Committee III
Female Urology
Prof. Mohamed Salah Professor of Urology, Cairo University
Prof. Sherif Mourad Professor of Urology, Ain Shams University
Dr. Wally Mahfouz Assistant Professor of Urology Alexandria University
Dr. Hussien Aly Hussien Assistant Professor of Urology Cairo University
Dr. Ahmed Farouk Assistant Professor of Urology. Ain Shams University
Dr. Ahmed Maher Higazy Assistant Lecturer of Urology. Ain Shams University
Contents
- III.1 Abbreviations
- III.2 Abstract.
- III.3 Introduction
- III.4.1 Guidelines Statements on SUI.
- III.5 Diagnosis and Treatment of Overactive Bladder (OAB) in Females.
- III.6 Pelvic Organ Prolapse (POP)
- III.7 Female urethral diverticulae (UD)
- III.8 Female Urethral injury
- III.9 Uro-gynecological fistulae
- III.10 Bladder Pain Syndrome (BPS).
- III.11 Female Bladder Outlet Obstruction (BOO).
- III.12 Geriatric urinary incontinence.
- III.13 Female Sexual Dysfunctions (FSD).
- III.14 Conclusions.
- III.15 References.
III.1 Abbreviations
- ALPP - Abdominal Leak Point Pressure
- ASC - Abdominal Sacrocolpopexy
- AUA - American Urological Association
- MUI - Mixed Urinary Incontinence
- MS - Multiple Sclerosis
- NLUTD - Neurogenic Lower Urinary Tract Dysfunction
- SUI - Anti-Stress Urinary Incontinence
- OAB - Overactive Bladder
- BOO - Bladder Outlet Obstruction
- PFME - Pelvic Floor Muscle Exercises
- BPS - Bladder Pain Syndrome
- PFMT - Pelvic Floor Muscle Training
- POP - Pelvic Organ Prolapse
- PTNS - Percutaneous Tibial Nerve Stimulation
- CIC - Clean Intermittent Catheterization
- PGAD - Persistent genital arousal disorder
- DHIC - Detrusor Hyperactivity with Impaired Contractility
- PFME - Pessaries and Pelvic Floor Muscle Exercises
- DO - Detrusor Overactivity
- PVR - Post Void Residual
- DSD - Detrusor Sphincter Dyssynergia
- PFSAD - Psychological arousal disorder
- DUA - Detrusor Underactivity
- PVS - Pubovaginal Sling
- DSM-5 - Diagnostic and Statistical Manual for Mental Disorders
- QoL - Quality of Life
- ER - Extended Release
- RVF - Rectovaginal fistula
- FI - Fecal Incontinence
- SNS - Sacral Neuromodulation
- FOD - Female Orgasmic Disorders
- SSRI - selective serotonin reuptake inhibitor
- FSAD - Female sexual arousal disorders
- SUI - Stress Urinary Incontinence
- FSD - Female Sexual Dysfunctions
- SCI - Suprasacral Spinal Cord Injuries
- FSFI - Female Sexual Function Index
- AUA - The American Urological Association
- PDE5Is - Phosphodiesterase 5 Inhibitors
- FM - Fibomyalgia
- EUG - The Egyptian Urological Guidelines
- GFSAD - Genital arousal disorder
- ICSI - The Interstitial Cystitis Symptom Index
- GU - Genitourinary
- GRA - Global Response Assessment
- TENS - Transcutaneous Electrical Nerve Stimulation
- GAG - Glycosaminoglycan
- TCAs - Tricyclic Antidepressants
- HSDD - Hypoactive sexual desire disorder
- UD - Urethral Diverticulae
- IR - Immediate Release
- UPP - Urethral Pressure Profilometry
- ICI - International Consultation on Incontinence
- ICS - International Continence Society
- UUI - Urgency Urinary Incontinence
- IUGA - International Uro-Gynecological Association
- UI - Urinary incontinence
- ISD - Intrinsic Sphincteric Deficiency
- UTIs - Urinary Tract Infections <
- LUTS - Lower Urinary Tract Symptoms
- VUDS - Videourodynamics
- MRI - Magnetic Resonance Imaging
- VAS - Visual Analogue Score
- MUCP - Maximal Urethral Closure Pressure
- VCUG - Voiding Cystourethrogram
- MUS - Mid Urethral Synthetic Slings
III.2 Abstract.
III.2.1 Objectives
III.2.2 Methods
III.2.3 Results
III.2.4 Conclusion
III.3 Introduction
Urinary incontinence (UI) is an extremely common complaint all over the globe. It causes great social distress and embarrassment, as well as significant costs, to individuals and societies. Estimates of prevalence vary according to the definition of incontinence and the population studied. However, there is universal agreement about the importance of the problem in terms of human suffering and economic cost. There are many types of UI, including stress urinary incontinence (SUI), urgency urinary incontinence (UUI) and mixed urinary incontinence (MUI). Uro-gynecological fistulae are common in Egypt and considered a cause of UI in females. Bladder pain syndrome (BPS), previously known as interstitial cystitis, has common symptoms with overactive bladder (OAB), thus needs to be diagnosed accurately to ensure the correct management. -
Bladder outlet obstruction (BOO) in females is an under-reported and underdiagnosed problem. Diagnosis of this condition is crucial as the presenting lower urinary tract symptoms (LUTS) always intermingle. Another important topic is management of geriatric incontinence in females, and the considerations taken in the management of such patients. Female sexual dysfunction (FSD) is an entity always neglected in the urogynecology practice, with no definite guidelines or recommendations available.
III.3.1 Aims and Objectives.
III.3.2 Methodology
III.4.1 Guidelines Statements on SUI.
o Inability to reach definitive diagnosis based on symptoms and initial evaluation
o No clinically demonstrable SUI
o Known or suspected neurogenic lower urinary tract dysfunction (NLUTD)
o Abnormal urinalysis such as pyuria or hematuria
o Urgency-predominant MUI
o Raised PVR or obstructive urinary symptoms
o High-stage POP (stage 3 or higher) and SUI is not demonstrable clinically after POP reduction
o Failure of prior anti-incontinence surgery
o Prior POP repair surgery
o Observation
o Pelvic floor muscle training with or without biofeedback o Other non-surgical options (e.g., continence pessary)
o Surgical intervention
• Urologists should counsel patients on potential complications specific to each treatment option (LE 1a)
• In patients with SUI or stress-predominant MUI, physicians may offer non-surgical treatment options such as continence pessaries and pelvic floor muscle exercises (PFME) (LE 3)
• In female patients willing to undergo anti-SUI surgery, urologists may offer mid-urethral synthetic slings (MUS), pubovaginal sling (PVS), Burch colposuspension or bulking agents (LE 1a)
• Urologists must discuss the specific risks and benefits of MUS placement as well as the available alternative options (LE 3)
• Urologists may offer either the retropubic (TVT) or transobturator (TOT) MUS for female patients willing to perform MUS surgery (LE 1a)
• Urologists may consider retropubic (TVT) MUS, PVS or bulking agents for female patients with ISD and willing to perform MUS surgery (LE 3)
• Urologists should not place a synthetic MUS if the urethra is inadvertently injured at the time of planned MUS procedure (LE 3)
• Urologists should not place a synthetic MUS in patients undergoing concomitant urethral diverticulectomy, repair of urethrovaginal fistulae, or simultaneously during urethral mesh excision (LE 3)
• Urologists should counsel patients on potential complications specific to each treatment option (LE 1a)
• In patients with SUI or stress-predominant MUI, physicians may offer non-surgical treatment options such as continence pessaries and pelvic floor muscle exercises (PFME) (LE 3)
• In female patients willing to undergo anti-SUI surgery, urologists may offer mid-urethral synthetic slings (MUS), pubovaginal sling (PVS), Burch colposuspension or bulking agents (LE 1a)
• Urologists must discuss the specific risks and benefits of MUS placement as well as the available alternative options (LE 3)
• Urologists may offer either the retropubic (TVT) or transobturator (TOT) MUS for female patients willing to perform MUS surgery (LE 1a)
• Urologists may consider retropubic (TVT) MUS, PVS or bulking agents for female patients with ISD and willing to perform MUS surgery (LE 3)
• Urologists should not place a synthetic MUS if the urethra is inadvertently injured at the time of planned MUS procedure (LE 3)
• Urologists should not place a synthetic MUS in patients undergoing concomitant urethral diverticulectomy, repair of urethrovaginal fistulae, or simultaneously during urethral mesh excision (LE 3)
• Synthetic MUS should be avoided in patients undergoing SUI surgery who have poor wound healing (e.g., irradiated patients, presence of significant scarring and fibrosis, poor tissue quality and immunocompromised patients) (LE 3)
• Urologists may offer patients with SUI and concomitant NLUTD surgical treatment of SUI after appropriate evaluation and dedicated counselling (LE 3)
• Urologists may offer synthetic MUS slings to female patients planning to get pregnant, diabetics, morbidly obese patients and geriatric females, after appropriate evaluation and dedicated counselling (LE 3)
• During the early postoperative period following anti-SUI procedures, patients should be examined for significant voiding problems, pain, occurrence of hematuria, any sign of mesh extrusion, wound healing or other unanticipated events (LE 2a)
• Patients should be seen and examined by their urologist within six months post-operatively of their anti-SUI procedure (LE 2b)
• The subjective outcome of anti-SUI surgery, as perceived by the patient, should be assessed and documented (LE 1a)
• Patients should be asked about residual incontinence, ease of voiding/force of stream, recent urinary tract infection (UTI), pain, sexual function and new onset or worsened OAB symptoms (LE 1a)
• A physical exam, including examination of all surgical incision sites, should be performed to evaluate healing, tenderness, mesh extrusion (in the case of synthetic MUS), and any other potential abnormalities. This should be coupled with PVR estimation (LE 2a)
III.4.2 Statement on the Use of Vaginal Mesh for the Surgical Treatment of SUI
• Both the Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction (SUFU) and the American Urological Association (AUA) recognize synthetic polypropylene monofilament MUS as a suitable treatment option for SUI in properly selected patients who are appropriately counseled regarding this surgical procedure, by surgeons who are trained in the placement of such devices, as well as the recognition and management of potential complications associated with their use.
III.5 Diagnosis and Treatment of Overactive Bladder (OAB) in Females.
• Urgency is the hallmark of OAB. It is defined as the "complaint of a sudden, compelling desire to pass urine which is difficult to defer."(4)
• Urinary frequency can be reliably measured with a voiding diary. Traditionally, up to seven micturition episodes during waking hours has been considered normal, (5) however this number is highly variable based upon hours of sleep, fluid intake and comorbid medical conditions. It is the patient’s perception that he/she voids too much as compared to their previous usual pattern.
• Nocturia is the complaint of interruption of sleep one or more times because of the need to void. (4) Three or more episodes of nocturia constitute moderate or major bother. (6) Nocturia is a multifactorial symptom which is often due to factors unrelated to OAB (e.g., excessive nighttime urine production, sleep apnea).
III.5.1 Epidemiology
III.5.2 Differential diagnosis.
• The clinical presentation of interstitial cystitis/ bladder pain syndrome (BPS) shares the symptoms of urinary frequency and urgency, with or without UUI; however, bladder and/or pelvic pain, including dyspareunia, is a crucial component of its presentation in contradistinction to OAB.
III.5.3 Guidelines statement on OAB.
• OAB is not a disease; it is a symptom complex that generally is not a life-threatening condition (LE 3)
• Urologists should educate patients regarding normal lower urinary tract function, natural history of OAB and the available treatment options with their benefits/risks (LE 3)
• Acceptable symptom control may require trials of multiple therapeutic options before it is achieved (LE 3)
• Urologists should offer behavioral therapies (e.g., bladder training, bladder control strategies, PFME, fluid management) as first line therapy to all patients with OAB (LE 1b)
• Behavioral therapies may be combined with pharmacologic management in patients with OAB (LE 2b)
• Oral anti-muscarinics or oral β3-adrenoceptor agonists should be offered as second-line therapy for OAB treatment (LE 1a)
• Extended release (ER) formulations of anti-muscarinics are preferred over immediate release (IR) formulations because of lower incidence of dry mouth (LE 2a)
• Dose modification of the same anti-muscarinic or a different anti-muscarinic medication or a β3-adrenoceptor agonist may be tried if a patient experiences inadequate symptom control and/or intolerable adverse drug events with one anti-muscarinic medication (LE 2b)
• Urologists may consider combination therapy with an anti-muscarinic and β3-adrenoceptor agonist for patients, who are refractory to monotherapy with either anti-muscarinics or β3adrenoceptor agonists (LE 2a)
• Anti-muscarinics should be used with extreme caution in patients with narrow-angle glaucoma, impaired gastric emptying or a history of urinary retention (LE 3)
• If an anti-muscarinic is effective in controlling OAB symptoms but with resultant occurrence of constipation or dry mouth as an adverse event, a trial to manage these side effects is considered before abandoning effective anti-muscarinic therapy. Management may include bowel management, fluid management, dose modification or alternative antimuscarinic. (LE 3)
• Urologists should be aware of the cumulative anticholinergic load in patients using other medications with anti-cholinergic properties. (LE 3)
• Urologists may offer intradetrusor onabotulinum toxin A (100U) as third-line treatment option in carefully selected and thoroughly counseled patients who has been refractory to first- and second line OAB treatments. (LE 2a)
• Patients willing to undergo intradetrusor onabotulinum toxin A injection must return for frequent PVR estimation and be able to perform clean intermittent catheterization (CIC) if necessary. (LE 2a)
• Urologists may offer percutaneous tibial nerve stimulation (PTNS) as third-line treatment in carefully selected patient population. (LE 2b)
• Sacral neuromodulation (SNS) may be offered as third-line treatment in refractory OAB. (LE 3)
• Augmentation cystoplasty or urinary diversion may be considered for severe, refractory OAB patients, not responding to any of the first, second or third-line treatment options, after careful and detailed counselling about the irreversible nature of the procedure, the possible complications and the need for CIC to empty their bladders. (LE 3)
• Indwelling urinary catheters (including transurethral and suprapubic catheters) are not recommended as a management option for OAB because of the adverse risks. They could be considered as a last resort in selected patients. (LE 3)
III.6 Pelvic Organ Prolapse (POP)
III.6.1 Guidelines statements on POP
• Take a detailed history to include symptoms of POP, urinary, bowel and sexual function in the initial assessment of POP (LE 1a)
• Perform a complete pelvic examination in the standing and supine position, to document presence of POP, the degree of prolapse of the anterior, central and posterior vaginal compartments of the pelvic floor, using the POP-Q (Pelvic Organ Prolapse Quantification) system (LE 1a)
• Do not routinely perform imaging to document the presence of vaginal prolapse if a prolapse is detected by physical examination (LE 3)
• Do not perform dynamic MRI in the initial assessment of POP (LE 3) • Perform dynamic MRI of the pelvis to exclude presence of rectal intussusception or rectal prolapse. If not available, perform cystocolpodefecography (LE 3)
• Offer females with low grade POP non-surgical treatment options as losing weight if BMI >30, minimize lifting heavy objects and treating constipation (LE 1a)
• Consider topical vaginal estrogen for females with POP and signs of vulvovaginal atrophy (LE 2a)
• Consider PFME for at least 16 weeks as a first option for females with symptomatic POPQ stage 1 or stage 2 (LE 2b)
• Offer a vaginal pessary for females with symptomatic POP (LE 2b) • When considering vaginal pessary for POP, advise patients about the effects of pessaries on sexual activity, risk of vaginitis and vaginal erosions, and the need for exchange every 3 months (LE 2b)
• Offer surgery for POP to females whose symptoms have not improved after non-surgical treatment (LE 1b)
• Patients willing to undergo surgery for POP should be advised about the risks and benefits of each procedure and the risk of recurrent prolapse (LE 1a)
• In patients who will undergo ASC for treatment of POP, they should be informed about the use of intra-abdominal synthetic mesh for fixation, and that risk of erosion is less than that with vaginally placed meshes (LE 2b)
• For female patients with apical uterine prolapse, offer surgical treatment in the form of ASC, vaginal sacrospinous fixation (SSF) or vaginal hysterectomy with or without vaginal SSF (LE 2a)
• Offer females with vault prolapse ASC or vaginal SSF (LE 2a)
• Consider colpocleisis for apical prolapse in sexually inactive elderly females who do not intend to have penetrative vaginal sex (LE 3)
• Offer anterior or posterior repair without mesh to females with anterior vaginal wall prolapse or posterior vaginal wall prolapse respectively (LE 2b)
• Offer females a follow-up visit six months after surgery for POP. Follow-up visit should include a vaginal examination and, if mesh was used, check for mesh exposure (LE 1a)
• When performing ASC for apical POP in females with concomitant SUI, it is advisable to perform ASC alone and evaluate SUI symptom after six months (LE 3)
• Perform cystourethroscopy in suspected vaginal erosion, urethral perforation, bladder perforation, uro-gynecological fistulae, stone on mesh (LE 3)
• Perform imaging of the pelvis (vaginal ultrasound or MRI) in suspected mesh exposure or perforation (LE 3)
• Discuss treatment with topical vaginal estrogen cream in females who have a single area of vaginal mesh exposure that is smaller than 1 cm2 (LE 2b)
• Consider partial or complete surgical removal of the vaginal portion of mesh if the area of vaginal mesh exposure is 1 cm2 or larger, or if there has been no response to non-surgical treatment after a period of 3 months, or in immunocompromised patients (LE 2b)
• Complete removal of the vaginal portion of mesh is associated with a greater risk of recurrent SUI than partial removal (LE 3)
• Partial removal of the mesh is associated with a higher rate of further mesh extrusion (LE 2b)
• Complete removal of the vaginal mesh is not always possible (LE 3)
• Perform sling release in females who have voiding difficulty after mesh sling surgery. If failed, sling incision is an alternative option (LE 2a)
• Refer females who are candidates for excision of mesh sling for persistent voiding dysfunction to a specialized tertiary center in the management of mesh-related complications (LE 2b)
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III.6.2 References.
1. McKenzie S, Watson T, Thompson J et al: Stress urinary incontinence is highly prevalent in recreationally active women attending gyms or exercise classes. Int Urogynecol J 2016; 27:1175.
2. Dmochowski RR, Blaivas JM, Gormley EA et al: Update of AUA guideline on the surgical management of female stress urinary incontinence. J Urol 2010; 183: 1906.
3. Holroyd-Leduc JM, Tannenbaum C, Thorpe KE et al: What type of urinary incontinence does this woman have? JAMA 2008; 299: 1446.
4. Haylen BT, de Ridder D, Freeman RM et al: An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female pelvic floor dysfunction. Neurourol Urodyn 2010; 29: 4.
5. Fitzgerald MP and Brubaker L: Variability of 24-hour voiding diary variables among asymptomatic women. J Urol 2003; 169: 207.
6. Tikkinen KA, Johnson TM, Tammela TL et al: Nocturia frequency, bother and quality of life: how often is too often? A population-based study in Finland. Eur Urol 2010; 57: 488.
7. Choo MS, Ku JH, Lee JB et al: Cross-cultural differences for adapting overactive bladder symptoms: results of an epidemiologic survey in Korea. World J Uro 2007; 25: 505.
8. Corcos J and Schick E: Prevalence of overactive bladder and incontinence in Canada. Can J Urol 2004; 11: 2278.
9. Coyne KS, Sexton CC, Vats V et al: National community prevalence of overactive bladder in the United States stratified by sex and age. Urology 2011; 77: 1081.
10. Tikkinen, KA, Auvinen A, Tiitinen A. et al: Reproductive factors associated with nocturia and urinary urgency inin women: A population-based study in Finland. Am J Obstet Gynecol 2008: 199: 153 e1.
11. Irwin DE, Milsom I, Hunskaar S et al: Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: Results of the EPIC study. Eur Urol 2006; 50: 1306.
12. Stewart WF, Van Rooyen JB, Cundiff GW et al: Prevalence and burden of overactive bladder in the United States. World J Uro 2003; 20: 327.
13. Herschorn S, Gajewski J, Schulz J, et al: A population-based study of urinary symptoms and incontinence: The Canadian Urinary Bladder Survery. BJU Int 2008; 101; 52.
14. Milsom I, Abrams P, Cardozo L et al: How widespread are the symptoms of an overactive bladder and how are they managed? A population-based prevalence study. BJU Intl 2001; 87: 760.
15. Donaldson MM, Thompson JR, Matthews RJ et al: The natural history of overactive bladder and stress urinary incontinence in older women in the community: a 3-year prospective cohort study. Neurourol Urodyn 2006; 25: 709.
16. Moller LA, Lose G and Jorgensen T: The prevalence and bothersomeness of lower urinary tract symptoms in women 40-60 years of age. Acta Obstet Gynecol Scand 2000; 79: 298.
17. Abrams P, Cardozo L, Fall M et al: The standardization of terminology of lower urinary tract function: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 2002; 21: 167.
18. Van Kerrebroeck P, Abrams P, Chaikin D et al: The standardisation of teminology in nocturia: Report from the standardization sub-committee of the International Continence Society. Neurourol Urodyn 2002; 21: 179.
19.Brown JS, Waetjen LE, Subak LL, Thom DH, Van Den Eeden S, Vittinghoff E (2002) Pelvic organ prolapse surgery in the United States. Am J Obstet Gynecol 186:712–716
20. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL (1997) Epidemiology of surgically managed POP and urinary incontinence. Obstet Gynecol 89:501–506
21. Elliott DS, Frank I, DiMarco DS, Chow GK (2004) Gynecologic use of robotically assisted laparoscopic sacrocolpopexy for the treatment of high-grade vaginal vault prolapse. Am J Surg 188(4A Suppl):52S–56S
22.Dietz HP, Hansell NK, Grace ME, Eldridge AM, Clarke B, Martin NG (2005) Bladder neck mobility is a heritable trait. BJOG 112:334–339
23. Chen B, Wen Y, Polan ML (2004) Elastolytic activity in women with stress urinary incontinence and pelvic organ prolapse. Neurourol Urodyn 23:119–126
24. Maher C, Feiner B, Baessler K, Schmid C (2013) Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev 30(4):CD004014. https ://doi.org/10.1002/14651 858. CD004 014
25. Van Der Ploeg JM, Van Der Steen A, Rengerink KO, Van Der Vaart CH, Roovers JP (2014) Prolapse surgery with or without stress incontinence surgery for pelvic organ prolapse: a systematic review and meta-analysis of randomised trials. BJOG 121:537–547
26. Jha S, Cutner A, Moran P (2018) The UK National Prolapse Survey: 10 years on. Int Urogynecol J 22:517–528
27. Raman SV, Raker CA, Sung VW (2014) Concomitant apical prolapse repair and incontinence procedures: trends from 2001– 2009 in the United States. Am J Obstet Gynecol 211: e1–e5
28. Urinary incontinence and pelvic organ prolapse in women: management NICE guideline Published: 2 April 2019 www.nice.org.uk/guidance/ng123
III.7 Female urethral diverticulae (UD)
III.7.1 Definition.
III.7.2 Etiology.
There is controversy regarding the exact origin. However, infection of the peri-urethral glands ± abscess formation ± gland rupture into the urethra is considered the most accepted theory 1. Mechanical trauma during vaginal delivery has been reported to be a cause of UD (2) Congenital urethral diverticulum is relatively uncommon; however, it has been reported. No accurate estimate of the prevalence but it is estimated to be 1-6% of adult females (3).
III.7.3 Evaluation and diagnosis.
III.7.3.1 Symptoms.
• Anterior vaginal mass
• Vaginal pain or urethral pain
• Dysuria
• Dyspareunia
• Urinary frequency, urgency and urinary incontinence (UI)
• Post-voiding dribbling
• Sense of incomplete emptying, double voiding and hesitancy
• Vaginal and urethral discharge (3)
III.7.3.2 Signs.
• Recurrent urinary tract infections (UTIs) and hematuria
• Urine expression upon compression of the vaginal swelling, and if infected, pus may be expressed
• Anterior vaginal cystic swelling and vaginal tenderness
• Urinary retention
• Urethral discharge with stripping of anterior vaginal wall (3)
Most UD are located posterolaterally over the middle and proximal portion of the urethra. During examination, evaluation for stress urinary incontinence (SUI) should be performed as well as the assessment for any concomitant pelvic organ prolapse (POP) (4)
III.7.4 Investigations.
• Urine analysis/culture: Most common organism is E. coli. Proper treatment of infection is mandatory before any surgical intervention (3)
• Voiding cystourethrogram (VCUG): It provides an excellent imaging of UD (4). However, it doesn’t show the actual spatial configuration of the UD.
• Ultrasonography (transvaginal or trans-labial): UD appear as an anechoic or hypoechoic area. It is a noninvasive modality with no radiation that does not requires voiding. However, may not produce an image with precise anatomy (5).
• Magnetic resonance imaging (MRI) with postvoid films: Noninvasive, high resolution imaging appears as decreased signal intensity in T1 images with high signal intensity in T2 (6). This is considered the imaging modality of choice to show the number, the site and complexity of the UD.
• Urodynamic study in patient with significant voiding dysfunction: Can accurately differentiate SUI from post micturition drippling, vaginal voiding and double micturition form a urine filled UD (7).
• Diagnostic urethroscopy is highly sensitivity however it is invasive 8 and may not show the ostium of the UD in most of the cases.
III.7.5 Differential diagnosis:
• Vaginal leiomyoma
• Skene gland abnormalities
• Gartner duct abnormalities
• Urethral mucosal prolapse
• Urethral carbuncle
• Bulking agent (9)
III.7.3.1 Symptoms.
• Anterior vaginal mass
• Vaginal pain or urethral pain
• Dysuria
• Dyspareunia
• Urinary frequency, urgency and urinary incontinence (UI)
• Post-voiding dribbling
• Sense of incomplete emptying, double voiding and hesitancy
• Vaginal and urethral discharge (3)
III.7.3.2 Signs.
• Recurrent urinary tract infections (UTIs) and hematuria
• Urine expression upon compression of the vaginal swelling, and if infected, pus may be expressed
• Anterior vaginal cystic swelling and vaginal tenderness
• Urinary retention
• Urethral discharge with stripping of anterior vaginal wall (3)
• Voiding cystourethrogram (VCUG): It provides an excellent imaging of UD (4). However, it doesn’t show the actual spatial configuration of the UD.
• Ultrasonography (transvaginal or trans-labial): UD appear as an anechoic or hypoechoic area. It is a noninvasive modality with no radiation that does not requires voiding. However, may not produce an image with precise anatomy (5).
• Magnetic resonance imaging (MRI) with postvoid films: Noninvasive, high resolution imaging appears as decreased signal intensity in T1 images with high signal intensity in T2 (6). This is considered the imaging modality of choice to show the number, the site and complexity of the UD.
• Urodynamic study in patient with significant voiding dysfunction: Can accurately differentiate SUI from post micturition drippling, vaginal voiding and double micturition form a urine filled UD (7).
• Diagnostic urethroscopy is highly sensitivity however it is invasive 8 and may not show the ostium of the UD in most of the cases.
• Skene gland abnormalities
• Gartner duct abnormalities
• Urethral mucosal prolapse
• Urethral carbuncle
• Bulking agent (9)
III.7.6 Treatment.
III.7.6.1 Asymptomatic and/or poor medical condition and/or refusing surgical intervention:
III.7.6.2 In symptomatic patients:
• In absence of voiding dysfunction proceed for transvaginal repair.
• If associated with voiding dysfunction, UDS is recommended to evaluate the presence of SUI. If present, transvaginal repair of UD with anti-incontinence surgery, but avoid using synthetic tapes. Preoperative preparation includes treatment of UTI, topical estrogen cream for several weeks in case of postmenopausal atrophic vaginitis (3,10).
• Cystourethroscopy is performed to visualize the UD ostium as well as to evaluate for other causes of LUTS. UD excision and reconstruction are the preferred surgical technique.
• Transvaginal marsupialization may reduce operative time and blood loss with less recurrence; however, it may be associated with dyspareunia and should be reserved only for distal UD. Synthetic slings should not be placed concomitantly at the time of urethral diverticulectomy. A well vascularized vascular flag (e.g., Martius Flap) may reduce the risk of wound breakdown. A peri-catheter VCUG is done 2 to 3 weeks postoperatively before catheter removal (3,10,11).
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III.8 Female Urethral injury
III.8.1 Etiology.
Female urethral injuries are often associated with vaginal injuries. It is a common complication of obstructed labor in rural and slum areas. Iatrogenic injury usually occurs during insertion of a synthetic sub-urethral sling for the treatment of SUI. Also, pelvic fracture may be associated with urethral disruption (12).
III.8.2 Diagnostic evaluation.
• History of relevant trauma
• Examination
• Inability to void is usually a sign of a complete injury
• Incomplete injuries are associated with pain on urination, hematuria or blood present at the vaginal introitus in female patients with pelvic fractures and co-existing urethral injuries
• Cysto-urethroscopy is the preferred diagnostic modality in case of suspected female urethral injury
• VCUG may be needed in late diagnosis and to outline any associated urinary bladder, bladder neck injuries or uro-genital fistulae.
III.8.3 Surgical management.
III.8.3.1 Early diagnosis (Within 1st two weeks)
• In case of hemodynamic instability, provide urinary diversion by suprapubic catherization or a single attempt of urethral catheterization.
• In case of pelvic fracture induced urethral injuries, early repair within seven days has the highest success rate and the lowest complication rate in comparison with delayed repair or early endoscopic re-alignment.
• In case of urethral injury during sling procedure, synthetic mesh should be removed and immediate urethral repair (12). III.8.3.2 Late diagnosis (Two weeks’ post trauma)
• It is preferred to do urinary diversion for three months then repair (12).
Table III:3 Recommendations for female urethral injury.
Recommendation
strength rating
1. History of trauma and examination is the method of diagnosis with need of VCUG in certain indications Weak
2. Cystourethroscopy is the preferred diagnostic modality Strong
3. Treatment may be immediate reconstruction or urinary diversion depending on timing of diagnosis, hemodynamic status of the patient and available facilities (12) Strong
III.9 Uro-gynecological fistulae
III.9.1 Causes.
o In developed countries. Non-obstetric (surgical) fistula is considered the most common cause of uro-gynecological fistulae (e.g., post abdominal hysterectomy, POP repair surgery, anti-incontinent surgery)
o In the developing countries. Obstetric fistula is considered the most common cause due to prolonged obstructed labor (13,14)
o Risk factors for obstetric fistula include lack of prenatal care, young age of first marriage, low socio-economical class, short stature, poor nutrition, lack of proper surgical training for obstetrician (13,14)
III.9.2 Different types of uro-gynecological fistula.
o Vesicovaginal fistula (VVF)
o Urethrovaginal fistula (UVF)
o Rectovaginal fistula (RVF)
o Ureterovaginal fistula
o Vesicouterine fistula
o Sometimes more than one type of fistula may occur at the same time (Complex fistula)
III.9.3 Diagnosis.
Unfortunately, intraoperative diagnosis of a genitourinary (GU) is made in only about half of the cases that result in fistula. Clinical diagnosis of leakage of urine is the hallmark sign of a fistula. The leakage is usually painless, may be intermittent if its position is independent, or maybe constant (15).
The diagnosis of VVF usually requires clinical assessment often in combination with appropriate imaging or laboratory studies. Direct visual inspection, cystoscopy, retrograde bladder filling with a coloured fluid or placement of a tampon into the vagina to identify staining may facilitate the diagnosis of a VVF. A double-dye test is used to differentiate between ureterovaginal and VVF in some cases (15). Cyclic hematuria may be pathognomonic sign of vesico-uterine fistula.
Testing the creatinine level in either the extravasated fluid or the accumulated ascites and comparing this to the serum creatinine levels will confirm urinary leakage. Contrast-enhanced CT with late excretory phase reliably diagnoses urinary fistulae and provides information about ureteric integrity and the presence of associated urinoma (16).
III.9.4 Treatment.
III.9.4.1 Management of vesicovaginal fistula.
III.9.4.1.1 Conservative management.
It may tend to close spontaneously in small sized fistula before complete epithelialization of the fistulous tract, provided that the natural outflow is unobstructed or if urine is diverted. Hence, immediate management should be by urinary catheterization or diversion (17,18)
III.9.4.1.2 Surgical management.
The most important points to be considered in fistula repair are fistula location, fistula size and dimensions, number of fistulae, extent of vaginal scarring, surgical approach and technique used (19).
III.9.4.1.2.1 Timing of surgery.
Findings from uncontrolled case series suggest no difference in success rates for early versus delayed closure of VVF. Tailor the timing of fistula repair to the individual patient and surgeon requirements once any edema, inflammation, tissue necrosis, or infection are resolved (20,21).
III.9.4.1.2.2 Surgical principles.
The best chance for successful fistula closure is at the first operation and closure rates tend to diminish with each subsequent attempt at operative repair (18).
The ureters should be identified and protected to ensure they are not cut or ligated during the fistula repair 19. The fistula should be mobilized from the surrounding tissues at the time of repair. The fistula should be closed without tension at the site of repair. The repair must be watertight. To ensure this, a dye test is performed intra-operatively and, if there is still leakage, the repair is sutured again (19).
A single randomized controlled trial compared trimming of the fistula edge with no trimming showed no difference in success rates, but failed repairs in trimmed cases ended up with larger recurrences than untrimmed cases (22).
A Martius flap in primary obstetric fistula repair is debatable with no clear evidence of its value and is usually reserved for recurrent cases, fistulae secondary to radiation or in case of associated urethral reconstruction (19).
One prospective randomized controlled trial compared the use of a Martius flap “as an interposition flap” to the use of a self-made fibrin glue. There was no statistical difference in outcome, but the authors stated that the use of fibrin glue allowed the fistula repair to be quicker (23).
III.9.4.1.2.3 Surgical approaches.
III.9.4.1.2.3.1 Vaginal procedures.
There are two main types of closure techniques applied to the repair of urinary fistulae, the classical saucerisation/partial colpocleisis and the more commonly used dissection and repair in layers or ‘flap- splitting’ technique. There are no data comparing their outcomes (24,25).
III.9.4.1.2.3.2 Abdominal procedures.
Repair is indicated when high fistulae are fixed in the vault and are inaccessible through the vagina. A trans-vesical repair has the advantage of being entirely extraperitoneal. A simple transperitoneal repair is used less often although it is favoured by some surgeons using the laparoscopic approach. A combined transperitoneal and transvesical procedure is favoured by many urologists and is particularly useful for fistula repair following Caesarean section.
There are no randomised studies comparing abdominal and vaginal approaches. When concurrent ureteric re-implantation or augmentation cystoplasty are required, the abdominal approach is necessary.
III.9.4.1.2.4 Post-operative management.
Catheter drainage for at least 10 days and longer periods in radiation associate fistulae (up to 3 weeks). No sexual intercourse for one month. Surgical treatment of postoperative SUI should only be considered six months after the fistula repair.
III.9.4.2 Management of radiation fistula.
Successful repair of irradiated fistulae requires prior urinary diversion and the use of non-irradiated tissues to ensure successful repair (26).
III.9.4.3 Management of ureteric fistula.
III.9.4.3.1 Endoscopic management.
Is often possible (16) by retrograde stenting, percutaneous nephrostomy and antegrade stenting if there is pelvicalyceal dilatation, or by ureteroscopy (17).
III.9.4.3.2 Surgical management.
III.9.4.3.2.1.1 Timing of repair.
If early discovery within two weeks, immediate repair of any injury should be performed observing the principles of debridement, adequate blood supply and tension free anastomosis with internal drainage using stents (27).
In case of delayed presentation of upper tract injury, conservative management is still possible with internal or external drainage, endoluminal management using nephrostomy and stenting where available, and early (< 3 months) or delayed (> 6 months) surgical repair when required (14).
If endoluminal techniques fail or result in secondary stricture, the abdominal approach to repair is the standard and requires re-implantation into the bladder with or without psoas hitch or Boari flap, or replacement with bowel segments with or without reconfiguration (28,29).
Functional and anatomical imaging should be used to follow up patients after repair to guard against late upper tract deterioration (14).
III.9.4.4 Management of vesicouterine fistula.
Surgical repair through abdominal approach whether by open or laparoscopic techniques, which can be preceded by cystoscopy and gauging of the fistulous tract using ureteric catheter. Hysterectomy may be considered in multiparous women (30,31).
III.9.4.5 Management of urethro-vaginal fistula.
Principles of reconstruction include identifying the fistula, creation of a plane between vaginal wall and urethra, watertight closure of urethral wall, eventual interposition of tissue, and closure of the vaginal wall (32).
Table III:4 Recommendations for uro-gynecological fistulae.
Recommendation
strength rating
1.Uro-gynecological fistulae can be diagnosed mainly by clinical examination which can be complemented by some radiological investigation as VCUG, or CT urography in some types of fistula and cystoscopy Strong
2.The commonest of uro-gynecological fistulae is VVF, which is managed mainly by surgical repair whether through vaginal or abdominal approaches Strong
3.Small VVF less 5 mm may close spontaneously by urinary catheterization or diversion provided that natural outflow is unobstructed
Weak
4.Timing of repair has no difference in the success of surgery Weak
5.Tailor the timing of fistula repair to the individual patient and surgeon requirements once any oedema, inflammation, tissue necrosis, or infection, are resolved Weak
6.There is no high-quality evidence of differing success rates for repair of vesicovaginal fistulae by vaginal, abdominal, trans-vesical or transperitoneal approaches Weak
7.Trimming of the edges of VVF has no difference in success rates but failed repairs in trimmed cases ended up with larger recurrences than untrimmed cases Strong
8.A Martius flap in primary obstetric fistula repair is debatable with no clear evidence of its value and usually reserved for recurrent cases, fistulae secondary to radiation or in case of associated urethral reconstruction Weak
9.Endoscopic management is the cornerstone in treatment of uretro-vaginal fistula. Otherwise, open or laparoscopic ureteric re-implantation may be performed Weak
10.Vesico-uterine fistula repair is mainly through abdominal approach, whether by open or laparoscopic techniques Strong
11.Attention should be given as appropriate to skin care, nutrition, rehabilitation, counselling and support prior to, and following, fistula repair Weak
12.Successful repair of irradiated fistulae requires prior urinary diversion and the use of non-irradiated tissues to ensure successful repair Weak
13.There is no high-level evidence to support any particular practice in postoperative management, but most reported series used catheter drainage for at least ten days and longer periods in radiation-associated fistulae up to three weeks Weak
III.9.5 References.
1. Chapple C. Female urology. Vol. 21, Current Opinion in Urology. 2011. 267 p.
2. Mitchell JD. Diverticulum of the Female Urethra11The opinions and assertions contained herein are the private views of the writers and are not to be considered as official or reflecting the views of the Navy Department or the Naval Service at large. J Urol [Internet]. 1936;51(4):411–23. Available from: http://dx.doi.org/10.1016/S0022-5347(17)70372-2
3. Lee JWS, Fynes MM. Female urethral diverticula. Best Pract Res Clin Obstet Gynaecol. 2005;19(6):875–93.
4. Ganabathi K, Leach GE, Zimmern PE, Dmochowski R. Experience with the Management of Urethral Diverticulum in 63 Women. J Urol [Internet]. 1994 Nov;152(5 Part 1):1445–52. Available from: http://www.jurology.com/doi/10.1016/S0022-5347%2817%2932442-4
5. Ultrasonography T, Pulsed W, Of CD, Urethral F. Translabial ultrasonography with pulsed colour-doppler in the diagnosis of female urethral diverticula. 1994;101–4.
6. Dinkelaar W, Dohle GR, Krestin GP, Rs D, Dinkelaar W, Wcj H. Diagnosis in Symptomatic Women. 2011;(September):676–82.
7. Bradley CS, Rovner ES. URODYNAMICALLY DEFINED STRESS URINARY INCONTINENCE AND BLADDER OUTLET OBSTRUCTION COEXIST IN WOMEN. 2004; 171:757–61.
8. Saito S. Usefulness of Diagnosis by the Urethroscopy Under Anesthesia and Effect of Transurethral Electrocoagulation in Symptomatic Female Urethral Diverticula. 2000; 14(5):455– 7.
9. Leach GE. BENIGN FEMALE PERIURETHRAL MASSES. J Urol [Internet]. 1994; 152(6):1943–51. Available from: http://dx.doi.org/10.1016/S0022-5347 (17)32276-0
10. Vakili B, Wai C, Nihira M. Anterior Urethral Diverticulum in the Female: Diagnosis and Surgical Approach. 2003; 102(5).
11. Gasthuis SF. P OI N T OF T E C H NI QU E Management of female urethral diverticula by transurethral incision. 1996; 745–6.
12. Patel DN, Fok CS, Webster GD, Anger JT. Female urethral injuries associated with pelvic fracture: a systematic review of the literature. BJU Int. 2017; 120(6):766–73.
13. Bettez M, Breault G, Carr L, Tu LM. Case report Early versus delayed repair of vesicouterine fistula. 2011; 5(4):52–5.
14. Murray C, Goh JT, Fynes M, Carey MP. Urinary and faecal incontinence following delayed primary repair of obstetric genital fistula. 2002; 109(July):828–32.
15. Æ JHÆTPP. Vesico-vaginal fistula : report of 220 cases. 2009; 299–302.
16. Exhibit E. Fistulas in Malignant Gynecologic Disease : Etiology, Imaging, and. 2009; 1073–84.
17. Faso B. Fistulas in the Developing World. : 1419–58.
18. Bazi T. Spontaneous closure of vesicovaginal fistulas after bladder drainage alone : review of the evidence. 2007; 329–33.
19. Mourad S. Vesico-vaginal fistula in the developing world. 2020;
20. Waaldijk K. The imediate surgical management of fresh obstetric fistulas with catheter and / or early closure. 1994; 11–6.
21. Vierhout ME. Prospective results after first-time surgery for obstetric fistulas in East African women. 2008; (November 2002):73–9.
22. Shaker H, Saafan A, Yassin M, Idrissa A, Mourad MS. Obstetric Vesico-Vaginal Fistula Repair: Should We Trim The Fistula Edges ? A Randomized Prospective Study. 2011; 305(July 2010):302–5.
23. Safan A, Shaker H, Abdelaal A, Mourad MS, Albaz M. Fibrin Glue Versus Martius Flap Interpositioning in the Repair of Complicated Obstetric Vesicovaginal Fistula. A Prospective Multi-Institution Randomized Trial. 2009; 441(May):438–41.
24. Kumar S, Pal ÆBC. Latzko repair for vesicovaginal fistula revisited in the era of minimal-access surgery. 2008; 317–20.
25. Wall LL. Dr. George Hayward (1791 – 1863): a forgotten pioneer of reconstructive pelvic surgery. 2005; 330–3.
26. Langkilde NC, Pless TK, Lundbeck F, Nerstrøm B. Surgical Repair of Vesicovaginal Fistulae. 1999;
27. Brandes S, Coburn M, Armenakas N, Mcaninch J. The Consensus on Genitourinary by a team of experts under the Diagnosis and management of ureteric injury: an evidence-based. 2004;
28. Shaw MBK, Tomes M, Rix DA, Dorkin TJ, Murthy LNS, Pickard RS. The Management of Bilateral Ureteric Injury following Radical Hysterectomy. 2008; 2008.
29. Narang V, Sinha T, Karan SC. Ureteroscopy: Savior to the gynecologist ?— Ureteroscopic management of post laparoscopic-assisted vaginal hysterectomy ureterovaginal fistulas. 2007 ;( 1):345–7.
30. Rajamaheswari N, Chhikara AB. Vesicouterine fistulae: Our experience of 17 cases and literature review. Int Urogynecol J Pelvic Floor Dysfunct. 2013; 24(2):275–9.
31. Milani R, Cola A, Frigerio M, Manodoro S. Repair of a vesicouterine fistula following cesarean section. Int Urogynecol J. 2018; 29(2):309–11.
32. Pushkar DY, Dyakov V V, Kosko JW, Kasyan GR. Management of Urethrovaginal Fistulas. 2006; 50:1000–5.
III.10 Bladder Pain Syndrome (BPS).
III.10.1 Definition.
• It is the occurrence of persistent or recurrent pain perceived in the urinary bladder region, accompanied by at least one other symptom, such as pain worsening with bladder filling and daytime and/or night-time urinary frequency with no proven infection or other obvious local pathology for a period more than six weeks. (1)
• Pain characteristics include pain, pressure or discomfort perceived to be related to the bladder, increasing with increasing bladder volume. It is located suprapubically, sometimes radiating to the groins, vagina, rectum or sacrum. It is relieved by voiding but soon returns (2,3). It could be aggravated by food or drink. (3)
• Bladder pain syndrome is often associated with negative cognitive, behavioral, sexual or emotional consequence. BPS is believed to represent a heterogeneous spectrum of disorders. Localization of the pain can be difficult by examination. Cystoscopy with hydrodistension and biopsy may be indicated to define phenotypes. Recently, ESSIC has suggested a standardized scheme of sub-classifications (4) to acknowledge differences and make it easier to compare various studies. Other terms that have been used include “interstitial cystitis”, “painful bladder syndrome”, and “PBS/IC” or “BPS/IC”. These terms are no longer recommended.
• Prevalence varies largely, along with the diagnostic criteria and populations studied. Recent reports range from 0.06% to 30% (5-14). There is a female preponderance of about 10:1 (9) but no difference in race or ethnicity (15,16). The relative proportions of classic and nonlesion disease are unclear and their incidence in studies has ranged from 5 to 50% (16-20). Children under the age of eighteen may be affected as well, although prevalence figures are low (21).
III.10.1.1 Risk factors.
• The cause of BPS is proposed to be an unidentified insult to the bladder, leading to urothelial damage, neurogenic inflammation and pain. BPS might be a local manifestation of a systemic disorder. No infection has been incriminated in the pathogenesis of BBS (1).
• Pancystitis, with associated perineural inflammatory infiltrates, and mastocytosis is an essential part of BPS type 3 C (22), but is scant in non-lesion BPS (23,24). Cystoscopic and biopsy findings in both lesion and non-lesion BPS are consistent with defects in the urothelial glycosaminoglycan (GAG) layer which might expose submucosal structures to noxious urine components (25-31) and a consequent cytotoxic effect (32,33). Autonomic dysfunction with sympathetic predominance may be implicated in BPS (34,35).
• An association has been reported between BPS and non-bladder syndromes such as fibomyalgia (FM), inflammatory bowel syndrome, vulvodynia, depression, panic disorders, migraine, sicca syndrome, temporomandibular joint disorder, allergy, asthma and systemic lupus erythematosus (36-40). Risk of BPS correlates with a number of nonbladder syndromes in each patient (41). Recent research showing non-lesion BPS to have significantly more FM, migraine, temporomandibular joint disorder and depression than BPS type 3C patients, emphasizes the need for subtyping (42).
III.10.1.2 Diagnosis.
• This is mainly a disease of exclusion. The clinical examination often serves to confirm what we have gained from the history taking. Besides the local examination, a general musculoskeletal and neurological examination should be considered an integral part of the assessment. There is no specific diagnostic test for BPS, therefore, procedures are directed towards identification and exclusion of specific diseases associated with pelvic pain, and for phenotypic description.
• Ultrasound on the abdomen and pelvis is done to exclude gross pelvic pathology, but with limited value to diagnose PBS. Urine dipstick and urine culture (including culture for tuberculosis if sterile pyuria) are recommended in all patients suspected of having BPS. Urine cytology is also recommended to exclude malignancy (1).
• Symptom scores may help to assess the patient and act as outcome measures. The O’LearySant Symptom Index, also known as the Interstitial Cystitis Symptom Index (ICSI) was validated for use (43).
• Objective findings from cystoscopy are important for diagnosis, prognosis and ruling out other treatable conditions (44). Endoscopically, BPS type 3 displays reddened mucosal areas often associated with small vessels radiating towards a central scar, sometimes covered by a small clot or fibrin deposit - the Hunner ulcer (2). The scar ruptures with increasing bladder distension, producing a characteristic waterfall type of bleeding. There is a strong association between BPS type 3 and reduced bladder capacity under anaesthesia. Nonlesion disease displays a normal bladder mucosa at initial cystoscopy. The development of glomerulations after hydrodistension is considered to be a positive diagnostic sign although they can be observed without BPS. Biopsies are helpful in establishing or supporting the clinical diagnosis of both classic and non-lesion types of the disease (26,44-47). Important differential diagnoses to exclude, by histological examination, are carcinoma in situ and tuberculous cystitis
III.10.2 Management.
• Treatment is usually multimodal (1). It includes lifestyle interventions such as fluid intake modifications, smoking cessation, exercise and no wearing of tight clothes. Another aspect is pain education and education about the causes of pain. Dietary restrictions alone do not produce significant symptomatic relief and scientific data are limited, however, consider the involvement of a dietician.
• The physiotherapist is part of the pain management team, together with the pain doctor and the psychologist. Physiotherapists can either specifically treat the pathology of the pelvic floor muscles, or more generally treat myofascial pain if it is part of the pelvic pain syndrome (48). Efficacy and safety of pelvic floor myofascial physical therapy has been compared with global therapeutic massage in women with BPS; global response assessment (GRA) rate was 59% and 26%, respectively. Pain, urgency and frequency ratings, and symptoms decreased in both groups during follow-up, and did not differ significantly between the groups. This suggests that myofascial physical therapy is beneficial in women with BPS (49).
• Psychological interventions are directed at pain itself or at adjustment to pain in terms of function and mood. Ideally, treatment follows general principles and practice in the field of chronic pain (49). Two systematic reviews and meta-analyses of the few heterogeneous trials of psychologically based treatment for pelvic pain (50,51) found some short-term benefits for pain, of around 50%, comparable to that from pharmacotherapy, but this was not sustained at follow-up.
• Medical therapy includes many option modalities. Histamine receptor antagonists have been used to block the H1 and H2 receptor subtypes (52), with unsatisfactory results (53). Amitriptyline is a tricyclic antidepressant. Several reports have indicated improvement of BPS symptoms after oral amitriptyline (54,55). Drowsiness is a side effect of amitriptyline. Subjective improvement of pain, urgency, frequency, but not nocturia, has been reported with use of Pentosane polysulphate (56,57). It has a more favorable effect in BPS type 3C than in non-lesion disease (58). Immunosuppressants have been tried. Azathioprine and cyclocporin A (59,60) treatment have resulted in disappearance of pain and urinary frequency. Corticosteroids are not recommended in the management of patients with BPS because of lack of evidence.
• Intravesical route is an appealing mode of delivery in PBS. Intravesical drugs are administered due to poor oral bioavailability, establishing high drug concentrations within the bladder, with few systemic side-effects. Disadvantages include the need for intermittent catheterization which can be painful in BPS patients, cost and risk of infection (61). Several drugs have been tried. There are sporadic reports of successful treatment of BPS with intravesical lidocaine (62,63). Combination of heparin, lidocaine and sodium bicarbonate gave immediate symptom relief in 94% of patients and sustained relief after two weeks in 80% (64). Intravesical instillation of alkalized lidocaine for five consecutive days resulted in significantly sustained symptom relief for up to one month (65). Hyaluronic acid and chondroitin sulphate are described to repair defects in the GAG layer (66). Most of the studies are uncontrolled and with a small number of patients and most studies are nonrandomized and with few numbers (67). Symptomatic improvement was reported in 80% of BPS patients with intravesical heparin (67,68).
• There are treatments which are of limited value in BPS. These include cimetidine, with limited data to suggest that cimetidine improves symptoms of BPS in the short-term. These treatments also include misoprostol, which is a prostaglandin, oral L-arginine, intravesical oxybutynin and duloxetine (69-74). None of these drugs have proven to be recommended for treatment of BPS.
• Neuromodulation.
• The role of neuromodulation in the management of chronic pelvic pain (CPP) should only be considered by specialists in pelvic pain management. These techniques are used as part of a broader management plan and require regular follow-up. These are expensive interventional tools for patients who are refractory to other therapies. There has been growing evidence, but more detailed, high quality research is required (75). Two recent systematic reviews have evaluated neuromodulation techniques for CPP (76,77). Both studies concluded that neuromodulation may be effective in reducing pain and improving QoL in patients with CPP, however studies were of a low quality and long-term results were needed.
• Transcutaneous Electrical Nerve Stimulation (TENS) is a non-invasive technique used in many pain conditions. All RCTs demonstrated a significant reduction in pain following twelve weeks of treatment for pain conditions including CPP. There was conflicting data with regard to improvement of quality of life (QoL) following TENS; where validated questionnaires were used. TENS could offer an effective non- invasive treatment option for patients with CPP. • Percutaneous Tibial Nerve Stimulation (PTNS) is a minimally invasive technique that can be use in an outpatient setting. Two trials have shown that PTNS is effective in reducing pain in patients with CPP (76,77). Adverse events were rare and minor including temporary slight pain at application site and haematoma.
• Sacral nerve stimulation (77) is an invasive technique requiring sedation or general anaesthesia for implantation of a device following trial stimulation. All studies reported an improvement in pain and QoL. There was a large variation in adverse events reported ranging from 0-50%.
• Re-operation rate ranged between 11-50% for complications including lead migration, systemic infection, intrathecal implantation, loss of efficacy and erosion.
• Although bladder hydrodistension is a common treatment for BPS, the scientific justification is scarce. It can be part of the diagnostic evaluation but has limited therapeutic role. Diagnostic hydrodistention is done under general anesthesia for 2 minutes and with height of fluid above the bladder of 81cmH2O. Therapeutic hydrodistension is done under same circumstances but for 8 minutes (78). Treatment with hydrodistension and hydrodistension plus intravesical botulinum toxin A (BTX-A) has been compared (79). There was symptomatic improvement in all patients. However, in the hydrodistension-only group, 70% returned to their previous symptoms after one month, while in the BTX-Atreated patients, visual analogue score (VAS) score and functional and cystometric bladder capacity improved at three months. BTX-A trigonal-only injection seems effective and long-lasting as 87% of patients reported improvement after three months’ follow-up (80). Over 50% reported continued benefit nine months after the first treatment. When retreatment was needed, similar results were obtained. Adverse effects of BTX-A administration for IC/BPS were significantly less than for overactive bladder syndrome (81). The American Urological Association (AUA) guidelines panel has upgraded BTX-A treatment from fifth to a fourth line treatment (82).
• Endourological destruction of bladder tissue aims to eliminate urothelial lesions, mostly Hunner ulcer. Resection and fulguration have been reported to achieve symptom relief, often for more than three years (83,84). Prolonged amelioration of pain and urgency has been described for transurethral laser ablation as well (85). Laser fulgration is preferred due to chronicity of the disease and need for refulgration, with possible bladder fibrosis and shrinkage.
• There is no evidence that open surgery for PBS relieves pain. Surgery for refractory BPS is only appropriate as a last resort for patients with refractory end-stage disease. Urinary diversion without cystectomy (86) is performed to minimise the duration and complexity of surgery, but complications related to the retained bladder commonly occur. Supratrigonal cystectomy with bladder augmentation represents the most favoured continence preserving surgical technique particularly in younger patients (87). Subtrigonal or simple cystectomy refers to removal of the entire bladder at the level of the bladder neck. This approach has the benefit of removing the trigone as a possible disease site, but at the cost of requiring ureteric re-implantation. Trigonal disease is reported in 50% of patients and surgical failure has been blamed on the trigone being left in place (88), especially in patients with non-ulcer type disease (89,90).
Table III:5 Recommendations for bladder pain syndrome (BPS).
Recommendation
strength rating
1.Basic assessment should include history taking, physical examination, and laboratory examination to rule in symptoms that characterize BPS and exclude other confusable disorders Strong
2.Patients should be educated about normal bladder function, what is known and not known about IC/ BPS, the benefits versus risks/burdens of the available treatment alternatives, the fact that no single treatment has been found effective for the majority of patients, and the fact that acceptable symptom control may require trials of multiple therapeutic options Strong
3.Multiple, simultaneous treatments may be considered if it is in the best interests of the patient Weak
4.Perform general anaesthetic rigid cystoscopy in patients with bladder pain to subtype and rule out confusable disease Strong
5.Cystoscopy under anesthesia with short-duration, low-pressure hydrodistension may be undertaken if first- and second-line treatments have not provided acceptable symptom control and quality of life Strong
6.Always consider offering multimodal behavioural, physical and psychological techniques alongside oral or invasive treatments of BPS Strong
7.Offer dietary advice Weak
8.Amitriptyline, cimetidine or hydroxyzine may be administered as first-line oral medications . Weak
9.Administer amitriptyline 25mg-50mg for treatment of BPS Strong
10.Intravesical heparin, lidocaine, hyaluronic acid or chondroitin sulfate may be administered as second line intravesical treatments Weak
11.Offer intravesical hyaluronic acid or chondroitin sulphate before more invasive measures. Weak
12.Offer intravesical lidocaine plus sodium bicarbonate plus heparin prior to more invasive methods Weak
13. Offer intravesical heparin before more invasive measures alone or in combination treatment Weak
14.If Hunner’s lesions are present, then laser fulguration and/or injection of triamcinolone should be performed. This should be performed in BPS type 3 C only Strong
15.Offer submucosal bladder wall and trigonal injection of BTX-A plus hydrodistension if intravesical instillation therapies have failed Strong
16.Do not recommend oral corticosteroids for long-term treatment Strong
17. Use long-acting phosphodiesterase 5 inhibitors as a single treatment for patients with bothersome, moderate to severe LUTS secondary to BPH (AUA-SI score ≥ 8) whether they suffer from erectile dysfunction or not Strong
III.10.3 References.
1- D. Engeler, A.P. Baranowski, B. Berghmans et al. EAU Guidelines on chronic pelvic pain. European Guidelines 2020.
2- Fall, M., et al. Chronic interstitial cystitis: a heterogeneous syndrome. J Urol, 1987. 137: 35.
3- Warren, J.W., et al. Evidence-based criteria for pain of interstitial cystitis/painful bladder syndrome in women. Urology, 2008. 71: 444.
4- van de Merwe, J.P., et al. Diagnostic criteria, classification, and nomenclature for painful bladder syndrome/interstitial cystitis: an ESSIC proposal. Eur Urol, 2008. 53: 60.
5- Bade, J.J., et al. Interstitial cystitis in The Netherlands: prevalence, diagnostic criteria and therapeutic preferences. J Urol, 1995. 154: 2035.
6- Burkman, R.T. Chronic pelvic pain of bladder origin: epidemiology, pathogenesis and quality of life. J Reprod Med, 2004. 49: 225.
7- Curhan, G.C., et al. Epidemiology of interstitial cystitis: a population-based study. J Urol, 1999. 161: 549.
8- Held, P., et al., Interstitial Cystitis. In: Epidemiology of interstitial cystitis. Hanno PM, Staskin DR, Krane RJ, Wein AJ, eds. 1990, Springer Verlag: London.
9- Jones, C., et al. Prevalence of interstitial cystitis in the United States. Proc Am Urol Ass J Urol, 1994. 151 (Suppl).
10- Leppilahti, M., et al. Prevalence of clinically confirmed interstitial cystitis in women: a population-based study in Finland. J Urol, 2005. 174: 581.
11- Oravisto, K.J. Epidemiology of interstitial cystitis. Ann Chir Gynaecol Fenn, 1975. 64: 75.
12- Parsons, C.L., et al. Prevalence of interstitial cystitis in young women. Urology, 2004. 64: 866.
13- Roberts, R.O., et al. Incidence of physician-diagnosed interstitial cystitis in Olmsted County: a community-based study. BJU Int, 2003. 91: 181.
14- Temml, C., et al. Prevalence and correlates for interstitial cystitis symptoms in women participating in a health screening project. Eur Urol, 2007. 51: 803.
15- Berry, S.H., et al. Prevalence of symptoms of bladder pain syndrome/interstitial cystitis among adult females in the United States. J Urol, 2011. 186: 540.
16- Song, Y., et al. Prevalence and correlates of painful bladder syndrome symptoms in Fuzhou Chinese women. Neurourol Urodyn, 2009. 28: 22.
17- Koziol, J.A., et al. Discrimination between the ulcerous and the nonulcerous forms of interstitial cystitis by noninvasive findings. J Urol, 1996. 155: 87.
18- Messing, E.M., et al. Interstitial cystitis: early diagnosis, pathology, and treatment. Urology, 1978. 12: 381.
19- Parsons, C. Interstitial cystitis: clinical manifestations and diagnostic criteria in over 200 cases. Neurourol Urodyn, 1990. 9.
20- Peeker, R., et al. Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease. J Urol, 2002. 167: 2470.
21- Mattox, T.F. Interstitial cystitis in adolescents and children: a review. J Pediatr Adolesc Gynecol, 2004. 17: 7.
22- Richter, B., et al. YKL-40 and mast cells are associated with detrusor fibrosis in patients diagnosed with bladder pain syndrome/interstitial cystitis according to the 2008 criteria of the European Society for the Study of Interstitial Cystitis. Histopathology, 2010. 57: 371.
23- Dundore, P.A., et al. Mast cell counts are not useful in the diagnosis of nonulcerative interstitial cystitis. J Urol, 1996. 155: 885.
24- Peeker, R., et al. Recruitment, distribution and phenotypes of mast cells in interstitial cystitis. J Urol, 2000.163: 1009.
25- Anderstrom, C.R., et al. Scanning electron microscopic findings in interstitial cystitis. Br J Urol, 1989. 63: 270.
26- Johansson, S.L., et al. Clinical features and spectrum of light microscopic changes in interstitial cystitis. J Urol, 1990. 143: 1118.
27- Logadottir, Y.R., et al. Intravesical nitric oxide production discriminates between classic and nonulcer interstitial cystitis. J Urol, 2004. 171: 1148.
28- Lokeshwar, V.B., et al. Urinary uronate and sulfated glycosaminoglycan levels: markers for interstitial cystitis severity. J Urol, 2005. 174: 344.
29- Parsons, C.L., et al. Epithelial dysfunction in nonbacterial cystitis (interstitial cystitis). J Urol, 1991. 145: 732.
30- Parsons, C.L., et al. Successful therapy of interstitial cystitis with pentosan polysulfate. J Urol, 1987. 138: 513.
31- Sanchez-Freire, V., et al. Acid-sensing channels in human bladder: expression, function and alterations during bladder pain syndrome. J Urol, 2011. 186: 1509.
32- Hang, L., et al. Cytokine repertoire of epithelial cells lining the human urinary tract. J Urol, 1998. 159: 2185.
33- Parsons, C.L., et al. Cyto-injury factors in urine: a possible mechanism for the development of interstitial cystitis. J Urol, 2000. 164: 1381.
34- Chelimsky, G., et al. Autonomic Testing in Women with Chronic Pelvic Pain. J Urol, 2016. 196: 429.
35- Charrua, A., et al. Can the adrenergic system be implicated in the pathophysiology of bladder pain syndrome/ interstitial cystitis? A clinical and experimental study. Neurourol Urodyn, 2015. 34: 489.
36- Alagiri, M., et al. Interstitial cystitis: unexplained associations with other chronic disease and pain syndromes. Urology, 1997. 49: 52.
37- Buffington, C.A. Comorbidity of interstitial cystitis with other unexplained clinical conditions. J Urol, 2004. 172: 1242.
38- Erickson, D.R., et al. Nonbladder related symptoms in patients with interstitial cystitis. J Urol, 2001. 166: 557.
39- Warren, J.W., et al. Antecedent nonbladder syndromes in case-control study of interstitial cystitis/painful bladder syndrome. Urology, 2009. 73: 52.
40- Weissman, M., et al. Interstitial Cystitis and Panic Disorder - A Potential Genetic Syndrome. Arch Gen Psych, 2004. 61.
41- Warren, J.W., et al. Numbers and types of nonbladder syndromes as risk factors for interstitial cystitis/painful bladder syndrome. Urology, 2011. 77: 313.
42- Peters, K.M., et al. Are ulcerative and nonulcerative interstitial cystitis/painful bladder syndrome 2 distinct diseases? A study of coexisting conditions. Urology, 2011. 78: 301.
43- Lubeck, D.P., et al. Psychometric validation of the O'leary-Sant interstitial cystitis symptom index in a clinical trial of pentosan polysulfate sodium. Urology, 2001. 57: 62.
44- Aihara, K., et al. Hydrodistension under local anesthesia for patients with suspected painful bladder syndrome/interstitial cystitis: safety, diagnostic potential and therapeutic efficacy. Int J Urol, 2009. 16: 947.
45- Parsons, C.L. The role of a leaky epithelium and potassium in the generation of bladder symptoms in interstitial cystitis/overactive bladder, urethral syndrome, prostatitis and gynaecological chronic pelvic pain. BJU Int, 2011. 107: 370.
46- Geurts, N., et al. Bladder pain syndrome: do the different morphological and cystoscopic features correlate? Scand J Urol Nephrol, 2011. 45: 20.
47- Johansson, S.L., et al. Pathology of interstitial cystitis. Urol Clin North Am, 1994. 21: 55.
48- Loving, S., et al. Does evidence support physiotherapy management of adult female chronic pelvic pain? Scan J Pain, 2012. 3: 70.
49- FitzGerald, M.P., et al. Randomized multicenter clinical trial of myofascial physical therapy in women with interstitial cystitis/painful bladder syndrome and pelvic floor tenderness. J Urol, 2012. 187: 2113.
50- Cheong, Y.C., et al. Non-surgical interventions for the management of chronic pelvic pain. Cochrane Database Syst Rev, 2014. 3: CD008797.
51- Champaneria, R., et al. Psychological therapies for chronic pelvic pain: Systematic review of randomized controlled trials. Acta Obstet Gynecol Scand, 2012. 91: 281.
52- Seshadri, P., et al. Cimetidine in the treatment of interstitial cystitis. Urology, 1994. 44: 614.
53- Sant, G.R., et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol, 2003. 170: 810.
54- Hanno, P.M., et al. Use of amitriptyline in the treatment of interstitial cystitis. J Urol, 1989. 141: 846.
55- Foster, H.E., Jr., et al. Effect of amitriptyline on symptoms in treatment naive patients with interstitial cystitis/ painful bladder syndrome. J Urol, 2010. 183: 1853.
56- Hwang, P., et al. Efficacy of pentosan polysulfate in the treatment of interstitial cystitis: a metaanalysis. Urology, 1997. 50: 39.
57- Mulholland, S.G., et al. Pentosan polysulfate sodium for therapy of interstitial cystitis. A doubleblind placebocontrolled clinical study. Urology, 1990. 35: 552.
58- Fritjofsson, A., et al. Treatment of ulcer and nonulcer interstitial cystitis with sodium pentosan polysulfate: a multicenter trial. J Urol, 1987. 138: 508.
59- Oravisto, K.J., et al. Treatment of interstitial cystitis with immunosuppression and chloroquine derivatives. Eur Urol, 1976. 2: 82.
60- Forsell, T., et al. Cyclosporine in severe interstitial cystitis. J Urol, 1996. 155: 1591.
61- Barua, J.M., et al. A systematic review and meta-analysis on the efficacy of intravesical therapy for bladder pain syndrome/interstitial cystitis. Int Urogynecol J, 2016. 27: 1137.
62- Asklin, B., et al. Intravesical lidocaine in severe interstitial cystitis. Case report. Scand J Urol Nephrol, 1989. 23: 311.
63- Giannakopoulos, X., et al. Chronic interstitial cystitis. Successful treatment with intravesical idocaine. Arch Ital Urol Nefrol Androl, 1992. 64: 337.
64- Parsons, C.L. Successful downregulation of bladder sensory nerves with combination of heparin and alkalinized lidocaine in patients with interstitial cystitis. Urology, 2005. 65: 45.
65- Nickel, J.C., et al. Intravesical alkalinized lidocaine (PSD597) offers sustained relief from symptoms of interstitial cystitis and painful bladder syndrome. BJU Int, 2009. 103: 910.
66- Hammouda Sherif, Ahmed Sebay, Wael Kandeel, Tarek Othman, Abdallah Fathi, Ahmed Mohey, and Ali Eshazly. Safety and efficacy of Intravesical hyaluronic acid/chondroitin sulfate in the treatment of refractory painful bladder syndrome. Turk J Urol. 2019 Jul; 45(4): 296–301.
67- Pyo, J.S., et al. Systematic Review and Meta-Analysis of Intravesical Hyaluronic Acid and Hyaluronic Acid/Chondroitin Sulfate Instillation for Interstitial Cystitis/Painful Bladder Syndrome. Cell Physiol Biochem, 2016. 39: 1618.
68- Parsons, C.L., et al. Treatment of interstitial cystitis with intravesical heparin. Br J Urol, 1994. 73: 504.
69- Thilagarajah, R., et al. Oral cimetidine gives effective symptom relief in painful bladder disease: a prospective, randomized, double-blind placebo-controlled trial. BJU Int 2001. 87: 207.
70- Kelly, J.D., et al. Clinical response to an oral prostaglandin analogue in patients with interstitial cystitis. Eur Urol 1998. 34: 53. 71- Korting, G.E., et al. A randomized double-blind trial of oral L-arginine for treatment of interstitial cystitis. J Urol 1999. 161: 558.
72- Cartledge, J.J., et al. A randomized double-blind placebo-controlled crossover trial of the efficacy of L-arginine in the treatment of interstitial cystitis. BJU Int, 2000. 85: 421.
73- Barbalias, G.A., et al. Interstitial cystitis: bladder training with intravesical oxybutynin. J Urol, 2000. 163: 1818.
74- van Ophoven, A., et al. The dual serotonin and noradrenaline reuptake inhibitor duloxetine for the treatment of interstitial cystitis: results of an observational study. J Urol, 2007. 177: 552.
75- Fariello, J.Y., et al. Sacral neuromodulation stimulation for IC/PBS, chronic pelvic pain, and sexual dysfunction. Int Urogynecol J, 2010. 21: 1553.
76- Cottrell, A.M., et al. Benefits and Harms of Electrical Neuromodulation for Chronic Pelvic Pain: A Systematic Review. Eur Urol Focus, 2019.
77- Tutolo, M., et al. Efficacy and Safety of Sacral and Percutaneous Tibial Neuromodulation in NonNeurogenic Lower Urinary Tract Dysfunction and Chronic Pelvic Pain: A Systematic Review of the Literature. Eur Urol, 2018. 73: 406.
78- El-Hefnawy AS, Makharita MY, Abed A, Amr YM, Salah El-Badry M, Shaaban AA. Anesthetic Bladder Hydrodistention Is Superior to Superior Hypogastric Plexus Neurolysis in Treatment of Interstitial Cystitis-bladder Pain Syndrome: A Prospective Randomized Trial. Urology. 2015 May;85(5):1039-1044.
79- Kuo, H.C., et al. Comparison of intravesical botulinum toxin type A injections plus hydrodistention with hydrodistention alone for the treatment of refractory interstitial cystitis/painful bladder syndrome. BJU Int, 2009. 104: 657.
80- Pinto, R., et al. Trigonal injection of botulinum toxin A in patients with refractory bladder pain syndrome/interstitial cystitis. Eur Urol, 2010. 58: 360.
81- Kuo, Y.C., et al. Adverse Events of Intravesical Onabotulinum Toxin A Injection between Patients with Overactive Bladder and Interstitial Cystitis-Different Mechanisms of Action of Botox on Bladder Dysfunction? Toxins, 2016. 8
82- Hanno, P.M., et al. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol, 2015. 193: 1545.
83- Kerr, W.S., Jr. Interstitial cystitis: treatment by transurethral resection. J Urol, 1971. 105: 664.
84- Peeker, R., et al. Complete transurethral resection of ulcers in classic interstitial cystitis. Int Urogynecol J Pelvic Floor Dysfunct, 2000. 11: 290.
85- Rofeim, O., et al. Use of the neodymium: YAG laser for interstitial cystitis: a prospective study. J Urol, 2001. 166: 134.
86- Freiha, F.S., et al. The surgical treatment of intractable interstitial cystitis. J Urol, 1980. 123: 632.
87- Kim, H.J., et al. Efficacy and safety of augmentation ileocystoplasty combined with supratrigonal cystectomy for the treatment of refractory bladder pain syndrome/interstitial cystitis with Hunner's lesion. Int J Urol, 2014. 21 Suppl 1: 69.
88- Nurse, D.E., et al. The problems of substitution cystoplasty. Br J Urol, 1988. 61: 423.
89- Peeker, R., et al. The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease. J Urol, 1998. 159: 1479.
90- Rossberger, J., et al. Long-term results of reconstructive surgery in patients with bladder pain syndrome/interstitial cystitis: subtyping is imperative. Urology, 2007. 70: 638.
III.11 Female Bladder Outlet Obstruction (BOO).
III.11.1 Definition and Background.
• BOO in females is an under-reported and underdiagnosed problem worldwide due to paucity of clinical studies and lack of well-defined diagnostic criteria. (1) Prevalence of BOO among females undergoing urodynamics (UDS) for lower urinary tract symptoms (LUTS) range from 2.7% to 29%. (2-5). This is attributed to many definitions used to diagnose BOO in these studies. Different nomograms based on urodynamic parameters have been reproduced, but none was approved worldwide for use. (2,6,7)
• Symptoms of female BOO are mostly non-specific and the classic voiding LUTS of impaired urine flow, hesitancy, intermittent stream, straining and even retention may be less apparent, making diagnosis difficult. (1,8) Other presenting symptoms, e.g. irritative voiding complaints, may be secondary to BOO. Urethral pain and recurrent urinary tract infections (UTIs) are other presenting symptoms as well. Bending forward to void or having to change positions to empty effectively usually indicates an element of obstruction in post anti-stress urinary incontinence (SUI) operations (8). This raises the importance of high level of suspicion for BOO in women. Finally, this problem is often not suspected in women, and so its management is typically delayed. (1)
• Female BOO can be caused by anatomical or functional causes. Furthermore, anatomical causes include extrinsic and intrinsic (luminal) factors. (9) Extrinsic causes include pelvic organ prolapse (POP), iatrogenic post anti-incontinence procedure and skene gland abscess or cyst, while intrinsic causes include urethral stricture or fibrosis, urethral diverticulum, excessive bulking agent, urethral tumour, condyloma accuminata, urethral stone, urethral caruncle or urethral prolapse. Functional causes include primary bladder neck obstruction, pseudo-dyssynergia known as Hinman’s syndrome and detrusor sphincter dyssynergia (DSD). (1,8)
• Detrusor failure or acontractility should be excluded, and pressure-flow study could be of help in the diagnosis. However, there are currently no nomograms that accurately assesses detrusor underactivity (DUA) in women. (1,9)
• In a study by Greenwell et al (1), 192 females with BOO were diagnosed. Anatomical obstruction was found in 64% and functional obstruction was present in 36%. The most common anatomical cause of BOO was previous anti-SUI surgery (21%), followed by urethral stricture (20%).
III.11.2 Diagnosis.
• Urine analysis is an important initial tool to exclude infections. Urine culture and sensitivity is recommended specially in the context of recurrent UTIs. Renal function tests could be elevated if condition is severe or chronic with elevated postvoid residual (PVR). Bladder scan is indicated to estimate PVR. Imaging is indicated when renal function is impaired or when organic cause is suspected. Role of cystourethroscopy is crucial, especially if associated with difficult catheterization or previous anti-incontinence procedures. (1,8)
• Many nomograms have been utilized, with different prevalence rates. Ferrar et al. diagnosed BOO based only on Qmax of <15 mL/s with prevalence of BOO of 6.7%. (3) Massey and Abrams diagnosed BOO in only 2.7% of 5948 females based on 2 or more of the following criteria: Qmax <12 mL/s, pdet @Qmax >50 cmH2O, urethral resistance (pdet @Qmax/ 2Qmax) >0.2, and significant PVR. (4) Lemack and Zimmern used cut-off values of Qmax ≤15 mL/s and pdet@ Qmax>20 cmH2O, diagnosing BOO in 20% of the patients. (7) Blaivas and Groutz created a nomogram to diagnose BOO and classify its severity based on pressure–flow criteria of a free Qmax ≤12 mL/s and a Pdet @Qmax ≥20 cmH2O, in association with radiographic evidence of obstruction, and reported a prevalence of 8.3%.(2)
• Elmissiry et al. categorized females with BOO into three different subtypes based on urodynamic patterns (early, compensated and late obstruction). They recommended that UDS should be combined with the clinical presentation and estimation of PVR for an accurate diagnosis of BOO. (10)
• The role of pressure flow studies alone to diagnose female BOO is questioned because voiding dynamics in females are different from those in males, and most of the females void predominantly by pelvic floor relaxation or abdominal straining with low detrusor pressures. Nitti et al. introduced the role of videourodynamics (VUDS), combined with clinical suspicion of BOO, with an overall prevalence of 29%. (11,12)
III.11.3 Treatment.
• Treatment usually depends on treatment of the cause. (8) Prolapse correction in cases of POP. (12, 14) In cases of iatrogenic post-tape obstruction, CIC could be tried for the first week. Tape release could be tried initially within the first 10 days. If failed, tape incision could be done in the first two months (15), with urethrolysis being a last resort in some refractory cases. (16,17)
• Most urethral strictures or fibrosis in women are iatrogenic and can result from previous urethral or periurethral surgery, or in some cases from previous urethral dilatation. Many females experience urethral strictures from previous obstructed labors. Options include urethral dilatations, better under brief anesthesia, cystourethroscopy, or in resistant recurrent cases, urethroplasty with vaginal flap or buccal mucosal grafts is indicated but in highly specialized referral centers. (8,18,19)
• Primary bladder neck obstruction is caused by lack of relaxation of the smooth muscle of the bladder neck during voiding, and it responds well to alpha blockers. CIC could be an option if medications fail. Transurethral incision of the bladder neck is definitive, but with increased risks of postoperative incontinence. Neuromodulation is of help in these cases. (20-24)
• Pseudo-dyssynergia or Hinman’s syndrome results from an external sphincter that does not relax during voiding in an otherwise neurologically intact woman. First-line treatment consists of pelvic floor relaxation. Skeletal muscle relaxants such as diazepam can be used as well, but the side-effects limit their applicability. Intrasphincter botulinum injection is successful in many cases, but this is off-label use. Finally, sacral neuromodulation has been used successfully.
• DSD occurs when the external sphincter contracts during a detrusor contraction in a neurologically impaired individual. It is common in patients with suprasacral spinal cord injuries (SCI) and multiple sclerosis (MS). Introduction of botulinum toxin injections into the external sphincter of these patients is successful. (8,25)
Table III:6 Recommendations for female bladder outlet obstruction (BOO).
Recommendation
strength rating
1. Role of VUDS, combined with the clinical symptoms of BOO, is more accurate in diagnosing BOO and determining the site of obstruction
Strong
2. Pressure-flow study is of low yield in diagnosing female BOO Weak
3. Suspect BOO in females who underwent slings recently if they experience deNovo storage symptoms, or if they report change in position when they void (lean forward or squat) Weak
4. Estimation of PVR in patients suspected with BOO is mandatory
Strong
5. Perform cystourethroscopy in female patients suspected with BOO Weak
6.Offer alpha blockers initially in cases diagnosed with primary bladder neck obstruction Strong
7. Urethral dilatations, better under general anesthesia, is of help in cases of urethral strictures or fibrosis in women Strong
8. Transurethral incision or resection of the bladder neck is definitive in primary bladder neck obstruction, but with increased risks of postoperative incontinence Weak
9. Offer initially pelvic floor muscle exercises in patients suspected with Hinman’s syndrome Strong
10. Offer skeletal muscle relaxants such as diazepam in patients diagnosed with Hinman’s syndrome, but the side effects limit their applicability Weak
11. Offer intrasphincter botulinum injection in cases of Hinman’s syndrome, pseudodyssynergia and DSD, with better results in DSD patients Weak
III.11.4 References.
1- Malde S, Solomon E, Spilotros M, Mukhtar B, Pakzad M, Hamid R, Ockrim J, Greenwell T. Female bladder outlet obstruction: Common symptoms masking an uncommon cause. Low Urin Tract Symptoms. 2019 Jan; 11(1):72-77.
2- Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn. 2000; 19(5):553–564.
3- Farrar DJ, Osborne JL, Stephenson TP, et al. A urodynamic view of bladder outflow obstruction in the female: factors influencing the results of treatment. Br J Urol. 1975; 47(7):815–822.
4- Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol. 1988; 61(1):36–39.
5- Rees DL, Whitfield HN, Islam AK, Doyle PT, Mayo ME, Wickham JE. Urodynamic findings in adult females with frequency and dysuria. Br J Urol. 1975; 47(7):853–860.
6- Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS, Zimmern PE. Proposed cutoff values to define bladder outlet obstruction in women. Urology. 1998; 51(3):408–411.
7- Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying women with outflow obstruction. J Urol. 2000; 163 (6):1823–1828.
8- Goldman HB, Zimmern PE. The treatment of female bladder outlet obstruction. BJU Int. 2006 Sep; 98 Suppl 1:17-23
9- Are There Pharmacotherapeutic Options for Underactive Bladder? Osman NI, Chapple CR. Eur Urol Focus. 2018 Jan; 4(1):6-7.
10- Elmissiry MM, Ali AG, Ali GA. Different urodynamic patterns in female bladder outlet obstruction: Can urodynamics alone reach the diagnosis? Arab J Urol. 2013 Jun; 11(2):127-30.
11- Patel R, Nitti V. Bladder outlet obstruction in women: prevalence, recognition and management. Curr Urol Rep. 2001; 2(5):379–387.
12- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol. 1999; 161(5):1535–1540.
13- Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999; 161: 581–6
14- Gilleran JP, Lemack GE, Zimmern PE. Reduction of moderate-to-largecystocele during urodynamic evaluation using a vaginal gauze pack: 8-year experience. BJU Int 2006; 97: 292–5
15- Goldman HB. Simple sling incision for the treatment of iatrogenic urethral obstruction. Urology 2003; 62: 714–8
16- Goldman HB. Urethrolysis. Atlas Urol Clinics 2004; 12: 197–204
17- Carey JM, Chon JK, Leach GE. Urethrolysis with Martius labial fat pad graft for iatrogenic bladder outlet obstruction. Urology 2003; 61(Suppl.4):21–5
18- Nnenaya Agochukwu-Mmonu, Sudarshan Srirangapatanam. Andrew Cohen, Benjamin Breyer.Female Urethral Strictures: Review of Diagnosis, Etiology, and Management. J Med Case Rep. 2018; 12: 382.
19- Lemack G, Zimmern PE. Voiding difficulties. In Shaw R, Soutter WP, Stanton SL eds, Gynaecology, 3rd edn. Edinburgh: Churchill Livingstone, 2003: 803–12
20- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999; 161: 1535–40
21- Kumar A, Mandhani A, Gogoi S, Srivastava A. Management of functional bladder neck obstruction in women: use of alpha-blockers and pediatric resectoscope for bladder neck incision. J Urol 1999; 162: 2061-5
22- Blaivas J, Flisser AJ, Tash JA. Treatment of primary bladder neck obstruction in women with transurethral resection of the bladder neck. J Urol 2004; 171: 1172–5
23- Peng CH, Kuo HC. Transurethral incision of bladder neck in treatment of bladder neck obstruction in women. Urology 2005; 65: 275–8
24- Hourieh Sharifian, Mahtab Zargham, Mohamad Hatef Khorami et al. Internal urethrotomy in treatment of female with anatomical bladder outlet obstruction. Adv Biomed Res. 2019; 8: 36.
25- Moore C, Rackley R, Goldman H. Urologic applications of botox. Curr Urol Rep 2005; 6: 419–23
III.12 Geriatric urinary incontinence.
• Urinary incontinence (UI) can be considered both a specific diagnosis and a geriatric syndrome. This is particularly of significance in frail elderly population, with multiple chronic morbid conditions. (1)
• Geriatric syndromes are defined as common conditions seen in the elderly that are complex in nature, are usually multifactorial, and can have clinical or other negative health outcomes for affected patients. (2)
• The incidence and prevalence of UI increase in the elderly population. However, incontinence should not be considered a normal or inevitable aging event. This is a common myth among both health care providers and patients. (3)
• UI is accompanied with social isolation, stigmatization, depression, aversion from sexual life and embarrassment. Skin irritation and cracking from urine, development of pressure ulcers, recurrent urinary tract infections (UTIs), falls and fractures are all substantial physical problems. (4) UI has a stronger negative influence on overall levels of happiness than diabetes, hypertension, arthritis, and osteoporosis. (5)
• Economic data has shown an estimated national cost of evaluation and care for wetoveractive bladder (OAB) of $65.9 billions in 2007, with estimated increase to $76.2 billions in 2015 and $82.6 billions in 2020. (6) The degree of incontinence in the elderly as measured by severity appears to be more influential on health-related quality of life (QoL) outcomes than type of UI. (7)
III.12.1 Transient urinary incontinence.
III.8.2 Diagnostic evaluation.
• Examination
• Inability to void is usually a sign of a complete injury
• Incomplete injuries are associated with pain on urination, hematuria or blood present at the vaginal introitus in female patients with pelvic fractures and co-existing urethral injuries
• Cysto-urethroscopy is the preferred diagnostic modality in case of suspected female urethral injury
• VCUG may be needed in late diagnosis and to outline any associated urinary bladder, bladder neck injuries or uro-genital fistulae.
III.8.3 Surgical management.
• In case of hemodynamic instability, provide urinary diversion by suprapubic catherization or a single attempt of urethral catheterization.
• In case of pelvic fracture induced urethral injuries, early repair within seven days has the highest success rate and the lowest complication rate in comparison with delayed repair or early endoscopic re-alignment.
• In case of urethral injury during sling procedure, synthetic mesh should be removed and immediate urethral repair (12).
Recommendation |
strength rating |
|---|---|
III.9 Uro-gynecological fistulae
III.9.1 Causes.
o In developed countries. Non-obstetric (surgical) fistula is considered the most common cause of uro-gynecological fistulae (e.g., post abdominal hysterectomy, POP repair surgery, anti-incontinent surgery)
o In the developing countries. Obstetric fistula is considered the most common cause due to prolonged obstructed labor (13,14)
o Risk factors for obstetric fistula include lack of prenatal care, young age of first marriage, low socio-economical class, short stature, poor nutrition, lack of proper surgical training for obstetrician (13,14)
III.9.2 Different types of uro-gynecological fistula.
o Vesicovaginal fistula (VVF)
o Urethrovaginal fistula (UVF)
o Rectovaginal fistula (RVF)
o Ureterovaginal fistula
o Vesicouterine fistula
o Sometimes more than one type of fistula may occur at the same time (Complex fistula)
III.9.3 Diagnosis.
Unfortunately, intraoperative diagnosis of a genitourinary (GU) is made in only about half of the cases that result in fistula. Clinical diagnosis of leakage of urine is the hallmark sign of a fistula. The leakage is usually painless, may be intermittent if its position is independent, or maybe constant (15).
The diagnosis of VVF usually requires clinical assessment often in combination with appropriate imaging or laboratory studies. Direct visual inspection, cystoscopy, retrograde bladder filling with a coloured fluid or placement of a tampon into the vagina to identify staining may facilitate the diagnosis of a VVF. A double-dye test is used to differentiate between ureterovaginal and VVF in some cases (15). Cyclic hematuria may be pathognomonic sign of vesico-uterine fistula.
Testing the creatinine level in either the extravasated fluid or the accumulated ascites and comparing this to the serum creatinine levels will confirm urinary leakage. Contrast-enhanced CT with late excretory phase reliably diagnoses urinary fistulae and provides information about ureteric integrity and the presence of associated urinoma (16).
III.9.4 Treatment.
III.9.4.1 Management of vesicovaginal fistula.
III.9.4.1.1 Conservative management.
It may tend to close spontaneously in small sized fistula before complete epithelialization of the fistulous tract, provided that the natural outflow is unobstructed or if urine is diverted. Hence, immediate management should be by urinary catheterization or diversion (17,18)
III.9.4.1.2 Surgical management.
The most important points to be considered in fistula repair are fistula location, fistula size and dimensions, number of fistulae, extent of vaginal scarring, surgical approach and technique used (19).
III.9.4.1.2.1 Timing of surgery.
Findings from uncontrolled case series suggest no difference in success rates for early versus delayed closure of VVF. Tailor the timing of fistula repair to the individual patient and surgeon requirements once any edema, inflammation, tissue necrosis, or infection are resolved (20,21).
III.9.4.1.2.2 Surgical principles.
The best chance for successful fistula closure is at the first operation and closure rates tend to diminish with each subsequent attempt at operative repair (18).
The ureters should be identified and protected to ensure they are not cut or ligated during the fistula repair 19. The fistula should be mobilized from the surrounding tissues at the time of repair. The fistula should be closed without tension at the site of repair. The repair must be watertight. To ensure this, a dye test is performed intra-operatively and, if there is still leakage, the repair is sutured again (19).
A single randomized controlled trial compared trimming of the fistula edge with no trimming showed no difference in success rates, but failed repairs in trimmed cases ended up with larger recurrences than untrimmed cases (22).
A Martius flap in primary obstetric fistula repair is debatable with no clear evidence of its value and is usually reserved for recurrent cases, fistulae secondary to radiation or in case of associated urethral reconstruction (19).
One prospective randomized controlled trial compared the use of a Martius flap “as an interposition flap” to the use of a self-made fibrin glue. There was no statistical difference in outcome, but the authors stated that the use of fibrin glue allowed the fistula repair to be quicker (23).
III.9.4.1.2.3 Surgical approaches.
III.9.4.1.2.3.1 Vaginal procedures.
There are two main types of closure techniques applied to the repair of urinary fistulae, the classical saucerisation/partial colpocleisis and the more commonly used dissection and repair in layers or ‘flap- splitting’ technique. There are no data comparing their outcomes (24,25).
III.9.4.1.2.3.2 Abdominal procedures.
Repair is indicated when high fistulae are fixed in the vault and are inaccessible through the vagina. A trans-vesical repair has the advantage of being entirely extraperitoneal. A simple transperitoneal repair is used less often although it is favoured by some surgeons using the laparoscopic approach. A combined transperitoneal and transvesical procedure is favoured by many urologists and is particularly useful for fistula repair following Caesarean section.
There are no randomised studies comparing abdominal and vaginal approaches. When concurrent ureteric re-implantation or augmentation cystoplasty are required, the abdominal approach is necessary.
III.9.4.1.2.4 Post-operative management.
Catheter drainage for at least 10 days and longer periods in radiation associate fistulae (up to 3 weeks). No sexual intercourse for one month. Surgical treatment of postoperative SUI should only be considered six months after the fistula repair.
III.9.4.2 Management of radiation fistula.
Successful repair of irradiated fistulae requires prior urinary diversion and the use of non-irradiated tissues to ensure successful repair (26).
III.9.4.3 Management of ureteric fistula.
III.9.4.3.1 Endoscopic management.
Is often possible (16) by retrograde stenting, percutaneous nephrostomy and antegrade stenting if there is pelvicalyceal dilatation, or by ureteroscopy (17).
III.9.4.3.2 Surgical management.
III.9.4.3.2.1.1 Timing of repair.
If early discovery within two weeks, immediate repair of any injury should be performed observing the principles of debridement, adequate blood supply and tension free anastomosis with internal drainage using stents (27).
In case of delayed presentation of upper tract injury, conservative management is still possible with internal or external drainage, endoluminal management using nephrostomy and stenting where available, and early (< 3 months) or delayed (> 6 months) surgical repair when required (14).
If endoluminal techniques fail or result in secondary stricture, the abdominal approach to repair is the standard and requires re-implantation into the bladder with or without psoas hitch or Boari flap, or replacement with bowel segments with or without reconfiguration (28,29).
Functional and anatomical imaging should be used to follow up patients after repair to guard against late upper tract deterioration (14).
III.9.4.4 Management of vesicouterine fistula.
Surgical repair through abdominal approach whether by open or laparoscopic techniques, which can be preceded by cystoscopy and gauging of the fistulous tract using ureteric catheter. Hysterectomy may be considered in multiparous women (30,31).
III.9.4.5 Management of urethro-vaginal fistula.
Principles of reconstruction include identifying the fistula, creation of a plane between vaginal wall and urethra, watertight closure of urethral wall, eventual interposition of tissue, and closure of the vaginal wall (32).
Table III:4 Recommendations for uro-gynecological fistulae.
Recommendation
strength rating
1.Uro-gynecological fistulae can be diagnosed mainly by clinical examination which can be complemented by some radiological investigation as VCUG, or CT urography in some types of fistula and cystoscopy Strong
2.The commonest of uro-gynecological fistulae is VVF, which is managed mainly by surgical repair whether through vaginal or abdominal approaches Strong
3.Small VVF less 5 mm may close spontaneously by urinary catheterization or diversion provided that natural outflow is unobstructed
Weak
4.Timing of repair has no difference in the success of surgery Weak
5.Tailor the timing of fistula repair to the individual patient and surgeon requirements once any oedema, inflammation, tissue necrosis, or infection, are resolved Weak
6.There is no high-quality evidence of differing success rates for repair of vesicovaginal fistulae by vaginal, abdominal, trans-vesical or transperitoneal approaches Weak
7.Trimming of the edges of VVF has no difference in success rates but failed repairs in trimmed cases ended up with larger recurrences than untrimmed cases Strong
8.A Martius flap in primary obstetric fistula repair is debatable with no clear evidence of its value and usually reserved for recurrent cases, fistulae secondary to radiation or in case of associated urethral reconstruction Weak
9.Endoscopic management is the cornerstone in treatment of uretro-vaginal fistula. Otherwise, open or laparoscopic ureteric re-implantation may be performed Weak
10.Vesico-uterine fistula repair is mainly through abdominal approach, whether by open or laparoscopic techniques Strong
11.Attention should be given as appropriate to skin care, nutrition, rehabilitation, counselling and support prior to, and following, fistula repair Weak
12.Successful repair of irradiated fistulae requires prior urinary diversion and the use of non-irradiated tissues to ensure successful repair Weak
13.There is no high-level evidence to support any particular practice in postoperative management, but most reported series used catheter drainage for at least ten days and longer periods in radiation-associated fistulae up to three weeks Weak
III.9.5 References.
1. Chapple C. Female urology. Vol. 21, Current Opinion in Urology. 2011. 267 p.
2. Mitchell JD. Diverticulum of the Female Urethra11The opinions and assertions contained herein are the private views of the writers and are not to be considered as official or reflecting the views of the Navy Department or the Naval Service at large. J Urol [Internet]. 1936;51(4):411–23. Available from: http://dx.doi.org/10.1016/S0022-5347(17)70372-2
3. Lee JWS, Fynes MM. Female urethral diverticula. Best Pract Res Clin Obstet Gynaecol. 2005;19(6):875–93.
4. Ganabathi K, Leach GE, Zimmern PE, Dmochowski R. Experience with the Management of Urethral Diverticulum in 63 Women. J Urol [Internet]. 1994 Nov;152(5 Part 1):1445–52. Available from: http://www.jurology.com/doi/10.1016/S0022-5347%2817%2932442-4
5. Ultrasonography T, Pulsed W, Of CD, Urethral F. Translabial ultrasonography with pulsed colour-doppler in the diagnosis of female urethral diverticula. 1994;101–4.
6. Dinkelaar W, Dohle GR, Krestin GP, Rs D, Dinkelaar W, Wcj H. Diagnosis in Symptomatic Women. 2011;(September):676–82.
7. Bradley CS, Rovner ES. URODYNAMICALLY DEFINED STRESS URINARY INCONTINENCE AND BLADDER OUTLET OBSTRUCTION COEXIST IN WOMEN. 2004; 171:757–61.
8. Saito S. Usefulness of Diagnosis by the Urethroscopy Under Anesthesia and Effect of Transurethral Electrocoagulation in Symptomatic Female Urethral Diverticula. 2000; 14(5):455– 7.
9. Leach GE. BENIGN FEMALE PERIURETHRAL MASSES. J Urol [Internet]. 1994; 152(6):1943–51. Available from: http://dx.doi.org/10.1016/S0022-5347 (17)32276-0
10. Vakili B, Wai C, Nihira M. Anterior Urethral Diverticulum in the Female: Diagnosis and Surgical Approach. 2003; 102(5).
11. Gasthuis SF. P OI N T OF T E C H NI QU E Management of female urethral diverticula by transurethral incision. 1996; 745–6.
12. Patel DN, Fok CS, Webster GD, Anger JT. Female urethral injuries associated with pelvic fracture: a systematic review of the literature. BJU Int. 2017; 120(6):766–73.
13. Bettez M, Breault G, Carr L, Tu LM. Case report Early versus delayed repair of vesicouterine fistula. 2011; 5(4):52–5.
14. Murray C, Goh JT, Fynes M, Carey MP. Urinary and faecal incontinence following delayed primary repair of obstetric genital fistula. 2002; 109(July):828–32.
15. Æ JHÆTPP. Vesico-vaginal fistula : report of 220 cases. 2009; 299–302.
16. Exhibit E. Fistulas in Malignant Gynecologic Disease : Etiology, Imaging, and. 2009; 1073–84.
17. Faso B. Fistulas in the Developing World. : 1419–58.
18. Bazi T. Spontaneous closure of vesicovaginal fistulas after bladder drainage alone : review of the evidence. 2007; 329–33.
19. Mourad S. Vesico-vaginal fistula in the developing world. 2020;
20. Waaldijk K. The imediate surgical management of fresh obstetric fistulas with catheter and / or early closure. 1994; 11–6.
21. Vierhout ME. Prospective results after first-time surgery for obstetric fistulas in East African women. 2008; (November 2002):73–9.
22. Shaker H, Saafan A, Yassin M, Idrissa A, Mourad MS. Obstetric Vesico-Vaginal Fistula Repair: Should We Trim The Fistula Edges ? A Randomized Prospective Study. 2011; 305(July 2010):302–5.
23. Safan A, Shaker H, Abdelaal A, Mourad MS, Albaz M. Fibrin Glue Versus Martius Flap Interpositioning in the Repair of Complicated Obstetric Vesicovaginal Fistula. A Prospective Multi-Institution Randomized Trial. 2009; 441(May):438–41.
24. Kumar S, Pal ÆBC. Latzko repair for vesicovaginal fistula revisited in the era of minimal-access surgery. 2008; 317–20.
25. Wall LL. Dr. George Hayward (1791 – 1863): a forgotten pioneer of reconstructive pelvic surgery. 2005; 330–3.
26. Langkilde NC, Pless TK, Lundbeck F, Nerstrøm B. Surgical Repair of Vesicovaginal Fistulae. 1999;
27. Brandes S, Coburn M, Armenakas N, Mcaninch J. The Consensus on Genitourinary by a team of experts under the Diagnosis and management of ureteric injury: an evidence-based. 2004;
28. Shaw MBK, Tomes M, Rix DA, Dorkin TJ, Murthy LNS, Pickard RS. The Management of Bilateral Ureteric Injury following Radical Hysterectomy. 2008; 2008.
29. Narang V, Sinha T, Karan SC. Ureteroscopy: Savior to the gynecologist ?— Ureteroscopic management of post laparoscopic-assisted vaginal hysterectomy ureterovaginal fistulas. 2007 ;( 1):345–7.
30. Rajamaheswari N, Chhikara AB. Vesicouterine fistulae: Our experience of 17 cases and literature review. Int Urogynecol J Pelvic Floor Dysfunct. 2013; 24(2):275–9.
31. Milani R, Cola A, Frigerio M, Manodoro S. Repair of a vesicouterine fistula following cesarean section. Int Urogynecol J. 2018; 29(2):309–11.
32. Pushkar DY, Dyakov V V, Kosko JW, Kasyan GR. Management of Urethrovaginal Fistulas. 2006; 50:1000–5.
III.10 Bladder Pain Syndrome (BPS).
III.10.1 Definition.
• It is the occurrence of persistent or recurrent pain perceived in the urinary bladder region, accompanied by at least one other symptom, such as pain worsening with bladder filling and daytime and/or night-time urinary frequency with no proven infection or other obvious local pathology for a period more than six weeks. (1)
• Pain characteristics include pain, pressure or discomfort perceived to be related to the bladder, increasing with increasing bladder volume. It is located suprapubically, sometimes radiating to the groins, vagina, rectum or sacrum. It is relieved by voiding but soon returns (2,3). It could be aggravated by food or drink. (3)
• Bladder pain syndrome is often associated with negative cognitive, behavioral, sexual or emotional consequence. BPS is believed to represent a heterogeneous spectrum of disorders. Localization of the pain can be difficult by examination. Cystoscopy with hydrodistension and biopsy may be indicated to define phenotypes. Recently, ESSIC has suggested a standardized scheme of sub-classifications (4) to acknowledge differences and make it easier to compare various studies. Other terms that have been used include “interstitial cystitis”, “painful bladder syndrome”, and “PBS/IC” or “BPS/IC”. These terms are no longer recommended.
• Prevalence varies largely, along with the diagnostic criteria and populations studied. Recent reports range from 0.06% to 30% (5-14). There is a female preponderance of about 10:1 (9) but no difference in race or ethnicity (15,16). The relative proportions of classic and nonlesion disease are unclear and their incidence in studies has ranged from 5 to 50% (16-20). Children under the age of eighteen may be affected as well, although prevalence figures are low (21).
III.10.1.1 Risk factors.
• The cause of BPS is proposed to be an unidentified insult to the bladder, leading to urothelial damage, neurogenic inflammation and pain. BPS might be a local manifestation of a systemic disorder. No infection has been incriminated in the pathogenesis of BBS (1).
• Pancystitis, with associated perineural inflammatory infiltrates, and mastocytosis is an essential part of BPS type 3 C (22), but is scant in non-lesion BPS (23,24). Cystoscopic and biopsy findings in both lesion and non-lesion BPS are consistent with defects in the urothelial glycosaminoglycan (GAG) layer which might expose submucosal structures to noxious urine components (25-31) and a consequent cytotoxic effect (32,33). Autonomic dysfunction with sympathetic predominance may be implicated in BPS (34,35).
• An association has been reported between BPS and non-bladder syndromes such as fibomyalgia (FM), inflammatory bowel syndrome, vulvodynia, depression, panic disorders, migraine, sicca syndrome, temporomandibular joint disorder, allergy, asthma and systemic lupus erythematosus (36-40). Risk of BPS correlates with a number of nonbladder syndromes in each patient (41). Recent research showing non-lesion BPS to have significantly more FM, migraine, temporomandibular joint disorder and depression than BPS type 3C patients, emphasizes the need for subtyping (42).
III.10.1.2 Diagnosis.
• This is mainly a disease of exclusion. The clinical examination often serves to confirm what we have gained from the history taking. Besides the local examination, a general musculoskeletal and neurological examination should be considered an integral part of the assessment. There is no specific diagnostic test for BPS, therefore, procedures are directed towards identification and exclusion of specific diseases associated with pelvic pain, and for phenotypic description.
• Ultrasound on the abdomen and pelvis is done to exclude gross pelvic pathology, but with limited value to diagnose PBS. Urine dipstick and urine culture (including culture for tuberculosis if sterile pyuria) are recommended in all patients suspected of having BPS. Urine cytology is also recommended to exclude malignancy (1).
• Symptom scores may help to assess the patient and act as outcome measures. The O’LearySant Symptom Index, also known as the Interstitial Cystitis Symptom Index (ICSI) was validated for use (43).
• Objective findings from cystoscopy are important for diagnosis, prognosis and ruling out other treatable conditions (44). Endoscopically, BPS type 3 displays reddened mucosal areas often associated with small vessels radiating towards a central scar, sometimes covered by a small clot or fibrin deposit - the Hunner ulcer (2). The scar ruptures with increasing bladder distension, producing a characteristic waterfall type of bleeding. There is a strong association between BPS type 3 and reduced bladder capacity under anaesthesia. Nonlesion disease displays a normal bladder mucosa at initial cystoscopy. The development of glomerulations after hydrodistension is considered to be a positive diagnostic sign although they can be observed without BPS. Biopsies are helpful in establishing or supporting the clinical diagnosis of both classic and non-lesion types of the disease (26,44-47). Important differential diagnoses to exclude, by histological examination, are carcinoma in situ and tuberculous cystitis
III.10.2 Management.
• Treatment is usually multimodal (1). It includes lifestyle interventions such as fluid intake modifications, smoking cessation, exercise and no wearing of tight clothes. Another aspect is pain education and education about the causes of pain. Dietary restrictions alone do not produce significant symptomatic relief and scientific data are limited, however, consider the involvement of a dietician.
• The physiotherapist is part of the pain management team, together with the pain doctor and the psychologist. Physiotherapists can either specifically treat the pathology of the pelvic floor muscles, or more generally treat myofascial pain if it is part of the pelvic pain syndrome (48). Efficacy and safety of pelvic floor myofascial physical therapy has been compared with global therapeutic massage in women with BPS; global response assessment (GRA) rate was 59% and 26%, respectively. Pain, urgency and frequency ratings, and symptoms decreased in both groups during follow-up, and did not differ significantly between the groups. This suggests that myofascial physical therapy is beneficial in women with BPS (49).
• Psychological interventions are directed at pain itself or at adjustment to pain in terms of function and mood. Ideally, treatment follows general principles and practice in the field of chronic pain (49). Two systematic reviews and meta-analyses of the few heterogeneous trials of psychologically based treatment for pelvic pain (50,51) found some short-term benefits for pain, of around 50%, comparable to that from pharmacotherapy, but this was not sustained at follow-up.
• Medical therapy includes many option modalities. Histamine receptor antagonists have been used to block the H1 and H2 receptor subtypes (52), with unsatisfactory results (53). Amitriptyline is a tricyclic antidepressant. Several reports have indicated improvement of BPS symptoms after oral amitriptyline (54,55). Drowsiness is a side effect of amitriptyline. Subjective improvement of pain, urgency, frequency, but not nocturia, has been reported with use of Pentosane polysulphate (56,57). It has a more favorable effect in BPS type 3C than in non-lesion disease (58). Immunosuppressants have been tried. Azathioprine and cyclocporin A (59,60) treatment have resulted in disappearance of pain and urinary frequency. Corticosteroids are not recommended in the management of patients with BPS because of lack of evidence.
• Intravesical route is an appealing mode of delivery in PBS. Intravesical drugs are administered due to poor oral bioavailability, establishing high drug concentrations within the bladder, with few systemic side-effects. Disadvantages include the need for intermittent catheterization which can be painful in BPS patients, cost and risk of infection (61). Several drugs have been tried. There are sporadic reports of successful treatment of BPS with intravesical lidocaine (62,63). Combination of heparin, lidocaine and sodium bicarbonate gave immediate symptom relief in 94% of patients and sustained relief after two weeks in 80% (64). Intravesical instillation of alkalized lidocaine for five consecutive days resulted in significantly sustained symptom relief for up to one month (65). Hyaluronic acid and chondroitin sulphate are described to repair defects in the GAG layer (66). Most of the studies are uncontrolled and with a small number of patients and most studies are nonrandomized and with few numbers (67). Symptomatic improvement was reported in 80% of BPS patients with intravesical heparin (67,68).
• There are treatments which are of limited value in BPS. These include cimetidine, with limited data to suggest that cimetidine improves symptoms of BPS in the short-term. These treatments also include misoprostol, which is a prostaglandin, oral L-arginine, intravesical oxybutynin and duloxetine (69-74). None of these drugs have proven to be recommended for treatment of BPS.
• Neuromodulation.
• The role of neuromodulation in the management of chronic pelvic pain (CPP) should only be considered by specialists in pelvic pain management. These techniques are used as part of a broader management plan and require regular follow-up. These are expensive interventional tools for patients who are refractory to other therapies. There has been growing evidence, but more detailed, high quality research is required (75). Two recent systematic reviews have evaluated neuromodulation techniques for CPP (76,77). Both studies concluded that neuromodulation may be effective in reducing pain and improving QoL in patients with CPP, however studies were of a low quality and long-term results were needed.
• Transcutaneous Electrical Nerve Stimulation (TENS) is a non-invasive technique used in many pain conditions. All RCTs demonstrated a significant reduction in pain following twelve weeks of treatment for pain conditions including CPP. There was conflicting data with regard to improvement of quality of life (QoL) following TENS; where validated questionnaires were used. TENS could offer an effective non- invasive treatment option for patients with CPP. • Percutaneous Tibial Nerve Stimulation (PTNS) is a minimally invasive technique that can be use in an outpatient setting. Two trials have shown that PTNS is effective in reducing pain in patients with CPP (76,77). Adverse events were rare and minor including temporary slight pain at application site and haematoma.
• Sacral nerve stimulation (77) is an invasive technique requiring sedation or general anaesthesia for implantation of a device following trial stimulation. All studies reported an improvement in pain and QoL. There was a large variation in adverse events reported ranging from 0-50%.
• Re-operation rate ranged between 11-50% for complications including lead migration, systemic infection, intrathecal implantation, loss of efficacy and erosion.
• Although bladder hydrodistension is a common treatment for BPS, the scientific justification is scarce. It can be part of the diagnostic evaluation but has limited therapeutic role. Diagnostic hydrodistention is done under general anesthesia for 2 minutes and with height of fluid above the bladder of 81cmH2O. Therapeutic hydrodistension is done under same circumstances but for 8 minutes (78). Treatment with hydrodistension and hydrodistension plus intravesical botulinum toxin A (BTX-A) has been compared (79). There was symptomatic improvement in all patients. However, in the hydrodistension-only group, 70% returned to their previous symptoms after one month, while in the BTX-Atreated patients, visual analogue score (VAS) score and functional and cystometric bladder capacity improved at three months. BTX-A trigonal-only injection seems effective and long-lasting as 87% of patients reported improvement after three months’ follow-up (80). Over 50% reported continued benefit nine months after the first treatment. When retreatment was needed, similar results were obtained. Adverse effects of BTX-A administration for IC/BPS were significantly less than for overactive bladder syndrome (81). The American Urological Association (AUA) guidelines panel has upgraded BTX-A treatment from fifth to a fourth line treatment (82).
• Endourological destruction of bladder tissue aims to eliminate urothelial lesions, mostly Hunner ulcer. Resection and fulguration have been reported to achieve symptom relief, often for more than three years (83,84). Prolonged amelioration of pain and urgency has been described for transurethral laser ablation as well (85). Laser fulgration is preferred due to chronicity of the disease and need for refulgration, with possible bladder fibrosis and shrinkage.
• There is no evidence that open surgery for PBS relieves pain. Surgery for refractory BPS is only appropriate as a last resort for patients with refractory end-stage disease. Urinary diversion without cystectomy (86) is performed to minimise the duration and complexity of surgery, but complications related to the retained bladder commonly occur. Supratrigonal cystectomy with bladder augmentation represents the most favoured continence preserving surgical technique particularly in younger patients (87). Subtrigonal or simple cystectomy refers to removal of the entire bladder at the level of the bladder neck. This approach has the benefit of removing the trigone as a possible disease site, but at the cost of requiring ureteric re-implantation. Trigonal disease is reported in 50% of patients and surgical failure has been blamed on the trigone being left in place (88), especially in patients with non-ulcer type disease (89,90).
Table III:5 Recommendations for bladder pain syndrome (BPS).
Recommendation
strength rating
1.Basic assessment should include history taking, physical examination, and laboratory examination to rule in symptoms that characterize BPS and exclude other confusable disorders Strong
2.Patients should be educated about normal bladder function, what is known and not known about IC/ BPS, the benefits versus risks/burdens of the available treatment alternatives, the fact that no single treatment has been found effective for the majority of patients, and the fact that acceptable symptom control may require trials of multiple therapeutic options Strong
3.Multiple, simultaneous treatments may be considered if it is in the best interests of the patient Weak
4.Perform general anaesthetic rigid cystoscopy in patients with bladder pain to subtype and rule out confusable disease Strong
5.Cystoscopy under anesthesia with short-duration, low-pressure hydrodistension may be undertaken if first- and second-line treatments have not provided acceptable symptom control and quality of life Strong
6.Always consider offering multimodal behavioural, physical and psychological techniques alongside oral or invasive treatments of BPS Strong
7.Offer dietary advice Weak
8.Amitriptyline, cimetidine or hydroxyzine may be administered as first-line oral medications . Weak
9.Administer amitriptyline 25mg-50mg for treatment of BPS Strong
10.Intravesical heparin, lidocaine, hyaluronic acid or chondroitin sulfate may be administered as second line intravesical treatments Weak
11.Offer intravesical hyaluronic acid or chondroitin sulphate before more invasive measures. Weak
12.Offer intravesical lidocaine plus sodium bicarbonate plus heparin prior to more invasive methods Weak
13. Offer intravesical heparin before more invasive measures alone or in combination treatment Weak
14.If Hunner’s lesions are present, then laser fulguration and/or injection of triamcinolone should be performed. This should be performed in BPS type 3 C only Strong
15.Offer submucosal bladder wall and trigonal injection of BTX-A plus hydrodistension if intravesical instillation therapies have failed Strong
16.Do not recommend oral corticosteroids for long-term treatment Strong
17. Use long-acting phosphodiesterase 5 inhibitors as a single treatment for patients with bothersome, moderate to severe LUTS secondary to BPH (AUA-SI score ≥ 8) whether they suffer from erectile dysfunction or not Strong
III.10.3 References.
1- D. Engeler, A.P. Baranowski, B. Berghmans et al. EAU Guidelines on chronic pelvic pain. European Guidelines 2020.
2- Fall, M., et al. Chronic interstitial cystitis: a heterogeneous syndrome. J Urol, 1987. 137: 35.
3- Warren, J.W., et al. Evidence-based criteria for pain of interstitial cystitis/painful bladder syndrome in women. Urology, 2008. 71: 444.
4- van de Merwe, J.P., et al. Diagnostic criteria, classification, and nomenclature for painful bladder syndrome/interstitial cystitis: an ESSIC proposal. Eur Urol, 2008. 53: 60.
5- Bade, J.J., et al. Interstitial cystitis in The Netherlands: prevalence, diagnostic criteria and therapeutic preferences. J Urol, 1995. 154: 2035.
6- Burkman, R.T. Chronic pelvic pain of bladder origin: epidemiology, pathogenesis and quality of life. J Reprod Med, 2004. 49: 225.
7- Curhan, G.C., et al. Epidemiology of interstitial cystitis: a population-based study. J Urol, 1999. 161: 549.
8- Held, P., et al., Interstitial Cystitis. In: Epidemiology of interstitial cystitis. Hanno PM, Staskin DR, Krane RJ, Wein AJ, eds. 1990, Springer Verlag: London.
9- Jones, C., et al. Prevalence of interstitial cystitis in the United States. Proc Am Urol Ass J Urol, 1994. 151 (Suppl).
10- Leppilahti, M., et al. Prevalence of clinically confirmed interstitial cystitis in women: a population-based study in Finland. J Urol, 2005. 174: 581.
11- Oravisto, K.J. Epidemiology of interstitial cystitis. Ann Chir Gynaecol Fenn, 1975. 64: 75.
12- Parsons, C.L., et al. Prevalence of interstitial cystitis in young women. Urology, 2004. 64: 866.
13- Roberts, R.O., et al. Incidence of physician-diagnosed interstitial cystitis in Olmsted County: a community-based study. BJU Int, 2003. 91: 181.
14- Temml, C., et al. Prevalence and correlates for interstitial cystitis symptoms in women participating in a health screening project. Eur Urol, 2007. 51: 803.
15- Berry, S.H., et al. Prevalence of symptoms of bladder pain syndrome/interstitial cystitis among adult females in the United States. J Urol, 2011. 186: 540.
16- Song, Y., et al. Prevalence and correlates of painful bladder syndrome symptoms in Fuzhou Chinese women. Neurourol Urodyn, 2009. 28: 22.
17- Koziol, J.A., et al. Discrimination between the ulcerous and the nonulcerous forms of interstitial cystitis by noninvasive findings. J Urol, 1996. 155: 87.
18- Messing, E.M., et al. Interstitial cystitis: early diagnosis, pathology, and treatment. Urology, 1978. 12: 381.
19- Parsons, C. Interstitial cystitis: clinical manifestations and diagnostic criteria in over 200 cases. Neurourol Urodyn, 1990. 9.
20- Peeker, R., et al. Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease. J Urol, 2002. 167: 2470.
21- Mattox, T.F. Interstitial cystitis in adolescents and children: a review. J Pediatr Adolesc Gynecol, 2004. 17: 7.
22- Richter, B., et al. YKL-40 and mast cells are associated with detrusor fibrosis in patients diagnosed with bladder pain syndrome/interstitial cystitis according to the 2008 criteria of the European Society for the Study of Interstitial Cystitis. Histopathology, 2010. 57: 371.
23- Dundore, P.A., et al. Mast cell counts are not useful in the diagnosis of nonulcerative interstitial cystitis. J Urol, 1996. 155: 885.
24- Peeker, R., et al. Recruitment, distribution and phenotypes of mast cells in interstitial cystitis. J Urol, 2000.163: 1009.
25- Anderstrom, C.R., et al. Scanning electron microscopic findings in interstitial cystitis. Br J Urol, 1989. 63: 270.
26- Johansson, S.L., et al. Clinical features and spectrum of light microscopic changes in interstitial cystitis. J Urol, 1990. 143: 1118.
27- Logadottir, Y.R., et al. Intravesical nitric oxide production discriminates between classic and nonulcer interstitial cystitis. J Urol, 2004. 171: 1148.
28- Lokeshwar, V.B., et al. Urinary uronate and sulfated glycosaminoglycan levels: markers for interstitial cystitis severity. J Urol, 2005. 174: 344.
29- Parsons, C.L., et al. Epithelial dysfunction in nonbacterial cystitis (interstitial cystitis). J Urol, 1991. 145: 732.
30- Parsons, C.L., et al. Successful therapy of interstitial cystitis with pentosan polysulfate. J Urol, 1987. 138: 513.
31- Sanchez-Freire, V., et al. Acid-sensing channels in human bladder: expression, function and alterations during bladder pain syndrome. J Urol, 2011. 186: 1509.
32- Hang, L., et al. Cytokine repertoire of epithelial cells lining the human urinary tract. J Urol, 1998. 159: 2185.
33- Parsons, C.L., et al. Cyto-injury factors in urine: a possible mechanism for the development of interstitial cystitis. J Urol, 2000. 164: 1381.
34- Chelimsky, G., et al. Autonomic Testing in Women with Chronic Pelvic Pain. J Urol, 2016. 196: 429.
35- Charrua, A., et al. Can the adrenergic system be implicated in the pathophysiology of bladder pain syndrome/ interstitial cystitis? A clinical and experimental study. Neurourol Urodyn, 2015. 34: 489.
36- Alagiri, M., et al. Interstitial cystitis: unexplained associations with other chronic disease and pain syndromes. Urology, 1997. 49: 52.
37- Buffington, C.A. Comorbidity of interstitial cystitis with other unexplained clinical conditions. J Urol, 2004. 172: 1242.
38- Erickson, D.R., et al. Nonbladder related symptoms in patients with interstitial cystitis. J Urol, 2001. 166: 557.
39- Warren, J.W., et al. Antecedent nonbladder syndromes in case-control study of interstitial cystitis/painful bladder syndrome. Urology, 2009. 73: 52.
40- Weissman, M., et al. Interstitial Cystitis and Panic Disorder - A Potential Genetic Syndrome. Arch Gen Psych, 2004. 61.
41- Warren, J.W., et al. Numbers and types of nonbladder syndromes as risk factors for interstitial cystitis/painful bladder syndrome. Urology, 2011. 77: 313.
42- Peters, K.M., et al. Are ulcerative and nonulcerative interstitial cystitis/painful bladder syndrome 2 distinct diseases? A study of coexisting conditions. Urology, 2011. 78: 301.
43- Lubeck, D.P., et al. Psychometric validation of the O'leary-Sant interstitial cystitis symptom index in a clinical trial of pentosan polysulfate sodium. Urology, 2001. 57: 62.
44- Aihara, K., et al. Hydrodistension under local anesthesia for patients with suspected painful bladder syndrome/interstitial cystitis: safety, diagnostic potential and therapeutic efficacy. Int J Urol, 2009. 16: 947.
45- Parsons, C.L. The role of a leaky epithelium and potassium in the generation of bladder symptoms in interstitial cystitis/overactive bladder, urethral syndrome, prostatitis and gynaecological chronic pelvic pain. BJU Int, 2011. 107: 370.
46- Geurts, N., et al. Bladder pain syndrome: do the different morphological and cystoscopic features correlate? Scand J Urol Nephrol, 2011. 45: 20.
47- Johansson, S.L., et al. Pathology of interstitial cystitis. Urol Clin North Am, 1994. 21: 55.
48- Loving, S., et al. Does evidence support physiotherapy management of adult female chronic pelvic pain? Scan J Pain, 2012. 3: 70.
49- FitzGerald, M.P., et al. Randomized multicenter clinical trial of myofascial physical therapy in women with interstitial cystitis/painful bladder syndrome and pelvic floor tenderness. J Urol, 2012. 187: 2113.
50- Cheong, Y.C., et al. Non-surgical interventions for the management of chronic pelvic pain. Cochrane Database Syst Rev, 2014. 3: CD008797.
51- Champaneria, R., et al. Psychological therapies for chronic pelvic pain: Systematic review of randomized controlled trials. Acta Obstet Gynecol Scand, 2012. 91: 281.
52- Seshadri, P., et al. Cimetidine in the treatment of interstitial cystitis. Urology, 1994. 44: 614.
53- Sant, G.R., et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol, 2003. 170: 810.
54- Hanno, P.M., et al. Use of amitriptyline in the treatment of interstitial cystitis. J Urol, 1989. 141: 846.
55- Foster, H.E., Jr., et al. Effect of amitriptyline on symptoms in treatment naive patients with interstitial cystitis/ painful bladder syndrome. J Urol, 2010. 183: 1853.
56- Hwang, P., et al. Efficacy of pentosan polysulfate in the treatment of interstitial cystitis: a metaanalysis. Urology, 1997. 50: 39.
57- Mulholland, S.G., et al. Pentosan polysulfate sodium for therapy of interstitial cystitis. A doubleblind placebocontrolled clinical study. Urology, 1990. 35: 552.
58- Fritjofsson, A., et al. Treatment of ulcer and nonulcer interstitial cystitis with sodium pentosan polysulfate: a multicenter trial. J Urol, 1987. 138: 508.
59- Oravisto, K.J., et al. Treatment of interstitial cystitis with immunosuppression and chloroquine derivatives. Eur Urol, 1976. 2: 82.
60- Forsell, T., et al. Cyclosporine in severe interstitial cystitis. J Urol, 1996. 155: 1591.
61- Barua, J.M., et al. A systematic review and meta-analysis on the efficacy of intravesical therapy for bladder pain syndrome/interstitial cystitis. Int Urogynecol J, 2016. 27: 1137.
62- Asklin, B., et al. Intravesical lidocaine in severe interstitial cystitis. Case report. Scand J Urol Nephrol, 1989. 23: 311.
63- Giannakopoulos, X., et al. Chronic interstitial cystitis. Successful treatment with intravesical idocaine. Arch Ital Urol Nefrol Androl, 1992. 64: 337.
64- Parsons, C.L. Successful downregulation of bladder sensory nerves with combination of heparin and alkalinized lidocaine in patients with interstitial cystitis. Urology, 2005. 65: 45.
65- Nickel, J.C., et al. Intravesical alkalinized lidocaine (PSD597) offers sustained relief from symptoms of interstitial cystitis and painful bladder syndrome. BJU Int, 2009. 103: 910.
66- Hammouda Sherif, Ahmed Sebay, Wael Kandeel, Tarek Othman, Abdallah Fathi, Ahmed Mohey, and Ali Eshazly. Safety and efficacy of Intravesical hyaluronic acid/chondroitin sulfate in the treatment of refractory painful bladder syndrome. Turk J Urol. 2019 Jul; 45(4): 296–301.
67- Pyo, J.S., et al. Systematic Review and Meta-Analysis of Intravesical Hyaluronic Acid and Hyaluronic Acid/Chondroitin Sulfate Instillation for Interstitial Cystitis/Painful Bladder Syndrome. Cell Physiol Biochem, 2016. 39: 1618.
68- Parsons, C.L., et al. Treatment of interstitial cystitis with intravesical heparin. Br J Urol, 1994. 73: 504.
69- Thilagarajah, R., et al. Oral cimetidine gives effective symptom relief in painful bladder disease: a prospective, randomized, double-blind placebo-controlled trial. BJU Int 2001. 87: 207.
70- Kelly, J.D., et al. Clinical response to an oral prostaglandin analogue in patients with interstitial cystitis. Eur Urol 1998. 34: 53. 71- Korting, G.E., et al. A randomized double-blind trial of oral L-arginine for treatment of interstitial cystitis. J Urol 1999. 161: 558.
72- Cartledge, J.J., et al. A randomized double-blind placebo-controlled crossover trial of the efficacy of L-arginine in the treatment of interstitial cystitis. BJU Int, 2000. 85: 421.
73- Barbalias, G.A., et al. Interstitial cystitis: bladder training with intravesical oxybutynin. J Urol, 2000. 163: 1818.
74- van Ophoven, A., et al. The dual serotonin and noradrenaline reuptake inhibitor duloxetine for the treatment of interstitial cystitis: results of an observational study. J Urol, 2007. 177: 552.
75- Fariello, J.Y., et al. Sacral neuromodulation stimulation for IC/PBS, chronic pelvic pain, and sexual dysfunction. Int Urogynecol J, 2010. 21: 1553.
76- Cottrell, A.M., et al. Benefits and Harms of Electrical Neuromodulation for Chronic Pelvic Pain: A Systematic Review. Eur Urol Focus, 2019.
77- Tutolo, M., et al. Efficacy and Safety of Sacral and Percutaneous Tibial Neuromodulation in NonNeurogenic Lower Urinary Tract Dysfunction and Chronic Pelvic Pain: A Systematic Review of the Literature. Eur Urol, 2018. 73: 406.
78- El-Hefnawy AS, Makharita MY, Abed A, Amr YM, Salah El-Badry M, Shaaban AA. Anesthetic Bladder Hydrodistention Is Superior to Superior Hypogastric Plexus Neurolysis in Treatment of Interstitial Cystitis-bladder Pain Syndrome: A Prospective Randomized Trial. Urology. 2015 May;85(5):1039-1044.
79- Kuo, H.C., et al. Comparison of intravesical botulinum toxin type A injections plus hydrodistention with hydrodistention alone for the treatment of refractory interstitial cystitis/painful bladder syndrome. BJU Int, 2009. 104: 657.
80- Pinto, R., et al. Trigonal injection of botulinum toxin A in patients with refractory bladder pain syndrome/interstitial cystitis. Eur Urol, 2010. 58: 360.
81- Kuo, Y.C., et al. Adverse Events of Intravesical Onabotulinum Toxin A Injection between Patients with Overactive Bladder and Interstitial Cystitis-Different Mechanisms of Action of Botox on Bladder Dysfunction? Toxins, 2016. 8
82- Hanno, P.M., et al. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol, 2015. 193: 1545.
83- Kerr, W.S., Jr. Interstitial cystitis: treatment by transurethral resection. J Urol, 1971. 105: 664.
84- Peeker, R., et al. Complete transurethral resection of ulcers in classic interstitial cystitis. Int Urogynecol J Pelvic Floor Dysfunct, 2000. 11: 290.
85- Rofeim, O., et al. Use of the neodymium: YAG laser for interstitial cystitis: a prospective study. J Urol, 2001. 166: 134.
86- Freiha, F.S., et al. The surgical treatment of intractable interstitial cystitis. J Urol, 1980. 123: 632.
87- Kim, H.J., et al. Efficacy and safety of augmentation ileocystoplasty combined with supratrigonal cystectomy for the treatment of refractory bladder pain syndrome/interstitial cystitis with Hunner's lesion. Int J Urol, 2014. 21 Suppl 1: 69.
88- Nurse, D.E., et al. The problems of substitution cystoplasty. Br J Urol, 1988. 61: 423.
89- Peeker, R., et al. The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease. J Urol, 1998. 159: 1479.
90- Rossberger, J., et al. Long-term results of reconstructive surgery in patients with bladder pain syndrome/interstitial cystitis: subtyping is imperative. Urology, 2007. 70: 638.
III.11 Female Bladder Outlet Obstruction (BOO).
III.11.1 Definition and Background.
• BOO in females is an under-reported and underdiagnosed problem worldwide due to paucity of clinical studies and lack of well-defined diagnostic criteria. (1) Prevalence of BOO among females undergoing urodynamics (UDS) for lower urinary tract symptoms (LUTS) range from 2.7% to 29%. (2-5). This is attributed to many definitions used to diagnose BOO in these studies. Different nomograms based on urodynamic parameters have been reproduced, but none was approved worldwide for use. (2,6,7)
• Symptoms of female BOO are mostly non-specific and the classic voiding LUTS of impaired urine flow, hesitancy, intermittent stream, straining and even retention may be less apparent, making diagnosis difficult. (1,8) Other presenting symptoms, e.g. irritative voiding complaints, may be secondary to BOO. Urethral pain and recurrent urinary tract infections (UTIs) are other presenting symptoms as well. Bending forward to void or having to change positions to empty effectively usually indicates an element of obstruction in post anti-stress urinary incontinence (SUI) operations (8). This raises the importance of high level of suspicion for BOO in women. Finally, this problem is often not suspected in women, and so its management is typically delayed. (1)
• Female BOO can be caused by anatomical or functional causes. Furthermore, anatomical causes include extrinsic and intrinsic (luminal) factors. (9) Extrinsic causes include pelvic organ prolapse (POP), iatrogenic post anti-incontinence procedure and skene gland abscess or cyst, while intrinsic causes include urethral stricture or fibrosis, urethral diverticulum, excessive bulking agent, urethral tumour, condyloma accuminata, urethral stone, urethral caruncle or urethral prolapse. Functional causes include primary bladder neck obstruction, pseudo-dyssynergia known as Hinman’s syndrome and detrusor sphincter dyssynergia (DSD). (1,8)
• Detrusor failure or acontractility should be excluded, and pressure-flow study could be of help in the diagnosis. However, there are currently no nomograms that accurately assesses detrusor underactivity (DUA) in women. (1,9)
• In a study by Greenwell et al (1), 192 females with BOO were diagnosed. Anatomical obstruction was found in 64% and functional obstruction was present in 36%. The most common anatomical cause of BOO was previous anti-SUI surgery (21%), followed by urethral stricture (20%).
III.11.2 Diagnosis.
• Urine analysis is an important initial tool to exclude infections. Urine culture and sensitivity is recommended specially in the context of recurrent UTIs. Renal function tests could be elevated if condition is severe or chronic with elevated postvoid residual (PVR). Bladder scan is indicated to estimate PVR. Imaging is indicated when renal function is impaired or when organic cause is suspected. Role of cystourethroscopy is crucial, especially if associated with difficult catheterization or previous anti-incontinence procedures. (1,8)
• Many nomograms have been utilized, with different prevalence rates. Ferrar et al. diagnosed BOO based only on Qmax of <15 mL/s with prevalence of BOO of 6.7%. (3) Massey and Abrams diagnosed BOO in only 2.7% of 5948 females based on 2 or more of the following criteria: Qmax <12 mL/s, pdet @Qmax >50 cmH2O, urethral resistance (pdet @Qmax/ 2Qmax) >0.2, and significant PVR. (4) Lemack and Zimmern used cut-off values of Qmax ≤15 mL/s and pdet@ Qmax>20 cmH2O, diagnosing BOO in 20% of the patients. (7) Blaivas and Groutz created a nomogram to diagnose BOO and classify its severity based on pressure–flow criteria of a free Qmax ≤12 mL/s and a Pdet @Qmax ≥20 cmH2O, in association with radiographic evidence of obstruction, and reported a prevalence of 8.3%.(2)
• Elmissiry et al. categorized females with BOO into three different subtypes based on urodynamic patterns (early, compensated and late obstruction). They recommended that UDS should be combined with the clinical presentation and estimation of PVR for an accurate diagnosis of BOO. (10)
• The role of pressure flow studies alone to diagnose female BOO is questioned because voiding dynamics in females are different from those in males, and most of the females void predominantly by pelvic floor relaxation or abdominal straining with low detrusor pressures. Nitti et al. introduced the role of videourodynamics (VUDS), combined with clinical suspicion of BOO, with an overall prevalence of 29%. (11,12)
III.11.3 Treatment.
• Treatment usually depends on treatment of the cause. (8) Prolapse correction in cases of POP. (12, 14) In cases of iatrogenic post-tape obstruction, CIC could be tried for the first week. Tape release could be tried initially within the first 10 days. If failed, tape incision could be done in the first two months (15), with urethrolysis being a last resort in some refractory cases. (16,17)
• Most urethral strictures or fibrosis in women are iatrogenic and can result from previous urethral or periurethral surgery, or in some cases from previous urethral dilatation. Many females experience urethral strictures from previous obstructed labors. Options include urethral dilatations, better under brief anesthesia, cystourethroscopy, or in resistant recurrent cases, urethroplasty with vaginal flap or buccal mucosal grafts is indicated but in highly specialized referral centers. (8,18,19)
• Primary bladder neck obstruction is caused by lack of relaxation of the smooth muscle of the bladder neck during voiding, and it responds well to alpha blockers. CIC could be an option if medications fail. Transurethral incision of the bladder neck is definitive, but with increased risks of postoperative incontinence. Neuromodulation is of help in these cases. (20-24)
• Pseudo-dyssynergia or Hinman’s syndrome results from an external sphincter that does not relax during voiding in an otherwise neurologically intact woman. First-line treatment consists of pelvic floor relaxation. Skeletal muscle relaxants such as diazepam can be used as well, but the side-effects limit their applicability. Intrasphincter botulinum injection is successful in many cases, but this is off-label use. Finally, sacral neuromodulation has been used successfully.
• DSD occurs when the external sphincter contracts during a detrusor contraction in a neurologically impaired individual. It is common in patients with suprasacral spinal cord injuries (SCI) and multiple sclerosis (MS). Introduction of botulinum toxin injections into the external sphincter of these patients is successful. (8,25)
Table III:6 Recommendations for female bladder outlet obstruction (BOO).
Recommendation
strength rating
1. Role of VUDS, combined with the clinical symptoms of BOO, is more accurate in diagnosing BOO and determining the site of obstruction
Strong
2. Pressure-flow study is of low yield in diagnosing female BOO Weak
3. Suspect BOO in females who underwent slings recently if they experience deNovo storage symptoms, or if they report change in position when they void (lean forward or squat) Weak
4. Estimation of PVR in patients suspected with BOO is mandatory
Strong
5. Perform cystourethroscopy in female patients suspected with BOO Weak
6.Offer alpha blockers initially in cases diagnosed with primary bladder neck obstruction Strong
7. Urethral dilatations, better under general anesthesia, is of help in cases of urethral strictures or fibrosis in women Strong
8. Transurethral incision or resection of the bladder neck is definitive in primary bladder neck obstruction, but with increased risks of postoperative incontinence Weak
9. Offer initially pelvic floor muscle exercises in patients suspected with Hinman’s syndrome Strong
10. Offer skeletal muscle relaxants such as diazepam in patients diagnosed with Hinman’s syndrome, but the side effects limit their applicability Weak
11. Offer intrasphincter botulinum injection in cases of Hinman’s syndrome, pseudodyssynergia and DSD, with better results in DSD patients Weak
III.11.4 References.
1- Malde S, Solomon E, Spilotros M, Mukhtar B, Pakzad M, Hamid R, Ockrim J, Greenwell T. Female bladder outlet obstruction: Common symptoms masking an uncommon cause. Low Urin Tract Symptoms. 2019 Jan; 11(1):72-77.
2- Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn. 2000; 19(5):553–564.
3- Farrar DJ, Osborne JL, Stephenson TP, et al. A urodynamic view of bladder outflow obstruction in the female: factors influencing the results of treatment. Br J Urol. 1975; 47(7):815–822.
4- Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol. 1988; 61(1):36–39.
5- Rees DL, Whitfield HN, Islam AK, Doyle PT, Mayo ME, Wickham JE. Urodynamic findings in adult females with frequency and dysuria. Br J Urol. 1975; 47(7):853–860.
6- Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS, Zimmern PE. Proposed cutoff values to define bladder outlet obstruction in women. Urology. 1998; 51(3):408–411.
7- Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying women with outflow obstruction. J Urol. 2000; 163 (6):1823–1828.
8- Goldman HB, Zimmern PE. The treatment of female bladder outlet obstruction. BJU Int. 2006 Sep; 98 Suppl 1:17-23
9- Are There Pharmacotherapeutic Options for Underactive Bladder? Osman NI, Chapple CR. Eur Urol Focus. 2018 Jan; 4(1):6-7.
10- Elmissiry MM, Ali AG, Ali GA. Different urodynamic patterns in female bladder outlet obstruction: Can urodynamics alone reach the diagnosis? Arab J Urol. 2013 Jun; 11(2):127-30.
11- Patel R, Nitti V. Bladder outlet obstruction in women: prevalence, recognition and management. Curr Urol Rep. 2001; 2(5):379–387.
12- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol. 1999; 161(5):1535–1540.
13- Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999; 161: 581–6
14- Gilleran JP, Lemack GE, Zimmern PE. Reduction of moderate-to-largecystocele during urodynamic evaluation using a vaginal gauze pack: 8-year experience. BJU Int 2006; 97: 292–5
15- Goldman HB. Simple sling incision for the treatment of iatrogenic urethral obstruction. Urology 2003; 62: 714–8
16- Goldman HB. Urethrolysis. Atlas Urol Clinics 2004; 12: 197–204
17- Carey JM, Chon JK, Leach GE. Urethrolysis with Martius labial fat pad graft for iatrogenic bladder outlet obstruction. Urology 2003; 61(Suppl.4):21–5
18- Nnenaya Agochukwu-Mmonu, Sudarshan Srirangapatanam. Andrew Cohen, Benjamin Breyer.Female Urethral Strictures: Review of Diagnosis, Etiology, and Management. J Med Case Rep. 2018; 12: 382.
19- Lemack G, Zimmern PE. Voiding difficulties. In Shaw R, Soutter WP, Stanton SL eds, Gynaecology, 3rd edn. Edinburgh: Churchill Livingstone, 2003: 803–12
20- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999; 161: 1535–40
21- Kumar A, Mandhani A, Gogoi S, Srivastava A. Management of functional bladder neck obstruction in women: use of alpha-blockers and pediatric resectoscope for bladder neck incision. J Urol 1999; 162: 2061-5
22- Blaivas J, Flisser AJ, Tash JA. Treatment of primary bladder neck obstruction in women with transurethral resection of the bladder neck. J Urol 2004; 171: 1172–5
23- Peng CH, Kuo HC. Transurethral incision of bladder neck in treatment of bladder neck obstruction in women. Urology 2005; 65: 275–8
24- Hourieh Sharifian, Mahtab Zargham, Mohamad Hatef Khorami et al. Internal urethrotomy in treatment of female with anatomical bladder outlet obstruction. Adv Biomed Res. 2019; 8: 36.
25- Moore C, Rackley R, Goldman H. Urologic applications of botox. Curr Urol Rep 2005; 6: 419–23
III.12 Geriatric urinary incontinence.
• Urinary incontinence (UI) can be considered both a specific diagnosis and a geriatric syndrome. This is particularly of significance in frail elderly population, with multiple chronic morbid conditions. (1)
• Geriatric syndromes are defined as common conditions seen in the elderly that are complex in nature, are usually multifactorial, and can have clinical or other negative health outcomes for affected patients. (2)
• The incidence and prevalence of UI increase in the elderly population. However, incontinence should not be considered a normal or inevitable aging event. This is a common myth among both health care providers and patients. (3)
• UI is accompanied with social isolation, stigmatization, depression, aversion from sexual life and embarrassment. Skin irritation and cracking from urine, development of pressure ulcers, recurrent urinary tract infections (UTIs), falls and fractures are all substantial physical problems. (4) UI has a stronger negative influence on overall levels of happiness than diabetes, hypertension, arthritis, and osteoporosis. (5)
• Economic data has shown an estimated national cost of evaluation and care for wetoveractive bladder (OAB) of $65.9 billions in 2007, with estimated increase to $76.2 billions in 2015 and $82.6 billions in 2020. (6) The degree of incontinence in the elderly as measured by severity appears to be more influential on health-related quality of life (QoL) outcomes than type of UI. (7)
III.12.1 Transient urinary incontinence.
o In developed countries. Non-obstetric (surgical) fistula is considered the most common cause of uro-gynecological fistulae (e.g., post abdominal hysterectomy, POP repair surgery, anti-incontinent surgery)
o In the developing countries. Obstetric fistula is considered the most common cause due to prolonged obstructed labor (13,14)
o Risk factors for obstetric fistula include lack of prenatal care, young age of first marriage, low socio-economical class, short stature, poor nutrition, lack of proper surgical training for obstetrician (13,14)
III.9.2 Different types of uro-gynecological fistula.
o Vesicovaginal fistula (VVF)
o Urethrovaginal fistula (UVF)
o Rectovaginal fistula (RVF)
o Ureterovaginal fistula
o Vesicouterine fistula
o Sometimes more than one type of fistula may occur at the same time (Complex fistula)
III.9.3 Diagnosis.
Unfortunately, intraoperative diagnosis of a genitourinary (GU) is made in only about half of the cases that result in fistula. Clinical diagnosis of leakage of urine is the hallmark sign of a fistula. The leakage is usually painless, may be intermittent if its position is independent, or maybe constant (15).
The diagnosis of VVF usually requires clinical assessment often in combination with appropriate imaging or laboratory studies. Direct visual inspection, cystoscopy, retrograde bladder filling with a coloured fluid or placement of a tampon into the vagina to identify staining may facilitate the diagnosis of a VVF. A double-dye test is used to differentiate between ureterovaginal and VVF in some cases (15). Cyclic hematuria may be pathognomonic sign of vesico-uterine fistula.
Testing the creatinine level in either the extravasated fluid or the accumulated ascites and comparing this to the serum creatinine levels will confirm urinary leakage. Contrast-enhanced CT with late excretory phase reliably diagnoses urinary fistulae and provides information about ureteric integrity and the presence of associated urinoma (16).
III.9.4 Treatment.
o Urethrovaginal fistula (UVF)
o Rectovaginal fistula (RVF)
o Ureterovaginal fistula
o Vesicouterine fistula
o Sometimes more than one type of fistula may occur at the same time (Complex fistula)
III.9.3 Diagnosis.
The diagnosis of VVF usually requires clinical assessment often in combination with appropriate imaging or laboratory studies. Direct visual inspection, cystoscopy, retrograde bladder filling with a coloured fluid or placement of a tampon into the vagina to identify staining may facilitate the diagnosis of a VVF. A double-dye test is used to differentiate between ureterovaginal and VVF in some cases (15). Cyclic hematuria may be pathognomonic sign of vesico-uterine fistula.
Testing the creatinine level in either the extravasated fluid or the accumulated ascites and comparing this to the serum creatinine levels will confirm urinary leakage. Contrast-enhanced CT with late excretory phase reliably diagnoses urinary fistulae and provides information about ureteric integrity and the presence of associated urinoma (16).
III.9.4 Treatment.
III.9.4.1 Management of vesicovaginal fistula.
III.9.4.1.1 Conservative management.
III.9.4.1.2 Surgical management.
III.9.4.1.2.1 Timing of surgery.
III.9.4.1.2.2 Surgical principles.
The ureters should be identified and protected to ensure they are not cut or ligated during the fistula repair 19. The fistula should be mobilized from the surrounding tissues at the time of repair. The fistula should be closed without tension at the site of repair. The repair must be watertight. To ensure this, a dye test is performed intra-operatively and, if there is still leakage, the repair is sutured again (19).
A single randomized controlled trial compared trimming of the fistula edge with no trimming showed no difference in success rates, but failed repairs in trimmed cases ended up with larger recurrences than untrimmed cases (22).
A Martius flap in primary obstetric fistula repair is debatable with no clear evidence of its value and is usually reserved for recurrent cases, fistulae secondary to radiation or in case of associated urethral reconstruction (19).
One prospective randomized controlled trial compared the use of a Martius flap “as an interposition flap” to the use of a self-made fibrin glue. There was no statistical difference in outcome, but the authors stated that the use of fibrin glue allowed the fistula repair to be quicker (23).
III.9.4.1.2.3 Surgical approaches.
III.9.4.1.2.3.1 Vaginal procedures.
III.9.4.1.2.3.2 Abdominal procedures.
There are no randomised studies comparing abdominal and vaginal approaches. When concurrent ureteric re-implantation or augmentation cystoplasty are required, the abdominal approach is necessary.
III.9.4.1.2.4 Post-operative management.
III.9.4.2 Management of radiation fistula.
III.9.4.3 Management of ureteric fistula.
III.9.4.3.1 Endoscopic management.
III.9.4.3.2 Surgical management.
In case of delayed presentation of upper tract injury, conservative management is still possible with internal or external drainage, endoluminal management using nephrostomy and stenting where available, and early (< 3 months) or delayed (> 6 months) surgical repair when required (14).
If endoluminal techniques fail or result in secondary stricture, the abdominal approach to repair is the standard and requires re-implantation into the bladder with or without psoas hitch or Boari flap, or replacement with bowel segments with or without reconfiguration (28,29).
Functional and anatomical imaging should be used to follow up patients after repair to guard against late upper tract deterioration (14).
III.9.4.4 Management of vesicouterine fistula.
III.9.4.5 Management of urethro-vaginal fistula.
Recommendation |
strength rating |
|---|---|
III.9.5 References.
2. Mitchell JD. Diverticulum of the Female Urethra11The opinions and assertions contained herein are the private views of the writers and are not to be considered as official or reflecting the views of the Navy Department or the Naval Service at large. J Urol [Internet]. 1936;51(4):411–23. Available from: http://dx.doi.org/10.1016/S0022-5347(17)70372-2
3. Lee JWS, Fynes MM. Female urethral diverticula. Best Pract Res Clin Obstet Gynaecol. 2005;19(6):875–93.
4. Ganabathi K, Leach GE, Zimmern PE, Dmochowski R. Experience with the Management of Urethral Diverticulum in 63 Women. J Urol [Internet]. 1994 Nov;152(5 Part 1):1445–52. Available from: http://www.jurology.com/doi/10.1016/S0022-5347%2817%2932442-4
5. Ultrasonography T, Pulsed W, Of CD, Urethral F. Translabial ultrasonography with pulsed colour-doppler in the diagnosis of female urethral diverticula. 1994;101–4.
6. Dinkelaar W, Dohle GR, Krestin GP, Rs D, Dinkelaar W, Wcj H. Diagnosis in Symptomatic Women. 2011;(September):676–82.
7. Bradley CS, Rovner ES. URODYNAMICALLY DEFINED STRESS URINARY INCONTINENCE AND BLADDER OUTLET OBSTRUCTION COEXIST IN WOMEN. 2004; 171:757–61.
8. Saito S. Usefulness of Diagnosis by the Urethroscopy Under Anesthesia and Effect of Transurethral Electrocoagulation in Symptomatic Female Urethral Diverticula. 2000; 14(5):455– 7.
9. Leach GE. BENIGN FEMALE PERIURETHRAL MASSES. J Urol [Internet]. 1994; 152(6):1943–51. Available from: http://dx.doi.org/10.1016/S0022-5347 (17)32276-0
10. Vakili B, Wai C, Nihira M. Anterior Urethral Diverticulum in the Female: Diagnosis and Surgical Approach. 2003; 102(5).
11. Gasthuis SF. P OI N T OF T E C H NI QU E Management of female urethral diverticula by transurethral incision. 1996; 745–6.
12. Patel DN, Fok CS, Webster GD, Anger JT. Female urethral injuries associated with pelvic fracture: a systematic review of the literature. BJU Int. 2017; 120(6):766–73.
13. Bettez M, Breault G, Carr L, Tu LM. Case report Early versus delayed repair of vesicouterine fistula. 2011; 5(4):52–5.
14. Murray C, Goh JT, Fynes M, Carey MP. Urinary and faecal incontinence following delayed primary repair of obstetric genital fistula. 2002; 109(July):828–32.
15. Æ JHÆTPP. Vesico-vaginal fistula : report of 220 cases. 2009; 299–302.
16. Exhibit E. Fistulas in Malignant Gynecologic Disease : Etiology, Imaging, and. 2009; 1073–84.
17. Faso B. Fistulas in the Developing World. : 1419–58.
18. Bazi T. Spontaneous closure of vesicovaginal fistulas after bladder drainage alone : review of the evidence. 2007; 329–33.
19. Mourad S. Vesico-vaginal fistula in the developing world. 2020;
20. Waaldijk K. The imediate surgical management of fresh obstetric fistulas with catheter and / or early closure. 1994; 11–6.
21. Vierhout ME. Prospective results after first-time surgery for obstetric fistulas in East African women. 2008; (November 2002):73–9.
22. Shaker H, Saafan A, Yassin M, Idrissa A, Mourad MS. Obstetric Vesico-Vaginal Fistula Repair: Should We Trim The Fistula Edges ? A Randomized Prospective Study. 2011; 305(July 2010):302–5.
23. Safan A, Shaker H, Abdelaal A, Mourad MS, Albaz M. Fibrin Glue Versus Martius Flap Interpositioning in the Repair of Complicated Obstetric Vesicovaginal Fistula. A Prospective Multi-Institution Randomized Trial. 2009; 441(May):438–41.
24. Kumar S, Pal ÆBC. Latzko repair for vesicovaginal fistula revisited in the era of minimal-access surgery. 2008; 317–20.
25. Wall LL. Dr. George Hayward (1791 – 1863): a forgotten pioneer of reconstructive pelvic surgery. 2005; 330–3.
26. Langkilde NC, Pless TK, Lundbeck F, Nerstrøm B. Surgical Repair of Vesicovaginal Fistulae. 1999;
27. Brandes S, Coburn M, Armenakas N, Mcaninch J. The Consensus on Genitourinary by a team of experts under the Diagnosis and management of ureteric injury: an evidence-based. 2004;
28. Shaw MBK, Tomes M, Rix DA, Dorkin TJ, Murthy LNS, Pickard RS. The Management of Bilateral Ureteric Injury following Radical Hysterectomy. 2008; 2008.
29. Narang V, Sinha T, Karan SC. Ureteroscopy: Savior to the gynecologist ?— Ureteroscopic management of post laparoscopic-assisted vaginal hysterectomy ureterovaginal fistulas. 2007 ;( 1):345–7.
30. Rajamaheswari N, Chhikara AB. Vesicouterine fistulae: Our experience of 17 cases and literature review. Int Urogynecol J Pelvic Floor Dysfunct. 2013; 24(2):275–9.
31. Milani R, Cola A, Frigerio M, Manodoro S. Repair of a vesicouterine fistula following cesarean section. Int Urogynecol J. 2018; 29(2):309–11.
32. Pushkar DY, Dyakov V V, Kosko JW, Kasyan GR. Management of Urethrovaginal Fistulas. 2006; 50:1000–5.
III.10 Bladder Pain Syndrome (BPS).
III.10.1 Definition.
• It is the occurrence of persistent or recurrent pain perceived in the urinary bladder region, accompanied by at least one other symptom, such as pain worsening with bladder filling and daytime and/or night-time urinary frequency with no proven infection or other obvious local pathology for a period more than six weeks. (1)
• Pain characteristics include pain, pressure or discomfort perceived to be related to the bladder, increasing with increasing bladder volume. It is located suprapubically, sometimes radiating to the groins, vagina, rectum or sacrum. It is relieved by voiding but soon returns (2,3). It could be aggravated by food or drink. (3)
• Bladder pain syndrome is often associated with negative cognitive, behavioral, sexual or emotional consequence. BPS is believed to represent a heterogeneous spectrum of disorders. Localization of the pain can be difficult by examination. Cystoscopy with hydrodistension and biopsy may be indicated to define phenotypes. Recently, ESSIC has suggested a standardized scheme of sub-classifications (4) to acknowledge differences and make it easier to compare various studies. Other terms that have been used include “interstitial cystitis”, “painful bladder syndrome”, and “PBS/IC” or “BPS/IC”. These terms are no longer recommended.
• Prevalence varies largely, along with the diagnostic criteria and populations studied. Recent reports range from 0.06% to 30% (5-14). There is a female preponderance of about 10:1 (9) but no difference in race or ethnicity (15,16). The relative proportions of classic and nonlesion disease are unclear and their incidence in studies has ranged from 5 to 50% (16-20). Children under the age of eighteen may be affected as well, although prevalence figures are low (21).
III.10.1.1 Risk factors.
• The cause of BPS is proposed to be an unidentified insult to the bladder, leading to urothelial damage, neurogenic inflammation and pain. BPS might be a local manifestation of a systemic disorder. No infection has been incriminated in the pathogenesis of BBS (1).
• Pancystitis, with associated perineural inflammatory infiltrates, and mastocytosis is an essential part of BPS type 3 C (22), but is scant in non-lesion BPS (23,24). Cystoscopic and biopsy findings in both lesion and non-lesion BPS are consistent with defects in the urothelial glycosaminoglycan (GAG) layer which might expose submucosal structures to noxious urine components (25-31) and a consequent cytotoxic effect (32,33). Autonomic dysfunction with sympathetic predominance may be implicated in BPS (34,35).
• An association has been reported between BPS and non-bladder syndromes such as fibomyalgia (FM), inflammatory bowel syndrome, vulvodynia, depression, panic disorders, migraine, sicca syndrome, temporomandibular joint disorder, allergy, asthma and systemic lupus erythematosus (36-40). Risk of BPS correlates with a number of nonbladder syndromes in each patient (41). Recent research showing non-lesion BPS to have significantly more FM, migraine, temporomandibular joint disorder and depression than BPS type 3C patients, emphasizes the need for subtyping (42).
III.10.1.2 Diagnosis.
• This is mainly a disease of exclusion. The clinical examination often serves to confirm what we have gained from the history taking. Besides the local examination, a general musculoskeletal and neurological examination should be considered an integral part of the assessment. There is no specific diagnostic test for BPS, therefore, procedures are directed towards identification and exclusion of specific diseases associated with pelvic pain, and for phenotypic description.
• Ultrasound on the abdomen and pelvis is done to exclude gross pelvic pathology, but with limited value to diagnose PBS. Urine dipstick and urine culture (including culture for tuberculosis if sterile pyuria) are recommended in all patients suspected of having BPS. Urine cytology is also recommended to exclude malignancy (1).
• Symptom scores may help to assess the patient and act as outcome measures. The O’LearySant Symptom Index, also known as the Interstitial Cystitis Symptom Index (ICSI) was validated for use (43).
• Objective findings from cystoscopy are important for diagnosis, prognosis and ruling out other treatable conditions (44). Endoscopically, BPS type 3 displays reddened mucosal areas often associated with small vessels radiating towards a central scar, sometimes covered by a small clot or fibrin deposit - the Hunner ulcer (2). The scar ruptures with increasing bladder distension, producing a characteristic waterfall type of bleeding. There is a strong association between BPS type 3 and reduced bladder capacity under anaesthesia. Nonlesion disease displays a normal bladder mucosa at initial cystoscopy. The development of glomerulations after hydrodistension is considered to be a positive diagnostic sign although they can be observed without BPS. Biopsies are helpful in establishing or supporting the clinical diagnosis of both classic and non-lesion types of the disease (26,44-47). Important differential diagnoses to exclude, by histological examination, are carcinoma in situ and tuberculous cystitis
III.10.2 Management.
• Treatment is usually multimodal (1). It includes lifestyle interventions such as fluid intake modifications, smoking cessation, exercise and no wearing of tight clothes. Another aspect is pain education and education about the causes of pain. Dietary restrictions alone do not produce significant symptomatic relief and scientific data are limited, however, consider the involvement of a dietician.
• The physiotherapist is part of the pain management team, together with the pain doctor and the psychologist. Physiotherapists can either specifically treat the pathology of the pelvic floor muscles, or more generally treat myofascial pain if it is part of the pelvic pain syndrome (48). Efficacy and safety of pelvic floor myofascial physical therapy has been compared with global therapeutic massage in women with BPS; global response assessment (GRA) rate was 59% and 26%, respectively. Pain, urgency and frequency ratings, and symptoms decreased in both groups during follow-up, and did not differ significantly between the groups. This suggests that myofascial physical therapy is beneficial in women with BPS (49).
• Psychological interventions are directed at pain itself or at adjustment to pain in terms of function and mood. Ideally, treatment follows general principles and practice in the field of chronic pain (49). Two systematic reviews and meta-analyses of the few heterogeneous trials of psychologically based treatment for pelvic pain (50,51) found some short-term benefits for pain, of around 50%, comparable to that from pharmacotherapy, but this was not sustained at follow-up.
• Medical therapy includes many option modalities. Histamine receptor antagonists have been used to block the H1 and H2 receptor subtypes (52), with unsatisfactory results (53). Amitriptyline is a tricyclic antidepressant. Several reports have indicated improvement of BPS symptoms after oral amitriptyline (54,55). Drowsiness is a side effect of amitriptyline. Subjective improvement of pain, urgency, frequency, but not nocturia, has been reported with use of Pentosane polysulphate (56,57). It has a more favorable effect in BPS type 3C than in non-lesion disease (58). Immunosuppressants have been tried. Azathioprine and cyclocporin A (59,60) treatment have resulted in disappearance of pain and urinary frequency. Corticosteroids are not recommended in the management of patients with BPS because of lack of evidence.
• Intravesical route is an appealing mode of delivery in PBS. Intravesical drugs are administered due to poor oral bioavailability, establishing high drug concentrations within the bladder, with few systemic side-effects. Disadvantages include the need for intermittent catheterization which can be painful in BPS patients, cost and risk of infection (61). Several drugs have been tried. There are sporadic reports of successful treatment of BPS with intravesical lidocaine (62,63). Combination of heparin, lidocaine and sodium bicarbonate gave immediate symptom relief in 94% of patients and sustained relief after two weeks in 80% (64). Intravesical instillation of alkalized lidocaine for five consecutive days resulted in significantly sustained symptom relief for up to one month (65). Hyaluronic acid and chondroitin sulphate are described to repair defects in the GAG layer (66). Most of the studies are uncontrolled and with a small number of patients and most studies are nonrandomized and with few numbers (67). Symptomatic improvement was reported in 80% of BPS patients with intravesical heparin (67,68).
• There are treatments which are of limited value in BPS. These include cimetidine, with limited data to suggest that cimetidine improves symptoms of BPS in the short-term. These treatments also include misoprostol, which is a prostaglandin, oral L-arginine, intravesical oxybutynin and duloxetine (69-74). None of these drugs have proven to be recommended for treatment of BPS.
• Neuromodulation.
• The role of neuromodulation in the management of chronic pelvic pain (CPP) should only be considered by specialists in pelvic pain management. These techniques are used as part of a broader management plan and require regular follow-up. These are expensive interventional tools for patients who are refractory to other therapies. There has been growing evidence, but more detailed, high quality research is required (75). Two recent systematic reviews have evaluated neuromodulation techniques for CPP (76,77). Both studies concluded that neuromodulation may be effective in reducing pain and improving QoL in patients with CPP, however studies were of a low quality and long-term results were needed.
• Transcutaneous Electrical Nerve Stimulation (TENS) is a non-invasive technique used in many pain conditions. All RCTs demonstrated a significant reduction in pain following twelve weeks of treatment for pain conditions including CPP. There was conflicting data with regard to improvement of quality of life (QoL) following TENS; where validated questionnaires were used. TENS could offer an effective non- invasive treatment option for patients with CPP. • Percutaneous Tibial Nerve Stimulation (PTNS) is a minimally invasive technique that can be use in an outpatient setting. Two trials have shown that PTNS is effective in reducing pain in patients with CPP (76,77). Adverse events were rare and minor including temporary slight pain at application site and haematoma.
• Sacral nerve stimulation (77) is an invasive technique requiring sedation or general anaesthesia for implantation of a device following trial stimulation. All studies reported an improvement in pain and QoL. There was a large variation in adverse events reported ranging from 0-50%.
• Re-operation rate ranged between 11-50% for complications including lead migration, systemic infection, intrathecal implantation, loss of efficacy and erosion.
• Although bladder hydrodistension is a common treatment for BPS, the scientific justification is scarce. It can be part of the diagnostic evaluation but has limited therapeutic role. Diagnostic hydrodistention is done under general anesthesia for 2 minutes and with height of fluid above the bladder of 81cmH2O. Therapeutic hydrodistension is done under same circumstances but for 8 minutes (78). Treatment with hydrodistension and hydrodistension plus intravesical botulinum toxin A (BTX-A) has been compared (79). There was symptomatic improvement in all patients. However, in the hydrodistension-only group, 70% returned to their previous symptoms after one month, while in the BTX-Atreated patients, visual analogue score (VAS) score and functional and cystometric bladder capacity improved at three months. BTX-A trigonal-only injection seems effective and long-lasting as 87% of patients reported improvement after three months’ follow-up (80). Over 50% reported continued benefit nine months after the first treatment. When retreatment was needed, similar results were obtained. Adverse effects of BTX-A administration for IC/BPS were significantly less than for overactive bladder syndrome (81). The American Urological Association (AUA) guidelines panel has upgraded BTX-A treatment from fifth to a fourth line treatment (82).
• Endourological destruction of bladder tissue aims to eliminate urothelial lesions, mostly Hunner ulcer. Resection and fulguration have been reported to achieve symptom relief, often for more than three years (83,84). Prolonged amelioration of pain and urgency has been described for transurethral laser ablation as well (85). Laser fulgration is preferred due to chronicity of the disease and need for refulgration, with possible bladder fibrosis and shrinkage.
• There is no evidence that open surgery for PBS relieves pain. Surgery for refractory BPS is only appropriate as a last resort for patients with refractory end-stage disease. Urinary diversion without cystectomy (86) is performed to minimise the duration and complexity of surgery, but complications related to the retained bladder commonly occur. Supratrigonal cystectomy with bladder augmentation represents the most favoured continence preserving surgical technique particularly in younger patients (87). Subtrigonal or simple cystectomy refers to removal of the entire bladder at the level of the bladder neck. This approach has the benefit of removing the trigone as a possible disease site, but at the cost of requiring ureteric re-implantation. Trigonal disease is reported in 50% of patients and surgical failure has been blamed on the trigone being left in place (88), especially in patients with non-ulcer type disease (89,90).
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III.10.3 References.
1- D. Engeler, A.P. Baranowski, B. Berghmans et al. EAU Guidelines on chronic pelvic pain. European Guidelines 2020.
2- Fall, M., et al. Chronic interstitial cystitis: a heterogeneous syndrome. J Urol, 1987. 137: 35.
3- Warren, J.W., et al. Evidence-based criteria for pain of interstitial cystitis/painful bladder syndrome in women. Urology, 2008. 71: 444.
4- van de Merwe, J.P., et al. Diagnostic criteria, classification, and nomenclature for painful bladder syndrome/interstitial cystitis: an ESSIC proposal. Eur Urol, 2008. 53: 60.
5- Bade, J.J., et al. Interstitial cystitis in The Netherlands: prevalence, diagnostic criteria and therapeutic preferences. J Urol, 1995. 154: 2035.
6- Burkman, R.T. Chronic pelvic pain of bladder origin: epidemiology, pathogenesis and quality of life. J Reprod Med, 2004. 49: 225.
7- Curhan, G.C., et al. Epidemiology of interstitial cystitis: a population-based study. J Urol, 1999. 161: 549.
8- Held, P., et al., Interstitial Cystitis. In: Epidemiology of interstitial cystitis. Hanno PM, Staskin DR, Krane RJ, Wein AJ, eds. 1990, Springer Verlag: London.
9- Jones, C., et al. Prevalence of interstitial cystitis in the United States. Proc Am Urol Ass J Urol, 1994. 151 (Suppl).
10- Leppilahti, M., et al. Prevalence of clinically confirmed interstitial cystitis in women: a population-based study in Finland. J Urol, 2005. 174: 581.
11- Oravisto, K.J. Epidemiology of interstitial cystitis. Ann Chir Gynaecol Fenn, 1975. 64: 75.
12- Parsons, C.L., et al. Prevalence of interstitial cystitis in young women. Urology, 2004. 64: 866.
13- Roberts, R.O., et al. Incidence of physician-diagnosed interstitial cystitis in Olmsted County: a community-based study. BJU Int, 2003. 91: 181.
14- Temml, C., et al. Prevalence and correlates for interstitial cystitis symptoms in women participating in a health screening project. Eur Urol, 2007. 51: 803.
15- Berry, S.H., et al. Prevalence of symptoms of bladder pain syndrome/interstitial cystitis among adult females in the United States. J Urol, 2011. 186: 540.
16- Song, Y., et al. Prevalence and correlates of painful bladder syndrome symptoms in Fuzhou Chinese women. Neurourol Urodyn, 2009. 28: 22.
17- Koziol, J.A., et al. Discrimination between the ulcerous and the nonulcerous forms of interstitial cystitis by noninvasive findings. J Urol, 1996. 155: 87.
18- Messing, E.M., et al. Interstitial cystitis: early diagnosis, pathology, and treatment. Urology, 1978. 12: 381.
19- Parsons, C. Interstitial cystitis: clinical manifestations and diagnostic criteria in over 200 cases. Neurourol Urodyn, 1990. 9.
20- Peeker, R., et al. Toward a precise definition of interstitial cystitis: further evidence of differences in classic and nonulcer disease. J Urol, 2002. 167: 2470.
21- Mattox, T.F. Interstitial cystitis in adolescents and children: a review. J Pediatr Adolesc Gynecol, 2004. 17: 7.
22- Richter, B., et al. YKL-40 and mast cells are associated with detrusor fibrosis in patients diagnosed with bladder pain syndrome/interstitial cystitis according to the 2008 criteria of the European Society for the Study of Interstitial Cystitis. Histopathology, 2010. 57: 371.
23- Dundore, P.A., et al. Mast cell counts are not useful in the diagnosis of nonulcerative interstitial cystitis. J Urol, 1996. 155: 885.
24- Peeker, R., et al. Recruitment, distribution and phenotypes of mast cells in interstitial cystitis. J Urol, 2000.163: 1009.
25- Anderstrom, C.R., et al. Scanning electron microscopic findings in interstitial cystitis. Br J Urol, 1989. 63: 270.
26- Johansson, S.L., et al. Clinical features and spectrum of light microscopic changes in interstitial cystitis. J Urol, 1990. 143: 1118.
27- Logadottir, Y.R., et al. Intravesical nitric oxide production discriminates between classic and nonulcer interstitial cystitis. J Urol, 2004. 171: 1148.
28- Lokeshwar, V.B., et al. Urinary uronate and sulfated glycosaminoglycan levels: markers for interstitial cystitis severity. J Urol, 2005. 174: 344.
29- Parsons, C.L., et al. Epithelial dysfunction in nonbacterial cystitis (interstitial cystitis). J Urol, 1991. 145: 732.
30- Parsons, C.L., et al. Successful therapy of interstitial cystitis with pentosan polysulfate. J Urol, 1987. 138: 513.
31- Sanchez-Freire, V., et al. Acid-sensing channels in human bladder: expression, function and alterations during bladder pain syndrome. J Urol, 2011. 186: 1509.
32- Hang, L., et al. Cytokine repertoire of epithelial cells lining the human urinary tract. J Urol, 1998. 159: 2185.
33- Parsons, C.L., et al. Cyto-injury factors in urine: a possible mechanism for the development of interstitial cystitis. J Urol, 2000. 164: 1381.
34- Chelimsky, G., et al. Autonomic Testing in Women with Chronic Pelvic Pain. J Urol, 2016. 196: 429.
35- Charrua, A., et al. Can the adrenergic system be implicated in the pathophysiology of bladder pain syndrome/ interstitial cystitis? A clinical and experimental study. Neurourol Urodyn, 2015. 34: 489.
36- Alagiri, M., et al. Interstitial cystitis: unexplained associations with other chronic disease and pain syndromes. Urology, 1997. 49: 52.
37- Buffington, C.A. Comorbidity of interstitial cystitis with other unexplained clinical conditions. J Urol, 2004. 172: 1242.
38- Erickson, D.R., et al. Nonbladder related symptoms in patients with interstitial cystitis. J Urol, 2001. 166: 557.
39- Warren, J.W., et al. Antecedent nonbladder syndromes in case-control study of interstitial cystitis/painful bladder syndrome. Urology, 2009. 73: 52.
40- Weissman, M., et al. Interstitial Cystitis and Panic Disorder - A Potential Genetic Syndrome. Arch Gen Psych, 2004. 61.
41- Warren, J.W., et al. Numbers and types of nonbladder syndromes as risk factors for interstitial cystitis/painful bladder syndrome. Urology, 2011. 77: 313.
42- Peters, K.M., et al. Are ulcerative and nonulcerative interstitial cystitis/painful bladder syndrome 2 distinct diseases? A study of coexisting conditions. Urology, 2011. 78: 301.
43- Lubeck, D.P., et al. Psychometric validation of the O'leary-Sant interstitial cystitis symptom index in a clinical trial of pentosan polysulfate sodium. Urology, 2001. 57: 62.
44- Aihara, K., et al. Hydrodistension under local anesthesia for patients with suspected painful bladder syndrome/interstitial cystitis: safety, diagnostic potential and therapeutic efficacy. Int J Urol, 2009. 16: 947.
45- Parsons, C.L. The role of a leaky epithelium and potassium in the generation of bladder symptoms in interstitial cystitis/overactive bladder, urethral syndrome, prostatitis and gynaecological chronic pelvic pain. BJU Int, 2011. 107: 370.
46- Geurts, N., et al. Bladder pain syndrome: do the different morphological and cystoscopic features correlate? Scand J Urol Nephrol, 2011. 45: 20.
47- Johansson, S.L., et al. Pathology of interstitial cystitis. Urol Clin North Am, 1994. 21: 55.
48- Loving, S., et al. Does evidence support physiotherapy management of adult female chronic pelvic pain? Scan J Pain, 2012. 3: 70.
49- FitzGerald, M.P., et al. Randomized multicenter clinical trial of myofascial physical therapy in women with interstitial cystitis/painful bladder syndrome and pelvic floor tenderness. J Urol, 2012. 187: 2113.
50- Cheong, Y.C., et al. Non-surgical interventions for the management of chronic pelvic pain. Cochrane Database Syst Rev, 2014. 3: CD008797.
51- Champaneria, R., et al. Psychological therapies for chronic pelvic pain: Systematic review of randomized controlled trials. Acta Obstet Gynecol Scand, 2012. 91: 281.
52- Seshadri, P., et al. Cimetidine in the treatment of interstitial cystitis. Urology, 1994. 44: 614.
53- Sant, G.R., et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol, 2003. 170: 810.
54- Hanno, P.M., et al. Use of amitriptyline in the treatment of interstitial cystitis. J Urol, 1989. 141: 846.
55- Foster, H.E., Jr., et al. Effect of amitriptyline on symptoms in treatment naive patients with interstitial cystitis/ painful bladder syndrome. J Urol, 2010. 183: 1853.
56- Hwang, P., et al. Efficacy of pentosan polysulfate in the treatment of interstitial cystitis: a metaanalysis. Urology, 1997. 50: 39.
57- Mulholland, S.G., et al. Pentosan polysulfate sodium for therapy of interstitial cystitis. A doubleblind placebocontrolled clinical study. Urology, 1990. 35: 552.
58- Fritjofsson, A., et al. Treatment of ulcer and nonulcer interstitial cystitis with sodium pentosan polysulfate: a multicenter trial. J Urol, 1987. 138: 508.
59- Oravisto, K.J., et al. Treatment of interstitial cystitis with immunosuppression and chloroquine derivatives. Eur Urol, 1976. 2: 82.
60- Forsell, T., et al. Cyclosporine in severe interstitial cystitis. J Urol, 1996. 155: 1591.
61- Barua, J.M., et al. A systematic review and meta-analysis on the efficacy of intravesical therapy for bladder pain syndrome/interstitial cystitis. Int Urogynecol J, 2016. 27: 1137.
62- Asklin, B., et al. Intravesical lidocaine in severe interstitial cystitis. Case report. Scand J Urol Nephrol, 1989. 23: 311.
63- Giannakopoulos, X., et al. Chronic interstitial cystitis. Successful treatment with intravesical idocaine. Arch Ital Urol Nefrol Androl, 1992. 64: 337.
64- Parsons, C.L. Successful downregulation of bladder sensory nerves with combination of heparin and alkalinized lidocaine in patients with interstitial cystitis. Urology, 2005. 65: 45.
65- Nickel, J.C., et al. Intravesical alkalinized lidocaine (PSD597) offers sustained relief from symptoms of interstitial cystitis and painful bladder syndrome. BJU Int, 2009. 103: 910.
66- Hammouda Sherif, Ahmed Sebay, Wael Kandeel, Tarek Othman, Abdallah Fathi, Ahmed Mohey, and Ali Eshazly. Safety and efficacy of Intravesical hyaluronic acid/chondroitin sulfate in the treatment of refractory painful bladder syndrome. Turk J Urol. 2019 Jul; 45(4): 296–301.
67- Pyo, J.S., et al. Systematic Review and Meta-Analysis of Intravesical Hyaluronic Acid and Hyaluronic Acid/Chondroitin Sulfate Instillation for Interstitial Cystitis/Painful Bladder Syndrome. Cell Physiol Biochem, 2016. 39: 1618.
68- Parsons, C.L., et al. Treatment of interstitial cystitis with intravesical heparin. Br J Urol, 1994. 73: 504.
69- Thilagarajah, R., et al. Oral cimetidine gives effective symptom relief in painful bladder disease: a prospective, randomized, double-blind placebo-controlled trial. BJU Int 2001. 87: 207.
70- Kelly, J.D., et al. Clinical response to an oral prostaglandin analogue in patients with interstitial cystitis. Eur Urol 1998. 34: 53. 71- Korting, G.E., et al. A randomized double-blind trial of oral L-arginine for treatment of interstitial cystitis. J Urol 1999. 161: 558.
72- Cartledge, J.J., et al. A randomized double-blind placebo-controlled crossover trial of the efficacy of L-arginine in the treatment of interstitial cystitis. BJU Int, 2000. 85: 421.
73- Barbalias, G.A., et al. Interstitial cystitis: bladder training with intravesical oxybutynin. J Urol, 2000. 163: 1818.
74- van Ophoven, A., et al. The dual serotonin and noradrenaline reuptake inhibitor duloxetine for the treatment of interstitial cystitis: results of an observational study. J Urol, 2007. 177: 552.
75- Fariello, J.Y., et al. Sacral neuromodulation stimulation for IC/PBS, chronic pelvic pain, and sexual dysfunction. Int Urogynecol J, 2010. 21: 1553.
76- Cottrell, A.M., et al. Benefits and Harms of Electrical Neuromodulation for Chronic Pelvic Pain: A Systematic Review. Eur Urol Focus, 2019.
77- Tutolo, M., et al. Efficacy and Safety of Sacral and Percutaneous Tibial Neuromodulation in NonNeurogenic Lower Urinary Tract Dysfunction and Chronic Pelvic Pain: A Systematic Review of the Literature. Eur Urol, 2018. 73: 406.
78- El-Hefnawy AS, Makharita MY, Abed A, Amr YM, Salah El-Badry M, Shaaban AA. Anesthetic Bladder Hydrodistention Is Superior to Superior Hypogastric Plexus Neurolysis in Treatment of Interstitial Cystitis-bladder Pain Syndrome: A Prospective Randomized Trial. Urology. 2015 May;85(5):1039-1044.
79- Kuo, H.C., et al. Comparison of intravesical botulinum toxin type A injections plus hydrodistention with hydrodistention alone for the treatment of refractory interstitial cystitis/painful bladder syndrome. BJU Int, 2009. 104: 657.
80- Pinto, R., et al. Trigonal injection of botulinum toxin A in patients with refractory bladder pain syndrome/interstitial cystitis. Eur Urol, 2010. 58: 360.
81- Kuo, Y.C., et al. Adverse Events of Intravesical Onabotulinum Toxin A Injection between Patients with Overactive Bladder and Interstitial Cystitis-Different Mechanisms of Action of Botox on Bladder Dysfunction? Toxins, 2016. 8
82- Hanno, P.M., et al. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol, 2015. 193: 1545.
83- Kerr, W.S., Jr. Interstitial cystitis: treatment by transurethral resection. J Urol, 1971. 105: 664.
84- Peeker, R., et al. Complete transurethral resection of ulcers in classic interstitial cystitis. Int Urogynecol J Pelvic Floor Dysfunct, 2000. 11: 290.
85- Rofeim, O., et al. Use of the neodymium: YAG laser for interstitial cystitis: a prospective study. J Urol, 2001. 166: 134.
86- Freiha, F.S., et al. The surgical treatment of intractable interstitial cystitis. J Urol, 1980. 123: 632.
87- Kim, H.J., et al. Efficacy and safety of augmentation ileocystoplasty combined with supratrigonal cystectomy for the treatment of refractory bladder pain syndrome/interstitial cystitis with Hunner's lesion. Int J Urol, 2014. 21 Suppl 1: 69.
88- Nurse, D.E., et al. The problems of substitution cystoplasty. Br J Urol, 1988. 61: 423.
89- Peeker, R., et al. The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease. J Urol, 1998. 159: 1479.
90- Rossberger, J., et al. Long-term results of reconstructive surgery in patients with bladder pain syndrome/interstitial cystitis: subtyping is imperative. Urology, 2007. 70: 638.
III.11 Female Bladder Outlet Obstruction (BOO).
III.11.1 Definition and Background.
• Symptoms of female BOO are mostly non-specific and the classic voiding LUTS of impaired urine flow, hesitancy, intermittent stream, straining and even retention may be less apparent, making diagnosis difficult. (1,8) Other presenting symptoms, e.g. irritative voiding complaints, may be secondary to BOO. Urethral pain and recurrent urinary tract infections (UTIs) are other presenting symptoms as well. Bending forward to void or having to change positions to empty effectively usually indicates an element of obstruction in post anti-stress urinary incontinence (SUI) operations (8). This raises the importance of high level of suspicion for BOO in women. Finally, this problem is often not suspected in women, and so its management is typically delayed. (1)
• Female BOO can be caused by anatomical or functional causes. Furthermore, anatomical causes include extrinsic and intrinsic (luminal) factors. (9) Extrinsic causes include pelvic organ prolapse (POP), iatrogenic post anti-incontinence procedure and skene gland abscess or cyst, while intrinsic causes include urethral stricture or fibrosis, urethral diverticulum, excessive bulking agent, urethral tumour, condyloma accuminata, urethral stone, urethral caruncle or urethral prolapse. Functional causes include primary bladder neck obstruction, pseudo-dyssynergia known as Hinman’s syndrome and detrusor sphincter dyssynergia (DSD). (1,8)
• Detrusor failure or acontractility should be excluded, and pressure-flow study could be of help in the diagnosis. However, there are currently no nomograms that accurately assesses detrusor underactivity (DUA) in women. (1,9)
• In a study by Greenwell et al (1), 192 females with BOO were diagnosed. Anatomical obstruction was found in 64% and functional obstruction was present in 36%. The most common anatomical cause of BOO was previous anti-SUI surgery (21%), followed by urethral stricture (20%).
III.11.2 Diagnosis.
• Many nomograms have been utilized, with different prevalence rates. Ferrar et al. diagnosed BOO based only on Qmax of <15 mL/s with prevalence of BOO of 6.7%. (3) Massey and Abrams diagnosed BOO in only 2.7% of 5948 females based on 2 or more of the following criteria: Qmax <12 mL/s, pdet @Qmax >50 cmH2O, urethral resistance (pdet @Qmax/ 2Qmax) >0.2, and significant PVR. (4) Lemack and Zimmern used cut-off values of Qmax ≤15 mL/s and pdet@ Qmax>20 cmH2O, diagnosing BOO in 20% of the patients. (7) Blaivas and Groutz created a nomogram to diagnose BOO and classify its severity based on pressure–flow criteria of a free Qmax ≤12 mL/s and a Pdet @Qmax ≥20 cmH2O, in association with radiographic evidence of obstruction, and reported a prevalence of 8.3%.(2)
• Elmissiry et al. categorized females with BOO into three different subtypes based on urodynamic patterns (early, compensated and late obstruction). They recommended that UDS should be combined with the clinical presentation and estimation of PVR for an accurate diagnosis of BOO. (10)
• The role of pressure flow studies alone to diagnose female BOO is questioned because voiding dynamics in females are different from those in males, and most of the females void predominantly by pelvic floor relaxation or abdominal straining with low detrusor pressures. Nitti et al. introduced the role of videourodynamics (VUDS), combined with clinical suspicion of BOO, with an overall prevalence of 29%. (11,12)
III.11.3 Treatment.
• Most urethral strictures or fibrosis in women are iatrogenic and can result from previous urethral or periurethral surgery, or in some cases from previous urethral dilatation. Many females experience urethral strictures from previous obstructed labors. Options include urethral dilatations, better under brief anesthesia, cystourethroscopy, or in resistant recurrent cases, urethroplasty with vaginal flap or buccal mucosal grafts is indicated but in highly specialized referral centers. (8,18,19)
• Primary bladder neck obstruction is caused by lack of relaxation of the smooth muscle of the bladder neck during voiding, and it responds well to alpha blockers. CIC could be an option if medications fail. Transurethral incision of the bladder neck is definitive, but with increased risks of postoperative incontinence. Neuromodulation is of help in these cases. (20-24)
• Pseudo-dyssynergia or Hinman’s syndrome results from an external sphincter that does not relax during voiding in an otherwise neurologically intact woman. First-line treatment consists of pelvic floor relaxation. Skeletal muscle relaxants such as diazepam can be used as well, but the side-effects limit their applicability. Intrasphincter botulinum injection is successful in many cases, but this is off-label use. Finally, sacral neuromodulation has been used successfully.
• DSD occurs when the external sphincter contracts during a detrusor contraction in a neurologically impaired individual. It is common in patients with suprasacral spinal cord injuries (SCI) and multiple sclerosis (MS). Introduction of botulinum toxin injections into the external sphincter of these patients is successful. (8,25)
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III.11.4 References.
1- Malde S, Solomon E, Spilotros M, Mukhtar B, Pakzad M, Hamid R, Ockrim J, Greenwell T. Female bladder outlet obstruction: Common symptoms masking an uncommon cause. Low Urin Tract Symptoms. 2019 Jan; 11(1):72-77.
2- Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn. 2000; 19(5):553–564.
3- Farrar DJ, Osborne JL, Stephenson TP, et al. A urodynamic view of bladder outflow obstruction in the female: factors influencing the results of treatment. Br J Urol. 1975; 47(7):815–822.
4- Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol. 1988; 61(1):36–39.
5- Rees DL, Whitfield HN, Islam AK, Doyle PT, Mayo ME, Wickham JE. Urodynamic findings in adult females with frequency and dysuria. Br J Urol. 1975; 47(7):853–860.
6- Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS, Zimmern PE. Proposed cutoff values to define bladder outlet obstruction in women. Urology. 1998; 51(3):408–411.
7- Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying women with outflow obstruction. J Urol. 2000; 163 (6):1823–1828.
8- Goldman HB, Zimmern PE. The treatment of female bladder outlet obstruction. BJU Int. 2006 Sep; 98 Suppl 1:17-23
9- Are There Pharmacotherapeutic Options for Underactive Bladder? Osman NI, Chapple CR. Eur Urol Focus. 2018 Jan; 4(1):6-7.
10- Elmissiry MM, Ali AG, Ali GA. Different urodynamic patterns in female bladder outlet obstruction: Can urodynamics alone reach the diagnosis? Arab J Urol. 2013 Jun; 11(2):127-30.
11- Patel R, Nitti V. Bladder outlet obstruction in women: prevalence, recognition and management. Curr Urol Rep. 2001; 2(5):379–387.
12- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol. 1999; 161(5):1535–1540.
13- Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999; 161: 581–6
14- Gilleran JP, Lemack GE, Zimmern PE. Reduction of moderate-to-largecystocele during urodynamic evaluation using a vaginal gauze pack: 8-year experience. BJU Int 2006; 97: 292–5
15- Goldman HB. Simple sling incision for the treatment of iatrogenic urethral obstruction. Urology 2003; 62: 714–8
16- Goldman HB. Urethrolysis. Atlas Urol Clinics 2004; 12: 197–204
17- Carey JM, Chon JK, Leach GE. Urethrolysis with Martius labial fat pad graft for iatrogenic bladder outlet obstruction. Urology 2003; 61(Suppl.4):21–5
18- Nnenaya Agochukwu-Mmonu, Sudarshan Srirangapatanam. Andrew Cohen, Benjamin Breyer.Female Urethral Strictures: Review of Diagnosis, Etiology, and Management. J Med Case Rep. 2018; 12: 382.
19- Lemack G, Zimmern PE. Voiding difficulties. In Shaw R, Soutter WP, Stanton SL eds, Gynaecology, 3rd edn. Edinburgh: Churchill Livingstone, 2003: 803–12
20- Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999; 161: 1535–40
21- Kumar A, Mandhani A, Gogoi S, Srivastava A. Management of functional bladder neck obstruction in women: use of alpha-blockers and pediatric resectoscope for bladder neck incision. J Urol 1999; 162: 2061-5
22- Blaivas J, Flisser AJ, Tash JA. Treatment of primary bladder neck obstruction in women with transurethral resection of the bladder neck. J Urol 2004; 171: 1172–5
23- Peng CH, Kuo HC. Transurethral incision of bladder neck in treatment of bladder neck obstruction in women. Urology 2005; 65: 275–8
24- Hourieh Sharifian, Mahtab Zargham, Mohamad Hatef Khorami et al. Internal urethrotomy in treatment of female with anatomical bladder outlet obstruction. Adv Biomed Res. 2019; 8: 36.
25- Moore C, Rackley R, Goldman H. Urologic applications of botox. Curr Urol Rep 2005; 6: 419–23
III.12 Geriatric urinary incontinence.
• Geriatric syndromes are defined as common conditions seen in the elderly that are complex in nature, are usually multifactorial, and can have clinical or other negative health outcomes for affected patients. (2)
• The incidence and prevalence of UI increase in the elderly population. However, incontinence should not be considered a normal or inevitable aging event. This is a common myth among both health care providers and patients. (3)
• UI is accompanied with social isolation, stigmatization, depression, aversion from sexual life and embarrassment. Skin irritation and cracking from urine, development of pressure ulcers, recurrent urinary tract infections (UTIs), falls and fractures are all substantial physical problems. (4) UI has a stronger negative influence on overall levels of happiness than diabetes, hypertension, arthritis, and osteoporosis. (5)
• Economic data has shown an estimated national cost of evaluation and care for wetoveractive bladder (OAB) of $65.9 billions in 2007, with estimated increase to $76.2 billions in 2015 and $82.6 billions in 2020. (6) The degree of incontinence in the elderly as measured by severity appears to be more influential on health-related quality of life (QoL) outcomes than type of UI. (7)
III.12.1 Transient urinary incontinence.
• A wide variety of conditions can lead to associated transient UI. UTI can cause urinary frequency and in some cases UI. This should be considered symptomatic and should be evaluated and treated appropriately. True asymptomatic bacteriuria does not by itself cause UI and does not require antibiotic therapy. Atrophic vaginitis or urethritis is common in elderly females and may be associated with dysuria or a burning sensation with voiding. Treatment with vaginal estrogens can help ameliorate symptoms of this condition and may help improve UI and decrease incidence of UTIs. (10)
• Fecal impaction is frequently caused by slow transit time through the gut or increased water reuptake in the colon. Fecal incontinence (FI) and diarrhea may be presenting symptoms because liquid stool proximal to the impaction moves around the impacted stool bolus. Disimpaction often results in resolution of both urinary and fecal symptoms. Chronic constipation is a common problem in older adults. Treatment and prevention with a bowel regimen can help. (11)
• Different medications can cause transient incontinence the elderly including psychotropics, diuretics, benzodiazepines, calcium channel blockers, tricyclic antidepressants (TCAs), αblockers, and narcotic analgesics. Diuretics increase urinary output leading to urinary urgency, frequency, and UUI. Opioids and narcotic analgesics tend to decrease detrusor contractility and can cause urinary retention with associated incontinence. TCAs have pronounced anticholinergic effect and decrease detrusor contractility, leading to difficulty voiding or urinary retention. Alcohol and other substance abuse are also causing UI. (12,13
• Other causes of transient incontinence include depression, anxiety, delirium, dementia, Alzheimer’s disease, mobility impairment, excess urinary output and polyuria. (3)
III.12.2 Established Urinary Incontinence.
• Urgency urinary incontinence (UUI) is the most common form of established incontinence among elderly people. (15) The term precipitancy has been used to describe the symptom that occurs with detrusor overactivity (DO) in older adults. In patients with no sensation of warning, precipitant leakage may be experienced as an unconscious or reflex episode of incontinence. (16)
• One form of bladder dysfunction that is unique in the geriatric population is detrusor hyperactivity with impaired contractility (DHIC). Patients experience DO with bladder filling, which is associated with the typical symptoms of urinary urgency, frequency, and UUI. However, during voiding the bladder does not contract efficiently to completely empty. Successful treatment often requires multimodal therapy including behavioral interventions and medications to inhibit DO and clean intermittent catheterization (CIC) to empty the bladder. (17)
• Stress urinary incontinence (SUI) is common in the elderly, and urethral atrophy associated with decreased tissue estrogenization and other age-related factors can exacerbate sphincteric competency, leading to intrinsic sphincteric deficiency (ISD). (3) Detrusor underactivity (DUA), sometimes called underactive bladder, can be caused by a wide variety of conditions. Often the cause is idiopathic. Pelvic atherosclerosis is associated with diminished arterial blood flow to the bladder, which could cause ischemic changes. (18)
• Targeted protocols to treat UI in long-term care settings have proven quite successful. Prompted toileting can be used in patients with adequate mobility and cognitive function to use toilet facilities independently. Patients are prompted by caregivers or staff to use the toilet on a regular schedule. Timing is adjusted based on specific individual needs. In those older adults with mobility and/or cognitive impairment, assisted toileting procedures may be necessary. The use of assistive toileting devices such as handheld urinals or bedside commodes may be necessary depending on functional status. (19,20)
• Evaluation should be individually tailored to the clinical needs and goals of the patient and his or her caregivers. It includes detailed history taking, review of medical records, identifying the most bothersome component of UI. Physical examination, including pelvic examination in women, is essential. (3) Many elderlies do not completely empty the bladder with voiding. Elevated PVR is common in the elderly, however, no specific volume is considered pathologic and there is a great deal of controversy surrounding the importance of elevated PVR volume in older adult patients. (21) Urinalysis and urine cultures should be obtained when clinically indicated and can help to identify underlying comorbidity. (22)
• Urodynamic studies can be useful in the evaluation of select elderly patients with UI and other forms of voiding dysfunction. Indications for urodynamic studies, in the elderly, include failed prior therapy and underlying neurologic or other comorbid conditions. Pressure-flow urodynamic testing can be particularly helpful to differentiate between functional obstruction and poor contractility. (23,24)
III.12.3 Treatment.
• Timed or scheduled toileting can be quite useful in some patients with urgency and frequency. Many older adults have worse symptoms near full bladder capacity. Voiding on a more regular schedule before reaching capacity may help. Bladder retraining to increase the intervoiding interval, can be useful in select cases. (28)
• Most older adults require specific pelvic floor muscle training (PFMT). Cognitive impairment may limit practicality of this therapy in some patients. It requires a motivated patient who is willing to do the exercises and is able to follow guided instruction. PFMT is often used in combination with other forms of behavioral or pharmacologic therapies. (29,30)
• Medications are widely used in treatment of UI. Duloxetine, a balanced serotonin and noradrenaline reuptake inhibitor, also has α-adrenergic properties and has been considered as a possible treatment option for SUI. (31)
• Anticholinergics are the main stay of pharmacological treatment in OAB. Adverse effects on the central nervous system (CNS) include cognitive impairment, acceleration of neurodegenerative processes, appearance of psychotic or confusional symptoms and functionality disturbances. On the other hand, adverse effects on the PNS include dry mouth, urinary retention, constipation and paralytic ileus, increased heart rate and blurred vision. (32)
• Improved selectivity of muscarinic receptor binding is another focus in drug development. The goal is to target the bladder (M2 and M3) but avoid the salivary gland and bowel (both M3), which may help reduce the risk of dry mouth and constipation. (33-34) Some experts suggest that there is little evidence regarding the reversibility of anticholinergic cognitive effect through discontinuation and question the safety of this measure. Different studies have proposed conflicting hypotheses regarding the reversibility of cognitive effects after discontinuation. Abrupt discontinuation is not recommended due to the risk of a cholinergic rebound, i.e., symptoms of agitation, diarrhea, vomiting, lacrimation, tachycardia, insomnia and movement disorders after withdrawal. (35) Tolterodine and oxybutynin are the UI drugs with the highest anticholinergic load. (36) Oxybutynin has the highest blood-brain barrier permeability and trospium chloride the lowest.
• Mirabegron is a B3 agonist with no side effects of the anticholinergics. This acts on detrusor smooth muscle to decrease contractility and reduce symptoms associated with overactivity. In the PILLAR study (37), efficacy of mirabegron in the elderly for the treatment of wetOAB in patients aged > 65 years was tested. Results revealed good clinical efficacy, relatively few side effects and tolerability consistent with the known safety profile of the drug over 12 weeks.
• A number of different forms of surgical therapy is used for treatment of UI in older adults. These include surgical procedures for both SUI and UUI. Many older adults want to avoid surgery as a possible treatment option for UI. Age alone is rarely a significant risk factor for postoperative outcomes. (38)
• A number of published studies have examined safety and efficacy of sling procedures for treatment of SUI in geriatric patients. These have shown good outcomes in general, with no significant difference in complication rates compared with younger patients. (39)
• Use of indwelling catheters is usually avoided in older adults because of the associated risks of UTI, catheter colonization, urinary tract stones, or tissue erosion. Catheters should be removed as soon as feasible to help prevent negative outcomes. Cystoscopy is recommended on at least an annual basis, particularly after the first several years of use, to evaluate for any mucosal changes such as squamous metaplasia or development of stones. If patients have problems with urinary leakage around the catheter or from the urethra, treatment should be focused on reducing bladder contractions with antimuscarinics. It is strongly recommended that providers don’t increase the caliber of the tube. Increasing the diameter of the catheter will not solve the underlying cause of the urinary leakage and will serve only to dilate the suprapubic tract or urethra. This can lead to severe problems with erosion and catheter extrusion. Catheters of 16 or 18 Fr are typically adequate for use as a suprapubic tube. (40-42)
• Urine containment and absorbent products are also valid options to help manage urinary leakage. Although these should not be considered a curative treatment option, they can be quite useful for management of symptomatic urine loss. Absorbent pads come in many designs and range from small pads to extra absorbent briefs and can be used for both light and heavier volumes of urinary leakage. (43) Gel-based products may offer better odor control and have good overall absorbency, although they may not be able to control large volume leakage. Pads and absorbent products are used in UI management scheme of nursing home residents. (3)
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III.12.4 References.
III.13 Female Sexual Dysfunctions (FSD).
III.13.1 Definition.
• FSD is an umbrella term that entails distressing situations which interfere with a woman’s ability to enjoy a satisfying sexual life. It is defined as persistent or recurrent inability to engage in satisfying sexual activity leading to marked distress or interpersonal difficulty after excluding general medical conditions, psychiatric issues, substance abuse and medications. Duration of at least 6 months is required to apply a diagnosis except in the case of medication-induced sexual dysfunction (1).
• Prevalence of sexual problems in the general female population is unknown (2) due to selection bias, limited data collection, and variation/disagreement about what constitutes a sexual problem. Prevalence in the general population varies widely from 23% to 82% (3-8).
• FSD has been linked to increasing age (9,10), menopausal symptoms (10-12), absence of partner (12), age of partner (10), partner sexual dysfunction (9,13), urinary incontinence (UI) (14,15), depression (14,16), tobacco use (11), sedentary lifestyle (17), hypothyroidism (18), diabetes (19) and poor general health (9,12).
III.13.2 Evaluation of sexual health in women.
• Sexuality and sexual health are sensitive topics that many patients are hesitant to discuss with their health care providers. In a study by Nusbeum et al in 2000 (20), 98% of females seeking routine gynecological care had sexual concerns, yet, both physicians and patients are reluctant to ask. Physicians’ questioning increases patients’ reporting of sexual dysfunction, where 14% of females report spontaneously, and 55% of patients reports FSD after direct questioning. Approximately 43% of American women have sexual complaints.
• FSD is more difficult to diagnose and manage, and even more challenging than male sexual dysfunction. Inquiry about sexual health can be incorporated into a general urologic clinic visit. Normalizing statements (e.g., “Many patients have questions about their sexual life”) may help the patient to feel at ease discussing their sexual complaints (21). A simple, openended question (e.g., “What concerns do you have about sexuality?”) is recommended as an initial screen (22). Yes/no questions (e.g., “Are there any problems with your sexual life that you wish to discuss with me?” “Are you satisfied with your sexual life?”) may be a more practical way to screen for sexual problems.
• Evaluation of the partner is another pivotal issue. Sexual distress is linked to incompatibility with the partner (23) and therefore involvement of the sexual partner is mandatory in the management of any sexuality problem. Education of the partner may be of particular importance given the generally low knowledge of female sexual response in the community (24).
• A general physical examination is required. The patient should be assessed for evidence of endocrinopathy, nerve injury, diabetes, or obesity (24,25). Evaluation of the genitals should start with careful inspection of the external genitalia including mons pubis, labia majora, labia minora, clitoris, and the vulva. This superficial examination may show genital lesions, erythema that may predispose to sexual pain disorders, redundancy of the labia, or atrophy of the external genitalia (24,25). Vulvar skin conditions are common and can lead to a variety of sexual concerns. Examples include eczema, contact dermatitis, fungal infections, apthous ulcers, and drug reactions.
• Testing for genital neuropathy may be accomplished by application of heat/cold stimuli, vibration, and/or application of a toothpick. A simple assessment for stress urinary incontinence (SUI) as performing cough test is mandatory. Urinary symptoms are associated with sexual problems and are within the scope of practice for urologists to manage. Bimanual examination of the vagina is performed to assess for pelvic organ prolapse (POP) and ovarian pathology (24). Assessment of the levator ani muscles should be included as part of the bimanual examination (26). A speculum examination should be considered. Assessment of vaginal pH is a simple and inexpensive test. High pH signifies disruption of the normal vaginal microbiome; this may have relevance to recurrent infection and vulvovaginal atrophy collectively known as genitourinary syndrome of menopause (27).
• The role of laboratory studies in evaluation of FSD is controversial (24,25). Serum lipids, and glycosylated hemoglobin should be assayed, as these are low-risk tests for common problems relevant to female sexual function. Assessment of sex steroids particularly, serum estradiol and testosterone (T), should be considered (28,29). Most widely available assays for T are not precise in women (30). The timing of assay with respect to menstrual cycle should be clearly defined. T should be assayed in the morning between days 8 and 14 of a 28-day menstrual cycle (31). The decision to measure serum T should only be made after consultation with the patient about the unknowns and with a clear sense of what will be done with the data if the test result is concerning for androgen insufficiency (32,33). Elevated prolactin is associated with decreased sexual desire and suppression of serum T levels (18).
• Many questionnaires are developed to diagnose FSD. The most widely used and cited research in urologic sexual medicine is the Female Sexual Function Index (FSFI) (34). The FSFI is a 19-item questionnaire that assesses 6 domains of female sexual experience (desire, arousal, lubrication, orgasm, satisfaction, and pain). In most studies, a total FSFI score of less than 26.55 has been used as a marker for a higher risk of FSD. The FSFI has been shown to be more reliable in predicting treatment success in studies of sexual dysfunctions. An abbreviated six-item version of the FSFI has been reported (35).
III.13.3 Classification of FSD.
• FSD is classified in the fifth edition of the Diagnostic and Statistical Manual for Mental Disorders (DSM-5) into (36):
1. Female sexual interest/arousal disorder which includes desire and arousal disorders.
2. Female orgasmic disorder.
3. Genito-pelvic pain/penetration disorder” which includes dyspareunia and vaginismus.
III.13.3.1 Female sexual interest/arousal disorders.
They include.
III.13.3.1.1 Hypoactive sexual desire disorder (HSDD).
• It is the most common disorder, and it is defined as diminished feelings of sexual interest or desire, absence of sexual thoughts, and/or lack of receptivity to sexual activity.
• Common precipitating factors include hormonal changes, medication use, changes in relationship status, or life stressors (37). It is very common for women to experience a reactive decline in sexual desire in the presence of other impediments to sexual activity.
• Hypoestrogenism has been clearly linked to decreased sexual desire in women, primarily in association with menopause (38). Androgen deficiency has also been linked to decreased sexual interest in women (39). Psychosocial stressors have a marked effect on sexual interest in women. Depression is prevalent and includes a well-known association with HSDD (40). Aging is associated with declines in sexual desire (38). The use of medications, particularly antidepressants of the SSRI class, is associated with HSDD (40).
• There is no approved pharmacotherapy for HSDD in women. Stress reduction strategies, maintenance of general health, and addressing relationship issues are generally regarded as positive interventions. Psychosexual therapy encompasses numerous mental health approaches to addressing HSDD in women. The general goals of therapy include education on sexual physiology and response, determination of type and frequency of sexual activity that is personally desired and developing interpersonal communication skills (22). If it is selective serotonin reuptake inhibitor (SSRI)-related medication, cessation of the drug or modulation of the dose would be beneficial (41). A meta-analysis of adjunctive treatments for SSRI-induced sexual dysfunction confirmed that twice-daily dosing with bupropion 150 mg improved sexual function outcomes (42). On-demand use of sildenafil enhances orgasmic function in women taking SSRIs for depression (43).
• Correction of estrogen deficiency has been associated with improvement in female sexual function, including desire (44). Supplementation with T increases sexual desire in women with low libido and low serum androgen levels (45). Currently there is no approved androgen-based treatment for sexual-interest disorders in women in the United States. Other drugs increase androgens such as tibolone which is a synthetic hormone that is metabolized to several forms with estrogenic activity (46). Flibanserin is an agonist against the 5HT1A receptor and antagonist against the 5HT2A receptor. It exerts dopaminergic and noradrenergic actions. These CNS effects may enhance sexual interest. High doses of flibanserin (100 mg/day) are consistently associated with statistically significant positive changes in sexuality (particularly desire) (47). However adverse events include somnolence, headache, vertigo, and nausea.
III.13.3.1.2 Female sexual arousal disorders (FSAD)
III.13.3.1.2.1 Genital arousal disorder (GFSAD).
Impaired genital arousal with minimal vulvar swellings and vaginal lubrication from genital stimulation. (25)
III.13.3.1.2.1.1 Psychological arousal disorder (PFSAD).
Absent or markedly diminished feelings of excitement or pleasure in response to sexual stimulation.
III.13.3.1.2.1.2 Mixed arousal disorder.
It includes GFSAD and PFSAD.
III.13.3.1.2.2 Persistent genital arousal disorder (PGAD).
Persistent, recurrent, intrusive, and/or distressing sensations of genital arousal not related to sexual stimulation that do not resolve after orgasm. It may last for hours to days.
III.13.3.1.3 Pathogenesis.
Vascular or neurologic disease may contribute to GFSAD (48). Pelvic surgery (gynecologic, urologic, or colorectal) may also disrupt genital innervations (particularly the autonomic innervation of the pelvic nerve) and vascular supply (49). Smoking is associated with impairment of genital response due to effect of nicotine (50). Diabetes represents a special risk factor for FSD, as it may be associated with neurologic, vascular, and/or hormonal defects (19). Antidepressants may also impair genital arousal responses. Although depression itself is a risk factor for FSD, some women may experience improvement in sexual satisfaction when treated with antidepressant drugs (51). Endocrinopathy is an important cause of GFSAD. Perturbation of genital response (thinning of vagina and dryness) is often related to hypoestrogenism from menopause (27). PFASD typically originates from psychological causes. Common examples include dissatisfaction with a sexual partner and depression (25).
III.13.3.1.4 Treatment.
Psychosocial therapy entails attention to psychosocial factors mediating FSAD. Eros Clitoral Therapy Device (52) is a battery-powered vacuum-driven suction device designed to be applied to the clitoris. It was shown to enhance sensation, arousal, and orgasmic potential in women. Phosphodiesterase 5 inhibitors (PDE5I) (53) have been of great interest in treating FSAD because of the similarities in the mechanisms of vascular engorgement between men and women. PDE5I are not approved for use in women and hence any use of these drugs in women is off label. Use of sexual lubricants is one of the simplest approaches to treat GFASD (54). There are innumerable formulations of sexual lubricants which vary in terms of lubricity, additives, durability, and cost. Transdermal prostaglandin E1 (PGE1) applied to the vulva and/or clitoris has been reported as a therapy for GFSAD. One gram of ointment containing 0.2% PGE1 applied to the external genitalia produced a pronounced genital response when compared to placebo ointment (55). Estrogens and tibolone may prove efficacious in treating FSAD (46).
III.13.3.1.5 Persistent genital arousal disorder (PGAD).
Genital sensations associated with PGAD include throbbing, lubrication, pelvic congestion, sense of imminent orgasm without climax, and unprovoked orgasm (56). PGAD has been associated with a dysfunction of sexual beliefs (57) and restless legs syndrome (56). PGAD has also been associated with anxiety and obsessive-compulsive symptoms (58), withdrawal of SSRI medications (59), and pelvic arteriovenous malformations (60). The largest series of women with confirmed PGAD revealed high (55%) prevalence of pelvic varices (61). Clinical examination of these women demonstrated that two thirds of them had restless legs syndrome and/or overactive bladder (56). Many women also reported exacerbation of PGAD symptoms with stress. PGAD may be a manifestation of nonsexual “hyperexcitability” of the genitals.
Benzodiazepine drug, clonazepam (0.5 to 1.5 mg/day) is effective in reducing PGAD symptoms in 56% of treated subjects (61). Benefit was also reported in some women from treatment with tramadol 50 mg (56). Cognitive/behavioral treatments have been proposed, including training to direct attention away from genital sensations and the reduction of overall anxiety (58). Women with this poorly understood disorder have very positive responses to empathy and support from their providers (56).
III.13.3.2 Female orgasmic disorders (FOD)
It is defined as lack of experience of orgasm or diminished orgasm intensity despite high sexual arousal after a period of sufficient sexual stimulation and arousal. Primary orgasmic disorders are typically the result of sexual inexperience and are treated using cognitive behavioral therapy, directed masturbation (62), and sex education. Permission giving by the physician regarding sexual exploration and masturbation is hugely helpful to women with anorgasmia. Secondary anorgasmia, or acquired anorgasmia, is often the result of antidepressant medications. This can be treated by stopping the offending medication. There are no approved pharmacotherapies for FOD. PDE5I enhance orgasmic response in women with decreased sexual desire related to the use of SSRI drugs (43) and in postmenopausal women with orgasmic dysfunction. Use of these drugs in women is off label.
III.13.3.3 Genito-pelvic pain/penetration disorders.
III.13.3.3.1 Dyspareunnia
Is defined as persistent/recurrent pain with attempted/complete vaginal entry with a penis, finger, or another object. It could be superficial or deep. Introital or superficial type could be caused by vaginitis, decreased lubrication and superficial vestibulodynia. Deep dyspareunia could be due to endometriosis and pelvic inflammatory diseases.
Treatment of dyspareunia includes pelvic floor physical therapy with biofeedback and pelvic floor electrical stimulation. Vaginal dilators have all been used with reported clinical benefit but without scientific evidence. Postmenopausal women with pain secondary to atrophic vaginitis should be treated with topical estrogen, whereas women with vulvovaginitis should be treated with oral or transvaginal antifungal and/or antibacterial agents.
III.13.3.3.2 Vaginism
Is defined as vaginal spasm or pain in response to penetration with a penis, finger, or other object despite a desire for penetration to occur. Treatment includes topical lidocaine, gabapentin, botulinum toxin injection in the vagina, biofeedback and cognitive behavior.
Table III:8 Recommendations for female sexual dysfunctions (FSD).
Recommendation
strength rating
1. Inquiry about sexual health can be incorporated into a general urologic clinic visit Strong
2. Duration of sexual dysfunction for at least 6 months is required to apply a diagnosis Weak
3. Use normalizing statements (e.g., “Many patients have questions about their sexual life”). This may help patients feel comfortable during discussing their sexual complaints Srtrong
4. Ask simple, open-ended questions (e.g., “What concerns do you have about sexuality?”) as an initial screening Strong
5. Yes/No questions (e.g., “Are you satisfied with your sexual life?”) could be used to screen for sexual problems Strong
6. A complete history (medical, sexual, partner, etc.) and thorough physical examination (particularly of the genitals) is fundamental for the evaluation of sexual wellness in women Weak
7. Evaluate the male partner in cases of female sexual dysfunctions Strong
8. Education of the male partner may be of particular importance given the generally low knowledge of normal female sexual function Strong
9. Use validated FSFI in the initial assessment of FSD Strong
10. Psychosocial support is critical in the management of any sexual concern Strong
11. There are few approved pharmacotherapies for FSD; there are a number of treatments, but many of these are off label Weak
12. Twice daily-dosing of Bupropion 150 mg in SSRI-induced sexual dysfunction is associated with improved sexual function outcomes Strong
13. On-demand use of sildenafil enhances orgasmic function in women taking SSRIs for depression Strong
13. On-demand use of sildenafil enhances orgasmic function in women taking SSRIs for depression Strong
14. High doses of flibanserin (100 mg/day) are consistently associated with statistically significant positive changes in sexuality (particularly desire) but be aware of the side effects associated Weak
15. PDE5I could be used in treating FSAD, however they are not approved for use and they are considered off-label drugs Weak
17. Benzodiazepines (clonazepam 0.5 to 1.5 mg/day) is effective in reducing PGAD symptoms in 56% of patients. Benefit was also reported with tramadol 50 mg Weak
18. Postmenopausal women with pain secondary to atrophic vaginitis should be treated with topical estrogen Strong
19. Women with vulvovaginitis should be treated with oral or transvaginal antifungal and/or antibacterial agents Strong
20. Treatment of vaginismus includes topical lidocaine, gabapentin, botulinum toxin injection in the vagina, biofeedback and cognitive behavior Weak
III.14 Conclusions.
These guidelines provide practical evidence-based guidance on the clinical aspect of many urogynecological entities. The main target is entirely focused on assessment and treatment, reflecting the recommended clinical practice. This can provide the basis for thinking through patient’s management and also for planning and designing clinical services.
Early diagnosis of the different female urogynecological problems is fundamental before deciding any plan of management. Accordingly, tailoring and individualizing the plan of management follows, which ensures the best practice of clinical care offered to these patients. The role of these guidelines is to offer expert advice on how to manage these patients. .
III.15 References.
1- Alan W. Shindel and Irwin Goldstein. Sexual Function and Dysfunction in the Female. In: Wein A, Kavoussi L, Partin A, Peters C, editors. Campbell-Walsh Urology. 11th ed. Philadelphia (USA): 2016.
2- Laumann EO, Paik A, Glasser DB, et al. A cross-national study of subjective sexual well-being among older women and men: findings from the Global Study of Sexual Attitudes and Behaviors. Arch Sex Behav 2006; 35:145–61.
3- Nicolosi A, Buvat J, Glasser DB, et al. Sexual behaviour, sexual dysfunctions and related help seeking patterns in middle-aged and elderly Europeans: the global study of sexual attitudes and behaviors. World J Urol 2006a; 24:423–8.
4- Nicolosi A, Laumann EO, Glasser DB, et al. Sexual activity, sexual disorders and associated helpseeking behavior among mature adults in five Anglophone countries from the Global Survey of Sexual Attitudes and Behaviors (GSSAB). J Sex Marital Ther 2006b; 32:331–42.
5- Nicolosi A, Glasser DB, Kim SC, et al. Sexual behaviour and dysfunction and help-seeking patterns in adults aged 40-80 years in the urban population of Asian countries. BJU Int 2005; 95:609–14.
6- Blumel JE, Chedraui P, Baron G, et al. Sexual dysfunction in middle-aged women: a multicenter Latin American study using the Female Sexual Function Index. Menopause 2009; 16:1139–48.
7- Shindel AW, Eisenberg ML, Breyer BN, et al. Sexual function and depressive symptoms among female North American medical students. J Sex Med 2011; 8:391–9.
8- Shindel AW, Rowen TS, Lin TC, et al. An Internet survey of demographic and health factors associated with risk of sexual dysfunction in women who have sex with women. J Sex Med 2012; 9:1261–71.
9- Blumel JE, Chedraui P, Baron G, et al. Sexual dysfunction in middle-aged women: a multicenter Latin American study using the Female Sexual Function Index. Menopause 2009; 16:1139–48.
10- Chedraui P, Perez-Lopez FR, San Miguel G, et al. Assessment of sexuality among middle-aged women using the Female Sexual Function Index. Climacteric 2009; 12:213–21.
11- Oksuz E, Malhan S. Prevalence and risk factors for female sexual dysfunction in Turkish women. J Urol 2006; 175:654–8, discussion 658.
12- Valadares AL, Pinto-Neto AM, Osis MJ, et al. Prevalence of sexual dysfunction and its associated factors in women aged 40-65 years with 11 years or more of formal education: a population-based household survey. Clinics 2008; 63:775–82.
13- Zhang H, Yip PS. Female sexual dysfunction among young and middle-aged women in Hong Kong: prevalence and risk factors. J Sex Med 2012;9: 2911–8.
14- Rosen RC, Link CL, O’Leary MP, et al. Lower urinary tract symptoms and sexual health: the role of gender, lifestyle and medical comorbidities. BJU Int 2009b;103(Suppl. 3):42–7.
15- Kim YH, Kim SM, Kim JJ, et al. Does metabolic syndrome impair sexual function in middle- to old-aged women? J Sex Med 2011; 8:1123–30.
16- West SL, D’Aloisio AA, Agans RP, et al. Prevalence of low sexual desire and hypoactive sexual desire disorder in a nationally representative sample of US women. Arch Intern Med 2008; 168:1441–9.
17- Esposito K, Maiorino MI, Bellastella G, et al. Determinants of female sexual dysfunction in type 2 diabetes. Int J Impot Res 2010; 22:179–84.
18- Atis G, Dalkilinc A, Altuntas Y, et al. Sexual dysfunction in women with clinical hypothyroidism and subclinical hypothyroidism. J Sex Med 2010; 7:2583–90.
19- Giraldi A, Kristensen E. Sexual dysfunction in women with diabetes mellitus. J Sex Res 2010; 47:199–211.
20- Nusbaum MR, Gamble G, Skinner B, Heiman J. The high prevalence of sexual concerns among women seeking routine gynecological care. J Fam Pract. 2000 Mar; 49(3):229-32.
21- Sadovsky R, Alam W, Enecilla M, et al. Sexual problems among a specific population of minority women aged 40-80 years attending a primary care practice. J Sex Med 2006; 3:795–803.
22- Kingsberg S, Althof SE. Evaluation and treatment of female sexual disorders. Int Urogynecol J Pelvic Floor Dysfunct 2009; 20(Suppl. 1): S33–43.
23- Witting K, Santtila P, Varjonen M, et al. Female sexual dysfunction, sexual distress, and compatibility with partner. J Sex Med 2008; 5:2587–99.
24- Goldstein I, Alexander JL. Practical aspects in the management of vaginal atrophy and sexual dysfunction in perimenopausal and postmenopausal women. J Sex Med 2005;2(Suppl. 3):154–65.
25- Basson R, Wierman ME, van Lankveld J, et al. Summary of the recommendations on sexual dysfunctions in women. J Sex Med 2010b; 7:314–26.
26- Rosenbaum TY, Owens A. The role of pelvic floor physical therapy in the treatment of pelvic and genital pain-related sexual dysfunction (CME). J Sex Med 2008; 5:513–23, quiz 524–5.
27- Bachmann GA, Ebert GA, Burd ID. Vulvovaginal complaints. In: Lobo RA, editor. Treatment of the postmenopausal woman: basic and clinical aspects. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 195–201.
28- Utian WH, Archer DF, Bachmann GA, et al. Estrogen and progestogen use in postmenopausal women: July 2008 position statement of The North American Menopause Society. Menopause 2008; 15:584–602.
29- Kingsberg SA. The sexual health benefits of oral low-dose estrogen plus progestogen and vaginal estrogen for postmenopausal women. Menopause 2009; 16:224–5.
30- Stanczyk FZ, Cho MM, Endres DB, et al. Limitations of direct estradiol and testosterone immunoassay kits. Steroids 2003; 68:1173–8.
31- Davison SL, Davis SR. Androgenic hormones and aging–the link with female sexual function Horm Behav 2011; 59:745–53.
32- Bachmann G, Bancroft J, Braunstein G, et al. Female androgen insufficiency: the Princeton consensus statement on definition, classification, and assessment. Fertil Steril 2002; 77:660–5.
33- Bachmann G, Oza D. Female androgen insufficiency. Obstet Gynecol Clin North Am 2006; 33:589–98.
34- Rosen R, Brown C, Heiman J, et al. The Female Sexual Function Index (FSFI): a multidimensional self-report instrument for the assessment of female sexual function. J Sex Marital Ther 2000; 26:191–208.
35- Isidori AM, Pozza C, Esposito K, et al. Development and validation of a 6-item version of the female sexual function index (FSFI) as a diagnostic tool for female sexual dysfunction. J Sex Med 2010;7: 1139–46.
36- Derogatis LR, Laan E, Brauer M, et al. Responses to the proposed DSM-V changes. J Sex Med 2010; 7:1998–2014.
37- Brotto LA, Bitzer J, Laan E, et al. Women’s sexual desire and arousal disorders. J Sex Med 2010; 7:586–614.
38- West SL, D’Aloisio AA, Agans RP, et al. Prevalence of low sexual desire and hypoactive sexual desire disorder in a nationally representative sample of US women. Arch Intern Med 2008; 168:1441–9.
39- Warnock JK, Bundren JC, Morris DW. Female hypoactive sexual desire disorder due to androgen deficiency: clinical and psychometric issues. Psycho pharmacol Bull 1997; 33:761–6.
40- Clayton AH, Maserejian NN, Connor MK, et al. Depression in premenopausal women with HSDD: baseline findings from the HSDD Registry for Women. Psychosom Med 2012; 74:305–11.
41- Ahrold TK, Meston CM. Effects of SNS activation on SSRI-induced sexual side effects differ by SSRI. J Sex Marital Ther 2009; 35:311–9.
42- Taylor MJ, Rudkin L, Bullemor-Day P, et al. Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database Syst Rev 2013;(5):CD003382.
43- Nurnberg HG, Hensley PL, Heiman JR, et al. Sildenafil treatment of women with antidepressantassociated sexual dysfunction: a randomized controlled trial. JAMA 2008; 300:395–404.
44- Nastri CO, Lara LA, Ferriani RA, et al. Hormone therapy for sexual function in perimenopausal and postmenopausal women. Cochrane Database Syst Rev 2013;(6):CD009672.
45- North American Menopause Society. The role of testosterone therapy in postmenopausal women: position statement of The North American Menopause Society. Menopause 2005; 12:496–511, quiz 649.
46- Laan E, van Lunsen RH, Everaerd W. The effects of tibolone on vaginal blood flow, sexual desire and arousability in postmenopausal women. Climacteric 2001; 4:28–41.
47- Derogatis LR, Komer L, Katz M, et al. Treatment of hypoactive sexual desire disorder in premenopausal women: efficacy of flibanserin in the VIOLET Study. J Sex Med 2012; 9:1074– 85.
48- Traish AM, Botchevar E, Kim NN. Biochemical factors modulating female genital sexual arousal physiology. J Sex Med 2010; 7:2925–46.
49- Raina R, Pahlajani G, Khan S, et al. Female sexual dysfunction: classification, pathophysiology, and management. Fertil Steril 2007; 88:1273–84
50- Harte CB, Meston CM. The inhibitory effects of nicotine on physiological sexual arousal in nonsmoking women: results from a randomized, double-blind, placebo-controlled, cross-over trial. J Sex Med 2008;5: 1184–97.
51- Ishak WW, Christensen S, Sayer G, et al. Sexual satisfaction and quality of life in major depressive disorder before and after treatment with citalopram in the STAR*D study. J Clin Psychiatry 2013; 74:256–61.
52- Billups KL, Berman L, Berman J, et al. A new non-pharmacological vacuum therapy for female sexual dysfunction. J Sex Marital Ther 2001; 27:435–41.
53- Munarriz R, Kim SW, Kim NN, et al. A review of the physiology and pharmacology of peripheral (vaginal and clitoral) female genital arousal in the animal model. J Urol 2003;170: S40–4, discussion S44–5.
54- Herbenick D, Reece M, Hensel D, et al. Association of lubricant use with women’s sexual pleasure, sexual satisfaction, and genital symptoms: a prospective daily diary study. J Sex Med 2011a; 8:202–12.
55- Bechara A, Bertolino MV, Casabe A, et al. Duplex Doppler ultrasound assessment of clitoral hemodynamics after topical administration of alprostadil in women with arousal and orgasmic disorders. J Sex Marital Ther 2003;29(Suppl. 1):1–10.
56- Waldinger MD, Schweitzer DH. Persistent genital arousal disorder in 18 Dutch women: part II. a syndrome clustered with restless legs and overactive bladder. J Sex Med 2009; 6:482–97.
57- Carvalho J, Verissimo A, Nobre PJ. Cognitive and emotional determinants characterizing women with persistent genital arousal disorder. J Sex Med 2013; 10:1549–58.
58- Leiblum SR, Chivers ML. Normal and persistent genital arousal in women: new perspectives. J Sex Marital Ther 2007; 33:357–73.
59- Leiblum SR, Goldmeier D. Persistent genital arousal disorder in women: case reports of association with anti-depressant usage and withdrawal. J Sex Marital Ther 2008; 34:150–9.
60- Goldstein I, De EJB, Johnson JA. Persistent sexual arousal syndrome and clitoral priapism. In: Goldstein I, Meston CM, Davis SR, et al, editors. Women’s sexual function and dysfunction: study, diagnosis and treatment. London: Taylor and Francis; 1995. p. 674–85.
61- Waldinger MD, van Gils AP, Ottervanger HP, et al. Persistent genital arousal disorder in 18 Dutch women: part I. MRI, EEG, and transvaginal ultrasonography investigations. J Sex Med 2009; 6:474–81.
62- Heiman JR, Meston CM. Empirically validated treatment for sexual dysfunction. Annu Rev Sex Res 1997; 8:148–94
• Prevalence of sexual problems in the general female population is unknown (2) due to selection bias, limited data collection, and variation/disagreement about what constitutes a sexual problem. Prevalence in the general population varies widely from 23% to 82% (3-8).
• FSD has been linked to increasing age (9,10), menopausal symptoms (10-12), absence of partner (12), age of partner (10), partner sexual dysfunction (9,13), urinary incontinence (UI) (14,15), depression (14,16), tobacco use (11), sedentary lifestyle (17), hypothyroidism (18), diabetes (19) and poor general health (9,12).
III.13.2 Evaluation of sexual health in women.
• FSD is more difficult to diagnose and manage, and even more challenging than male sexual dysfunction. Inquiry about sexual health can be incorporated into a general urologic clinic visit. Normalizing statements (e.g., “Many patients have questions about their sexual life”) may help the patient to feel at ease discussing their sexual complaints (21). A simple, openended question (e.g., “What concerns do you have about sexuality?”) is recommended as an initial screen (22). Yes/no questions (e.g., “Are there any problems with your sexual life that you wish to discuss with me?” “Are you satisfied with your sexual life?”) may be a more practical way to screen for sexual problems.
• Evaluation of the partner is another pivotal issue. Sexual distress is linked to incompatibility with the partner (23) and therefore involvement of the sexual partner is mandatory in the management of any sexuality problem. Education of the partner may be of particular importance given the generally low knowledge of female sexual response in the community (24).
• A general physical examination is required. The patient should be assessed for evidence of endocrinopathy, nerve injury, diabetes, or obesity (24,25). Evaluation of the genitals should start with careful inspection of the external genitalia including mons pubis, labia majora, labia minora, clitoris, and the vulva. This superficial examination may show genital lesions, erythema that may predispose to sexual pain disorders, redundancy of the labia, or atrophy of the external genitalia (24,25). Vulvar skin conditions are common and can lead to a variety of sexual concerns. Examples include eczema, contact dermatitis, fungal infections, apthous ulcers, and drug reactions.
• Testing for genital neuropathy may be accomplished by application of heat/cold stimuli, vibration, and/or application of a toothpick. A simple assessment for stress urinary incontinence (SUI) as performing cough test is mandatory. Urinary symptoms are associated with sexual problems and are within the scope of practice for urologists to manage. Bimanual examination of the vagina is performed to assess for pelvic organ prolapse (POP) and ovarian pathology (24). Assessment of the levator ani muscles should be included as part of the bimanual examination (26). A speculum examination should be considered. Assessment of vaginal pH is a simple and inexpensive test. High pH signifies disruption of the normal vaginal microbiome; this may have relevance to recurrent infection and vulvovaginal atrophy collectively known as genitourinary syndrome of menopause (27).
• The role of laboratory studies in evaluation of FSD is controversial (24,25). Serum lipids, and glycosylated hemoglobin should be assayed, as these are low-risk tests for common problems relevant to female sexual function. Assessment of sex steroids particularly, serum estradiol and testosterone (T), should be considered (28,29). Most widely available assays for T are not precise in women (30). The timing of assay with respect to menstrual cycle should be clearly defined. T should be assayed in the morning between days 8 and 14 of a 28-day menstrual cycle (31). The decision to measure serum T should only be made after consultation with the patient about the unknowns and with a clear sense of what will be done with the data if the test result is concerning for androgen insufficiency (32,33). Elevated prolactin is associated with decreased sexual desire and suppression of serum T levels (18).
• Many questionnaires are developed to diagnose FSD. The most widely used and cited research in urologic sexual medicine is the Female Sexual Function Index (FSFI) (34). The FSFI is a 19-item questionnaire that assesses 6 domains of female sexual experience (desire, arousal, lubrication, orgasm, satisfaction, and pain). In most studies, a total FSFI score of less than 26.55 has been used as a marker for a higher risk of FSD. The FSFI has been shown to be more reliable in predicting treatment success in studies of sexual dysfunctions. An abbreviated six-item version of the FSFI has been reported (35).
III.13.3 Classification of FSD.
1. Female sexual interest/arousal disorder which includes desire and arousal disorders.
2. Female orgasmic disorder.
3. Genito-pelvic pain/penetration disorder” which includes dyspareunia and vaginismus.
III.13.3.1 Female sexual interest/arousal disorders.
III.13.3.1.1 Hypoactive sexual desire disorder (HSDD).
• It is the most common disorder, and it is defined as diminished feelings of sexual interest or desire, absence of sexual thoughts, and/or lack of receptivity to sexual activity.
• Common precipitating factors include hormonal changes, medication use, changes in relationship status, or life stressors (37). It is very common for women to experience a reactive decline in sexual desire in the presence of other impediments to sexual activity.
• Hypoestrogenism has been clearly linked to decreased sexual desire in women, primarily in association with menopause (38). Androgen deficiency has also been linked to decreased sexual interest in women (39). Psychosocial stressors have a marked effect on sexual interest in women. Depression is prevalent and includes a well-known association with HSDD (40). Aging is associated with declines in sexual desire (38). The use of medications, particularly antidepressants of the SSRI class, is associated with HSDD (40).
• There is no approved pharmacotherapy for HSDD in women. Stress reduction strategies, maintenance of general health, and addressing relationship issues are generally regarded as positive interventions. Psychosexual therapy encompasses numerous mental health approaches to addressing HSDD in women. The general goals of therapy include education on sexual physiology and response, determination of type and frequency of sexual activity that is personally desired and developing interpersonal communication skills (22). If it is selective serotonin reuptake inhibitor (SSRI)-related medication, cessation of the drug or modulation of the dose would be beneficial (41). A meta-analysis of adjunctive treatments for SSRI-induced sexual dysfunction confirmed that twice-daily dosing with bupropion 150 mg improved sexual function outcomes (42). On-demand use of sildenafil enhances orgasmic function in women taking SSRIs for depression (43).
• Correction of estrogen deficiency has been associated with improvement in female sexual function, including desire (44). Supplementation with T increases sexual desire in women with low libido and low serum androgen levels (45). Currently there is no approved androgen-based treatment for sexual-interest disorders in women in the United States. Other drugs increase androgens such as tibolone which is a synthetic hormone that is metabolized to several forms with estrogenic activity (46). Flibanserin is an agonist against the 5HT1A receptor and antagonist against the 5HT2A receptor. It exerts dopaminergic and noradrenergic actions. These CNS effects may enhance sexual interest. High doses of flibanserin (100 mg/day) are consistently associated with statistically significant positive changes in sexuality (particularly desire) (47). However adverse events include somnolence, headache, vertigo, and nausea.
III.13.3.1.2 Female sexual arousal disorders (FSAD)
Absent or markedly diminished feelings of excitement or pleasure in response to sexual stimulation.
It includes GFSAD and PFSAD.
III.13.3.1.2.2 Persistent genital arousal disorder (PGAD).
III.13.3.1.3 Pathogenesis.
III.13.3.1.4 Treatment.
III.13.3.1.5 Persistent genital arousal disorder (PGAD).
Benzodiazepine drug, clonazepam (0.5 to 1.5 mg/day) is effective in reducing PGAD symptoms in 56% of treated subjects (61). Benefit was also reported in some women from treatment with tramadol 50 mg (56). Cognitive/behavioral treatments have been proposed, including training to direct attention away from genital sensations and the reduction of overall anxiety (58). Women with this poorly understood disorder have very positive responses to empathy and support from their providers (56).
III.13.3.2 Female orgasmic disorders (FOD)
III.13.3.3 Genito-pelvic pain/penetration disorders.
III.13.3.3.1 Dyspareunnia
Treatment of dyspareunia includes pelvic floor physical therapy with biofeedback and pelvic floor electrical stimulation. Vaginal dilators have all been used with reported clinical benefit but without scientific evidence. Postmenopausal women with pain secondary to atrophic vaginitis should be treated with topical estrogen, whereas women with vulvovaginitis should be treated with oral or transvaginal antifungal and/or antibacterial agents.
III.13.3.3.2 Vaginism
Recommendation |
strength rating |
|---|---|
III.14 Conclusions.
Early diagnosis of the different female urogynecological problems is fundamental before deciding any plan of management. Accordingly, tailoring and individualizing the plan of management follows, which ensures the best practice of clinical care offered to these patients. The role of these guidelines is to offer expert advice on how to manage these patients. .
III.15 References.
1- Alan W. Shindel and Irwin Goldstein. Sexual Function and Dysfunction in the Female. In: Wein A, Kavoussi L, Partin A, Peters C, editors. Campbell-Walsh Urology. 11th ed. Philadelphia (USA): 2016.
2- Laumann EO, Paik A, Glasser DB, et al. A cross-national study of subjective sexual well-being among older women and men: findings from the Global Study of Sexual Attitudes and Behaviors. Arch Sex Behav 2006; 35:145–61.
3- Nicolosi A, Buvat J, Glasser DB, et al. Sexual behaviour, sexual dysfunctions and related help seeking patterns in middle-aged and elderly Europeans: the global study of sexual attitudes and behaviors. World J Urol 2006a; 24:423–8.
4- Nicolosi A, Laumann EO, Glasser DB, et al. Sexual activity, sexual disorders and associated helpseeking behavior among mature adults in five Anglophone countries from the Global Survey of Sexual Attitudes and Behaviors (GSSAB). J Sex Marital Ther 2006b; 32:331–42.
5- Nicolosi A, Glasser DB, Kim SC, et al. Sexual behaviour and dysfunction and help-seeking patterns in adults aged 40-80 years in the urban population of Asian countries. BJU Int 2005; 95:609–14.
6- Blumel JE, Chedraui P, Baron G, et al. Sexual dysfunction in middle-aged women: a multicenter Latin American study using the Female Sexual Function Index. Menopause 2009; 16:1139–48.
7- Shindel AW, Eisenberg ML, Breyer BN, et al. Sexual function and depressive symptoms among female North American medical students. J Sex Med 2011; 8:391–9.
8- Shindel AW, Rowen TS, Lin TC, et al. An Internet survey of demographic and health factors associated with risk of sexual dysfunction in women who have sex with women. J Sex Med 2012; 9:1261–71.
9- Blumel JE, Chedraui P, Baron G, et al. Sexual dysfunction in middle-aged women: a multicenter Latin American study using the Female Sexual Function Index. Menopause 2009; 16:1139–48.
10- Chedraui P, Perez-Lopez FR, San Miguel G, et al. Assessment of sexuality among middle-aged women using the Female Sexual Function Index. Climacteric 2009; 12:213–21.
11- Oksuz E, Malhan S. Prevalence and risk factors for female sexual dysfunction in Turkish women. J Urol 2006; 175:654–8, discussion 658.
12- Valadares AL, Pinto-Neto AM, Osis MJ, et al. Prevalence of sexual dysfunction and its associated factors in women aged 40-65 years with 11 years or more of formal education: a population-based household survey. Clinics 2008; 63:775–82.
13- Zhang H, Yip PS. Female sexual dysfunction among young and middle-aged women in Hong Kong: prevalence and risk factors. J Sex Med 2012;9: 2911–8.
14- Rosen RC, Link CL, O’Leary MP, et al. Lower urinary tract symptoms and sexual health: the role of gender, lifestyle and medical comorbidities. BJU Int 2009b;103(Suppl. 3):42–7.
15- Kim YH, Kim SM, Kim JJ, et al. Does metabolic syndrome impair sexual function in middle- to old-aged women? J Sex Med 2011; 8:1123–30.
16- West SL, D’Aloisio AA, Agans RP, et al. Prevalence of low sexual desire and hypoactive sexual desire disorder in a nationally representative sample of US women. Arch Intern Med 2008; 168:1441–9.
17- Esposito K, Maiorino MI, Bellastella G, et al. Determinants of female sexual dysfunction in type 2 diabetes. Int J Impot Res 2010; 22:179–84.
18- Atis G, Dalkilinc A, Altuntas Y, et al. Sexual dysfunction in women with clinical hypothyroidism and subclinical hypothyroidism. J Sex Med 2010; 7:2583–90.
19- Giraldi A, Kristensen E. Sexual dysfunction in women with diabetes mellitus. J Sex Res 2010; 47:199–211.
20- Nusbaum MR, Gamble G, Skinner B, Heiman J. The high prevalence of sexual concerns among women seeking routine gynecological care. J Fam Pract. 2000 Mar; 49(3):229-32.
21- Sadovsky R, Alam W, Enecilla M, et al. Sexual problems among a specific population of minority women aged 40-80 years attending a primary care practice. J Sex Med 2006; 3:795–803.
22- Kingsberg S, Althof SE. Evaluation and treatment of female sexual disorders. Int Urogynecol J Pelvic Floor Dysfunct 2009; 20(Suppl. 1): S33–43.
23- Witting K, Santtila P, Varjonen M, et al. Female sexual dysfunction, sexual distress, and compatibility with partner. J Sex Med 2008; 5:2587–99.
24- Goldstein I, Alexander JL. Practical aspects in the management of vaginal atrophy and sexual dysfunction in perimenopausal and postmenopausal women. J Sex Med 2005;2(Suppl. 3):154–65.
25- Basson R, Wierman ME, van Lankveld J, et al. Summary of the recommendations on sexual dysfunctions in women. J Sex Med 2010b; 7:314–26.
26- Rosenbaum TY, Owens A. The role of pelvic floor physical therapy in the treatment of pelvic and genital pain-related sexual dysfunction (CME). J Sex Med 2008; 5:513–23, quiz 524–5.
27- Bachmann GA, Ebert GA, Burd ID. Vulvovaginal complaints. In: Lobo RA, editor. Treatment of the postmenopausal woman: basic and clinical aspects. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 195–201.
28- Utian WH, Archer DF, Bachmann GA, et al. Estrogen and progestogen use in postmenopausal women: July 2008 position statement of The North American Menopause Society. Menopause 2008; 15:584–602.
29- Kingsberg SA. The sexual health benefits of oral low-dose estrogen plus progestogen and vaginal estrogen for postmenopausal women. Menopause 2009; 16:224–5.
30- Stanczyk FZ, Cho MM, Endres DB, et al. Limitations of direct estradiol and testosterone immunoassay kits. Steroids 2003; 68:1173–8.
31- Davison SL, Davis SR. Androgenic hormones and aging–the link with female sexual function Horm Behav 2011; 59:745–53.
32- Bachmann G, Bancroft J, Braunstein G, et al. Female androgen insufficiency: the Princeton consensus statement on definition, classification, and assessment. Fertil Steril 2002; 77:660–5.
33- Bachmann G, Oza D. Female androgen insufficiency. Obstet Gynecol Clin North Am 2006; 33:589–98.
34- Rosen R, Brown C, Heiman J, et al. The Female Sexual Function Index (FSFI): a multidimensional self-report instrument for the assessment of female sexual function. J Sex Marital Ther 2000; 26:191–208.
35- Isidori AM, Pozza C, Esposito K, et al. Development and validation of a 6-item version of the female sexual function index (FSFI) as a diagnostic tool for female sexual dysfunction. J Sex Med 2010;7: 1139–46.
36- Derogatis LR, Laan E, Brauer M, et al. Responses to the proposed DSM-V changes. J Sex Med 2010; 7:1998–2014.
37- Brotto LA, Bitzer J, Laan E, et al. Women’s sexual desire and arousal disorders. J Sex Med 2010; 7:586–614.
38- West SL, D’Aloisio AA, Agans RP, et al. Prevalence of low sexual desire and hypoactive sexual desire disorder in a nationally representative sample of US women. Arch Intern Med 2008; 168:1441–9.
39- Warnock JK, Bundren JC, Morris DW. Female hypoactive sexual desire disorder due to androgen deficiency: clinical and psychometric issues. Psycho pharmacol Bull 1997; 33:761–6.
40- Clayton AH, Maserejian NN, Connor MK, et al. Depression in premenopausal women with HSDD: baseline findings from the HSDD Registry for Women. Psychosom Med 2012; 74:305–11.
41- Ahrold TK, Meston CM. Effects of SNS activation on SSRI-induced sexual side effects differ by SSRI. J Sex Marital Ther 2009; 35:311–9.
42- Taylor MJ, Rudkin L, Bullemor-Day P, et al. Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database Syst Rev 2013;(5):CD003382.
43- Nurnberg HG, Hensley PL, Heiman JR, et al. Sildenafil treatment of women with antidepressantassociated sexual dysfunction: a randomized controlled trial. JAMA 2008; 300:395–404.
44- Nastri CO, Lara LA, Ferriani RA, et al. Hormone therapy for sexual function in perimenopausal and postmenopausal women. Cochrane Database Syst Rev 2013;(6):CD009672.
45- North American Menopause Society. The role of testosterone therapy in postmenopausal women: position statement of The North American Menopause Society. Menopause 2005; 12:496–511, quiz 649.
46- Laan E, van Lunsen RH, Everaerd W. The effects of tibolone on vaginal blood flow, sexual desire and arousability in postmenopausal women. Climacteric 2001; 4:28–41.
47- Derogatis LR, Komer L, Katz M, et al. Treatment of hypoactive sexual desire disorder in premenopausal women: efficacy of flibanserin in the VIOLET Study. J Sex Med 2012; 9:1074– 85.
48- Traish AM, Botchevar E, Kim NN. Biochemical factors modulating female genital sexual arousal physiology. J Sex Med 2010; 7:2925–46.
49- Raina R, Pahlajani G, Khan S, et al. Female sexual dysfunction: classification, pathophysiology, and management. Fertil Steril 2007; 88:1273–84
50- Harte CB, Meston CM. The inhibitory effects of nicotine on physiological sexual arousal in nonsmoking women: results from a randomized, double-blind, placebo-controlled, cross-over trial. J Sex Med 2008;5: 1184–97.
51- Ishak WW, Christensen S, Sayer G, et al. Sexual satisfaction and quality of life in major depressive disorder before and after treatment with citalopram in the STAR*D study. J Clin Psychiatry 2013; 74:256–61.
52- Billups KL, Berman L, Berman J, et al. A new non-pharmacological vacuum therapy for female sexual dysfunction. J Sex Marital Ther 2001; 27:435–41.
53- Munarriz R, Kim SW, Kim NN, et al. A review of the physiology and pharmacology of peripheral (vaginal and clitoral) female genital arousal in the animal model. J Urol 2003;170: S40–4, discussion S44–5.
54- Herbenick D, Reece M, Hensel D, et al. Association of lubricant use with women’s sexual pleasure, sexual satisfaction, and genital symptoms: a prospective daily diary study. J Sex Med 2011a; 8:202–12.
55- Bechara A, Bertolino MV, Casabe A, et al. Duplex Doppler ultrasound assessment of clitoral hemodynamics after topical administration of alprostadil in women with arousal and orgasmic disorders. J Sex Marital Ther 2003;29(Suppl. 1):1–10.
56- Waldinger MD, Schweitzer DH. Persistent genital arousal disorder in 18 Dutch women: part II. a syndrome clustered with restless legs and overactive bladder. J Sex Med 2009; 6:482–97.
57- Carvalho J, Verissimo A, Nobre PJ. Cognitive and emotional determinants characterizing women with persistent genital arousal disorder. J Sex Med 2013; 10:1549–58.
58- Leiblum SR, Chivers ML. Normal and persistent genital arousal in women: new perspectives. J Sex Marital Ther 2007; 33:357–73.
59- Leiblum SR, Goldmeier D. Persistent genital arousal disorder in women: case reports of association with anti-depressant usage and withdrawal. J Sex Marital Ther 2008; 34:150–9.
60- Goldstein I, De EJB, Johnson JA. Persistent sexual arousal syndrome and clitoral priapism. In: Goldstein I, Meston CM, Davis SR, et al, editors. Women’s sexual function and dysfunction: study, diagnosis and treatment. London: Taylor and Francis; 1995. p. 674–85.
61- Waldinger MD, van Gils AP, Ottervanger HP, et al. Persistent genital arousal disorder in 18 Dutch women: part I. MRI, EEG, and transvaginal ultrasonography investigations. J Sex Med 2009; 6:474–81.
62- Heiman JR, Meston CM. Empirically validated treatment for sexual dysfunction. Annu Rev Sex Res 1997; 8:148–94