32 Nick Watkin and Asheesh Kaul St George’s Hospital, St George’s University of London, London, UK In this chapter, the common inflammatory disorders of the penis and urethra are discussed. Inflammation of the glans and prepuce (balanoposthitis) is classified as acute or chronic. Acute causes include bacterial and fungal infection and the sexually transmitted infections, herpes, syphilis, and trichomonas vaginalis. The chronic causes include lichen sclerosus, Zoon balanitis, and lichen planus. Urethral infection and trauma can give rise to urethral stricture disease. An in‐depth review of the management of urethral stricture disease, including the various urethroplasty techniques commonly in use, is described. Other urethro‐penile‐scrotal disorders including Fournier’s gangrene, paraphimosis, and genital warts are also discussed. Keywords urethra; penis; stricture; urethral stricture; balanitis; urethroplasty; Fournier’s gangrene; genital warts Inflammation of the urethra can be caused by either infection (Chlamydia trachomatis, Neisseria gonorrhoeae, Escherichia coli, Trichomonas vaginalis, Herpes, Ureaplasma, and Mycoplasma are the most common organisms), autoimmune disorders (i.e. Reiter syndrome, Wegener granulomatosis), or local irritants (i.e. foreign bodies, shower gel and soaps) [1, 2]. Patients commonly present with urethral discharge, dysuria, and pain at the urethral meatus, penile shaft, or perineal pain (prostatitis) [1, 2]. There may be associated urinary symptoms such as frequency, urgency, and a sense of incomplete emptying of the bladder. The condition may occasionally be asymptomatic. A thorough history, including sexual history, should be taken. Examination should look for other sites of possible infection, including kidneys, bladder, prostate, or external genitalia. Chlamydia is the more common organism, followed by N. gonorrhoeae and E. coli. Chlamydia has a long incubation period of 7–21 days. Symptoms usually have a gradual onset and mild. Gonorrhoea has a shorter incubation period of two to seven days, with a sudden onset of more severe symptoms. A urethral swab should be sent for culture and sensitivity. Gram staining and nucleic acid amplification tests (NAAT) by polymerase chain reaction (PCR) or ligase chain reactions can quickly identify the organism [1, 2]. The midstream urine and the first 20 ml of urine are also sent for enzyme immunoassay and culturing. Treatment is with antibiotics based on local guidelines. However, as the most common organisms are Chlamydia followed by Gonococcus, treatment is with dual antibiotics to cover both. For Chlamydia, a single dose of 1.5 g Azithromycin or Doxycycline 100 mg twice a day for 7–14 days is recommended [1, 2]. For Gonococcus, a single dose of Ceftriaxone 1 g, Cefixime 800 mg, or Ciprofloxacin 500 mg [1, 2]. Balanitis is inflammation of the glans penis and is termed balanoposthitis when it also involves the prepuce. Patients present with nonspecific itching and burning of the glans and prepuce with associated discoloration. There are several causes of balanitis that can be broadly classified as acute or chronic. When the presentation is acute, the most likely aetiology is fungal or bacterial infection. Predisposing factors include being uncircumcised (particularly when phimosis is present), poor hygiene, build‐up of smegma, diabetes, and immunosuppression [3]. General advice for all patients is to improve hygiene by retracting the prepuce and washing with warm water daily, using emollient creams, and avoiding soaps, which can cause further irritation. On clinical examination, the glans will appear erythematous, and in severe cases, there may be preputial oedema with discharge and a foul odour. It is recommended to obtain subpreputial cultures in all cases [4]. Ulcerated areas should be swabbed to specifically test for herpes. The main organism implicated in infectious balanitis is Candida albicans, accounting for up to 35% of all cases [5]. The treatment for candida balanitis is topical antifungal cream in the form of 1% clotrimazole or 2% miconazole applied twice daily until symptoms have settled [6, 7]. In severe cases, a single dose of oral fluconazole 150 mg can be given [6]. Bacterial organisms implicated are Streptococcus spp., Staphylococcus aureus, Gardnerella vaginalis, and anaerobes. Treatment of bacterial balanitis is dependent on the organism grown [8]. There are a number of sexually transmitted infections (STIs) that cause balanitis. These include herpes simplex virus (HSV), T. vaginalis, and syphilis. There are two subtypes of HSV (HSV‐1 and HSV‐2). HSV‐1 is currently the most common cause of primary genital herpes in Western countries [4, 9]. HSV‐2 was previously the most common cause of primary genital herpes but is still the form that is more likely to recur [10]. Infection can be primary, nonprimary (i.e. previous infection with a different herpes virus), or recurrent. The patient may be asymptomatic during initial infection. The infection is transmitted by sexual intercourse, especially orogenital contact. It gives rise to little or no illness in around 50% of patients who are infected. The remainder, after a week’s incubation period, develop local burning, itching, urethral discharge, and pain, sometimes with systemic fever and muscle aches resembling influenza. Small groups of 2‐mm red papules appear, form vesicles, and burst, leaving painful ulcers on the prepuce or glans, which scab over and heal but are succeeded by further waves of fresh infection. Headache, neck stiffness, and photophobia signify meningeal infection from which patients recover spontaneously. Infection of the sacral nerve roots may give pain in the thighs and difficulty in voiding. In patients who are immunosuppressed, these symptoms may be much more severe. Female partners of men with genital herpes incur an increased risk of carcinoma of the cervix. Primary infection is likely to cause systemic symptoms in the form of fever and myalgia. After the primary infection, the virus becomes latent in local sensory ganglia and periodically reactivates. Diagnosis of HSV is performed by swab of a lesion, which is then sent for HSV culture or DNA detection by PCR. Initial management includes saline bathing, analgesia, and topical lignocaine 5% ointment [4, 9]. An oral antiviral such as acyclovir 400 mg three times a day is indicated within five days of the start of symptoms and treatment should last five days [9, 11]. Syphilis is caused by the spirochete bacterium Treponema pallidum. It occurs predominantly in white men who have sex with men (MSM) [12]. The bacterium invades the mucosal surface by direct contact [13]. After an incubation period of approximately 21 days, the chancre of primary disease is formed. The classical Hunterian chancre starts as a dull red papule of variable size on the prepuce, glans or coronal sulcus. There may be more than one papule, mimicking herpes. The papule becomes an ulcer, which may become secondarily infected. Typically, there is an enlarged lymph node in the inguinal region. If left untreated, 25% will develop secondary syphilis, which results in a widespread muco‐cutaneous rash and lymphadenopathy. To a lesser degree, hepatitis, glomerulonephritis, and neurological complications can occur [14]. After a latent period of some 20–40 years, tertiary disease occurs consisting of cardiovascular, neurological, and gummatous disease (i.e. granulomatous lesion affecting skin and bone most often) [15]. Diagnosis is by dark ground microscopy or PCR of swabs from a chancre. Serological tests are performed for suspected latent disease. Penicillins are the antibiotic of choice for the treatment of syphilis. T. vaginalis is a flagellated protozoon. It should be considered in a case of balanoposthitis when the female partner has undiagnosed vaginal discharge. The most common presentation is with urethritis and urethral discharge, but this can develop into balanitis [16]. Diagnosis is made by urethral culture or first void urine culture [17]. Treatment is with metronidazole either as a 2 g single dose or 500 mg twice daily for five to seven days [18]. Male genital lichen sclerosus is a chronic inflammatory skin condition affecting the prepuce, glans, and urethra. This condition was originally termed balanitis xerotica obliterans (BXO) by Stuhmer in 1928; however, male genital lichen sclerosus is now the preferred terminology. The overall incidence of disease is difficult to establish because patients may present to various specialities. It is seen at any age, though relatively rare in children. The incidence of a general uncircumcised male population is about 1%, while reported to be as high as 15% in specialist dermatology clinics [19, 20]. The aetiology of disease is unclear and likely multifactorial with autoimmune disease, infection, metabolic disease, and contact with urine all implicated [21]. Histologically, there is a loss of the rete pegs that fix the epidermis to the dermis, so the dermis tends to flake off. There is a thickening of the collagen layer of the dermis into which lymphocytes invade, and this collagen tends to contract so that the skin shrinks. Clinical appearances are initially white flat‐topped plaques. As disease progresses, atrophic and sclerotic white patches (i.e. leukoderma) ensue (Figure 32.1). The most common presenting symptom is male dyspareunia as a consequence of preputial dysfunction [22]. Thickening of the prepuce results in difficulty with retraction (i.e. phimosis) with subsequent splitting, tearing, and bleeding of the prepuce or frenulum. Disease of the glans tends to cause pruritus and paraesthesia. Glanular disease can also extend to the meatus and urethra. Stricturing of the meatus and urethra leads to symptoms of bladder outflow obstruction and urinary retention in severe circumstances [23]. Figure 32.1 Lichen sclerosus. PK Saraswat, A Garg, D Mishra, S Garg, A Study of pattern of nonveneral genital dermatoses of male attending skin OPD at a tertiary care centre. Indian J Sex Transm Dis. 2014 Jul‐Dec; 35(2): 129–34. Conservative management measures include using soap alternatives for washing and the use of barrier creams to avoid contact with urine [24]. In early disease, treatment should begin with daily application of a medium‐strength topical corticosteroid (i.e. clobetasol proprionate 0.05%) for six to eight weeks. If there is a good response, application can reduce to alternate days for up to 16 weeks or a less potent steroid could be used [23]. Surgical management is by circumcision. This is can be curative, not only for disease of the prepuce, but also for the glans in the majority of cases [25]. When disease of the glans does not resolve, a glans‐resurfacing procedure with split‐thickness skin graft may be indicated [25]. Disease extending to the urethral meatus and urethra can be treated by urethroplasty with buccal mucosa. In some cases of severe pan‐urethral stricturing (image), a perineal urethrostomy may be indicated. Zoon balanitis consists of shiny red plaques with speckled areas (cayenne pepper spots) on the inner prepuce and glans that mirror one another (Figure 32.2). It is a disease of unknown aetiology affecting middle aged and elderly uncircumcised men. It is also known as ‘plasma cell balanitis’ because of the classical histological appearance of a band‐like infiltrate of lymphocytes and plasma cells [26]. Patients are often completely asymptomatic but may complain of a small amount of discharge from the affected area. Temporary relief may be gained from the use of topical antibiotic or steroid creams [27]. Definitive treatment is by circumcision, which completely cures the disease [28]. Figure 32.2 Zoon balanitis. PK Saraswat, A Garg, D Mishra, S Garg, A Study of pattern of nonveneral genital dermatoses of male attending skin OPD at a tertiary care centre. Indian J Sex Transm Dis. 2014 Jul‐Dec; 35(2): 129–34. Lichen planus is a chronic inflammatory dermatosis affecting skin, mucous membranes, scalp, and nails [29]. On the penis, these lesions appear as reddish‐purple annular plaques on the glans and coronal sulcus (Figure 32.3) [30]. Approximately 25% of patients with lichen planus have genital lesions [31]. Unlike lichen planus on other body parts, penile lesions are usually not itchy. Treatment is with a potent topical corticosteroid [29]. Figure 32.3 Lichen planus. PK Saraswat, A Garg, D Mishra, S Garg, A Study of pattern of nonveneral genital dermatoses of male attending skin OPD at a tertiary care centre. Indian J Sex Transm Dis. 2014 Jul‐Dec; 35(2): 129–34. Fournier’s gangrene is a fulminant form of infective necrotising fasciitis affecting the external genitalia, perineum, and a perianal region, which commonly affects men, but can also occur in women and children [32]. Baurienne first described necrotising fasciitis of the genital region in 1764 [33]. However, the disease is commonly credited to Parisian venerologist Jean‐Alfred Fournier who, in 1883, described several cases of fulminant gangrene of the penis and scrotum in young men [34]. Sources of infection include the gastrointestinal tract (30–50%), genitourinary tract (20–40%), and cutaneous injury (20%) [35]. There is a strong association with systemic comorbidities with diabetes reported in 20–70% and alcoholism associated with 25–50% of cases [36, 37]. The compromised immunity provides an environment for infection to initiate. Infection is polymicrobial, and it is thought that synergy between these bacteria allows rapid multiplication and spread of infection. The most commonly isolated organisms are E. coli, Klebsiella pneumonia, and S. aureus. The most commonly isolated anaerobe is Bacteroides fragilis [38]. An obliterative endarteritis develops which leads to subcutaneous vascular necrosis and localised ischaemia. Fascial destruction ensues at rates of up to 2–3 cm h−1 [39]. This usually starts in the superficial facial planes of the perineum (Colles fascia) and extends to the scrotum via dartos fascia, penis via Buck fascia, and abdominal wall via Scarpa fascia. Because of the attachments of Colles fascia to the perineal body posteriorly and pubic rami laterally, the extension of disease is limited in these areas [40]. Testicular involvement is rare because of the separate blood supply to the testes. Presentation is usually dramatic with perineal pain and swelling and signs of severe sepsis or septic shock, although an insidious onset is also possible. The systemic signs of infection are often out of proportion with the local disease, which can range from local cellulitis to large areas of necrotic tissue and slough in the scrotum and perineum. Crepitus of the subcutaneous is also a common sign because of the presence of gas forming organisms [38]. Management consists of haemodynamic stabilisation, broad‐spectrum antibiotics, and early surgical debridement. Debridement is often more extensive than first imagined because subcutaneous involvement is greater than cutaneous appearances might suggest. General surgical input may also be required if the source of infection is perianal and a defunctioning stoma is being considered. Subsequent debridement is usually required at an average of 3.5 per patient [41]. It may also be appropriate to involve plastics surgeons at this point to consider approaches for management of large soft‐tissue defects. Options for management of such defects include vacuum‐assisted closure (VAC), skin‐grafting techniques, or a combination of both. Despite advances in management, mortality remains high at 20–30% [42]. Periurethral abscesses can occur in patients undergoing urological procedures, such as cystoscopy and urethral catheterisation, whereby bacteria gain access through Buck’s fascia into the periurethral tissue. More commonly seen in uncontrolled diabetes or in patients who are immunocompromised. It can initially present with a painful lump, urethral discharge if the abscess bursts into the urethra, scrotal swelling if it tracks down, and obstructive urinary symptoms because of mass effect on the urethra. However, if left untreated, Fournier’s gangrene can develop and spread to the perineum, buttocks, and abdominal wall. Treatment is early recognition and incision and drainage of the abscess with debridement of any necrotic tissue. Urinary diversion with a supra pubic catheter might be required. Genital warts are caused by the human papilloma virus (HPV), of which there are more than 100 subtypes. The majority of warts are benign, caused by HPV subtypes 6 and 11. High‐risk subtypes 16 and 18 do not tend to cause warty lesions, but do cause dysplastic lesions and cancers. These high‐risk subtypes of HPV are implicated in penile and cervical cancer. Transmission is most often by sexual contact. Genital warts are classically described as cauliflower‐like lesions that can be single or multiple, affecting any part of the ano‐genital region. On mucosal surfaces, they tend to be soft and fleshy, on hair‐bearing skin firmer and keratinised. Other than the psychological impact of the growth, patients tend to be asymptomatic. Lesions can extend into the urethra resulting in haematuria. A rare subtype of genital wart called giant condyloma acuminatum (GCA) or by its eponymous name – Buschke‐Lowenstein tumour – can grow to a significant size and result in local infiltration and destruction. There are several topical treatments available, including podophyllotoxin, imiquimod, and cryotherapy. Surgical excision is reserved for treatment failure or for large masses such as GCA. Topical therapy with podophyllotoxin cream 0.15% is the first‐line treatment where warts are multiple. Where this fails, imiquimod cream 5% is the second‐line treatment of choice. Where there are single or few warts, cyrotherapy is considered first‐line treatment, with topical therapies second. In patients who are pregnant, podophyllotoxin and imiquimod should not be used [43]. Success rates for monotherapy with podophyllotoxin are 0.15%, imiquimod 5%, and cryotherapy are up to 70, 81, and 92%, respectively [43]. The organism Haemophilus ducreyi causes a large, sloughing ulcer of the penis and prepuce with secondary infection and inflammation of the regional inguinal lymph nodes which often supurate. H. ducreyi is cultured from the exudate. It responds to antibiotics, but the follow up must include tests for unsuspected syphilis. The lesion of granuloma inguinale on the penis produces a shallow painful ulcer with a bright red granulating base from which the typical ‘Donovan bodies’ – Donovania granulomatis in mononuclear cells, can be found in scrapings stained with Giemsa. The urologist is likely to make the diagnosis only in a biopsy. It responds rapidly to tetracyclines. Paraphimosis is a urological emergency, whereby the foreskin fails to protract back to the normal anatomical location. The foreskin becomes oedematous, making protracting it more difficult. In itself, a paraphimosis is not dangerous, however, if the oedema is sufficient enough to constrict the blood supply, then it becomes painful, and if not alleviated within the first few hours, it can lead to avascular necrosis injuries with small areas of ulcerations developing. A tight band can be felt under the glans. If the swelling progresses, the oedema can constrict the blood supply to the glans as well. Treatment is focused on attempting to protract the foreskin from its constricting retracted position just proximal to the glans. Penile block with 10 ml of 0.5% bupivacaine (long‐term effect) mixed with 10 ml of 1 or 2% lignocaine (short‐term effect) can help with the pain and manipulation. Attempt only one of these, and if it fails, a traditional dorsal slit should be made. This is performed by incising the tight band at the 12 o’clock position and then ensuring the foreskin protracts back to its anatomical position with ease. The edges of the foreskin are suture closed. A subsequent circumcision can be organised as a non‐emergency procedure. A urethral stricture is a narrowing in the lumen of the urethra caused by scarring of the corpus spongiosum, which surrounds the urethral epithelium. This process is known as ‘spongiofibrosis’ and only affects the anterior urethra which is surrounded by the corpus spongiosum. A stricture of the posterior urethra is more correctly referred to as ‘contracture’ or ‘stenosis’ and is a consequence of healing caused by scarring and fibrosis, leading to the narrowing of the urethral lumen [45]. The functional effect of urethral narrowing leads to obstruction of the lower urinary tract. It is predominantly a disease of men with a prevalence of 200 per 10 000 men in their 20s, rising to 900 per 100 000 men in their 70s [46, 47]. There are 17 000 hospital admissions annually in the UK at a cost of more than £10 M [46]. The urethra can be divided into anterior and posterior segments. The posterior includes the prostatic urethra and the membranous urethra (i.e. segment passing through the pelvic floor musculature). The anterior includes the bulbar urethra (i.e. segment enveloped by the bulbospongiosus muscle), penile urethra, glanular urethra (passing through the glans), and the urethral meatus (Figure 32.4). Figure 32.4 Normal urethrogram. Case courtesy of Dr Ian Bickle, Radiopaedia.org, rID: 22531. Traditionally, the most common cause for urethral strictures was bacterial urethritis caused by untreated gonorrhoea. Abscesses would form in paraurethral glands and discharge into the surrounding corpus spongiosum (Figure 32.5). Healing by fibrous tissue led to stricture. The sites affected by stricture are those with the largest number of paraurethral glands at the bulb (Figure 32.6). Bacterial urethritis now accounts for 20% of strictures [48]. The majority of urethral strictures are iatrogenic in nature, accounting for approximately 45% [49]. Iatrogenic causes include urethral catheterisation, transurethral procedures, and hypospadias repair. Iatrogenic strictures tend to occur at the junction of the bulbar and penile urethra and are thought to be ischaemic secondary to pressure exerted by the instrument in use. They may also be caused by direct trauma to the urothelium by the instrument. Idiopathic strictures are the next most common, accounting for approximately 30% [48]. In some cases, this may be as a result of unrecognised trauma in childhood, which manifests as a stricture later in life. The short strictures seen in adolescent and young adults may be congenital in nature [50, 51]. Other causes include pelvic fracture and lichen sclerosus. Figure 32.5 (a) Acute gonococcal inflammation of the paraurethral glands bursts out into the corpus spongiosum to produce inflammation (b) which heals by scarring – hence (c) the stricutre. Figure 32.6 Paraurethral glands are most numerous in the terminal centimetre and in the bulb of the urethra. Pelvic fractures tend to cause injury to the posterior urethra by causing distraction injury (i.e. the urethra is pulled apart and heals with scar tissue formation). Other causes of stricture to the posterior urethra include radiotherapy, brachytherapy, and focal therapies for prostate cancer. Symptoms generally start when the urethral calibre falls below 10‐ to 14‐Fr. Once stenosis occurs, infected urine accumulates under pressure upstream of the stenosis and extravasates into the corpus spongiosum. As a result, there is a tendency for the process of scarring and stricture to spread slowly in a retrograde direction (Figure 32.7). The main symptoms of a urethral stricture are those of lower urinary tract obstruction including poor and prolonged stream, incomplete emptying, and urinary frequency. Recurrent urinary tract infections (UTIs) may occur, including cystitis, prostatitis, or epididymo‐orchitis because of incomplete emptying [2]. Visible haematuria results because of the straining to force urine out, causing erosions of the strictured urothelium; patients may develop acute or chronic urinary retention. Obstructed ejaculation suggests stricture. Figure 32.7 Inflammatory stricture tends to creep up the urethra as infected urine is forced into the corpus spongiosum upstream of a stricture. Clinical examination is often unrevealing; however, the glans and prepuce should be inspected for lichen sclerosus (causing meatal stenosis or phimosis). Abdominal examination palpating for a grossly distended bladder. Strictures themselves are often impalpable, but induration may be felt if there is a periurethral abscess. In more severe cases, periurethral abscesses can lead to chronic fistulae, the so‐called ‘watering can perineum’. Figure 32.8 In the extravasation of urine, it is important to make sure that both compartments A and B of Colles fascia are drained. Figure 32.9 An infected paraurethral gland upstream of a stricture may cause an abscess which will discharge, giving rise to a urinary fistula which will persist so long as the stricture persists. After a clinical history and examination, uroflometry should be the first‐line investigation. This can give a typical box‐shaped curve with a sharp rise to maximum flow rate (Qmax), reduced flow rate, and a plateau appearance of the Qmax (Figure 32.10). Ultrasound is useful in assessing for the presence of any urinary retention or hydronephrosis as well as a thick‐walled trabeculated bladder indicating chronic obstruction. Urine dipstick testing can be used to rule out concomitant infection. Figure 32.10 Urethral stricture flow pattern, a ‘flat box‐shaped’ curve. If a urethral stricture is suspected, confirmation of the diagnosis is achieved either by direct visualisation (cystoscopy) or imaging (cystourethrogram). Images are taken in an oblique view to visualise the entire length of the urethra. A urethrogram is performed with the patient lying in a 30° oblique position with the bottom leg flexed. A 12‐Fr catheter is placed into the fossa navicularis and the balloon inflated with 2 ml of water. Up to 30 ml undiluted contrast is injected slowly whilst screening. Once the bladder is adequately distended with contrast, a voiding cystourethrogram can be performed. This investigation gives information on the site and length of stricture as well as the presence of a urethral diverticulum or fistula. Urethrograms are vital to establish a management plan because they can distinguish between, small (Figure 32.11), and long strictures (Figure 32.12), as well as panurethral strictures (Figure 32.13). Figure 32.11 Short penile urethral stricture. Figure 32.12 Bulbar urethral stricture longer than 2 cm. Figure 32.13 Panurethral stricutre. In some cases, cystoscopy can be used to dilate a soft stricture under vision using the scope at the same time as investigating. However, tight or long strictures will always require a urethrogram to gain information about the urethra upstream of the stricture before planning treatment. Never use force to dilate a stricture because one can cause more damage. If the presentation is retention of urine with failure of urethral catheterisation, a suprapubic catheter should be placed, followed by combined antegrade and retrograde urethrogram to assess the stricture. In pelvic fractures, a reconstructed computed tomography (CT) can help assess the fracture and how it relates to the urinary tract; however, a cystogram can easily demonstrate distraction injuries. Most strictures require treatment under general or spinal anaesthesia. The choice between urethrotomy and urethral dilatation is often one of preference of the surgeon, but it is influenced by how tight and how long the stricture is as well as location [47]. Nearly 50% of all strictures recur, but multiple, complex, or long strictures (>2 cm) are even more likely to recur. To treat a penile urethral stricture: To treat a bulbar urethral stricture: ‘The skill of the urologist is measured by his gentleness’ [52]. Urethral dilation has been practiced for thousands of years. Dilation is done to stretch the stricture without causing damage to lead to further scarring. This is evident when significant bleeding occurs which signifies tearing of the stricture. There are a number of instruments that can be used. Historically bougies and sounds have been used to dilate strictures. The term bougie is derived from the word Bujiyah – an Algerian port known for the best wax candles and thin wax tapers were found to make excellent dilators. In the recent history, thin pliable metal bougies – filiforms were used. Using this technique, multiple filiforms could be passed until the true lumen was identified. Then a series of flexible screw on dilators could be deployed, commonly known as ‘followers’ (Figures 32.14 and 32.15). Figure 32.14 The technique of using multiple filiforms. Figure 32.15 Filiform bougies, with flexible or rigid followers. The most common instrument found on cystoscopy sets are Clutton or Lister sounds (Figure 32.16). These are a series of curved metal instruments, sequentially increasing in diameter. These metal instruments were used for ‘sounding’ for bladder stones; hence, the name ‘sound’. Blind dilation with metal sounds should be performed with caution because there is a risk of producing a false passage, particularly with those of smaller diameter. With an easy stricture and a skilled surgeon, this method provided excellent results; however, strictures that were not easy and were often delegated to junior urologists of varying skill had a considerable morbidity [53]. It is often safer to start with a medium‐sized dilator to reduce the risk of this complication. These dilators are also useful in helping to identify the site of a stricture when performing an open reconstruction. The current trend is to perform urethral dilation using hydrophilic‐coated, S‐shaped curved dilators (Figure 32.17). These are inserted over a guidewire, which has been passed into the bladder cystoscopically. This all but negates the risk of causing a false passage and appears to be less traumatic. Figure 32.16 Clutton sounds. Source: From BAUS virtual museum. Figure 32.17 S‐curve dilators. Source: Courtesy of Cook medical. Direct vision internal urethrotomy (DVIU) is an endoscopic procedure. Using normal saline rather than water (in view of the risk of haemolysis if water is extravasated), the stricture is incised with a blade or laser under direct vision (Figure 32.18). Because this is controlled, the stricture is divided rather than torn or shorn, and healing is by re‐epithelializing of the cut surface. Where the urethra proximal to the stricture cannot be seen, a guidewire is passed to direct the incision. Figure 32.18 Internal urethrotomy. The knife or laser must cut right through all the scar tissue. After both dilation and urethrotomy, a catheter is usually placed for at least 24 hours to reduce infective complications associated with extravasation of urine [54]. Once the stricture has been divided or dilated, the patient might require regular intermittent self‐dilation. Following the procedure, cure can be expected in approximately 40–70% of patients [55]. There is no difference in recurrence rates between urethral dilation and DVIU [56]. However, it is safer to dilate a stricture after a transurethral resection of the prostate (TURP) that is near the sphincter to avoid damaging it and leading to incontinence. Once a stricture has recurred, further recurrence is almost inevitable requiring repeat DVIU every two years on average [10]. Many would argue that once a stricture has recurred, the next step in management should be urethroplasty [57]. Urethroplasty is the repair of an injury or defect in the wall of the urethra. The technique used is dependent on several factors. The most important consideration is the site of the stricture. The sites are broadly classified as penile, bulbar, or posterior urethra. The technique used can be classified as follows. The most commonly used graft is buccal mucosa, which can be used for both augmentation and substitution. Buccal mucosa has a pandermal plexus allowing it to be harvested and thinned without interrupting the vasculature [58]. Full‐thickness grafts (including the inner prepuce) contain a separate intradermal and subdermal plexus joined by communicating vessels. They must be treated with more care and kept free from haemolytic streptococcal infection, thus making them more fastidious than buccal mucosal grafts [59]. A pedicled skin flap can be used in a augmentation urethroplasty. This involves the mobilisation of a patch of skin while keeping its blood supply intact. It is not commonly used for bulbar urethral strictures because the adjacent scrotal skin used is hair bearing, which can lead to recurrent infections and stone formation. In this section, we will discuss which urethroplasty technique is most suitable based on the site of the stricture. With regards to the posterior urethra, the management of those caused by pelvic fracture, pelvic fracture urethral injury (PFUI), will be primarily discussed. There are several techniques for the management of bulbar urethral stricture. These are primarily anastomotic or augmentation urethroplasties. The technique used depends on the length of stricture and individual surgeon preference or experience. The initial approach is similar for all bulbar urethral strictures. The stricture can be assessed endoscopically with a 6‐ to 7.5‐Fr semi‐rigid ureteroscopy and a guidewire or 4‐Fr ureteral catheter deployed across the stricture. A perineal midline incision is made. The initial layers of dissection include skin, Campers fascia (fatty tissue), and Colles fascia which is a continuation of Scarpa facia in the abdominal wall. Next the bulbospongiosus muscle with its covering of deep perineal fascia (Gallaudet fascia) will be dissected. The distal extent of the stricture can be assessed by passing a Foley catheter or Clutton’s sound larger than the diameter of the stricture. The urethra can then be mobilised from the corporal bodies as necessary and the sound or catheter used to guide the site of urethral incision. This is the treatment of choice for short strictures of the bulbar urethra such as those caused by a fall astride injury (Figure 32.11). The urethra is mobilised from the corporal bodies, the strictured segment is excised, and the two ends spatulated and anastomosed (Figure 32.19). One must ensure a tension‐free anastomosis and good blood supply is maintained. Long‐term success rates for this procedure are high ranging from 91 to 99% [60–62]. The ideal stricture length for this procedure is generally accepted to be less than 2 cm [61]; however, some recommend a stricture length of no more than 1 cm due to the risk of chordee [63]. Attempts at longer stricture lengths of 2.5–5 cm have shown promise [64]. One common criticism of the anastomotic urethroplasty is the interruption of blood flow within the corpus spongiosum caused by complete transection. This can result in a lack of glans engorgement during erection. Figure 32.19 Excision and end‐to‐end anastomosis. The mobilised urethral ends are spatulated and anastomosed as an ellipse. To minimise disruption to the corpus spongiosum, the nontransecting anastomotic urethroplasty was developed [65, 66]. The bulbar urethra is mobilised and a dorsal stricturotomy made. The strictured segment is excised, leaving the ventral corpus spongiosum intact. The ventral surface of the urethra is anastomosed inside the urethra while the dorsal ends are closed transversely (i.e. stricturoplasty). This approach also allows for the option of an augmentation urethroplasty with a buccal mucosal graft if required. It is not recommended where there is complete obliteration of the lumen [65]. An augmentation urethroplasty is the treatment of choice for longer bulbar urethral strictures (>2 cm), where there is a limited degree of spongiofibrosis and a patent urethral lumen (Figure 32.12). In this procedure, a longitudinal stricturotomy is made, and an ellipse of graft is patched to the incised urethra, thus widening the lumen. The graft of choice is buccal mucosa. Debate remains as to whether dorsal or ventral stricturotomy and patch is preferable. Proponents of the dorsal approach argue that the graft is more secure because it is applied to the tunica albuginea of the corpora cavernosa allowing for better healing and less risk of sacculation. The corpus spongiosum is also thinner dorsally, resulting in less bleeding [67]. Conversely, a ventral incision allows for less mobilisation of the urethra and the corpus spongiosum can be closed over the graft to give support and a rich vascular bed. The ventral approach is also technically less challenging. The success rates are similar for both, 88–89% and 88–89% for dorsal and ventral grafting techniques, respectively [68, 69]. To perform a dorsal patch urethroplasty without mobilisation of the urethra, the transventral dorsal inlay urethroplasty technique was developed in 2001 (i.e. Asopa technique), with an average success rate of 87% [68, 70]. Palminteri took this one step further and performed a combination of dorsal and ventral grafting without mobilisation of the urethra, with an average success rate of 91% [68, 71]. Another technique to limit the amount of mobilisation for the urethra is the lateral onlay urethroplasty first described by Barbagli in 2005 [72]. Only one side of the urethra needs to be mobilised; therefore, blood supply to the corpus spongiosum is maintained on the contralateral side. This also avoids a ventral urethrotomy in the thickest part of the spongiosum, theoretically leading to less intraoperative blood loss. Barbagli described this procedure in six patients with a success rate of 83% at 77 months follow up [71]. Techniques for treatment of penile urethral strictures vary by the type of tissue used: pedicled flap, buccal mucosa, or full‐thickness skin and by whether a single‐stage or two‐staged approach is used. Anastomotic urethroplasty is not suitable in the penile urethra because of the risk of chordee. General considerations include the quality of the native tissue, the length of stricture, and aetiology of disease. For example, a single‐stage pedicled penile skin flap, such as the Orandi flap, is likely to be the best option in a long stricture where there have been no previous attempts at reconstruction and no lichen sclerosus. Where there is evidence of lichen sclerosus, this will undoubtedly recur in a graft made of genital skin. Where there has been previous hypospadias repair, the corpus spongiosum, dartos fascia, and ventral shaft skin are often deficient, and in this situation, a free graft substitution would be more appropriate. The clear benefit of a pedicled penile skin flap is the long length of stricture that can be treated and that it is a single‐stage procedure. As most of the described techniques involve ventral application of the skin flap, they are at risk of sacculation with resulting postvoid dribbling [73] (Figures 32.20 and 32.21). A skin graft may be taken from the prepuce (if available) or the penile shaft. Dissecting in the plane between the dartos muscle and the dermis provides the patch of skin with a vascular pedicle which promotes its survival (Figure 32.21). Once the flap of skin has been mobilised, the strictured segment of uretha is laid open and the skin graft anastomosed to the cut edges. Figure 32.20 For a stenosis some way down from the meatus a dartos‐pedicled patch of penile skin is raised and inserted into the opened up stricture. Figure 32.21 For longer penile strictures a pedicled graft from the shaft of the penis is raised on a dartos pedicle and inserted into the stricture. The skin patch may enlarge to form a pouch; this may take place upstream or downstream of a stenosis (Figure 32.22). Occasionally such a pouch acts as a valve to cause obstruction (Figure 32.23). Other complications include haematoma, skin necrosis, and fistula formation. Long‐term overall stricture free rates of a McAninch single‐stage penile skin flap for anterior urethral stricture are 95, 89, 84, and 79% at 1, 3, 5, and 10 years, respectively [74]. Figure 32.22 A pouch may form upstream or downstream of a restenosis. Figure 32.23 A pouch is apt to form in a skin urethroplasty in the presence of incontinence and can act as a valve to cause obstruction. The urethra is laid open by a ventral incision from the meatus until healthy urethra is encountered. If there is a healthy urethral plate, a single‐stage inlay of graft and closure can be performed. If this is not the case, a graft should be inlaid as a first stage procedure, allowed to mature for four to six months, followed by a second‐stage tubularisation procedure (Figure 32.24). Clearly a single‐stage approach is beneficial to the patient where possible because it avoids long periods of discomfort and disability. Again the most commonly used graft here is buccal mucosa. Full‐thickness grafts from genital skin are again contraindicated in lichen sclerosus. Manoj et al. have used postauricular full‐thickness grafts in 12 patients with lichen sclerosus with a 90% success rate [75]. Figure 32.24 Mature dorsal inlay of buccal graft mobilised and tubularised. It is rare for women to present with urethral strictures, and the urethra can usually be dilated with no need for more formal surgery. Injury to the urethra is associated with 5–25% of pelvic fractures, and these are predominantly injuries to the posterior urethra [76]. It is also more common in men than women due to lack of urethral attachments to the pubis in women [77]. The aetiology of injury is usually an accident involving great force with vehicular collision and fall from a great height as the most common type of accident [78]. The mechanism of injury is stretching of the urethra caused by cephalad movement of the bladder, prostate, and membranous urethra during the trauma. The membranous urethra is firmly attached to the pubis by the perineal membrane. Distal to this, attachments of the urethra are weak, resulting in a distraction defect between the bulbar and membranous urethra. If the dorsal vein ruptures, the resulting haematoma also contributes to the distraction defect. Once maximum elasticity is reached, rupture of the urethra occurs. This rupture, therefore, tends to occur at the bulbomembranous junction. Direct trauma to the urethra by a bony fragment is less common. The cardinal signs of a pelvic fracture urethral injury (PFUI) are blood at the urethral meatus, distended bladder, or inability to void. Where none of these signs are present, an attempt at urethral catheterisation can be made. If any of these signs are present, a urethrogram should be performed. In the acute setting, an ultrasound‐guided suprapubic catheter may need to be placed and urethrogram deferred. If the patient is being taken to theatre for management of other injuries, an on‐table urethrogram can be performed if the patient is stable. While under anaesthetic, an attempt at primary endoscopic realignment and urethral catheter insertion can be made with little risk of morbidity. Ultimately, a suprapubic catheter can always be sited if urethral catheterisation fails. The only indications for immediate exploration are the finding of concomitant injury to the bladder neck, vagina, or rectum and for removal of a bony fragment. When open exploration is performed in these instances, an attempt at urethral realignment can be made. Overall, primary realignment reduces stricture formation in approximately a third of cases [79]. Early open exploration does, however, result in higher rates of incontinence and erectile dysfunction [80]. The vast majority of patients will be managed with suprapubic catheterisation alone and urethroplasty performed after approximately three months once fractures have healed and haematoma resolved. This is currently the treatment gold standard for PFUI to the posterior urethra [81]. Based on the degree of rupture and urethrographic findings, a grading system for PFUI with recommended approaches to management has been devised (Table 32.1). Table 32.1 Grading system for pelvic fracture urethral injury. Delayed urethroplasty consists of excision of a large fibrotic mass and anastomosis between what is left of the bulbar and membranous urethra. Often the defect is quite wide, and extensive mobilisation of the urethra is required. Still the gap may be too wide, resulting excessive tension on the anastomosis. In these cases, adjunctive manoeuvres such as splitting of the crura or infrapubectomy can be used to reduce the distance between the two ends. When the stricture follows undisplaced fracture of the pelvis, the bulbar urethra is mobilised (Figure 32.25). The upper end is found by cutting down on a bougie introduced through the suprapubic cystostomy (Figure 32.26). A wide oval opening is made into the urethra through the scar tissue, and the spatulated bulbar urethra is then anastomosed to it. Figure 32.25 The bulbar urethra is mobilised. Figure 32.26 The upper end of the prostatic urethra is found by cutting down onto a bougie passed down through the suprapubic cystostomy. When the fracture of the pelvis has led to much dislocation of the bones, there is a longer gap between the ends of the urethra. The corpora cavernosa must be separated in the midline and retracted laterally to expose the lower part of the symphysis, which may be unusually broad because of the malunited fracture (Figure 32.27). Figure 32.27 (a) The corpora cavernosa are separated in the midline to (b) reveal the lower edge of the malunited symphysis pubis. After scraping the periosteum from the symphysis, a generous window is cut out from its inferior border (Figure 32.28). An oscillating bone saw is used which does not cut the periosteum on the pelvic surface of the bone. A bougie introduced through the suprapubic cystostomy is now felt through the periosteum (Figure 32.29). An ellipse is cut out from the anterior lower part of the symphysis, and an end‐to‐end anastomosis made after spatulating the urethra. An alternative technique removes the entire symphysis and enwraps the anastomosis in omentum to prevent scar formation. Figure 32.28 (a) The periosteum of the symphysis is incised with diathermy and scraped away. (b) An arch is cut out using an oscillating bone saw. Figure 32.29 (a) Removing the arch of bone reveals the inner layer of periosteum. (b) The inner layer of periosteum is incised onto a bougie passed down the suprapubic track. (c) After spatulating the prostatic and bulbar urethra, they are anastomosed. Erectile dysfunction is a common complication of PFUI, occurring in 34% of all patients, prior to any intervention other than suprapubic catheter placement [82]. The aetiology is primarily neurogenic but may be vasculogenic, associated with pudendal artery injury. There is currently controversy as to whether revascularisation before urethral reconstruction is of benefit. It may reduce the incidence of ischaemic restenosis and reduce long‐term erectile dysfunction [83, 84]. After delayed urethroplasty, the overall re‐stricture rate is less than 10% and the impotence rate approximately 5% [81].
Penis and Urethra Inflammation
Abstract
32.1 Urethral Inflammation
32.1.1 Urethritis
32.1.1.1 Infective Urethritis
32.2 Penile Inflammation
32.2.1 Balanitis
32.2.1.1 Introduction
32.2.1.2 Acute balanitis
32.2.1.2.1 Fungal and Bacterial Infection
32.2.1.2.2 Sexually Transmitted Infections Causing Balanitis
Herpes Simplex Virus
Syphilis
Trichomonas Vaginalis
32.2.1.3 Chronic balanitis
32.2.1.3.1 Lichen Sclerosus
Introduction
Incidence
Aetiology
Presentation
Management
32.2.1.4 Zoon Balanitis
32.2.1.5 Lichen Planus
32.3 Other Urethro‐Peno‐Scrotal Pathologies
32.3.1 Fournier’s Gangrene
32.3.1.1 Introduction
32.3.1.2 Aetiology
32.3.1.3 Pathogenesis
32.3.1.4 Presentation
32.3.1.5 Management
32.3.2 Periurethral Abscess
32.3.3 Condyloma Acuminata (Genital Warts)
32.3.3.1 Aetiology
32.3.3.2 Presentation
32.3.3.3 Treatment
32.3.4 Chancroid
32.3.5 Granuloma Inguinale
32.3.6 Paraphimosis
32.3.6.1 Conservative Measures
32.4 Stricture Disease of the Urethra
32.4.1 Definition and Incidence
32.4.2 Anatomy
32.4.3 Aetiology
32.4.4 Signs and Symptoms
32.4.5 Complications of Urethral Stricture
32.4.6 Investigations
32.4.7 Treatment
32.4.7.1 Urethral Dilation
32.4.7.2 Direct Vision Internal Urethrotomy
32.4.7.3 Urethroplasty
32.4.7.3.1 Introduction
32.4.7.3.2 Urethroplasty for Bulbar Urethral Stricture
The Approach
32.4.7.3.3 Anastomotic Urethroplasty
32.4.7.3.4 Nontransecting Anastomotic Urethroplasty
32.4.7.3.5 Augmentation Urethroplasty
32.4.7.4 Penile Urethra
32.4.7.4.1 Pedicled or Island Patch Urethroplasty
32.4.7.4.2 Free Graft Urethroplasty
32.4.8 Female Urethral Stricture
32.5 Pelvic Fracture Urethral Injury
32.5.1 Incidence
32.5.2 Aetiology
32.5.3 Mechanism
32.5.4 Assessment and Acute Management
Grade
Description
Appearance
Management
I
Stretch injury
Elongation of the urethra without extravasation
No treatment required
II
Contusion
Blood at the urethral meatus; no extravasation on urethrography
Grades II and III can be managed conservatively with suprapubic cystostomy or urethral catheterization
III
Partial disruption
Extravasation of contrast at injury site with contrast visualised in proximal urethra or bladder.
IV
Complete disruption
Extravasation of contrast at injury site without contrast visualised in proximal urethra or bladder.
Suprapubic cystostomy and delayed repair or primary endoscopic realignment in selected patients delayed repair
V
Complete or partial disruption of posterior urethra with associated tear of the bladder neck, rectum, or vagina
Extravasation of contrast at urethral injury site presence of blood in the vaginal introitus in women. Extravasation of contrast at bladder neck during suprapubic cystography rectal or vaginal filling with contrast material
Primary open repair
32.5.5 Surgical Considerations
32.5.6 Complications
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