: if the patient is systemically well, use an oral . : urethral, suprapubic, or in-and-out catheter. BACTERIAL PROSTATITIS 211 Complications Prostatic abscess Failure to respond to treatment (i.e. persistent symptoms a nd fever while on appropriate antibiotic therapy) suggests the development of a pros- tatic abscess. The majority are due to E. coli infection. Risk factors include diabetes mellitus , immunocompromise, renal failure, transurethral instru- mentation, and urethral catheteriz ation. Rectal examination demonstrates a tender, boggy-feeling prostate or an area of \202 uctuance. A transrectal USS or CT scan (if the former proves too painful) is the best way of diagnosing a prostatic abscess. Transurethral resection or deroo \201 ng of the abs cess is the optimal treatment. Alternatively, percutaneous drainage may be attempted. Chronic bacterial prostatitis De \201 ned as bacterial prostatitis where symptoms persist for \211 3 months. Caused by recurrent UTI. Chronic episodes of pain, voiding dysfunction, and ejaculatory problems may be a feature. Assessment Enquire about factors that may be contributing to infection: urinary symp- toms, history of renal tract stones, symptoms suggesting a colovesical \201 s- tula in at-risk patients (pneumaturia, history of diverticular disease, pelvic surgery, or radiotherapy). DRE may reveal a tender, enlarged, and boggy prostate. Investigation - - - - - - 9 cytology. Urinalysis, urine culture Segmented urine cultures (see Semen culture. Urethral swabs (to e xclude Flow rate and Individualized further investigation as indicated (e.g. renal tract im aging to identify stones). b p. 208). STI). PVR urine measurement. Treatment - Prescribe a 2-week course of antibiotics ( \202 uoroquinolone or trimethoprim)* and then r eassess. If initial cultures are positive or the patient has reported positive effects from the treatment, antibiotics can be continued for a total course of 4 \200\2236 weeks. A- adrenoceptor blockers may provide some bene \201 t. They act on the prostate and bladder n eck A-receptors, causing smooth muscle relaxation, improved urinary \202 ow, and reduced intraprostatic ductal re \202 ux. The use of \202 uoroquinolones is restricted in many hospitals due to the risk of Clostri dium dif \201 cile infection. Hospitals now have their own antibiotic protocols for most i nfections, or alternative- ly, discuss with your local microbiologist. Alternative antibiot ics include trimethoprim which has good prostatic penetration. However, trimethoprim has no activity against Pseudomonas, some Enterococci, and some Enterobacteriaceae. CHAPTER 6 Infections and in \202 ammatory conditions 212 Chronic pelvic pain syndrome Chronic prostatitis / chronic pelvic pain syndrome (CP/ CPPS) Refers to abacterial prostatitis (i.e. in \202 ammatory (IIIA) and non-in \202 am- matory (IIIB) types of prostatitis). Also referred to as \200\230prostate pain syn- drome \200 \231. The etiology and pathophysiology is unknown. Presentation (cid:116)- 3 months of localized pelvic pain (prostate/perineum, suprapubic, penile, groin, external genitalia, lower back). Pain with ejaculation. LUTS May be associat ed with erectile dysfunction. Symptoms can be dif \201 cult to treat. They can recur over time and severely affect the patient \200\231s quality of life. Younger men have a higher r isk of suffering severe symptoms. - - (dysuria, frequency, urgency, poor \202 ow). Basic evaluation - History, including enquiry into associated disorders and psychosocial assessment. Physical exam, pelvic \202 oor assessment (including tenderness), and DRE. NIH-CPSI Prostatitis Sy mptom Index). This scores three main symptom areas: pain (location, frequency, severity), v oiding (obstructive and irritative symptoms), and impact on quality of life. Uro \202 owme try and Segmented urine cultures and not reveal leucocytes, but for the diagnosis, EPS and post-prostatic massage urine (VB3) cultures should not identify any bacteria. questionnaire (National Institute of Health Chronic PVR urine volume. EPS. These specimens may or may Further evaluation (where clinically indicated) - - - - - Semen analysis and culture. Urethral swab for culture (to exclude Urine cytology (if suspic ion of bladder malignancy). Urodynamics (to investigate voiding dysfunction). Cystoscopy (i f suspicion of urethral stricture, pathology). TRUS PSA STI). BOO, or bladder Treatment Some groups of patients will bene \201 t more from speci \201 c therapies than others. Patients require a multimodal approach to treatment, guided by their main clinical features.1 Options include: - Conservative therapy stress reduction, psychotherapy, focused pelvic physiotherapy for tend erness of skeletal muscles, gentle exercise, avoid aggravating factors (i.e. certain foods or activities). : counseling, biofeedback, education, anxiety/ - adrenoceptor blockers: most useful for those with associated voiding symptoms and in newly diagnosed disease. CHRONIC PELVIC PAIN SYNDROME 213 Antibiotics diagnosis of in \202 ammatory CPPS (i.e. cipro \202 oxacin, levo \202 oxacin for 4 \200\2236 weeks). Antibiotics do not appear effective for longstanding, refractory d isease. Anti-in \202 ammatory drugs : some bene \201 t in patients presenting early with a new 5- -reductase inhibitors: anti-androgens (i.e. \201 nasteride, dutasteride) have the ab ility to reduce prostatic glandular tissue and improve intraductal re \202 ux and symptoms in selected cases. Phytotherapies and anti-in \202 ammatory properties); Cernilton (polle n abstract). Pentosan polysulphate sodium ( Analgesics Neuromodulatory therapies (pregabali n) \200\224shown to improve mean NIH-CPSI and pain scores. Muscle relaxants Prostatic massa ge therapy Local heat therapy : NSAIDs (i.e. ibuprofen). : Quercetin (polyphenolic bio \202 avonoid with antioxidant - PPS). : opioids may be trialed in collaboration with the pain team. : amitriptyline, gabapentinoid : diazepam. : 2/3 times per week for 6 weeks with antibiotic If no pathology is identi \201 ed and there is no response to initial treatments, referral to the pain team is advised. 1 Nickel JC, Shoskes DA (2010) Phenotypic approach to the management of the chronic prostat itis/chronic pelvic pain syndrome. BJU Int 106:1252 \200\22363. CHAPTER 6 Infections and in \202 ammatory conditions 214 Bladder pain syndrome (BPS) A chronic and debilitating disorder characterized by urinary fr equency, urgency, nocturia, and bladder and pelvic pain. It remains a diagnosis of exclusio n after all other causes for the symptoms have been ruled out (Table 6.5). The \200\230cla ssic \200\231 form is associated with bladder ulceration (Hunner \200\231s ulcers) and dest ructive in \202 ammation, with some developing a small-capacity \201 brotic bladder or u pper urinary tract out \202 ow obstruction. \200\230Non-ulcer \200\231 forms do not show the same progression. De \201 nitions Terminology has changed a number of times. It was formally known as inters titial cystitis (IC). The ICS, the European Society for the Study of Bladder Pain Syndrome/ Interstitial Cystitis (ESSIC), and the EAU use the term \200\230BPS \200\231.1,2 The AUA u se the term \200\230IC/BPS \200\231.2,3 ESSIC: \200\230chronic (>6 months) pelvic pain, pressure, or discomfort perceived to be re lated to the urinary bladder, accompanied by at least one other urinary symptom such as per sistent urge to void or frequency \200\231. 1,2 AUA: \200\230an unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with LUTS >6 weeks, in the absence of infection or other identi \201 able causes \200\231.2,3 Epidemiology Predominantly affects females (female : male ratio is >5:1). Reported prev- al ence varies widely, but is estimated to be 300 per 100 000 women and 30 \200\22360 per 100 000 men.2 Associated disorders Irritable bowel syndrome, allergies, \201 bromyalgia, chronic fatigu e syndrome, focal vulvitis, Sj gren \200\231s syndrome, in \202 ammatory bowel disease. Etiology BPS is now considered a generalized somatic disorder with multifactorial contribut ing factors, including: - Mast cells detrusor, blood vessels, nerves, and lymphatics. Activated mast cells release hi stamine, causing pain, hyperaemia, and \201 brosis in tissues. C- \201 bre activation De fective bladder epithelium urine constituents (including potassium) to leak past the lumina l surface, causing in \202 ammation in muscle layers. Neurogenic mechanisms causes release of neuropeptides, resulting in neurogenic in \202 ammation. : excessive sympathetic Re \202 ex sympathetic dystrophy of the bladder activity. Bladder autoimmune response Urin ary toxins or allergens : frequently associated with the BPS bladder, located around and substance P release. : an abnormal GAG layer may allow : abnormal activation of sensory nerves BLADDER PAIN SYNDROME (BPS) 215 Urine antiproliferative factor ( It inhibits bladder cell propagation and may predispose su sceptible individuals to BPS following other bladder insults. APF): is made by bladder urothelium. Presentation Urinary frequency, urgency and nocturia with associated suprapubic pain, press ure or discomfort related to bladder \201 lling (and typically relieved by bladder emptyi ng). Patients often describe pelvic pain (urethra, vagina, vulva, rectum) and pain in the l ower abdomen and back. Evaluation The \201 rst priority is to exclude other causes for symptoms (Table 6.5). - - - - - History . Focused physical examination Frequency \200\223volume chart Urinalysis and ur ine culture O \200\231Leary \200\223Sant Symptom Index symptoms and effectiveness of treatm ents. (treat any infection and reassess). is useful in assessing baseline Further investigations (if clinically indicated): - - - . Urine cytology Urodynamics . Cystoscopy malignancy. Bladder biopsy is only indicated to r ule out other pathologies. Around 10% of patients may have Hunner \200\231s ulcers, seen as pink or red areas on the bladder mucosa, often associated with small vessels radiating tow ards a central scar, occasionally covered by \201 brin deposit or clot. The scar ruptures with increasing bladder distension, producing \200\230waterfall \200\231 type bleeding. I t is clinically signi \201 cant as it is directly related to symptoms of pain and sensory urgency and destruction of the lesion can provide symptomatic relief. Low-pressure hydrodis tension is distended twice (to around 80cmH2O for 1 \200\2232min) and then reinspected for diffuse glomerulations (petechiae); >10 per quadrant in three of four bladder quadrants pre viously being described as diagnostic. Hydrodistension can have some therapeutic bene \201 t, but it is now thought that neither the presence nor severity of post- distension glomer ulations correlates with any of the primary symptoms of BPS. It is still used to help class ify disease.1 : indicated for investigation of haematuria and to exclude : under anesthesia, the bladder First-line treatment There should be a multidisciplinary team approach throughout from phys icians, dieticians, physiotherapists, pain specialists, psychologists, and patient support groups. - Patient education and support pelvic \202 oor relaxation techniques (avoid pelvic \202 oor exercises), referral to the pain team. Avoid triggers individual to the patient (i.e. c offee, citrus fruits). Aims are to optimize the quality of life and encourage realistic pat ient expectations. : bladder training, stress management, CHAPTER 6 Infections and in \202 ammatory conditions 216 Multimodal pain management potency NSAIDs), progressing to more potent forms if no bene \201 t. Opiates may be used when all other reasonable treatments have been tried and failed . Pain control should be reassessed throughout treatment, with input from specialist pain c linics. : initially use simple analgesia (low Second-line treatment - Oral medications antihistamine, and sedative effects; pentosan polysulphate is an anti- in \202 ammatory synthetic GAG analog; cimetidine (H2 histamine receptor anatagonist); hydrox yzine (H1 antagonist); gabapentin (antiepileptic used as an adjuvant in pain disorders). Tr y one drug at a time. Stop ineffective treatments and try an alternative. If there is only moderate improvement with one drug, add an adjuvant therapy. Repeated intravesical drug ins tallation (alkalinized) lignocaine; heparin. Sodium hyaluronate and pentosan polysulphate b oth repair the GAG layer (the potassium sensitivity test can help to predict the response t o GAG treatment). Instillation of lignocaine and dexamethsone can be given by electromotive drug administration (EMDA) which enhances drug penetration across the urothelium. : tricyclics (amitriptyline) have anticholinergic, : dimethyl sulphoxide (DMSO); Third-line treatment - Surgery Hunner \200\231s ulcers, bladder hydrodistension. : transurethral resection, laser coagulation or diathermy of Fourth-line treatment - - - - Sacral nerve neuromodulation . Botulinum toxin A injection Oral cyclosporine A . Reconstruc tion cystectomy. This can be considered earlier in the treatment strategy for end-stage, sm all \201 brotic bladders. Augmentation cystoplasty can be used for small capacity bladder s due to classical Hunner \200\231s ulcer disease, with complete relief of pain in 63% and improvement in 25%. However, warn patients that they may experience recurrence of pain in t heir augmented bladder or continent diversion (neobladder). into the bladder. : urinary diversion (ileal conduit) with or without Of note, it is recommended that patients are not given: long-term antibi- otics in the abse nce of proven infection or effectiveness; intravesical BCG; intravesical resiniferatoxin; h igh-pressure, long duration hydrodistension; or long-term oral glucocorticoids. BLADDER PAIN SYNDROME (BPS) 217 Table 6.5 NIDDK diagnostic criteria for \200\230interstitial cystitis \200\2314 Diagnostic criteria 1. Cystoscopic evidence of Hunner \200\231s ulcer Positive factors (supporting diagnosis) 1. Pain on bladder \201 lling, relieved by emptying 2. Pain (suprapubic, pelvic, urethral , vaginal, or perineal) 3. Glomerulations on cystoscopy 4. Decreased compliance on urodynamics Exclusion criteria 1. <18y old (controversial \200\224 children can be affected) 2. Benign or malignant bladder tumors 3. Radiation cystitis 4. Tuberculous cystitis 5. Bact erial cystitis 6. Vaginitis 7. Cyclophosphamide cystitis 8. Symptomatic urethral diverticul um 9. Uterine, cervical, vaginal, or urethral cancer 10. Active herpes 11. Bladder or lower ureteral calculi 12. Daytime frequency <5 times in 12h 13. Nocturia <2 times 14. Symptoms relieved by antibiotics, urinary antiseptics and analgesics, e.g. phenazopyridine hydrochloride 15. Duration <12 months (de \201 nitions now suggest shorter durations of >6 weeks are ass ociated with BPS) 16. Involuntary bladder contractions (on urodynamics) 17. Bladder capacity >400 mL (absence of sensory urgency) NIDDK: National Institute of Diabetes and Digestive and Kidney Diseases. Of note, it is rec ommended that these criteria are only used within the context of clinical trials as they ar e felt to be too restrictive for clinical use. 1 Van De Merwe J, Nordling J, Bouchelouche K, et al. (2008) Diagnostic criteria, classi \201 cation and nonmenclature for painful bladder syndrome/interstitial cystitis: An ESSIC proposal. Eur Urol 53:60 \200\2237. 2 Hanno P, Lin A, Nordling J, et al. (2010) Bladder Pain Syndrome International Consultatio n on Incontinence. Neurourol Urodyn 29:191 \200\2238. 3 Hanno PM, Burks DA, Clemens JQ, et al. (2011) AUA guidelines for the diagnosis and treatm ent of interstitial cystitis/bladder pain syndrome. J Urol 185:2162 \200\22370. 4 Gillenwater JY, Wein AJ (1988) Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis, National Institutes of Hea lth, Bethesda, Maryland, August 28-29,1987. J Urol 140:203 \200\2236. CHAPTER 6 Infections and in \202 ammatory conditions 218 Urological problems from ketamine misuse Ketamine is a sedative and an analgesic used clini cally for the induction and maintenance of anesthesia. Increasingly, it is being misused as a rec- reational drug (its class C status is under review). It is a non-competitive N-meth yl-D-aspartate receptor antagonist, excreted with its metabolites into the urine. It has ha llucinogenic effects, producing an out-of-body experience known as the \200\230K-hole \200 \231. Pathology In \202 ammation of bladder epithelium, denuding of urothelium, and neo- vascula rization and petechial hemorrhage of the bladder are reported.1 Histologically, it may mimi c the characteristics of carcinoma in situ.2 The exact mechanism of damage is not known. Th eories include a direct toxic effect of ketamine and its metabolites on the genitourinary t ract, microv- ascular reactions and damage, and autoimmune processes.5 Presentation - Lower urinary tract phenomenon, comprising severe urinary frequency, urgency, urge incontin ence, dysuria, and painful haematuria. Bladder emptying and urinary \202 ow rates appear unaffected. Upper urinary tract to ureteric transmural in \202 ammation and stricture form ation, VUR, papillary necrosis, and renal failure. : ketamine-induced cystitis is a recognized : unilateral and bilateral hydronephrosis secondary An association of these symptoms with hepatic dysfunction is reported.3 Assessment A full history of urinary symptoms and recreational drug use is essential, inclu ding doses and duration of use, as they impact on prognosis. Patients often use other subst ances at the same time. Investigation - - Renal function ( MSU of UTI. Urodynamics: demonstrated detrusor overactivity and reduced bl adder compliance. U & E; GFR). dipstick 9 microscopy and culture to detect and guide treatment CT- - urogram: to assess for upper urinary tract involvement. Cystoscopy and biopsy: clearly document any pathology (i.e. denuded urothelium) and measure bladder capacity. Treatment - Patients must be strongly encouraged to stop using ketamine. Taking the drug >3 times per w eek is associated with signi \201 cantly lower voided volumes.4 Pelvic pain, urgency, and frequency are reported to be signi \201 cantly higher for ketamine use for >24 months, com pared to use for short durations.4 Symptoms scores improve, directly related to UROLOGICAL PROBLEMS FROM KETAMINE MISUSE 219 the length of abstinence from the drug,4 and early functional changes have the potential to normalize after 1y of ketamine cessation.4 Reduced bene \201 t from abstinence is seen if ketamine is used at higher frequencies or for longer durations. Symptoms can persist for u p to 1y after stopping. Analgesia to control the symptoms. Pain control strategies that hav e been described include buprenorphine patches, co-codamol, and amitriptyline.3 Symptoms ar e often refractory to treatment with antibiotics, anticholinergics, and NSAIDs. Local suppo rt from drug and addiction services. Where indicated, nephrostomy or ureteric stents to pre serve renal function until de \201 nitive surgical correction of ureteric stricture. Surge ry is undertaken for refractory end-stage disease. Techniques include cystectomy (9 reconst ruction with neobladder)3 or substitution cystoplasty to increase bladder capacity. These p rocedures should be reserved for patients who have abstained from ketamine use. 1 Chu PS, Ma WK, Wong J, et al. (2008) The destruction of the lower urinary tract by ketami ne abuse: a new syndrome? BJU Int 2008;102:1616-22. 2 Oxley JD, Cottrell AM, Adams S, et al. (2009) Ketamine cystitis is a mimic of carcinoma i n situ. Histopathology 55:705 \200\2238. 3 Wood D, Cottrell A, Baker S, et al. (2011) Recreational ketamine: from pleasure to pain. BJU Int 107:1881 \200\2234. 4 Mak SK, Chan MT, Bower WF, et al. (2011) Lower urinary tract changes in young adults usin g ketamine. J Urol 186:610 \200\2234. CHAPTER 6 Infections and in \202 ammatory conditions 220 Genitourinary tuberculosis Tuberculosis (TB) of the genitourinary tract is caused by Mycoba cterium (M.) tuberculosis. TB was formerly predominantly seen in Asian popula- tions, but i s now seen with increasing incidence in those from other ethnic groups and immunocompromise d patients (i.e. with HIV infection). It has a higher incidence in males than females. Pathogenesis Primary TB: the primary granulomatous lesion forms in the mid to upper zone of the lung. It consists of a central area of caseation surrounded by epitheloid and Langhans \200\231 giant cells, accompanied by caseous lesions in the regional lymph nodes. There is early spread of bacilli via the bloodstream to the genitourinary tract, but immunity rapid ly develops and the infection remains quiescent. Acute diffuse systemic dissemination of tu bercle bacilli can result in symptomatic miliary TB. Post-primary TB: reactivation of infection is triggered by immune com- promise (including H IV). It is at this point that patients develop clinical manifestations. Effects on the genitourinary tract - Kidney : the most common site of extrapulmonary TB. Haematogenous spread causes granuloma f ormation in the renal cortex, associated with caseous necrosis of the renal papillae and de formity of the calyces, leading to the release of bacilli into the urine. This is followed by healing \201 brosis and calci \201 cation, which causes destruction of the renal arch itecture, resulting in a small, distorted kidney. In severe cases, this ultimately results in autonephrectomy. Ureters formation (VUJ, PUJ, and mid-ureteric) and ureteritis cystica. VUR may develop due to distortion of the ureteric ori \201 ces. Bladder TB can be caused b y intravesical Bacillus Calmette \200\223Gu rin (BCG), the treatment given for bladder can cer. The bladder wall becomes oedematous, red, and in \202 amed, with ulceration and tuber cles (yellow lesions with a red halo). Disease progression causes \201 brosis and contrac tion (resulting in a small capacity \200\230thimble \200\231 bladder), obstruction, calci \201 cation, and \201 stula formation. Prostate and seminal vesicles cavitation and calc i \201 cation, with palpable, hard-feeling structures. Fistulae may form to the rectum or perineum. Epididymis spread. Features include a \200\230beaded \200\231 cord which may be tender or asymptomatic and is usually unilateral. Complications include abscess, spread of infection to the testis, and infertility. Fallopian tubes with infertility, pelvic pain, ma ss, or abnormal bleeding. Penis : rare manifestation transmitted from sexual contact or loc al contamination, resulting in ulceration of the glans or a penile nodule. Biopsy con \201 rms the diagnosis. : spread is directly from the kidney and can result in stricture : usually secondary to renal infection, although iatrogenic : haematogenous spread causes : results from descending renal infection or haematogenous : may then spread to involve the uterus. It can present GENITOURINARY TUBERCULOSIS 221 Presentation Early symptoms include fever, lethargy, weight loss, night sweats, and UTI not responding to treatment. Later manifestations include LUTS, haema- turia, and \202 ank p ain. Investigation - - Urine dipstick test Urine culture required. A typical \201 nding is sterile pyuria (leuko cytes, but no growth). Ziehl \200\223Neelsen staining will identify these acid- and alcohol -fast bacilli (cultured on Lowenstein \200\223Jensen medium). Polymerase chain reaction (PC R) of urine, where available, is useful for TB detection. Urine cytology malignancy/carcino ma in situ). CXR and sputum culture. Tuberculin skin test suggests TB exposure. Renal tract imaging initially. Further investigation into urinary tract involvement and complications can include CTU or IVU. and biopsy. Cystoscopy : may show blood and leukocytes, but no nitrites. : at least three early morning urines (EMUs) are : to exclude other causes of sterile pyuria (i.e. bladder : a negative test excludes TB; a positive test : X-ray and USS of kidneys, ureters, and bladder Treatment Medical A multidisciplinary team approach is required, involving colleagues from respiratory, infectious diseases, and microbiology departments. Treatment is with 2 months of isoniazid, rifampicin, and pyrazinamide and ethambutol, followed by a continuation phase of 4 months of isoniazid and rifampicin. Longer treatments or modi \201 cation of drugs i s needed for complications and resistant organisms. Surgical A non-functioning, calci \201 ed kidney may need nephrectomy. Regular follow-up i maging with IVU is recommended to monitor for ureteric strictures which may need stenting, nephrostomies, or ureteric reimplan- tation. Severe bladder disease may require surgical au gmentation, urinary diversion or cystectomy, and neobladder reconstruction. For epididymal involvement, epididymectomy 9 orchidectomy is considered if pharmaco- therapy fails or exte nsive disease is present. CHAPTER 6 Infections and in \202 ammatory conditions 222 Parasitic infections Urinary schistosomiasis (bilharzia) This is caused by the parasitic tr ematode (or \202 atworm) called Schistosoma (S.) haematobium. It occurs in Africa (Egypt) and the Middle East. Other causes of schistosomiasis include S. mansoni, S. japonicum, S. mekongi, and S. intercalatum. They are mainly responsible for intestinal forms of disease. Life cycle of S. haematobium (Fig. 6.2) Infection is acquired by exposure to contaminated w ater. The parasite (cercariae form) penetrates the skin of the human host, shed their tails , and become schistosomula. They migrate \201 rst to the lung via venous cir- culation, t hen to the liver to mature. The adult worms couple (sexual reproductive phase), migrate to veins of the vesical plexus, and lay ferti- lized eggs. Most eggs (which typically have a t erminal spine) leave the body by penetrating the bladder and entering the urine. Some eggs are trapped in the tissues and those not destroyed by host responses can become calci \201 ed. The released eggs hatch in fresh water, releasing miracidia which \201 nd and enter the intermediate host, a fresh water Bulinus species snail. Through an asexual reproductive phase, sporocytes are created in the snail. These produce and later release larvae called cercariae, the free- swimming, infective form of the parasite, and the cycle is continued, with penetration into the human host. The disease has two main stages: active (when adult w orms are laying eggs) and inactive (when the adults have died and there is a reaction to th e remaining eggs). Pathology Lesions occur due to calci \201 cation of dead eggs trapped in tissues, trigger- ing a \201 brotic reaction. A T-cell-mediated immune response is stimulated also by the presence of the eggs, resulting in eosinophilic granuloma in the bladder, uterus, and genit alia. Clinical presentation - (cercarial dermatitis): may arise on the skin Maculopapular eruption at the site of cercari al penetration (within hours, lasting up to 3 days). \200\230Swimmer \200\231s itch \200 \231 may occur in individuals who are already sensitized and become re-infected. Acute schi stosomiasis reaction associated with the onset of egg-laying. Symptoms may include fever, m alaise, non-productive cough, lymphadenopathy, hepatosplenomegaly, haematuria, urinary freq uency, and terminal dysuria (onset 3 weeks \200\2234 months). Chronic and advanced disease : chronic local in \202 ammatory response to eggs trapped in host tissues results in in \202 ammatory and obstructive urinary tract sequelae, usually after several years. Obstruct ive features include \201 brosis and \200\230eggshell \200\231 calci \201 cation of the bladder, urinary retention, ureteric stenosis, hydronephrosis, renal failure, and stones. Seminal vesicle involvement can produce \200\230lumpy semen \200\231. (Katayama fever): is a generalized immune PARASITIC INFECTIONS 223 Investigation - Midday urine specimen terminal spine). Eggs may also be identi \201 ed in the feces. FBC c hronic and advanced disease. U & E Serology tests ( Cystoscopy Bladder and rectal biopsies urine or feces). X-ray, evidence of obstructive uropathy. USS bladder wall. : may contain eggs (distinguished by having a : eosinophilia in acute infection; anemia and thrombocytopenia in - - : raised creatinine in advanced disease (renal impairment). ELISA): identify speci \201 c antibodies. : identi \201 es eggs in the trigone ( \200\230sandy patches \200\231). : may identify eggs (if not already found in CT, or IVU: may show a calci \201 ed, contracted bladder and : in established disease may show hydronephrosis and a thickened Treatment Praziquantel 40mg/kg as a single or divided oral doses. Corticosteroids are an ad juvant therapy used to treat Katayama fever (within 2 months of freshwater contact). Patien ts should be followed up at 2 and 6 months with urinalysis and clinical assessment. Adult worms in venules of vesical plexus Schistosomulum Migrate and mature in the liver Human host Fertilized eggs pass through blood vessel walls and into the bladder Cercariae are released. They are free-swimming and penetrate skin of the human host Eggs shed into urine Sporocytes produce larvae called cercariae Eggs hatch in fresh water to form miracidia Develop into sporocytes in the snail Fresh water snail (Bulinus) Intermediate host Fig 6.2 Life cycle of Schistosoma haematobium. CHAPTER 6 Infections and in \202 ammatory conditions 224 Complications - SCC infection and the development of malignancy. Bladder contraction, calci \201 cation, a nd ulceration. Obstructive uropathy. Renal failure. Secondary bacterial of the bladder \200\224there can be a lag period of around 20y between - - UTI. Genitourinary hydatid disease - Infection occurs after ingestion of the dog parasite, granulosus (tapeworm). Sheep are the intermediate hosts. Occurs in the Middle East, Australia, and Argentina. Eggs come to rest in the genitourinary tract after passage through the portal system, heart, and pulmonary ci rculation. Large (hydatid) cysts form, which can be asymptomatic or present with pain. They can affect the kidneys, bladder, prostate, seminal vesicles, and epididymis. A peripheral eosinophilia is seen, with a positive hydatid complement \201 xation test. USS \202 uid - \201 lled spherical cyst with a calci \201 ed wall. Medical treatment is with albendazo le, mebendazole, or praziquantel. Where surgical excision is indicated, cysts can be \201 rst sterilized with chlorhexidine, alcohol, or hydrogen peroxide. Medical therapy is recom mended preoperative and post-operatively to reduce recurrence rates. Cyst rupture or spilla ge of cyst contents perioperatively can provoke systemic anaphylaxis. Echinococcus is usually diagnostic; X-rays and CT scans show a thick-walled, Genital \201 lariasis Lymphatic \201 lariasis caused by Wuchereria bancrofti infection is common in the tropics and is transmitted by mosquitoes. Genitourinary manifesta- tions, which may be delayed up to 5y, include funiculoepididymitis, orchitis, hydrocoele, scrotal and penile elephantitis, and lymph scrotum (oedema). Diagnosis is on thick \201 lm, serol ogy, or biopsy. Medical treatment is with diethylcarbamazine. Surgical excision of \201 b rotic and oedematous tissue may be needed for genital elephantitis. This page intentionally left blank CHAPTER 6 Infections and in \202 ammatory conditions 226 HIV in urological surgery Human immunode \201 ciency virus (HIV) Causes a spectrum of illn ess related to immune system de \201 ciency. HIV-1 is pandemic and accounts for signi \201 cant mortality in developing coun- tries. HIV-2 has less pathogenicity and is predomin ant in West Africa. Transmission is via unprotected sexual intercourse, contaminated needle s, mother-to-fetus transmission, infected blood, and blood products (blood transfusion risk s are now minimal). Pathogenesis HIV is a retrovirus. It possesses the enzyme, reverse transcriptase, that enab les viral RNA to be transcribed into DNA, which is then incorpo- rated into the host cell g enome. HIV binds to CD4 receptors on helper T-lymphocytes (CD4 cells), monocytes, and neura l cells. After an extended latent period (8 \200\22310y), CD4 counts decline. Acquired immu node \201 ciency syndrome (AIDS) is de \201 ned as HIV positivity and CD4 lymphocyte coun ts <200 x 106/L. The associated immunosuppression increases the risk of opportunistic infec tions and tumors. Diagnosis ELISA testing of serum detects antibodies against HIV antigens. The sec- ond con \201 rmatory test is Western blot. Informed consent is required for the test. Urological sequelae of HIV infection Renal - Opportunistic infections aspergillosis, mycobacteria, and cryptococcus infections. Can lead to pyelonephritis, acute tubular necrosis, and abscess formation. Renal impairment and fai lure Renal stones Tumors : including cytomegalovirus (CMV), - : HIV and AIDS-associated nephropathy. : secondary to indinavir (antiretroviral treatment). : Kaposi \200\231s sarcoma, lymphoma. Bladder - Voiding dysfunction toxoplasmosis), bladder overactivity or underactivity. Opportunistic in fections Tumors : urinary retention (associated with causing UTI. : squamous cell carcinoma, Kaposi \200\231s sarcoma, lymphoma. Urethra - Reiter \200\231s syndrome (urethritis, conjunctivitis, arthritis) is associated with AIDS. Bacterial urethritis. Prostate - - Bacterial prostatitis and abscesses (including opportunistic organisms). Reported increased progression rate for prostatic carcinoma. HIV IN UROLOGICAL SURGERY 227 External genitalia - - - - Chronic or recurrent genital herpes. Atypical syphilis. Opportunistic infections of testicl e and epididymis. Testicular cancers (increased risk of germ cell and non-germ cell tumors, lymphoma). Testicular atrophy Scrotal and penile Kaposi \200\231s sarcoma (seen as purple/ red lesions). Fournier \200\231s gangrene. Sexual dysfunction: due to the underlying neurop athy, encephalopathy, or lipodystrophy) and/or due to HIV drug therapies (antiretroviral th erapy). - - 9 hypogonadism. HIV pathology (HIV Of note, circumcision has been shown to reduce the risk of acquiring HIV infection in heter osexual men. Occupational needle stick injury The risk of HIV transmission after percutaneous exposure t o HIV-infected blood is 3 per 1000 injuries.1 Risks are increased if the patient has termin al HIV-related illness, a deep injury, visible blood on the device causing the injury, and injury with a needle previously placed in the source patient \200\231s vein or artery.1 Aft er mucocutaneous exposure, the risk is <1 in 1000.1 Management Immediately wash the area well and encourage free bleeding of puncture wounds. I rrigate exposed mucous membranes with water. Report to occu- pational health (A & E or equi valent out-of-hours service) for a risk assess- ment and baseline blood sample for storage. The source patient will be approached and counseled on undergoing HIV testing. Health care worker follow-up testing is recommended at 12 and 24 weeks post-exposure (or 24 weeks afte r antiretroviral prophylaxis if prescribed). Occupational HIV exposure is reported to the H PA Center for Infections. Post-exposure prophylaxis (PEP) is recommended if there has been sig- ni \201 cant occupat ional exposure to blood or another high-risk body \202 uid from a patient or other source , either known to be HIV-infected or con- sidered high risk of HIV infection (but where the result of a HIV test has not or cannot be obtained). PEP should be initiated ideally withi n 1h and continued for at least 28 days. The PEP starter pack contains one Truvada tablet ( tenofovir and emtricitabine) taken once a day plus two Kaletra tablets (lopinavir and riton avir) taken twice a day.1 1 Department of Health (2008) HIV post exposure prophylaxis: Guidance from the UK Chief Med ical Of \201 cers \200\231 Expert Advisory Group on AIDS [online]. Available from: M http: //www.dh.gov. uk/publications. CHAPTER 6 Infections and in \202 ammatory conditions 228 Phimosis A condition where the contracted foreskin (prepuce) has a tight, nar- rowed ori \201 ce and cannot be retracted back over glans of the penis. A physiological phimosis is p resent at birth due to adhesions between the epithelium of inner foreskin and glans. Penile growth, erections, and accu- mulation of epithelial debris (smegma) under the foreskin cau ses gradual separation. Ninety percent of foreskins are retractile at age 3.1 Few persist i nto adulthood (<1% phimosis at age 17).2 Recurrent balanitis and in \202 am- matory condit ions such as BXO in uncircumcised males can cause new pathological phimosis (see b p. 230). Presentation Physiological phimosis is usually asymptomatic. Patients may describe bal- loo ning of the foreskin on voiding and an inability to fully retract the fore- skin which, in sexually active men, may also cause skin trauma during sexual intercourse. In \202 ammatio n or infection (balanitis and balanoposthisis) may cause bleeding, pain, discharge, or dysu ria (see b p. 230). Phimosis associ- ated with BXO presents with white, itching plaques aff ecting the foreskin and glans and may have associated voiding problems. Treatment Adults: treat any associated infection. If symptomatic or a pathological phi- mos is, surgical treatment is circumcision (see b p. 750). Preputioplasty (longitudinal incisio n on foreskin which is closed transversely) is an alter- native for milder cases. It is eff ective in around 50%; a circumcision is then required for those who do not respond. It is n ot suitable for BXO. Children: older children with phimosis suffering infection (balanitis) can be treated with antibiotics and a course of topical 0.1% betamethasone (bet- novate) cream which acts to so ften the phimosis and allow foreskin retrac- tion. The recommendations are to avoid circumc ision where possible.1 Indications for circumcision in children include phimosis associated with recurrent balanit is, BXO, (recurrent) UTI associated with an underlying abnormality (i.e. VUR,3 posterior ur ethral valves, neuropathic bladder dys- function), recurrent UTI,3 failed medical therapy f or UTI, stone disease, and for religious reasons. Contraindications to (neonatal) circumcision include the presence of hypospadias (9 chordee or hooded foreskin), small penis, or large hernia or hydrocele (where repair after circumc ision may cause a buried penis or secondary phimosis). Complications of phimosis - Paraphimosis : the foreskin is retracted behind the glans, but cannot be replaced again. An existing degree of phimosis and/or prolonged retraction produces a tight ring of tissue at the corona, leading to venous congestion, oedema, and swelling of the glans, which can pro gress to arterial occlusion and necrosis (see b p. 533) Recurrent balanitis PHIMOSIS 229 Balanoposthitis in \202 ammatory secretions and pus are trapped in the foreskin by the phi motic band. Chronic in \202 ammation . Penile cancer (squamous cell carcinoma) uncircumcis ed males. Sexually transmitted infection transmission) in uncircumcised males (see b p. 227 ). : severe balanitis and infection of the foreskin, where : increased risk in : increased risk (including HIV 1 Gairdner D (1949) The fate of the foreskin. A study in circumcision. BMJ 2:1433 \200\2237 .