In prolonged, obstructed labor pressure necrosis of the anterior vaginal wall and underlying bladder neck or urethra occurs as the tissues are compressed between the fetal head and the posterior surface of the symphysis pubis. When the mother survives, the necrotic tissue sloughs away and is expelled after approximately 10 days, at which point incontinence ensues Indian Journal of Urology : IJU : Journal of the Urological Society of India
Medknow Publications
Vesicovaginal fistulae
Mary Garthwaite and Neil Harris
Additional article information
Abstract
Vesicovaginal fistula (VVF) formation represents a condition with devastating consequences for the patient and continues to pose a significant challenge to the surgeon. Quick and accurate diagnosis, followed by timely repair is essential to the successful management of these cases. A thorough understanding of the pathophysiology and anatomy of the fistula, potential factors that may compromise healing and experience in the fundamental principles of fistula repair are the vital tools of the fistula surgeon. This review was undertaken to provide an overview of the key areas in VVF investigation and management.
Keywords: Vesicovaginal fistula, pressure necrosis, management
INTRODUCTION
Regardless of the etiopathology, the development of a vesicovaginal fistula (VVF) has profound and devastating consequences for the patient’s physical and psychological health. First reports of successful repairs emerged in the literature around the mid-19th century when James Marion Sims described his technique of a transvaginal approach with the use of silver sutures and bladder drainage postoperatively.[1] Medical advances allowing transabdominal surgery heralded the development of modern-day fistula repair techniques. However, despite these advances VVF repair continues to present a major technical challenge for modern surgery.
ETIOLOGY
Worldwide, prolonged, obstructed labor is the leading cause of VVF. This, however, is an uncommon occurrence in the developed world, largely due to the availability of advanced obstetric practice.
In West Africa VVF is estimated to occur in up to three in 100,000 deliveries. Factors influencing this rate include young maternal age (physical immaturity of the mother’s body leads to cephalopelvic disproportion), a paucity of modern obstetric facilities and skills and ‘traditional’ practices such as female circumcision. In the developed world approximately 90% of VVF are secondary to accidental injury to the bladder during surgery. High-risk procedures include hysterectomy (75% of cases) and urological or lower gastrointestinal pelvic surgery (~2%).[2,3] In general, risk factors for VVF formation include previous uterine surgery, pelvic irradiation, endometriosis and anatomical distortion (such as a large fibroid uterus). A compounding factor is one that will compromise healing, such as anemia, malnutrition and steroid use. Other less common causes include pelvic malignancy, obstetric infections, erosion secondary to a foreign body and vaginal trauma.
PATHOGENESIS
In prolonged, obstructed labor pressure necrosis of the anterior vaginal wall and underlying bladder neck or urethra occurs as the tissues are compressed between the fetal head and the posterior surface of the symphysis pubis. When the mother survives, the necrotic tissue sloughs away and is expelled after approximately 10 days, at which point incontinence ensues VVF following hysterectomy is most likely to arise from an unrecognized bladder injury at the time of surgery, which results in the formation of a urinoma. Urine will then follow the path of least resistance and drain through the vaginal cuff suture line. A mucosa-lined tract will then establish between the bladder and the vagina. A second possible mechanism is pressure necrosis from incorrectly placed sutures between the vaginal cuff and posterior bladder. Hematoma and infection are often complicating factors
In prolonged, obstructed labor pressure necrosis of the anterior vaginal wall and underlying bladder neck or urethra occurs as the tissues are compressed between the fetal head and the posterior surface of the symphysis pubis. When the mother survives, the necrotic tissue sloughs away and is expelled after approximately 10 days, at which point incontinence ensues Indian Journal of Urology : IJU : Journal of the Urological Society of IndiaMedknow PublicationsVesicovaginal fistulaeMary Garthwaite and Neil HarrisAdditional article informationAbstractVesicovaginal fistula (VVF) formation represents a condition with devastating consequences for the patient and continues to pose a significant challenge to the surgeon. Quick and accurate diagnosis, followed by timely repair is essential to the successful management of these cases. A thorough understanding of the pathophysiology and anatomy of the fistula, potential factors that may compromise healing and experience in the fundamental principles of fistula repair are the vital tools of the fistula surgeon. This review was undertaken to provide an overview of the key areas in VVF investigation and management.Keywords: Vesicovaginal fistula, pressure necrosis, managementINTRODUCTIONRegardless of the etiopathology, the development of a vesicovaginal fistula (VVF) has profound and devastating consequences for the patient’s physical and psychological health. First reports of successful repairs emerged in the literature around the mid-19th century when James Marion Sims described his technique of a transvaginal approach with the use of silver sutures and bladder drainage postoperatively.[1] Medical advances allowing transabdominal surgery heralded the development of modern-day fistula repair techniques. However, despite these advances VVF repair continues to present a major technical challenge for modern surgery.ETIOLOGYWorldwide, prolonged, obstructed labor is the leading cause of VVF. This, however, is an uncommon occurrence in the developed world, largely due to the availability of advanced obstetric practice.In West Africa VVF is estimated to occur in up to three in 100,000 deliveries. Factors influencing this rate include young maternal age (physical immaturity of the mother’s body leads to cephalopelvic disproportion), a paucity of modern obstetric facilities and skills and ‘traditional’ practices such as female circumcision. In the developed world approximately 90% of VVF are secondary to accidental injury to the bladder during surgery. High-risk procedures include hysterectomy (75% of cases) and urological or lower gastrointestinal pelvic surgery (~2%).[2,3] In general, risk factors for VVF formation include previous uterine surgery, pelvic irradiation, endometriosis and anatomical distortion (such as a large fibroid uterus). A compounding factor is one that will compromise healing, such as anemia, malnutrition and steroid use. Other less common causes include pelvic malignancy, obstetric infections, erosion secondary to a foreign body and vaginal trauma.PATHOGENESISIn prolonged, obstructed labor pressure necrosis of the anterior vaginal wall and underlying bladder neck or urethra occurs as the tissues are compressed between the fetal head and the posterior surface of the symphysis pubis. When the mother survives, the necrotic tissue sloughs away and is expelled after approximately 10 days, at which point incontinence ensues VVF following hysterectomy is most likely to arise from an unrecognized bladder injury at the time of surgery, which results in the formation of a urinoma. Urine will then follow the path of least resistance and drain through the vaginal cuff suture line. A mucosa-lined tract will then establish between the bladder and the vagina. A second possible mechanism is pressure necrosis from incorrectly placed sutures between the vaginal cuff and posterior bladder. Hematoma and infection are often complicating factors
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