give effective palliation, but the basis of treatment remains pain control by analgesia.

Prognosis

The life expectancy of a patient with an incidental finding of focal carcinoma of the prostate is that of the normal population. With tumours localized to the prostate, a 15-year survival rate of 56–87% can be expected; if metastases are present, this falls to < 10%. PSA is a very useful marker to determine response to treatment in addition to monitoring disease progression or recurrence.

Summary Box 23.4 Prostatic cancer

• In the UK this is the second most common cancer in men, presents at a mean age of 70, and is increasing in incidence

• The carcinoma may be incidental (i.e. found on histological examination), clinically apparent (bladder outflow obstruction and a hard craggy prostate) or occult (metastatic disease)

• Metastatic spread may occur early; one-third of clinically confined cancers have spread to lymph nodes, and 10–15% of all new cases have bony spread (to lumbar spine and pelvis)

• Treatment of prostatic cancer varies:

° Incidental or focal cancer. If well differentiated, then life expectancy can be normal with a watch-and-wait policy. If the cancer contains undifferentiated cells, then either radical surgery or radiotherapy is considered

° Localized cancer with no evidence of bony metastases. Treated by either radical surgery or radiotherapy, keeping endocrine therapy in reserve

° Metastatic cancer. Treated by androgen depletion (orchiectomy) or androgen suppression (gonadotrophin releasing hormone analogues)

° Tumours localized to the prostate and amenable to radical curative treatment have a 10-year survival rate of 60–75%.

Benign prostatic hyperplasia

Pathology

From about the age of 40 years, the prostate undergoes enlargement as the result of hyperplasia of periurethral tissue, which forms adenomas in the transitional zone of the prostate. Normal prostatic tissue is compressed to form a surrounding shell or capsule. There is considerable variation in the growth rates of the adenomas and in the proportions of stromal and epithelial tissue. A prostate that has been infected previously or has a preponderance of stromal tissue is firm and fibrous on rectal examination. Adenomas with an epithelial preponderance can grow to form large discrete masses weighing more than 100 g, and have a characteristic rubbery consistency, referred to as benign prostatic hyperplasia (BPH). Enlarging adenomas lengthen and obstruct the prostatic urethra, causing outflow obstruction and detrusor muscle hypertrophy. The muscle bands of the bladder form trabeculae, between which saccules form diverticula (Fig. 23.19). Occasionally, a diverticulum may become quite large, even larger than the bladder. Bladder diverticula empty poorly and are liable to the three main complications of urinary stasis: infection, stones and tumour. With progressive inability to empty the bladder completely (chronic retention), the risk of urinary infection and stone formation increases. Eventually, the residual urine volume may exceed one litre, resulting in progressive obstruction and dilatation of the ureters (hydroureter) and pelvicalyceal system (hydronephrosis). This ultimately leads to obstructive renal failure.

Fig. 23.19 Late sequelae of prostatic obstruction.

Clinical features

Frequency, nocturia, urgency, dysuria and poor stream are common. Straining may cause vessels at the bladder neck to bleed. Clinical features may be due to obstruction (slow stream and hesitancy) and those due to detrusor instability (urgency and urge incontinence). In isolation, the latter symptoms are not an indication for prostatectomy. Increasing frequency may deceive the patient into believing that an adequate amount of urine is passed, whereas the bladder has a small functional capacity and may be almost full all of the time (chronic retention). Frequency may progress to continual dribbling incontinence leading over time to signs and symptoms of obstructive uraemia, including drowsiness, anorexia and personality changes. Urinary infection, cold weather, anticholinergic drugs or excessive alcohol intake can cause sufficient congestion of the bladder neck to provoke acute or acute-on-chronic retention. If the patient has a bladder stone, he may have obstructive symptoms during micturition, and there may also be bladder pain at the end of micturition. Examination reveals little except rubbery, symmetrical and smooth prostatic enlargement, with a median groove between the two lateral ‘lobes’. Asymmetry or a hard consistency raises the suspicion of malignancy. In a patient with acute painful retention of urine, the size of the prostate is more difficult to determine. In patients with chronic retention, the painless, enlarged bladder rises out of the pelvis, almost to the umbilicus. The overlying area will be dull on percussion. In addition, the patient with chronic retention may be ill from obstructive uraemia.

Investigations

A good history and examination are paramount. Further mandatory assessment includes blood for renal function, haemoglobin and electrolytes, urine culture and PSA. Prostatic cancer can occur with normal PSA values (0–4 ng/ml) while BPH can cause elevated values, so careful interpretation is required (Table 23.3). If digital rectal examination raises suspicion, needle biopsy is indicated. Ultrasound can detect bladder diverticula, intravesical stones and measure residual urine volume. A urine flow rate will quantify a reduction in urinary stream. A symptom score sheet will quantify the degree of inconvenience and bother. In some patients, especially the elderly, neurological or pharmacological causes for the changes in micturition must be considered. A pressure-flow urodynamic assessment may be necessary.

Table 23.3 Factors affecting the level of prostate-specific antigen (PSA)

Causes of increase in PSA

• Increase in age

• Acute retention of urine

• Urethral catheterization

• Transurethral resection of the prostate (TURP)

• Prostatitis

• Prostate cancer

• Large benign prostatic hyperplasia

• Prostatic biopsy

Cause of decrease in PSA

• Patient taking a 5-α reductase inhibitor (finasteride, dutasteride)

Management

Patients can be divided into three clinical groups, each requiring a different approach to management.

Symptomatic only

The patient’s assessment of the severity of symptoms is influenced by his age, the social inconvenience caused, and the frequency and progression of symptoms. A young man may be greatly inconvenienced by symptoms that are quite acceptable to one who is elderly. If the exact role of the prostate in causing symptoms is difficult to determine, urodynamic studies may be helpful, especially if the symptoms appear to be irritative rather than obstructive. Initial management should be medical once prostate carcinoma and renal failure are excluded and it is established that the prostate is the principal problem. Alpha-blockers can relax the smooth muscle of the bladder neck and prostatic capsule, and are useful in small prostates; 5α-reductase inhibitors block the intraprostatic conversion of testosterone to dihydrotestosterone, resulting in shrinking of the prostate, and are useful in large glands. Prostatectomy (transurethral or open) is reserved for medical failures.

Acute retention

This condition usually requires emergency admission to hospital. If there is a history of bladder outflow obstruction, conservative measures aimed at encouraging micturition (sedation, a warm bath) only delay the inevitable requirement for catheterization. A self-retaining Foley catheter (size 16 Fr) is passed using strict asepsis and connected to a closed drainage system. If it is not possible to pass a urethral catheter, the bladder is entered directly by puncture with a trocar/cannula (suprapubic cystostomy). A specimen of urine is cultured and, if there is microbiological evidence of an infection, antibiotics are given. If the history of urinary symptoms is short, the catheter can be removed after 12 hours (trial without catheter), following which normal voiding may occur. This is more likely if the patient is given α-blockers (EBM 23.3). If retention recurs, then definitive treatment with TURP is performed.

23.3 Benign prostatic hyperplasia: α-blockers in patients with acute urinary retention

‘Alfuzosin 10 mg/day increases the likelihood of successful trial without catheter (TWOC) in men with a first episode of spontaneous urinary retention.’

McNeill SA, et al. Urology 2005; 65(1):83–90.

Chronic retention

It is essential to determine whether the patient has any complications of obstruction, especially renal damage. Although the upper urinary tracts may be dilated, renal function is not necessarily impaired. If the patient is well, with no haematological or biochemical disturbance, there is no indication for preliminary bladder drainage and prostatectomy may be planned in the usual way. If the patient is uraemic, his general fitness for operation must be assessed. Uraemia alone is not a contraindication to surgery, but hyperkalaemia, dehydration or other evidence of fluid and electrolyte disturbance must be corrected. The bladder is catheterized and prostatectomy is carried out as soon as the patient is fit. Relief of chronic obstruction is almost always followed by a diuresis, due partly to an osmotic (urea) diuresis and partly to renal tubular changes resulting from back pressure. Accurate intake/output fluid charts in addition to daily weights can detect these losses. The blood pressure, both lying and standing, should be monitored and intravenous fluid replacement may be necessary. Medical therapy is contraindicated in patients who present with renal failure secondary to BPH; these patients should be managed either by long-term catheter or TURP.

Open prostatectomy

Open procedures are now reserved for very large adenomas. Apart from the length of hospitalization (7–10 days) and the presence of an abdominal wound, enucleation of smaller adenomas may damage the external sphincter and cause incontinence. This is a particular problem with more fibrous glands and those that contain a focus of cancer.

Closed (endoscopic) prostatectomy

During transurethral resection of the prostate (TURP), the prostate is removed piecemeal by electroresection using a resectoscope. The advantages are patient acceptance, short hospitalization (2–3 days) and the precision of removal of the obstructing tissue. However, serious damage can be inflicted on the prostatic sphincter mechanism by inexpert use of the resectoscope. Prolonged resection can result in excessive absorption of irrigating fluid and electrolyte imbalance (TURP syndrome). Recent alternatives using minimally invasive techniques to TURP include transurethral radiofrequency needle ablation (TUNA), transurethral microwave thermotherapy (TUMT), and transrectal high intensity focused ultrasound (HIFU). The focused energy within the prostate causes coagulative necrosis and subsequent sloughing of prostatic tissue. However, improvement in symptoms is only modest and no long-term outcome data are available. More favourable results are seen with laser prostatectomy but again no long-term follow-up data is available. The different types of laser prostatectomy are: holmium only laser ablation of the prostate (HoLAP), holmium laser resection of the prostate (HoLRP), and holmium laser enucleation of the prostate (HoLEP).

Retrograde ejaculation is a common sequel to any operative procedure on the prostate and all patients should be advised preoperatively of this effect. Any associated bladder stone may be crushed with a lithotriptor or removed by suprapubic lithotomy. After prostatectomy, the bladder must be allowed to drain freely via a urethral catheter while the prostatic bed heals and bleeding stops. After TURP, the catheter is normally removed on the second postoperative day and after an open procedure, the fifth postoperative day. The main postoperative hazard is bleeding. In an open procedure, blood vessels at the bladder neck are sutured but bleeding within the capsule is less easy to control. With TURP, coagulation of the blood vessels is more precise but not always complete. If postoperative bleeding is excessive, clot may lead to obstruction (clot retention). This hazard can be minimized by continuous irrigation through a three-way urethral catheter. The results of all forms of prostatectomy continue to improve, but TURP has the lowest morbidity and mortality (< 1%) and requires a shorter hospital stay (50% less) than other procedures.

Bladder neck obstruction

Occasionally, the obstruction to the outflow tract appears to be at the bladder neck and the prostate is often quite small. The cause may be an infective condition such as prostatitis or schistosomiasis, or a neurological disorder such as diabetes or a prolapsed intervertebral disc. Endoscopic incision or excision of the bladder neck is preferable to long-term drug treatment, but surgery is relatively contraindicated if the risk of retrograde ejaculation and hence infertility is of concern to the patient.

Urethral obstruction

Pathology

Obstruction of the urethra may be congenital, or due to a stricture or malignancy (Fig. 23.20). Foreign bodies, including urinary stones, may also be responsible. The complications include infection with periurethral abscess, fistulation and stone formation. Congenital valves in the posterior urethra occur only in boys. They lie at the level of the verumontanum and may cause gross obstructive changes in the bladder and upper urinary tracts at birth. Increasingly, this diagnosis is being established during pregnancy by ultrasound examination. If the diagnosis is established after birth, it is confirmed by micturating cystourethrography. Treatment consists of endoscopic incision of the valves. Urethral diverticulum is a rare cause of obstruction. More commonly, it is secondary to obstruction and infection in women. Urethral trauma or infection may result in a stricture, the severity of which is related to both the site and the extent of the insult. A posterior urethral stricture following major trauma may be surrounded by dense fibrous tissue, whereas healthy tissues may surround a stricture of the bulb of the urethra. The former requires major reconstructive surgery but urethral dilatation or incision can readily manage the latter. Rough inexpert use of any instrument (including a catheter) in the urethra can cause stricture formation. The principal organism responsible for inflammatory scarring and stricture of the urethra is Neisseria gonorrhoeae. Long-term use of a self-retaining catheter, although not necessarily associated with infection, can also cause an inflammatory reaction in the urethra.

Fig. 23.20 Common sites and causes of urethral stricture.

Clinical features

The diagnosis should be considered if there is a history of urethral infection, instrumentation or trauma. The external meatus must always be examined and, if the foreskin is present, it should be retracted for full inspection. The urethra is palpated. It is still possible for a patient to pass urine, albeit with difficulty, in the presence of a urethral stone.

Investigations

Urinary flow rate will help differentiate urethral strictures from bladder neck and prostatic obstruction, the former giving a uniformly low and prolonged (box-like) pattern (see Fig. 23.5). Post-micturition ultrasound may exclude an increased residual volume. An ascending and descending urethrogram will adequately demonstrate the urethral anatomy. The final investigation to assess a urethral lesion is cystourethroscopy.

Management

Many simple strictures are easily treated by repeated dilatation with metal bougies, or may be incised under direct vision using an urethrotome. Most short strictures in the region of the bulb respond well, but recurrence is common (50%) and operative reconstruction (urethroplasty) may be required. Short strictures can be excised and the healthy urethra re-anastomosed. Longer strictures can be patched with full-thickness skin flaps or buccal mucosal grafts, to restore normal calibre.

Disorders of micturition – incontinence

Overview

Incontinence is defined as the involuntary leakage of urine. It may be due to problems in storage, resulting in urge and stress incontinence or continual incontinence with fistulae, or to problems in emptying, resulting in chronic retention with overflow incontinence. In stress incontinence, leakage occurs because passive bladder pressure exceeds normal urethral pressure. This may be because of poor pelvic floor support, because of a weak urethral sphincter or an element of both. In urge incontinence, leakage usually occurs because detrusor overactivity produces an increase in bladder pressure that overcomes the urethral sphincter. A hypersensitive bladder (sensory urgency) resulting from urinary tract infection (UTI) or bladder stone may also drive urgency in the absence of overactive bladder contractions. Incontinence in these circumstances is less common. Stress incontinence and urge incontinence may coexist (mixed incontinence). All of the above terms, with the exception of a fistula, are descriptive only and do not accurately diagnose the underlying pathophysiology, which can only be determined by urodynamic testing.

Structural disorders

Clinical assessment

Abnormalities of function of the lower urinary tract are notoriously difficult to assess because there is frequently dual underlying pathology. Incontinence in an elderly man may be due to cerebral cortical degeneration, but could also be due to chronic outflow tract obstruction resulting from prostatic hyperplasia. The history is important but may be deceptive and the exact character of the urinary abnormality must be determined so that structural causes can be separated from neurological ones. Details of drug treatment are noted since diuretics and drugs with anticholinergic side-effects may tip the balance when there is already dysfunction. Urine is tested for glycosuria and infection. In addition to intravenous urography, there is now a range of more specific methods for assessing micturition, but not all are required for a diagnosis. They include radiology (cystourethrography), urodynamic studies (uroflowmetry, cystometrography and urethral pressure measurement) and direct inspection (cystourethroscopy and pelvic examination under anaesthesia). A full history and physical examination, with cystourethroscopy and bimanual examination, remain the basic initial investigation of structural disorders.

Structural causes of incontinence in males

Postprostatectomy

Disordered control of micturition occurs in 3–5% of patients after prostatectomy. In this operation, any inadvertent damage to the external sphincter can lead to difficulties with continence. Stress incontinence may occur, but as the damage to the sphincter is usually incomplete, it usually responds to physiotherapy. If not, insertion of an artificial urinary sphincter can be considered.

Chronic outflow obstruction

Changes within the bladder (detrusor hypertrophy) due to chronic obstruction commonly lead to secondary urgency and detrusor overactivity. Relief of obstruction alone is usually sufficient to correct the associated urgency and urge incontinence, but in about 10% of cases the instability is primary and antimuscarinics may be necessary. Chronic retention may also lead to overflow or dribbling incontinence. It must be emphasized that continence requires normal cortical control, and in an elderly patient this may be impaired. Possible abnormalities of both structure and innervation need to be considered in these patients.

Carcinoma of the prostate

Tumour may involve the external sphincter, preventing it from closing. Repeated transurethral resections for recurring obstruction may convert the posterior urethra into a rigid tube so that dribbling incontinence occurs. An indwelling catheter or condom incontinence appliance may be necessary.

Postmicturition dribble incontinence

This is very common, even in relatively young men, and is caused by a small amount of urine becoming trapped in the ‘U-bend’ of the bulbar urethra. This then leaks out passively when the patient moves. The condition is more pronounced if associated with a urethral diverticulum or urethral stricture.

Chronic illness and debility

Especially in the elderly, incontinence may arise from poor tone in the periurethral striated muscle of the pelvic floor and from difficulty in getting to the toilet. This may be worsened by loss of cortical inhibition of micturition.

Structural causes of incontinence in females

Incontinence is more prevalent than generally suspected; approximately 14% of all women have been incontinent at some time, half of them within the last 2 months. This figure rises rapidly in older patients, and reaches 50–70% in geriatric units. Only a proportion of younger women seek advice, either because of embarrassment or because of stoical acceptance of some incontinence as being normal.

Childbirth and operations

Multiparous women commonly lose some of the tone in the pelvic floor muscles with each pregnancy. Symptoms may range from occasional stress incontinence to almost continual dribbling incontinence. Examination shows weakening of the pelvic floor muscles and anterior vaginal wall (cystocoele). It is important to distinguish stress incontinence from urge incontinence. The former responds well to pelvic floor exercises and to surgical procedures designed to support the bladder neck, but the latter should be treated by bladder retraining and drug therapy. Stress incontinence is characterized by an involuntary loss of urine during coughing, laughing, sneezing or any other activity that suddenly raises the intra-abdominal pressure. A cough, however, may stimulate involuntary detrusor contractions (cough-induced detrusor instability), which causes urge incontinence. This differential diagnosis can be made only by urodynamic assessment. In parts of the world where obstetric services are poor, prolonged labour may lead to a vesicovaginal fistula, which presents as continuous dribbling incontinence. The association with delivery is usually clear, but a small fistula may be missed. Investigation of dribbling incontinence must distinguish between urethral damage and a fistula. Treatment consists of closing the fistula through a vaginal or suprapubic approach.

Cystitis

Cystitis is common in women and, in addition to causing frequency, urgency and dysuria, sometimes causes sensory urge incontinence. Treatment of both the infection and the bladder spasm is required. Interstitial cystitis (painful bladder syndrome) is a chronic inflammatory condition that, in addition to causing frequency and dysuria, may also cause urgency and urge incontinence. Treatment is often unsatisfactory. Hydrostatic dilatation may be effective.

Ectopic ureter

Dribbling incontinence in a child should raise the suspicion of an ectopic ureter, in which the lower of the two ureters opens outside the control of the urethral mechanism. The abnormal ureter must be relocated in the bladder.

Cervical cancer

Carcinoma of the cervix or its treatment by radiotherapy may cause vesicovaginal fistula and incontinence.

Neurogenic disorders

Clinical assessment

A full history, including an interview with relatives, is required. Examination must include assessment of the plantar reflexes and the sensation and tone of the anal canal. Glycosuria and urinary infection should be excluded. Urodynamic, radiological and electromyographic studies may all be required.

Aetiology of abnormal micturition

Impaired cortical control

Diseases affecting the frontal lobe can alter the pattern of micturition by increasing or decreasing its frequency, or by affecting the social awareness of incontinence. There may also be failure to inhibit initiation of micturition. The paracentral lobule controls the activity of skeletal muscle, so that lesions in this area may cause sustained pelvic and perineal muscular contraction. It must be remembered that a disorder of micturition may be accentuated by, or may even be due to, the physical inability to prepare for micturition such as poor mobility.

Emotional state

This may affect the postponement of micturition, giving rise to ‘giggle’ incontinence and possibly to enuresis in some patients. Incontinence with epilepsy is also due to a loss of inhibitory control. Excessive sensory stimuli, as with the pain of cystourethritis in women, may cause ‘sensory urge incontinence’.

Drugs

Drugs, including alcohol, may alter cortical control of micturition. Sedatives can affect the postponement phase and precipitate incontinence, especially at night. The intoxicated patient may lack the mental alertness to maintain continence, or may continually suppress the desire to void, leading to prostatic congestion and retention.

Damage to the spinal cord

Two aspects of disease or injury to the spinal cord influence disordered micturition: namely, the level of the disease and the completeness of the damage.

Injury at or below the sacral outflow (S2, 3, 4) may be due to a fracture of the spine at the level of T12 and L1 which damages the conus medullaris, a central prolapsed intervertebral disc leading to cauda equina injury, or to spinal stenosis. The bladder distends without sensation, the external sphincter is weak and little detrusor contraction is seen upon urodynamic assessment. The patient develops retention with overflow, but emptying is possible with abdominal straining or hand pressure.

Injury between the sacral segment and the pontine micturition centres (upper motor neuron lesions) may be due to fractures of the spine; tumours that compress the cord; surgical removal of such a tumour; and diseases of the cord itself, such as multiple sclerosis, transverse myelitis and cervical cord stenosis. If these central connections are disrupted, the patient develops a reflex bladder with impaired or absent cortical control; that is, the bladder loses the coordination imposed by the pontine micturition centre. The detrusor becomes overactive and attempted voiding results in detrusor contraction occurring synchronously with that of the external sphincter (detrusor-sphincter dyssynergia). The net result is poor bladder emptying and the development of a thick, trabeculated bladder wall. The resultant high-pressure bladder will, over time, lead to renal impairment. Usually the central connections are not completely disrupted and there may be some sensation and some cortical inhibition.

Damage to pelvic nerves may occur in the course of surgery, especially when dissection involves the side walls of the pelvis, as in radical dissection of the rectum or the uterus. Similarly, aneurysm surgery may disrupt neural pathways in the pelvis. Diseases affecting the autonomic system, principally diabetes mellitus, also affect the control of micturition. With the loss of sensation and contraction, the bladder becomes atonic, prone to the complication of stasis infection. The external sphincter remains closed by uninhibited tonic contractions, but the internal sphincter is partly open as it, to some extent, depends on detrusor activity.

Primary failure of the detrusor has been described, but it is usually secondary to chronic overdistension. Atonic myogenic bladder is caused by prolonged outlet obstruction and is found in the late stages of bladder decompensation. The most common cause is silent prostatic obstruction, where progressive loss of the desire to void results in overflow incontinence. In women, conscious postponement can lead to a large atonic bladder.

Principles of management

More than one mechanism may account for disordered micturition and urodynamic assessment is mandatory in all patients with a suspected or proven neuropathic bladder.

Neurologically intact patients

Patients with congenital defects or fistulae should have these repaired surgically if possible. If the fistula is malignant or the surrounding tissues are poor because of radiation, urinary diversion is preferable. Stress incontinence in both males and females should be treated initially with pelvic floor exercises. If it persists in males, it is best treated by the insertion of an artificial urinary sphincter. In females, the urethra and bladder neck should be returned to their natural positions and supported by means of colposuspension or a pubovaginal sling. The injection of bulking agents at the bladder neck can improve continence, but remains under evaluation. Urge incontinence should be treated initially by bladder retraining, supplemented by anticholinergic drugs. If this fails, good results can be obtained by intravesical injection of botulinum toxin type A via flexible cystoscopy. Alternatives are insertion of a sacral nerve stimulator device, a detrusor myectomy which typically involves stripping off a substantial proportion of the detrusor muscle (myectomy) or splitting the bladder in half and suturing a strip of small bowel to augment the bladder (clam ileocystoplasty). Patients with atonic bladders are best managed by regular intermittent self-catheterization (ISC).

Neuropathic patients

These patients are prone to urinary infection and renal impairment, and preservation of renal function takes priority. The patient’s overall condition is important and those that are poorly motivated or immobile with poor cognition and hand function are best managed by suprapubic catheterization or urinary diversion. Highly motivated intelligent patients should be treated in much the same way as the neurologically intact, although the results are often less good.

Summary Box 23.5 Micturition

• Micturition requires parasympathetic innervation (S2–S4) of the detrusor, sympathetic innervation (T10–L2) of the bladder neck and proximal urethra, and somatic innervation (S2–S4) of the bladder, pelvic floor and urethra

• Structural causes of disordered micturition in the male include prostatic enlargement, prostatectomy (dribble, stress and urge incontinence) and chronic illness/debility

• Structural causes of disordered micturition in the female include childbirth, surgery, radiotherapy and cystitis (infection, chronic interstitial cystitis and urethral syndrome)

• Neurogenic causes of disordered micturition are:

° impaired cortical control

° alcohol abuse and drugs

° spinal cord damage (at/below T12–L1 – flaccid bladder with overflow; above T12–L1 – overactive bladder with incoordination of urinary sphincter, which results in poor bladder emptying)

° pelvic nerve damage (surgery, diabetic autonomic neuropathy)

° atonic myogenic bladder (prolonged outlet obstruction).

External genitalia

Anatomy

In the male, these comprise the penis, testicles and scrotum; in the female, the mons pubis, labia majora, labia minora and the clitoris (Fig. 23.21).

Fig. 23.21 Anatomy of the external genitalia.

A Female. B Male. C Cross-section through the penis.

The penis consists of three cylinders of erectile tissue. The ventral corpus spongiosum is expanded proximally as the bulb and distally as the glans penis, and transmits the urethra. Two dorsolateral corpora cavernosa attach to each side of the inferior pubic arch as the crura. They form the body of the penis and become embedded in the glans.

The penile skin is hairless, free of fat, and extends over the glans as the prepuce or foreskin. Blood is supplied from the internal pudendal arteries. The scrotum is a thin rugose pouch of skin containing the two testicles. Each testicle is contained within a tough capsule (tunica albuginea) and has the epididymis attached to it posteriorly. This highly coiled tubular structure arises from the rete testis, where some 20 small tubules enter it. This head of epididymis is considerably larger than the lower tail, from which the vas deferens arises to traverse the spermatic cord and finally to open into the prostatic urethra as the ejaculatory duct. The testicle and epididymis are invaginated into the tunica vaginalis, which lies anteriorly, so providing a potential space where a hydrocoele may form. The testicular arteries supply the testes. Venous blood drains along the spermatic cord as the pampiniform plexus. The scrotum drains lymph to the inguinal lymph nodes, and the contents of the scrotum drain along the spermatic cord to nodes in the pelvis and abdomen.

In the female, the mons pubis is the fatty elevation over the pubis from which the labia run backwards, enclosing between them the vestibule into which open the vagina and urethra. The clitoris lies above the urethral opening and is a smaller replica of the penis, with the same erectile tissues.

Physiology

Parasympathetic stimulation leads to erection through the release of nitric oxide, with resultant vasodilatation of the arterioles, increased penile blood flow and passive closure of the venules. After sufficient stimulation, sperm from the epididymis and seminal fluid from the seminal vesicles are emptied into the prostatic urethra. Sympathetic stimulation is responsible for this emission, and also closes the bladder neck to prevent leakage of semen into the bladder. Ejaculation proper is due to rhythmic contraction of the bulbospongiosus muscles expelling the semen out through the urethra.

Circumcision

The foreskin is normally non-retractile for the first few months of life. By the end of the first year, half will retract, but it may be 3–4 years before all do so. Provided the parents are reassured, there is no reason, apart from religious grounds, to remove the foreskin within the first few years of life. In some children, the foreskin remains non-retractile and has to be treated by division of preputial adhesions or by circumcision. Otherwise, secretions collect under the foreskin, leading to infection (balanitis) and narrowing of the orifice (phimosis).

Severe phimosis may obstruct urinary flow and if a poorly retracting foreskin remains retracted, it can act as a tight band and cause engorgement and oedema of the glans (paraphimosis). This demands urgent treatment. It may be possible to compress the glans and draw the foreskin forwards, but if this fails, the tight band must be incised under general anaesthesia. Later, elective circumcision is advocated.

Congenital abnormalities of the penis

Hypospadias

Failure of the embryonic folds to fuse results in abnormal placing of the external urinary meatus on the ventral surface of the penis. The opening may be coronal, penile, scrotal or even perineal. The corpus spongiosum may be scarred and fibrosed, leading to a ventral curvature or chordee of the penis. The aim of treatment is to correct the chordee by excising the fibrosis, and then to construct a new urethral opening in the normal position on the glans. This procedure should be ideally completed before the boy goes to school.

Epispadias

In this condition the external urinary meatus opens on the dorsal surface of the penis. The extent of the malformation varies from an isolated penile abnormality to gross malformation of the bladder and urethra. The mucosa of the bladder and the ureteric orifices may be exposed and form the infraumbilical part of the abdominal wall (exstrophy). The urethra then lies opened out like a gutter. Other associated abnormalities include separation of the symphysis pubis and rectal prolapse. Reconstruction of these deformities is not always successful, and urinary incontinence may remain a major problem and require urinary diversion.

Disorders of erection (impotence)

Impotence may be psychogenic, organic or drug-induced. Psychogenic problems, the most common cause, can usually be established from a careful history that includes details of sexual habits. Organic impotence is associated with diabetes mellitus, neurogenic disorders, major pelvic injury or operations, vascular disease of the pelvic vessels (Leriche’s syndrome), priapism and Peyronie’s disease. Most of these conditions constitute irreversible impotence. Drug-induced impotence occurs with hormonal manipulation for prostatic cancer; some antihypertensive drugs may cause loss of erection or inability to ejaculate, and barbiturates, benzodiazepines, corticosteroids, phenothiazines and spironolactone may affect libido. Medical treatment is by oral sildenafil (Viagra), intracavernosal (self)-injection of papaverine, or prostaglandin E. Vacuum suction devices or a prosthesis implanted into the corpora cavernosa are effective alternatives.

Priapism

This is a painful maintained erection unassociated with sexual desire. It is associated with intracavernosal self-injection for impotence (the most common cause), leukaemia, disorders of coagulation, renal dialysis and sickle-cell trait, and is believed to be due to venous sludging in the corpora cavernosa. (The corpus spongiosum and glans are unaffected.) Aspiration and intracavernosal injections of vasoconstrictors (phenylephrine) may be effective, especially in self-injection cases. If these fail, the creation of a venous shunt within 6–12 hours gives satisfactory results, and the patient can achieve normal erections subsequently. If treatment is delayed or incomplete, the erectile tissue is damaged and the patient will be impotent.

Peyronie’s disease

This is the occurrence of a hard fibrous plaque (or plaques) in the wall of a corpus cavernosum, causing curvature of the penis. The cause is obscure but is possibly related to trauma, leading to the formation of hard scar tissue. In addition to the deformity, the patient complains of pain during intercourse. Various treatments, including cortisone injections, vitamins and radiotherapy, have met with little success. Excision of the plaque and replacement by a dermal patch graft, or excision of a wedge of tissue on the convex (opposite) border of the penis, may be effective.

Carcinoma of the penis

This uncommon tumour has a prevalence of 1.5 cases per 100 000 and is generally attributed to poor hygiene associated with a non-retractile foreskin (Fig. 23.22). It is very rare in circumcised men and almost always occurs in the elderly. The cancer may be a papillary or an ulcerating squamous cell carcinoma. Local spread occurs early and the tumour may ulcerate and fungate. Lymphatic spread to inguinal lymph nodes is common; associated infection may also lead to lymphadenopathy. The patient may present with a purulent or blood-stained discharge. Unfortunately, many patients do not seek help until the lesion is advanced – some only when much of the penis is already destroyed and the inguinal lymph nodes are involved. The diagnosis must be confirmed by biopsy. Circumcision may cure early tumours confined to the prepuce. Early tumours confined to the glans may be treated by excision of the glans and skin grafting. Advanced tumours will require partial or total penile amputation, and often bilateral block dissection of the inguinal lymph nodes. Inoperable tumours are treated by radiotherapy.

Fig. 23.22 Penile carcinoma.

Inflammation of the penis

Inflammation of the glans penis (balanitis) usually also involves the prepuce (posthitis) and is common in children with poorly retractile foreskins. Circumcision usually cures recurrent non-specific balanitis. Balanitis xerotica obliterans (BXO) is the local manifestation of lichen sclerosus et atrophicus of the glans and prepuce. It causes typical white scarring of the prepuce and glans, and may involve the urethral meatus and distal urethra. Meatal stenosis occurs as a result of recurrent infection, trauma or BXO. It may respond to removal of the inflammation (by circumcision) and meatal dilatation; alternatively, it may require meatotomy or meatoplasty.

Undescended testes (cryptorchidism)

Retractile testis

Normally, both testes are in the scrotum by 6 months of age. However, they may be excessively mobile and readily retract towards the external inguinal ring, even into the inguinal canal, especially when the patient is examined in a cold room. Such retractile testes may easily be misdiag-nosed as being incompletely descended. Care must be taken to examine the baby in a warm room or after a bath. True undescended testes are of two types:

1. Incomplete. Such a testis is arrested in its normal pathway to the scrotum. Usually this is within the inguinal canal, more rarely within the abdomen.

2. Ectopic. An ectopic testis has developed normally, but after passing through the external inguinal ring its further descent is impeded. It either remains in the superficial inguinal pouch (common) or is transposed to perineal, femoral or prepubic sites (rare).

Torsion of the testis

Torsion of the cord can occur where the visceral layer of the tunica vaginalis completely covers the testis so that it lies suspended within the parietal layer. The patient, usually a teenager, presents with sudden onset of testicular pain and swelling. There may be a history of minor trauma, or previous episodes of pain due to partial torsion. On examination there is a red, swollen hemiscrotum that is usually too tender to palpate. Misdiagnosis of the swelling as epididymo-orchitis, which is rare in teenagers, is a serious error. Torsion of the testis is a surgical emergency; if the blood supply is not restored within 12 hours, the testis infarcts and must then be excised. If at operation the testis is found to be viable, it is sutured to the parietal tunica to prevent recurrence. As the underlying abnormality of the tunica is bilateral, the other testis must be fixed at the same time.

Testicular tumours

Pathology

Tumours of the testes are uncommon, with a prevalence of 5 cases per 100 000. They most commonly affect men between 20 and 40 years of age. Seminoma and teratoma account for 85%; malignant lymphoma, yolk-sac tumours, interstitial cell tumours and Sertoli cell/mesenchyme tumours make up the remainder. Seminomas arise from seminiferous tubules and are of relatively low-grade malignancy. Metastases occur mainly via the lymphatics and may involve the lungs. Teratoma (non-seminomatous tumour) arises from primitive germinal cells. It may contain cartilage, bone, muscle, fat and a variety of other tissues, and is classified according to the degree of differentiation. Well-differentiated tumours are the least aggressive; at the other extreme, trophoblastic teratoma is highly malignant. Occasionally, teratoma and seminoma occur in the same testis. A history of undescended testis increases the risk of malignancy in the ipsilateral testis. Orchidopexy does not reduce this risk but it does allow the testis to be moved into a position where it allows regular self examination.

Clinical features

The most common presentation is the incidental discovery of a painless testicular lump. The history is often vague, however, and symptoms may be attributed to an injury, or there may be pain and swelling suggesting inflammation. The patient may have wrongly received treatment for ‘acute epididymitis’. Very rarely, patients with teratoma may complain of gynaecomastia. Irrespective of the history, any new painless testicular lump in a young man must be regarded with suspicion. A hydrocoele in a young man also demands investigation, as testicular tumours may be accompanied by blood-stained effusion in the tunica vaginalis.

Investigations

All suspicious scrotal lumps should be imaged by ultrasound, which provides a high degree of accuracy. As soon as a tumour is suspected, and before orchiectomy, serum levels of AFP, β-HCG and LDH should be determined. The levels of these ‘tumour markers’ are increased in extensive disease. Accurate staging is based on CT of the lungs, liver and retroperitoneal area, and an assessment of renal and pulmonary function (Table 23.4).

Table 23.4 Royal Marsden classification for testicular cancer

• Stage 1

Tumour confined to testis

• Stage 2

Tumour spread only to lymph nodes below diaphragm

• Stage 3

Tumour spread only to lymph nodes above and below diaphragm

• Stage 4

Tumour spread to inguinal lymph nodes or distant metastases

Management

Through an inguinal incision the spermatic cord is divided at the internal ring; only then is the testis removed. Radiotherapy is the treatment of choice for early-stage seminoma, as this tumour is very radiosensitive. The management of a teratoma depends on the stage of the disease. Early disease confined to the testes may be managed without further treatment, provided that there is close surveillance for at least 2 years; tumour progression is treated by chemotherapy. More advanced cancers are managed initially by chemotherapy, usually with a combination of bleomycin, etoposide and cisplatin. Retroperitoneal lymph node dissection is now only performed for residual or recurrent nodal masses. AFP, β-HCG and LDH each offer a valuable means of monitoring response to treatment and detecting recurrent disease. These markers should be monitored in all patients with testicular tumours for at least 2 years after they are considered to be tumour-free. CT is used to follow the response of enlarged lymph nodes to treatment.

Prognosis

The 5-year survival rate for patients with seminoma is 90–95%. The more variable prognosis of teratomas depends on tumour type, stage and volume. With more favourable tumours the 5-year survival rate may be as high as 95%, but in more advanced cases 60–70% is more usual.

Summary Box 23.6 Testicular tumours

• In the UK, there are about 1000 new cases of testicular tumour per year and the 20–40-year age group is predominantly affected

• Seminomas and teratomas account for 85% of all testicular tumours

• Seminomas arise from the seminiferous tubules, are of relatively low-grade malignancy, spread mainly via the lymphatic system and are very sensitive to radiotherapy

• Teratomas arise from germinal cells, their differentiation reflects their aggressiveness (well-differentiated tumours being the least aggressive) and they are not radiosensitive

• Treatment consists of radical orchiectomy (with division of the spermatic cord at the level of the deep inguinal ring). Radiotherapy is used if the tumour proves to be a seminoma, whereas chemotherapy (bleomycin, etoposide and cisplatin) is used for teratomas that are advanced or recurrent

• Seminomas have a 5-year survival rate of 90–95%, whereas teratomas have a more varied prognosis (60–95% 5-year survival rate).

Epididymo-orchitis

Acute epididymo-orchitis is usually the appropriate term, as both testis and epididymides are involved in the acute inflammatory reaction. The spermatic cord is also often thickened (funiculitis). After infection has subsided, the epididymis alone may remain thickened and irregular, so that chronic epididymitis may be diagnosed. Thus a late effect of tuberculosis is an irregularly hard (craggy) epididymis. Apparent involvement of the testis alone may be a feature of viral infections such as mumps orchitis. The usual cause of epididymo-orchitis is bacterial spread, either from infected urine or from gonococcal urethritis. The affected side of the scrotum is swollen, inflamed and very tender. In all cases, the urine or urethral discharge must be cultured. Sometimes there is no evidence of a bacterial cause and a viral aetiology is then likely. Treatment consists of antibiotics, analgesia, bed rest and a scrotal support. The choice of antibiotic depends on the results of culture and sensitivity determination of the organism responsible. If there is any doubt about the diagnosis, the testis should be explored. Abscess formation is now rare, but if signs of localization or fluctuation develops, the pus should be drained. Infertility is an important late complication of epididymo-orchitis.

Hydrocoele

This is a common condition, especially in older men, in which fluid collects in the tunica vaginalis, resulting in an enlarged but painless scrotum. The inconvenience of its size usually leads the patient to seek advice. The cause of most hydrocoeles is unknown (idiopathic). The fluid is straw-coloured and protein-rich. In some patients, a hydrocoele develops as a reaction to epididymo-orchitis. Rarely, it may develop with a malignant testis (secondary hydrocoele) and the fluid may then be blood-stained. On examination of the scrotum, a normal spermatic cord can be palpated above a smooth oval swelling. Typically, an idiopathic hydrocoele transilluminates (Fig. 23.23), but where it is long-standing this may be difficult to elicit, owing to fibrosis and thickening of its wall. It is important always to seek this physical sign and also to examine the neck of the scrotum carefully to exclude an inguinal hernia as the cause of the swelling. It may be possible to palpate the testis and confirm that it is normal, but this is unusual as it lies behind and is enveloped by the hydrocoele. If there is any doubt about the diagnosis, then an ultrasound should be performed. Injury to the scrotum may result in a swelling that resembles a hydrocoele but does not transilluminate because the tunica has filled with blood (haematocoele). Aspiration alone does not cure an idiopathic hydrocoele and the tunica soon refills. It is possible to obliterate the sac by injecting a sclerosant after aspiration, but surgical excision and eversion is associated with a much lower recurrence rate. If the hydrocoele fluid becomes infected, incision and drainage of the pus is necessary. Similarly, a haematocoele may require treatment by incision and drainage.