Chapter 13 Benign and urogynaecology

Endometrial polyps

Female genital cutting

Fibroids

Ovarian cysts

Pelvic inflammatory disease

Female urinary incontinence

Urinary frequency and urgency

Urinary retention (voiding diffiulty)

Urinary tract injury

Uterovaginal prolapse

Urodynamic investigation

Vaginal discharge

Vesicovaginal fistulae

Vulval pain and pruritus

Endometrial polyps

Endometrial polyps are focal overgrowths of the endometrium that protrude into the uterine cavity.

Endometrial polyps are thought to arise from small areas of the endometrium that do not cycle with the rest of the endometrium. They grow but do not slough during menstruating, eventually forming a polyp which projects into the endometrial cavity.

Such polyps are common. They are detected by outpatient hysteroscopy in about 11% of women referred for the investigation of menstrual symptoms (Alexopoulos et al. 1999). They typically occur in women aged over 40 years. After the menopause, the endometrium is normally atrophic, but hormone replacement therapy does provide endometrial stimulation, leading to polyp formation.

Tamoxifen (a partial oestrogen agonist with inhibitory effects on breast tissue) treatment for breast cancer, causes endometrial stimulation, sometimes leading to polyp formation or even endometrial hyperplasia and malignancy. With tamoxifen, the incidence of polyps rises to 27%. Pathology

• Polyps are multiple in 20% of cases.

• Smooth surfaced sessile or pedunculated with thick or slender stalk.

• Histologically, a polyp is a focal overgrowth of endometrial glands and stroma with intact overlying endometrium on three sides. Clinical issues

Although polyps can be asymptomatic, the tip of the polyp often ulcerates and bleeds, resulting in intermenstrual bleeding in younger women or postmenopausal bleeding in older women. Other clinical presentations include menorrhagia, menometrorrhagia, or vaginal discharge.

Endometrial polyps are benign lesions with low potential for malignant transformation. The reported incidence of malignancy is about 0.5%.

Diagnosis

• Ultrasound, where transvaginal sonography (TVS) is the modality of choice with 56–96% sensitivity and 82% specificity.

• Sonohysterography (SHG) can be considered when TVS is suboptimal.

• Hysteroscopy is the most accurate diagnostic tool (Alexopoulos et al. 1999; Goldstein 2002).

Management

The first priority is to exclude endometrial malignancy in case of abnormal bleeding. Hysteroscopy and Polypectomy can be performed in cases of benign polyps. Further reading

Alexopoulos ED, Fay TN, et al. A review of 2581 out-patient diagnostic hysteroscopies in the management of abnormal uterine bleeding. Gynaecol Endoscopy 1999;8:105–10.

Goldstein SR, Monteagudo A, et al. Evaluation of endometrial polyps. Am J Obstet Gynecol 2002;186:669–74.

Female genital cutting Definition

Female genital mutilation (FGM) also called female genital cutting (FGC) is defined by the World Health Organization as comprising all procedures that involve partial or total removal of the external female genitalia, or other injury to the female genital organs for non-medical reasons (WHO 1997).

In communities where the practice still occurs, the term ‘mutilation’ is considered negative and a hindrance to social change towards elimination of the practice. The less judgemental term, female genital mutilation/cutting (FGM/C) is used by some authorities. Classification

Female genital mutilation is classified into four main types with subdivisions (WHO 2008).

• Type I: partial or total removal of the clitoris and/or the prepuce (clitoridectomy)

• Type Ia—removal of the clitoral hood or prepuce only

• Type Ib—removal of the clitoris with the prepuce

• Type II: partial or total removal of the clitoris and the labia minora, with or without excision of the labia majora

• Type IIa—removal of the labia minora only

• Type IIb—partial or total removal of the clitoris and the labia minora

• Type IIc—partial or total removal of the of the clitoris, the labia minora, and the labia majora

• Type III: narrowing of the vaginal orifice with the creation of a covering seal by cutting and appositioning the labia minora and/or the labia majora, with or without excision of the clitoris (infibulation)

• Type IIIa—removal and apposition of the labia minora

• Type IIIb—removal and apposition of the labia majora.

• Type IV: unclassified; all other harmful procedures to the female genitalia for non-medical purposes, for example pricking, piercing, incising, scraping, and cauterizing. Prevalence

Prevalence is defined as the percentage of women aged 15–49 who have undergone any form of FGM/C. Data provided by the Demographic and Health Surveys (DHS) and Multiple Indicator Cluster Surveys (MICS) reveal a prevalence rate of 1% in Cameroon to as high as 98% in Somalia (Table 13.2.1).

The World Health Organization estimates between 100 and 140 million females worldwide have been subjected to female genital mutilation, and a further 3 million females in Africa are at risk of the procedure every year (WHO 2008).

The practice of female genital mutilation is common in some parts of Africa (mainly sub-Saharan Africa), the Middle East, and some parts of Asia. It has also been reported among the immigrant population in European countries such as the UK, France, Switzerland, Canada, America, and Australia.

In societies where FGM/C is common, it is mainly carried on young girls between infancy and age 15, and occasionally on adult women. In Nigeria, 85% of genital mutilation was carried out in infancy (www.measureddhs.com/pubs/pdf/FR148/13chapter13.pdf), in Egypt 90% of girls are cut between ages 4 and 14years (Demographic and Health survey, Egypt, 1995 and 2000). The procedure is carried out by traditional circumcisers, traditional birth attenders, nurses, and midwives and in some cases by medical doctors. Causes

The practice of FMG/C is perpetuated by a combination of cultural, religious, and social factors within families and communities.

• Social convention: there is pressure to conform to the society norm. Failure to do so may lead to condemnation, harassment and ostracization.

• FMG/C is considered necessary for proper raising of girls in preparation for adulthood and marriage (Yoder et al., 1999).

• It is enshrined by belief of what is considered appropriate sexual behaviour.

• Cultural belief of femininity and modesty also contribute to continuation of FGM/C The idea that girls are beautiful and more feminine after genital mutilation persist in some society (Talle 1993).

• Religious beliefs may be associated with the practice. None of the major religious script supports the practice. The attitude of community religious leaders towards FGM/C plays a significant role in eradicating the practice.

• New groups may start the practice after migration into area where the practice is common. Women and their children may be subject to FGM/C when they marry into communities where it is widely practised. Legal issues

FGM/C is recognized as a violation of the human rights of girls and women. Two important legally binding international human rights instruments address this issue:

• The 1979 Convention on the Elimination of All forms of Discrimination Against Women (CEDAW)

• The 1989 Convention on the Rights of the Child (CRC).

In Africa, where the majority of FGM/C occurs, the Maputo protocol (www.achr.org/english/women/protocolwomen.pdf) was adopted in 2003, and ratified by 27 member states of the African Union; it promotes women right and calls for an end to female genital mutilation. Some African countries have passed legislation abolishing the practice of female genital mutilation.

In the UK the 1985 Prohibition of Female Circumcision Act and the 2003 Female Genital Mutilation Act prohibits FGM/C in England, Scotland, and Wales. Similar legislation has been passed in countries such as Australia, Canada, Italy, New Zealand, Sweden, and the USA. Consequences of female genital mutilation

Female genital mutilation is associated with a series of health risks and consequences. In general, the risk associated with types I, II and III are similar, but the risks tend to be more common and severe the larger the amount of genital tissue excised.

The acute complications include

• severe pain

• haemorrhage

• acute urinary retention

• localized infection and abscess formation

• septicaemia

• tetanus

• hepatitis and HIV infection

• death.

Late gynaecological complications include

• apareunia

• superficial dyspareunia

• sexual dysfunction with anorgasmia

• chronic pain

• Keloid formation

• dysmenorrhoea (including haematocolpos)

• urinary flow obstruction

• recurrent urinary tract infection

• HIV and hepatitis infection

• implantation dermoid cyst

• pelvic infection

• labial fusion.

The gynaecological complications results in

• difficulty conceiving

• difficulty in gynaecological examination

• difficulty in cervical cytology screening

• Psychological sequelae including post-traumatic stress disorder with associated memory loss, anxiety, depression, and increased likelihood of fear of intercourse are common (Whitehorn 2002).

Obstetric complications associated with female genital mutilation are well documented (Lovel et al. 2000; Banks et al. 2006), and include

• fear of childbirth

• increased risk of postpartum haemorrhage, Caesarean section, episiotomies, and extensive vaginal tears

• difficulty in performing vaginal examination, applying fetal scalp electrodes, or performing fetal scalp blood sampling in labour.

Female genital mutilation is also associated with increased perinatal mortality (Banks et al. 2006).

In recognition of the increased maternal and perinatal morbidity and mortality, the Royal College of Obstetricians and Gynaecologists (RCOG) issued guideline on the management of women with female genital mutilation (RCOG 2009). It recommends the identification of pregnant women that have undergone FMG/C and provision of specialist care for these women.

In women who require defibulation before childbirth, this can be done during the antenatal period or in labour. Female genital mutilation is not a contraindication to vaginal delivery, and in fact most women who have suffered female genital mutilation prefer vaginal delivery, but recourse to Caesarean section may be necessary if the woman has a fear of childbirth. Eradication of female genital mutilation

In the last decade, the practice of FGM/C is showing a downward trend in some communities, but in others the prevalence has remained static (www.prb.org/pdf08/fgm-wallchart.pdf).

The eradication of FGM/C requires concerted effort at community, national, and global levels.

• Community level: successful community-based projects such as the Tostan project in Senegal, Guinea, Gambia, Burkina Faso, and Somalia (www.tostan.org/web/page/586/sectionid/547/pagelevel/3/interior.asp) has made a significant impact on the prevalence of FGM/C in these communities. This project is based on the promotion of human rights and emphasizes community participation. It guides the communities to define the problem and provide solutions themselves. It incorporates key elements necessary to a change social convention at the community level, including collective action, public declaration, and organized diffusion.

• National level: activity at the national level should promote a process of social change that leads to abandonment of FGM/C. These activities should involve traditional, religious, and government leaders, parliamentarians and civil society organizations. Media involvement is important for the dissemination of information about positive social change. Enactment of legislation on FGM/C at the national level serves the purpose of showing government disapproval, providing support to those who have or wish to abandon the practice and act as a deterrent. Improvements in the health, education, and the social and legal protection systems is also necessary to bring about lasting change in social conventions that perpetuate female genital mutilation/cutting.

• Regional level: the Maputo protocol adopted by members states of the African Union calls upon individual countries to create public awareness of the issue of female genital mutilation, introduce legislation to prohibit and sanction the practice of FGM/C, provide support for victims and protect women at risk of this and other harmful practices.

The Parliamentary Assembly of the council of Europe passed a resolution in 2001 calling for the introduction of national legislation, the promotion of awareness, the prosecution of those who perpetrate FGM/C, and the adoption of a more flexible approach in granting asylum to mothers and their children at risk of FGM/C.

FGM/C is a harmful practice that violates the fundamental human rights of women and children. The perpetuation of the practice in certain communities is borne out of deeply engrained sociocultural conventions. In the past decade the prevalence of FGM/C has declined, but more concerted efforts at community, national, regional, and global levels are necessary to eliminate the practice. Further reading

Banks E, Meirrik O, Farley T, et al. WHO study group on female genital mutilation and obstetrics outcome: WHO collaborative prospective study in six African countries. Lancet 2006;367:1835–41.

Demographic and Health survey, Egypt, 1995 and 2000.

Gruenbaum E. Socio-cultural dynamics of female genital cutting: research finding, gaps and directions. Culture Health Sexuality 2005;7:429–41.

Lovel H, McGettingan C, Mohammed Z. A systematic review of the health complication of female genital mutilation including sequelae in childbirth. Geneva: WHO 2000: www.who.int/reproductivehealth/docsa/systematic_review_health_complication_fgm.pdf

RCOG. Green-top guideline no. 53. May 2009.

Talle A. Transforming women into ‘pure’ agnate: aspects of female infibulation in Somalia. In: Broch-Due V, Rudie I, Bleie T (eds) Carved flesh, cast selves: gender symbols and social practices. Oxford: Berg 1993: 83–106.

Whitehorn J. Female genital mutilation: cultural and psychological implications. Sexual Relationship Therapy 2002;17:161–70.

WHO. Female genital mutilation. Fact Sheet no. 241. Geneva: WHO 2008.

WHO/UNFPA/UNICEF Female genital mutilation. A joint WHO/UNFPA/UNICEF statement. Geneva: WHO 1997.

World Health Organization (WHO). Eliminating female genital mutilation. An interagency statement UNAIDS, UNDP, UNECA, UNESCO, UNFPA, UNHCHR, UNHCR, UNICEF, UNIFEM, WHO. Geneva: WHO 2008.

Yoder PS, Camar PO, Soumaoro B, Female genital cutting and coming of age in Guinea. Calverton: Macro International 1999. Internet resources

www.measureddhs.com/pubs/pdf/FR148/13chapter13.pdf - accessed 1/11/09

www.prb.org/pdf08/fgm-wallchart.pdf

www.tostan.org/web/page/586/sectionid/547/pagelevel/3/interior.asp

www.achr.org/english/women/protocolwomen.pdf

Prohibition of Female Circumcision Act, 1985 United Kingdom. Female Genital mutilation Act 2003: www.hmso.gov.uk/acts/act2003/2003003.htm

Fibroids Introduction

Fibroids are well-circumscribed, benign tumours arising from myometrium and are the most common tumours of the female genital tract during the reproductive years. Aetiology

The incidence increases with age and fibroids may in present in 25–30% women between 35 and 50 years. Risk factors include nulliparity, obesity, family history, Afro-Caribbean race (develops at early age), and hypertension. Long-term use of oral contraceptive pills, Depo-provera injections for contraception and smoking are associated with reduced risk. Pathophysiology

Fibroid growth is related to genetic predisposition, hormonal influences, and various growth factors. Fibroids have been shown to have increased levels of both oestrogen and progesterone receptors than normal myometrium. They may enlarge in pregnancy or following treatment with tamoxifen. Fibroids shrink in size after the menopause due to reduced oestrogen exposure. Fibroids very rarely have malignant potential (0.2%), which can develop in the form of leiomyosarcoma, but most cases arise de novo.

They are composed of concentric whorls of mainly smooth muscle but may contain fibrous as well as connective tissue elements. There is a false capsule of compressed uterine muscle which allows easy enucleation of fibroids while performing myomectomy. As they enlarge they tend to outgrow the blood supply forming areas of cystic necrosis and central degeneration. Classification

Fibroids can be classified according to the site of development

• Subserosal (1%): originating from the serosal surface of the uterus. They may become pedunculated and lose their uterine attachment and gain a secondary blood supply (parasitic fibroid)

• Intramural (91–93%): within the uterine muscle

• Intraligamentry: in the broad ligament (secondary to heavy menstrual bleeding due to fibroids.

• Rapid growth of fibroids with suspicion of malignancy.

• Refusal of medical management by women.

• Side-effects of medical management.

Hysteroscopic myomectomy

This is hysteroscopic resection of submucous fibroid (grades 0 and 1). The indications include abnormal uterine bleeding, history of pregnancy loss, subfertility problems, and pain. Submucous fibroids of less than 3 cm have better outcome. A single dose of GnRH agonist if given 4 weeks before the procedure decreases the size of myoma, reduces endometrial thickness, and causes less fluid absorption during the procedure.

Abdominal myomectomy

Indicated when uterine preservation for childbearing is needed, but women should be counselled regarding the risk of requiring further intervention. It is also the procedure of choice for large solitary pedunculated subserous fibroids. Pretreatment with GnRH agonist can be used to shrink the size of fibroids and minimize the blood loss. Vasocontricting agents like vasopressin can be used at the time of surgery.

Laparoscopic myomectomy

This procedure can be performed in cases of pedunculated fibroids or with intramural fibroids. Laparoscopic-assisted myomectomy involves laparoscopic dissection of fibroids and can be removed through morcellator or mini-laparotomy incision. Multilayer uterine closure should be performed.

Hysterectomy

The definitive treatment for heavy menstrual loss due to fibroids in women who have completed their family and uterine preservation is not an issue. The usual route is abdominal, but vaginal hysterectomy can be performed. Hysterectomy is not recommended for routine management of treatment of asymptomatic fibroids. The complications include technical difficulty; bowel, ureteric, and bladder injury; infection; bleeding; risk of transfusion; and deep vein thrombosis. Hormone replacement therapy and fibroids

Oestrogen may stimulate fibroid growth and there is some evidence that Tibilone may be a better choice and may be associated with reduced fibroid growth. Fibroids and pregnancy

Seventy-eight per cent of fibroids are unchanged or may decrease in size in pregnancy. As there is an increased uterine blood supply in pregnancy, fibroids may undergo acute ischaemic necrosis and cystic degeneration. The potential effects of fibroids on pregnancy are

• subfertility due to either blockage of tubal ostia, distortion of uterine cavity, prevention of implantation of embryo

• miscarriage

• pain due to acute ischaemic necrosis (red degeneration)

• malpresentation

• cavity distortion, which can lead to increased incidence of placental abruption, retained placenta, premature rupture of membranes, and preterm labour.

• obstructed labour, cephalopelvic disproportion

• postpartum haemorrhage.

In conclusion, there is a wide range of treatment modalities for uterine fibroids but it is paramount to select an appropriate method of treatment to suit to the need of woman. Further reading

Becker E Jr, Lev-Toaff AS, Kaufman EP, et al. The added value of transvaginal sonohysterography over transvaginal sonography alone in women with known or suspected leiomyoma. J Ultrasound Med 2002;21:237–47.

Falcone T Falcone T, Gustilo-Ashby AM. Minimally invasive surgery for mass lesions. Clin Obstet Gynecol 2005;48:353–60.

Farquhar C, Arroll B, Ekeroma A, et al. Fibroids. Working Party of the New Zealand Guidelines Group. Aust NZ J Obstet Gynaecol 2001;41:125–40.

Gupta JK, Sinha AS, Lumsden MA, Hickey M. Uterine artery embolization for symptomatic uterine fibroids. Cochrane Database Syst Rev 2006; 25: CD005073.

Hricak H, Tscholakoff D, Heinrichs L, Fisher MR, et al. Uterine leiomyomas: correlation of MR, histopathologic findings, and symptoms. Radiology 1986;158:385–91.

Kaunitz. Progestin-releasing intrauterine systems and leiomyoma. Contraception. 2007;75 (6 Suppl): S130–3.

Lethaby A, Farquhar C, Cooke I. Antifibrinolytics for heavy menstrual bleeding. Cochrane.

Lethaby A, Vollenhoven B, Sowter M. Pre-operative GnRH analogue therapy before hysterectomy or myomectomy for uterine fibroids. Cochrane Database Syst Rev. 2000;(2): CD000547.

Lev-Toaff AS, Coleman BG, Arger PH, et al. Leiomyomas in pregnancy: sonographic study. Radiology 1987;164:375–80.

Monga AK, Woodhouse CR, Stanton SL. Pregnancy and fibroids causing simultaneous urinary retention and ureteric obstruction. Br J Urol 1996;77:606–7.

NICE. NICE guidance IPG094. Uterine artery embolisation for the treatment of fibroids. 2004.

NICE. NICE guidelines. CG44 Heavy menstrual bleeding: investigation and treatment. 2007.

Nowak RA. Fibroids: pathophysiology and current medical treatment. Baillieres Best Pract Res Clin Obstet Gynaecol 1999 13: 223–38.

Reinsch RC, Murphy AA, Morales AJ, Yen SS. The effects of RU 486 and leuprolide acetate on uterine artery blood flow in the fibroid uterus: a prospective, randomized study. Am J Obstet Gynecol 1994;170:1623–7.

Stewart EA, et al. Clinical outcome of focused ultrasound surgery for the treatment of uterine fibroids. Fertil Steril 2006;85:22–9.

Vollenhoven B. Introduction: the epidemiology of uterine leiomyomas. Baillieres Clin Obstet Gynaecol 1998;12:169–76.

Wallach E, et al. Uterine myomas: an overview of development clinical features, and management. Obstet Gynaecol 2004;104:393–406.

Wamsteker K, Emanuel MH, de Kruif JH Transcervical hysteroscopic resection of submucous fibroids for abnormal uterine bleeding: results regarding the degree of intramural extension. Obstet Gynecol 1993;82:736–40. Internet resources

NICE: www.nice.org.uk Patient resources

www.fibroids.co.uk

Ovarian cysts

Ovarian cysts are a common reason for gynaecology referral.

The incidence has increased with the use of transvaginal ultrasound and computed tomography. Pathophysiology

Cysts can occur at any age but differ in type. Germ cell tumours predominate in children. Functional cysts are more common in premenopausal women and the risk of malignancy increases after the menopause. Ninety per cent of ovarian cysts are benign, but this does vary with age.

Ovarian cysts are classified into non-neoplastic functional cysts (such as follicular and corpus luteal cysts) and neoplastic cysts. Clinical presentation

Many ovarian cysts are asymptomatic but some will present with abdominal/pelvic pain due to torsion, rupture, or haemorrhage.

The diagnosis is made from presenting symptoms, the clinical history, and examination findings. Pain can be described as radiating down the inner thigh to the knee (referred along the cutaneous branch of the obturator nerve).

Differential diagnosis

Pain may originate from the gastrointestinal tract or urinary tract. Pelvic inflammatory disease and ectopic pregnancy should be excluded.

Ovarian cyst accidents

• Torsion: this mainly occurs in premenopausal women with cysts >6 cm in size; benign teratomas are prone to torsion but polycystic ovaries can also tort. The enlarged ovary lifts out of the pelvis because of mobility of the supporting ligaments. Torsion is more common on the right. This is thought to be due to the presence of the rectosigmoid colon on the left. Complete arterial obstruction does not usually occur and the ischaemic–haemorrhagic appearance of the adnexa is due to venous and lymphatic stasis rather than gangrene.

• Rupture: the symptoms depend on the size of the cyst and its contents that are released into the abdominal cavity. Rupture of a small cyst may be asymptomatic or have localized pain. A larger cyst may present with peritonism, especially if the contents are irritant, such as dermoid or endometriotic cysts. Pseudomyxoma peritonei can result from rupture of a mucinous cystadenoma.

• Haemorrhage: The theca interna is prone to haemorrhage as is the corpus luteum during formation. Haemorrhage causes pain as the cyst capsule is stretched. If the cyst ruptures intraperitoneal bleeding can occur. Cyst rupture occurs more commonly on the right. Investigations

The aim of investigation is to exclude malignancy and triage women to the most appropriate place for them to be managed.

• Transvaginal sonography (TVS) is better than transabdominal sonography, giving better quality images of the ovaries. Dermoids and endometriomas have typical ultrasound appearances. Cysts are more likely to be malignant if there are solid components, papillary projections, and ascites, or if they are multilocular or bilateral. The specificity of TVS is not good enough for it to be used alone for screening for ovarian malignancy (NIH consensus). Colour flow Doppler studies can help to make a diagnosis of malignancy but have limited clinical application in isolation

• Magnetic resonance imaging (MRI): this is very useful to investigate further the nature of ovarian cysts suspected to be malignant. Vegetations in cystic tumours and necrosis in solid tumours can be identified. Contrast can be used to enhance images. Endometrioitic cysts have a homogenous high signal intensity on T1-weighted images and low signal intensity on T2-weighted images. Dermoid cysts also have a typical appearance on MRI.

Tumour markers

• CA125 is a glycoprotein antigen; levels usually rise with epithelial ovarian malignancies but it is not specific for ovarian cancer and can be raised in other benign intra-abdominal conditions such as endometriosis, during menstruation, pelvic inflammatory disease, and non-malignant ascites.

• α-Fetoprotein (AFP) and human chorionic gonadotrophin (hCG) levels are raised in germ cell tumours but also in pregnancy.

• Inhibin levels are raised in granulosa cell tumours.

• Risk of malignancy index (RMI) is a scoring system that combines menopausal status, ultrasound findings, and CA125 levels to give an estimate of the risk of malignancy. A score of >200 is considered high risk. There are two scoring systems, the RMI 2 score gives more weight to ultrasound findings and menopausal status than RMI 1 (Table 13.4.1).

• Ovarian crescent sign is the presence of normal ovarian tissue adjacent to a cyst on detailed TVS and may help to exclude invasive malignancy. Management

Table 13.4.1 Risk of malignancy index scoring system

Conservative management is appropriate for many women with a simple cyst, few symptoms, and a low RMI. Expectant management is particularly appropriate for haemorrhagic cysts. A TVS can be repeated 3 months later when a high proportion of these cysts will have resolved spontaneously. Recurrent functional cysts can be suppressed by the use of the combined oral contraceptive pill.

• Suspected ovarian torsion: the diagnosis is often delayed and surgery should take place as soon as possible and should be as conservative as possible if retention of fertility is required.

• Place of surgery: as the risk of malignancy increases, the appropriate location for management changes. Cysts with a high RMI >200 should be managed in a cancer centre.

• Transvaginal cyst aspiration: this leaves the cyst capsule intact and it usually reforms and is therefore not recommended except in selected cases, for example during infertility treatment, or if a patient is not medically fit for an anaesthetic.

• Laparoscopic management: many cysts can be managed laparoscopically, resulting in reduced postoperative pain, shorter hospital stay, better cosmetic result, and quicker return to normal. This is the treatment of choice for young women wishing to retain their fertility.

• Laparoscopic cystotomy and drainage of the cyst is not recommended because the capsule is left intact, the high recurrence rates, and spillage of the contents of the cyst.

• Laparoscopic cystectomy with removal of the cyst intact is the ideal treatment. The specimen is removed in an endobag to avoid spilling the contents into the peritoneal cavity. The risk of malignancy is low. After cystectomy the defect can be left open to heal, cauterized, or sutured. None of these techniques is superior for healing or the risk of postoperative adhesions. Ovarian cysts in pregnancy

The diagnosis of ovarian cysts has increased in pregnancy, especially in the first trimester. Most of these cysts will resolve spontaneously during the pregnancy and persistent cysts >6 cm are rare, reported in 0.07%. Ovarian cancer is very rare in women of reproductive age, and has been reported in 0.004–0.4% of pregnancies. Tumour markers are not as useful during pregnancy, α-fetoprotein, hCG, and inhibin levels are raised because of placental production. CA125 levels also rise in pregnancy and a level of 112 U/mL has been suggested as the upper limit of normal. MRI can be used to help differentiate benign from malignant cysts and avoids the need for radiation, associated with CT. Management is dependent on the clinical symptoms, size, and features of the cyst. Most cysts organisms include bacteroides, gardnerella, peptococcus, H. influenzae, enterococci and mycoplasma (70%) (Baveja 2001). Risk factors

The risk factors are important in both clinical diagnosis and prevention of PID. The factors associated with PID include:

• women the risk of infertility and ectopic pregnancy. As most PIDs are sexually transmitted, every effort should be made to reduce the patient’s sexual exposure by reducing the number of sexual partners, using barrier methods of contraception, etc. HIV testing and counselling should be offered. Further reading

Baveja G, Saini S, Sangwan K, Arora DR. A study of bacterial pathogens in acute pelvic inflammatory disease, Commun Dis 2001;33:121–5.

Bevan CD, Johal BJ, Mumtaz G, et al. Clinical laparoscopic and microbiological findings in acute salpingitis: report on a United Kingdom cohort. Br J Obstet Gynaecol 1995;102:407–14

Centers for Disease Control and Prevention sexually transmitted disease treatment guidelines.

Corsi PJ, Johnson SC, Gonik B, et al. Transvaginal ultrasound-guided aspiration of pelvic abscesses. Infect Dis Obstet Gynecol 1999;7:216–21.

Hillis SD, Joesoef R, Marchbanks PA, et al. Delayed care of pelvic inflammatory disease as a risk factor for impaired fertility. Am J Obstet Gynecol 1993;168:1503–9.

Lareau SM, Beigi RH. Pelvic inflammatory disease and tubo-ovarian abscess. Infect Dis Clin North Am. 2008;22:693–708

Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) Randomized Trial. Am J Obstet Gynecol 2002;186:929–37.

Pelvic inflammatory disease. NHS Library for Health. Clinical Knowledge Summaries: http://cks.library.nhs.uk

Ross JD. Outpatient antibiotics for pelvic inflammatory disease. BMJ 2001;322:251–2.

Royal College of Obstetricians and Gynaecologists (RCOG). Management of acute pelvic inflammatory disease. London: RCOG 2008: www.rcog.org.uk

Workowski KA, Berman SM. Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis 2007; 44 (Suppl 3): S73–6. Patient resources

www.rcog.org.uk/resources/public/pdf/Acute_PID_2004.pdf

RCOG Green Top guidelines No. 32. Management of Acute pelvic inflammatory disease. Nov 2008.

Sexually transmitted infections. Family Planning Association. www.fpa.org.uk Female urinary incontinence

Urinary incontinence (UI) is defined by the International Continence Society (ICS) as ‘any involuntary loss of urine’. (Abrams 2002).

UI affects both men and women of all ages; however, it is substantially more common in women. It is often detrimental to the social, psychological, and physical wellbeing of the sufferer, as well as impacting on their families and the health service (Brocklehurst 1993). The cost of UI in Sweden and the USA accounts for 2% of the healthcare budget (Milsom 2001). Assuming the current UK healthcare budget is £90 billion, this equates to approximately £1.2 billion. This does not account for patients’ own expenditure on support devices such as incontinence pads.

Considerable variation exists in the estimated prevalence of any UI with estimates from 8% to 69%, studies since 2000 are shown in Table 13.6.1. In a personal, population based, cross-sectional survey of 2500 women over the age of 21 in an English general practice in 2008, with a 60% response rate, there was a prevalence of any incontinence of 55%, with 10% of those women leaking ‘a lot’, or ‘a flood’. Women with an overactive bladder were more than three times more likely to seek help (42%) than those with stress urinary incontinence (SUI) (12.9%), perhaps indicating that it is a more disabling condition). Social isolation is demonstrated by 25% of patients who, due to embarrassment, delay seeking advice for 5 years (Norton 1988). Types of urinary incontinence

Urethral Conditions

• Urodynamic stress incontinence (USI) in which there is urethral sphincter incompetence diagnosed by urodynamics. SUI is the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing (Abrams 2002).

• Detrusor overactivity (DO) is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase which may be spontaneous or provoked (Abrams 2002). This is usually idiopathic. If associated with a neurological condition (e.g. Parkinson’s disease, multiple sclerosis), it is termed neurogenic detrusor activity. DO is associated with involuntary detrusor contractions leading to urgency, frequency, nocturia, with or without leakage (urge leakage). Urge urinary incontinence (UUI) is the complaint of involuntary leakage accompanied by or immediately preceded by urgency (Abrams 2002).

• Mixed incontinence is associated with an overactive bladder with an incompetent sphincter, with the patient complaining of both stress and urge incontinence. Mixed urinary incontinence (MUI) is the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing (Abrams 2002).

• Urinary retention with overflow. There is often no obvious cause. Chronic retention is often insidious especially in elderly people or those with neurological disease. This condition may be caused by either obstruction or more commonly in the female bladder atony. Dysfunctional voiding is characterized by an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the peri-urethral striated muscle during voiding in neurologically normal individuals (Abrams 2002) and may coexist with or precede retention. A non-relaxing urethral sphincter obstruction usually occurs in individuals with a neurological lesion and is characterized by a reduced urine flow (Abrams 2002).

• Other causes include urinary tract infections, faecal impaction, urethral diverticulae, psychological disorders, drugs (α-adrenergic blockers), restricted mobility, dementia, and rare congenital disorders (epispadias).

Non-urethral conditions

• These are associated with continuous UI. Causes include urinary fistulae (usually secondary to surgery in the Western world and obstructed childbirth in the developing world), pelvic radiotherapy, carcinoma, and congenital anomalies (ectopic ureter and bladder exstrophy). Risk factors for urinary incontinence

• Childbirth: parity has long been associated with UI. The Term Breech Trial noted that less UI occurred in the planned Caesarean section group (4.5%) than the planned vaginal delivery group (7.3%) at 3 months postpartum (Hannah 2002). Vaginal delivery does not appear to be associated with UUI.

• Age: the prevalence of UI increases with age. Younger women having a higher prevalence of SUI and older women more UUI and MUI. One study showing that women between the ages of 50 and 54 had more than twice the risk of severe UI than in women below 40 years (Danforth 2006).

Table 13.6.1 Summary table of prevalence studies published since 2000

• Race: being of Black, Hispanic, Japanese, and Chinese races appears to offer protection (Danforth 2006).

• Oestrogen deficiency. Oestrogen receptors are found in the urethra and bladder trigone. Urogenital atrophy because of oestrogen lack is at least partly responsible for sensory urinary symptoms, and lack of urethral coaptation.

• Smoking. The relationship between smoking and UI is unclear with some studies showing a positive correlation (Danforth 2006), and others no relationship (Parazzinia 2003).

• Body mass index (BMI). A raised BMI has been identified as an independent risk factor for incontinence of all types. It has been shown that a BMI of >30 kg/m² increases the odds of developing UI (Parazzinia 2003; Danforth 2006). In fact, of those complaining of incontinence 65–75% were overweight or obese (BMI >25) (Brown 1999). One explanation suggests that an increased intra-abdominal pressure with an increased BMI constantly stresses the pelvic floor muscles and weakens them. One study found that massive weight loss in morbidly obese people led to a decrease in the prevalence rate of SUI (from 61.2% to 11.6%) (Deitel 1988), another that a decrease in BMI by 5 resulted in a reduction in incontinence frequency of ≥50% (Subak 2002, 2005).

• Diabetes. There is some evidence that diabetes increases the incidence of UI by about 50% (Sampselle 2002; Hsieh 2008).

• Hysterectomy. There is evidence that women who have undergone hysterectomy are at a greater risk of developing UI (Parazzinia 2003; Hsieh 2008). A meta-analysis found that the increased risk of developing UI after hysterectomy was only significant in the over 60s, suggesting the risk is a long-term not an immediate risk (Brown 2000).

History: key points

• An adequate history will allow targeting of initial therapy. Points raised should determine the duration and type of leakage (e.g. stress, urge), the amount leaked, urinary frequency, nocturia, nocturnal enuresis, leaking with intercourse. Attention to the impact on quality of life is crucial.

• Symptoms of a urinary tract infection should be sought and antibiotic treatment initiated as appropriate.

• Attention should be paid to the patient’s medical history especially conditions impacting on the urinary system, e.g. diabetes, congestive heart failure, previous pelvic radiotherapy, multiple sclerosis, Parkinson’s disease, chronic obstructive pulmonary disease. Drug history should be sort, e.g. diuretics, antihypertensive drugs, sedatives, antidepressants. Caffeine and alcohol intake should be recorded.

• Past surgical history, especially previous gynaecological and urological procedures, should be obtained.

• Past obstetric history should be reviewed. This should include the number, type, and difficulty of deliveries, and perineal tears.

• It is crucial to rule out any urinary tract pathology. A history of haematuria should lead to an immediate referral to a urologist. Of concern would be a sudden onset of frequency and urgency, with or without leakage, in a smoker of over 50 years of age.

Examination: key points

• Attention should be paid to abdominal, pelvic, genital, and neurological examinations, as well as general status (e.g. mobility).

• Abdominal: masses, scars, distended bladder, renal tenderness.

• Pelvic and genital: hypo-oestrogenism, pelvic organ prolapse, cough test, pelvic floor squeeze.

• Neurological: mental and general neurological status, back for asymmetry, dimples and scars, evaluate the S2–S4 nerve roots by the bulbocaverosus reflex (contraction of the external anal sphincter and perineal muscles when pressure is applied to the clitoris), sensory status of the genital area, sensory, motor and tendon reflexes of the lower limbs (sensory loss may indicate diabetes, alcoholism; ankle clonus may indicate suprasacral cord lesions).

Investigation: key points

• Urinalysis. to exclude nitrites, pyuria, bacteriuria, glycocuria, and haematuria.

• Urine culture for infection.

• Voiding diary. This quantifies fluid intake, frequency of micturition and incontinence, frequency of nocturia and volume of urine passed. A 3-day diary appears to be adequate and is associated with improved compliance than those of longer duration diaries. The aim is to limit recall bias by collecting patients’ symptoms prospectively. It may also be useful in concentrating the patients mind on their symptoms.

• Assessment of post-void residual volume. This can be performed with a simple in–out catheter. However, newer ultrasound machines can accurately assess the bladder volume, avoiding the risks of catheterization.

• Perineal pad test. The 1-hour pad test has been standardized by the ICS. It is useful to grade the severity of incontinence and demonstrate leakage when other tests have failed to demonstrate incontinence.

• Pessary test. In patients with prolapse or voiding difficulties with prolapse, insertion of a pessary will mimic the post-surgical effect. This may reveal occult incontinence and will reveal the effect on urinary flow with correction of the prolapse.

• Imaging. Ultrasound of the urinary tract can be useful in detecting tumours and stones in the urinary tract as well as hydronephrosis, diverticulae, and bladder neck mobility. It is not required in the investigation of uncomplicated incontinence.

• Urodynamic evaluation. The ICS has recommended urodynamic testing prior to invasive procedures, after failed treatment, in surveillance of certain neurological dysfunctions and in complicated incontinence (Abrams 2002). This test measures bladder filling, storage, compliance, capacity, sensation during filling, and contractility. In combination with uroflowmery and residual testing, it will often allow an accurate diagnosis to be made. This is discussed in detail in Chapter xxxx.

In summary, diagnosis is made on the basis of an accurate history, detailed examination, augmented by investigations as required. Non-surgical therapy can usually be initiated on the basis of a presumptive diagnosis without the need for invasive urodynamic testing. Treatment of urinary incontinence

Surgical procedures for UI are described in Section 15.5, Continence procedures and will not be covered here.

Conservative treatment

Patients with uncomplicated UI should be offered a trial of conservative management prior to considering surgical remedies.

Lifestyle changes

Fluid intake: a normal intake should be encouraged, generally between 1.5 and 2.0 L per 24 hours. Excessive intake will contribute to frequency and urgency. Patients will often decrease their intake to try to decrease their risk of incontinence; however, this can lead to an excessively concentrated urine that can itself be an irritant, leading to a reduced functional bladder capacity, and encourage urinary tract infections. In elderly people with nocturnal symptoms, chronic medical conditions may be present, e.g. congestive cardiac failure with ankle oedema; in these patients elevation of the legs in the afternoon or even a small dose of furosemide in the early evening may encourage diuresis of dependent fluid prior to bedtime.

Dietary intake: drinks containing caffeine (direct bladder irritant and diuretic), alcohol, and carbonated drinks should be discouraged.

Weight: as obesity is a strong risk factor for both stress and MUI, weight loss should be encouraged. This is often a difficult subject to broach with patients as a strong element of denial of any weight problem may be present. It is important to discuss this in a non-judgmental and objective manner offering appropriate support to aid compliance.

Smoking: women who smoke should be educated about the possible role of smoking in all forms of incontinence.

Constipation: constipation and faecal impaction have been implicated as factors in both stress and urge incontinence. Instructions on fluid intake, fibre, laxatives, and enemas should be given aiming for a regular daily bowel habit.

Behavioural interventions

• Scheduled toileting: planned voiding by the clock whether or not a sensation is present. This may be particularly helpful in women with cognitive impairment.

• Bladder re-education: frequent urination in UUI can lead to a reduced bladder capacity, detrusor overactivity, and leakage. The patient voids at scheduled interval, gradually increasing the time between voids and hence bladder capacity. This is very helpful in detrusor overactivity and can help SUI.

• Pelvic floor muscle retraining: an increase in urethral pressure occurs with a pelvic floor contraction; the bladder base and urethra are approximated more closely to the symphysis pubis. Long-term training increases muscle bulk and may provide urethral support. Biofeedback can aid patients who have difficulty performing pelvic floor exercises (PFE), although cones have no additional benefit to PFE alone (Cooper 1999). Functional electrical stimulation offers some benefit, but only in those who are unable to locate and contract their pelvic floor. A trial of at least 3 months of PFE is recommended before considering surgical intervention in SUI, MUI, and UUI (NICE 2006).

• Catheterization: there is a role for catheterization for short-term relief of severe uncontrollable incontinence and also for those suffering from overflow incontinence. Ideally, this is performed as clean intermittent catheterization; occasionally an indwelling catheter is required. In the latter situation a suprapubic catheter is preferred.

Drug therapy

• SUI: Duloxetine, a combined serotonergic and noradrenaergic reuptake inhibitor, is often offered as an adjunct to PFE, or as an alternative to surgical treatment (Ghoniem 2005).

• UUI: if bladder training is ineffective then antimuscarinic drugs can be utilized. There are many available, most having similar efficacy with varying anticholinergic side-effects. Immediate-release oxybutynin is inexpensive and may be used as a first-line therapy, although the incidence of its adverse effects often lead to discontinuation. Alternatives include twice daily trospium, or once daily preparations such as extended-release oxybutynin tablets or patches, darifenacin, fesoterodine, solifenacin, or tolterodine. These drugs may be combined and will often require dose adjustment for maximal effect. Desmopressin has an important role in patients with troublesome nocturia (NICE 2006).

• MUI: drug treatment should be tailored to the most bothersome symptom. Antimuscarinic medication can be combined with duloxetine.

Surgery

This is discussed in Chapter 15.5, Continence procedures. Further reading

Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology of lower urinary tract function: report from th estandardisation sub-commitee of the International Continence Society. Neurourol Urodyn 2002;21:167–8.

Brocklehurst JC. Urinary incontinence in the community: analysis of a MORI poll. BMJ 1993;306:832–4.

Brown J, Grady D, Ouslander JG, et al. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart and Estrogen/Progestin Repalcement Study (HERS) Research Group. Obstet Gynecol 1999; 94: 66.

Brown JS, Sawaya G, Thom DH, Grady D. Hysterectomy and urinary incontinence: a systematic review. Lancet 2000;356:535–9.

Cooper JC, Monga AK. Issues 1, 2, 3, 4, 5, 6 & 7. Stress incontinence. Clinical evidence. London: BMJ Publishing Group & American College of Physicians—American Society of Internal Medicine.

Danforth KN, Townsend, MK, Lifford K, et al. Risk factors of urinary incontinence among middle aged women. Am J Obstet Gynecol 2006;194:339–45.

Deitel M, Stone E, Kassam HA, et al. Gynecologic-obstetric changes after loss of massive excess weight following bariatric surgery. J Am Coll Nutr 1988;7:147–53.

Ghoniem GM, Van Leeuwen JS, Elser DM, et al. A randomized controlled trial of duloxetine alone, pelvic floor muscle training alone, combined treatmet and no active treatment in women with stress urinary incontinence. J Urol 2005;173:1647–53.

Hannah ME, Pannuh HK, Hodnett ED, et al. Outcomes at 3 months after planned cesarean section vs planned vaginal delivery for breech presentation at term: The International Randomized Term Breech Trial. JAMA 2002;287:1822–31.

Hannested YS, Rortveit G, et al. Are smoking and other lifestyle factors associated with female urinary incontinence? The Norwegian EPINCOT Study. BMJ 2003;110:247–54.

Hsieh CH, Lee, MS, Lee MC, et al. Risk factor for urinary incontinence in Taiwanese women aged 20–59 years. Taiwan J Obstet Gynecol 2008;47:197–202.

Hunskaar S, Lose G, Sykes D, Voss S. The prevalence of urinary incontinence in women in four european countries. BJU Int 2004: 93; 324–30.

Irwin DE, Milsom I, Hunskar S, et al. Population based survey on urinary incontinence, overactive bladder and other lower urinary tract symptoms in five countries. Results of the EPIC study. Eur Urol 2006;50:1306–15.

McGrother CW, Donaldson MMK, Shaw C, et al. Storage symptoms of the bladder: prevalence, incidence and need for services in the UK. BJU Int 2004;93:763–9.

Milsom I, Abrams, P, Cardozo L, et al. How widespread are the symptoms of overactive bladder and how are they managed? A population based prevalence survey. BJU Int 2001: 87; 760–6.

National Institute of Clinical Excellence (NICE). Urinary Incontinence. The management of urinary incontinence in the female. Clinical Guideline 40. 2006: www.nice.org.uk/cg040

Norton P, McDonald, Sedgwick PM, Stanton SL. Distress and delay associated with urinary incontinence, frequency and urgency in women. BMJ 1988;297:1187–9.

Parazzinia, F, Chiaffarinoa, M, Lavezzaric V, Giambanco D and the VIVA Study Group. Risk factors for stress, urge or mixed urinary incontinence in Italy. Br J Obstet Gynaecol 2003;110:927–33.

Perry S. An epidemiological study to establish prevalence iof urinary symptoms and felt need in the community: the leicestershire MRC incontinencce study. J Public Health Med 1994;22:427–34.

Sampselle CM, Harlow SD, Skurnick J, et al. Urinary incontinence predictors and life impact in ethnically diverse perimenopausal women. Obstet Gynecol 2002;100:1230–8.

Subak LL, Johnson C, Whitcomb E, et al. Does weight loss improve incontinence in moderatley obese women? Int Urogynecol J 2002;13:40–3.

Subak LL, Whitcombe E, Shen H, et al. Weight loss: a novela and effective treatment for urinary incontinence. J Urol 2005;174:190–5.

Urinary frequency and urgency Definition

Urinary frequency is defined as voiding more than eight times per 24 hours. Urgency is defined as a sudden and compelling desire to void that is difficult to defer. The overactive bladder syndrome (OAB) is the combination of frequency and urgency with or without urge incontinence (incontinence preceded by urgency) and nocturia (Abrams and Cardozo 2002). Aetiology

A number of conditions can cause frequency and urgency, from within and outside the lower urinary tract.

Causes within the lower urinary tract

• Detrusor over activity

• Urinary tract infection

• Radiation cystitis

• High urinary residual

• Bladder calculus

• Bladder tumour

• Interstitial and chemical cystitis

• Sensory urgency

• Renal disease

• Urethral mucosal prolapse and caruncle

• Urethral tumour

• Urethral diverticulum.

Causes outside the lower urinary tract

• Excessive fluid intake

• Oestrogen deficiency

• Neurogenic bladder

• Uterovaginal prolapse

• Diabetes mellitus

• Diabetes insipidus

• Diuretic medication

• Pregnancy

• Pelvic mass. Epidemiology

Frequency and urgency are common symptoms, with up to 20% women reporting frequency and 15% reporting urgency. The symptoms have significant effects on quality of life. The incidence of OAB increases with age, reported as 5% in those 18–44 years old, increasing to 20% over the age of 44 years. Management

A number of conditions can result in frequency and urgency and it is essential that all patients have a stepwise evaluation to exclude any underlying cause.

History

A full urinary history should be taken to define any symptoms associated with the causes listed above. This will help assess the severity and how often symptoms occur. Other symptoms to consider include:

• urge incontinence

• stress-related incontinence: involuntary loss during physical examination such as coughing, running etc.

• nocturia/nocturnal enuresis

• coital incontinence

• continuous incontinence, which may be associated with a fistula or urinary retention

• drug history, including diuretic use

• neurological illness

• medical conditions such as diabetes mellitus/insipidus

• chronic/excessive drinking habits

• symptoms of prolapse

If pain or haematuria are present this needs further urgent investigation to exclude underlying urinary tract infection, bladder calculus, or tumour and any upper urinary tract lesion.

Examination

• Abdominal percussion to exclude urinary retention.

• A bimanual examination to exclude any pelvic masses such as fibroids, pregnancy or ovarian tumours.

• Perineal/vulval inspection to identify atrophic vaginitis and demonstrate any stress incontinence.

• A pelvic examination to assess any uterovaginal prolapse.

• The bladder base and urethra should be palpated to assess for tenderness which may be found in interstitial cystitis.

• Urethral examination to exclude any local lesions.

• Neurological examination to exclude any upper or lower motor neurone lesions particularly affecting the S2, S3, S4 nerve roots. This includes dorsiflexion of the toes (S3) and sensory innervations of the perineum (L1–2), lateral aspect of foot (S1), and thigh (S2).

Investigations

All patients should have the following investigations performed (as long as there is no strong suspicion of underlying malignancy).

• A midstream urine sample should be taken for an initial dipstick urinalysis to detect haematuria, glycosuria, pyuria, and bacteuria. The sample should then be sent for culture and sensitivity. The presence of red cells and haematuria should be followed up with a renal ultrasound and cystoscopy.

• Urine cytology if suspicion of malignancy and in high-risk groups, e.g. smokers, patients exposed to aniline/hair dyes.

• A frequency volume chart is a useful way to evaluate abnormal fluid intake, number of voids, functional bladder capacity and leakage episodes.

More specialized investigations are required if the above investigations have not revealed the cause of symptoms. Investigations to consider include the following.

• Urodynamics: this test measures the pressure–volume relationship during filling and voiding in relation to a patient’s symptoms. It should be performed when there is doubt regarding the aetiology of symptoms and in those who have had previous surgery, failed therapy and in those with voiding dysfunction. Most patients however can be treated for OAB empirically without the need for urodynamics.

• Detrusor overactivity is diagnosed on urodynamics as involuntary increases in detrusor pressure during filling or provocative manoeuvres such as coughing or running water. Low compliance may be found in the presence of a low capacity bladder. Poor voiding can be documented

• Cystoscopy: this can be performed using a rigid or flexible cystoscope. It should be performed if haematuria is present or there is a history suggestive of a urethral diverticulum or interstitial cystitis. It is also useful to measure true bladder capacity under anaesthetic.

• Imaging studies include renal ultrasound to assess for scarring, calculi, and to measure post-void urine volumes. An intravenous urogram can be performed if ultrasound suggests obstruction or a fistula. A CT scan is advocated on the presence of gross haematuria or if ultrasound has not been diagnostic,

Treatment

Treatment should be aimed at the underlying cause. For most patients with frequency urgency, treatment may be started empirically once any sinister underlying causes have been excluded and infection and high urinary residual treated (NICE 2006).

The mainstay of treatment is a combination of lifestyle changes, behavioural management, and antimuscarinic medication (Berghmans et al. 2000). Surgery is now only considered in those who have failed medical therapy.

Lifestyle changes

• Alteration in fluid intake such as avoidance of caffeine, fizzy drinks, and alcohol, which may exacerbate symptoms.

• Reduction in fluid intake to 2–2.5 L/day.

• Weight loss: this should be recommended in those with a BMI >30.

Behavioural management

This aims to teach a patient how to develop new voiding patterns by training the patient to actively increase the interval between voids and defer.

Antimuscarinic therapy

There are a number of drugs on the market that target the muscarinic receptors on the bladder wall, which are stimulated to acetylcholine released by the parasympathetic system causing bladder contraction. These drugs have been shown to have efficacy in reducing symptoms of urgency and urge incontinence (Chapple et al. 2008). Patients need to be warned about side-effects, which include dry mouth, constipation, headaches, and visual symptoms. They are contraindicated in those with a closed-angle glaucoma and myasthenia gravis.

The commonly used antimuscarinics include

• Oxybutynin: immediate release 2.5–5 mg bd/tds; extended release 5–30 mg/day

• Oxybutynin patch: 3.6 mg twice weekly

• Tolterodine: immediate release 1–2 mg/day; extended release 2–4 mg/day

• Solifenacin: extended release 5–10 mg/day

• Trospium: 20 mg bd

• Propiverine: 15 mg bd tds

• Darifenacin: 7.5–15 mg/day

• Fesoterodine: 4–8 mg/day

In those with troublesome nocturia a low dose antidepressant can be used, such as imipramine 25 mg nocte.

DDAVP (spray/tablets) can be used to reduce nocturnal urine production, although with caution in those over 65 years and with renal disease where a close review of renal function should be performed (Roxburgh et al. 2007).

Surgery

Over the last decade the surgical treatment for refractory urgency frequency has changed with newer less invasive approaches. Surgical procedures that have been used include the following.

• Augmentation cystoplasty: previously this was the procedure of choice and involved incising the bladder and inserting a portion of bowel to increase compliance. However, the procedure is associated with significant side-effects such as urinary retention, mucous production, stone formation, and malignant change within the transposed bowel.

• Detrusor myomectomy: this involves removing a portion of the detrusor from the bladder dome.

These procedures have now been superseded by the following techniques.

• Intradetrusor botulinum toxin: botulinum toxin is injected cystoscopically into the detrusor muscle or suburothelially. It is effective within a few weeks, with effects lasting on average 10 months, Side-effects include urinary retention. It is currently unlicensed for use in the bladder, although there is a large amount of research supporting its use in idiopathic and neurogenic detrusor overactivity.

• Sacroneuromodulation: this involves implantation of a pulsed generator in the S3 foramen and has 60–70% efficacy for frequency urgency (van Voskuilen et al. 2006).

Alternative therapy

A number of alternative therapies have been suggested such as acupuncture and hypnotherapy, although large good-quality studies are lacking (Emmons and Otto 2005). Further reading

Abrams P, Cardozo L, Fall, et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.

Berghmans LC, Hendriks HJ Conservative treatment of urge urinary incontinence in women: a systematic review of randomized clinical trials. BJU Int 2000;85:254–63.

Chapple CR, Khullar V, Gabriel Z, et al. The effects of antimuscarinic treatments in overactive bladder: an update of a systematic review and meta-analysis. Eur Urol 2008;54:543–62.

Emmons SL, Otto L. Acupuncture for overactive bladder: a randomized controlled trial. Obstet Gynecol 2005;106:138–43.

National Institute for Health and Clinical Excellence. Urinary incontinence: the management of urinary incontinence in women. Clinical Guideline 40. London: NICE 2006: www.nice.org.uk/cg40

Roxburgh C, Cook J, et al. Anticholinergic drugs versus other medications for overactive bladder syndrome in adults. Cochrane Database Syst Rev 2007; 4: CD003190.

van Voskuilen AC, Oerlemans DJ, Weil EH, et al. Long term results of neuromodulation by sacral nerve stimulation for lower urinary tract symptoms: a retrospective single center study. Eur Urol 2006;49:366–72. Internet resources

The International Continence Society: www.icsoffice.org Patient resources

www.bladderandbowelfoundation.org

Urinary retention (voiding difficulty) Introduction

Normal voiding occurs when a bladder contraction is initiated and the bladder neck and the urethra are synchronously relaxed. When the falling urethral pressure and increasing intravesical pressure equate, urine flow will commence.

The act of micturition is governed by a number of contributory factors: control from higher centres, the sacral reflex arc, the innervation of the bladder muscle and sphincter mechanisms, the outflow resistance, and the speed of contraction of the detrusor muscle fibres. Abnormalities of any component of this interactive mechanism may result in voiding dysfunction. Definitions and classification

Acute retention

Acute retention is the sudden onset of painful or painless inability to void over 12 hours, requiring catheterization with removal of a volume equal to or greater than normal bladder capacity. It is usually painful but may be painless in the presence of a neurological lesion or following an epidural anaesthetic.

Chronic retention

Chronic retention describes the insidious and painless failure of bladder emptying where catheterization yields a volume equal to at least 50% of normal bladder capacity. Chronic retention may cause urinary incontinence and occur without obvious cause.

There are usually two phases through which women pass before developing acute or chronic urinary retention. The first is asymptomatic voiding difficulty, where the woman is unaware of impaired bladder emptying. The urinary stream is reduced, and the peak flow rate is less than 15 mL/second. The maximum voiding pressure is usually normal, and there is no residual urine. The second stage is that of bladder decompensation, when symptoms of voiding difficulty appear such as hesitancy, poor stream, straining to void, and incomplete emptying, with or without urinary tract infection. The peak flow is less than 15 mL/second, the voiding pressure is reduced, and there is residual urine.

There is a paucity of data on the incidence or prevalence of voiding disorders in the absence of neuropathy. Of 600 women with symptoms of bladder dysfunction attending a urodynamic clinic, 2% had asymptomatic and 14% had symptomatic voiding difficulty. The symptomatic group tended to be older and were more likely to have had previous pelvic surgery. Aetiology and pathophysiology

In the female, voiding can occur via one of three mechanisms: contraction of the detrusor muscle, a rise in abdominal pressure, and relaxation of the urethral sphincter and pelvic floor musculature. Therefore, voiding disorders result when these mechanisms fail, that is when the detrusor muscle is unable to maintain an effective contraction, the urethra fails to relax and lower urethral resistance, or if there is a failure in the synchronization of these two actions, resulting in detrusor sphincter dyssynergia. The latter occurs in suprasacral neurological lesions

Pharmacological causes

Obstetric epidural anaesthesia is the commonest cause of voiding dysfunction. If retention is overlooked, overdistension injury may result in long-term voiding difficulty.

Anticholinergic agents used to treat urgency and frequency are frequent causes, for example Solifenacin or Fesoterodine. It is therefore vital to exclude urinary residual before prescribing this class of agent. In women with a combination of poor voiding and detrusor instability these drugs may be used in conjunction with intermittent self-catheterization. Ganglion-blocking drugs have a similar effect to anticholinergics, and α-adrenergic agents increase urethral resistance.

Inflammatory causes

The most frequent causes of inflammation are infective, chemical, or allergic (local or systemic allergens). Voiding difficulties may result from painful stimuli and may be aggravated by urethral oedema. Primary anogenital herpetic infection may produce urinary retention by the effect of local inflammatory lesions and lumbosacral meningomyelitis

Obstructive causes

Distal urethral stenosis usually results from urogenital atrophy in the postmenopausal woman but can result from chronic fibrosis following chronic inflammation, urethral instrumentation (e.g. urethrotomy), and scarring following surgery (e.g. anterior colporrhaphy).

Acute urethral oedema may occur after bladder neck surgery or, rarely, secondary to premenstrual fluid retention.

Foreign bodies and calculi

• Bladder neck surgery (e.g. sling procedures) may cause compression.

• Extrinsic causes of obstruction include impaction of a retroverted gravid uterus, pelvic masses, and faecal impaction.

• Haematocolpos associated with cryptomenorrhoea may present with retention due to urethral obstruction.

• Urethral distortion due to genital prolapsed; 33% of women with grades 3 and 4 prolapse have evidence of urethral obstruction.

Endocrine causes

Hypothyroidism and diabetes mellitus can cause peripheral neuropathy, resulting in urinary retention.

Overdistension

Bladder overdistension as a result of mismanagement of acute or chronic retention develops insidiously and is more frequent in women than in men. It often results after failure to detect retention after pelvic surgery (e.g. hysterectomy) or epidural anaesthesia. Overdistension may occur without obvious cause and is frequently observed in elderly women with large acontractile bladders.

Urethral sphincter hypertrophy

Fowler and Kirby have described a group of women who present with voiding difficulties due to a primary defect within the striated urethral sphincter.

Detrusor myopathy

Primary changes in the detrusor muscle have been reported as a cause of retention.

Psychogenic causes

Criteria for this diagnosis are an absence of neurological and or other significant organic disease, correlation of psychological disturbance with onset of symptoms, and a response to psychotherapy or psychopharmacological agents. Psychiatric diagnoses include hysteria and depression. Presentation

Symptoms

Impaired voiding may be asymptomatic in a few patients but the majority present with infrequent voiding, poor flow, intermittent stream, incomplete emptying, straining to void, and/or hesitancy. Others may present with overflow incontinence and frequency or urinary tract infection due to stasis. Acute retention may present with pain.

History taking should be directed towards determination of a primary cause. Neuropathy should be enquired about and a detailed drug, medical, and surgical history, including genital and urinary tract infection, should be obtained.

Signs

A careful general abdominal and pelvic examination should be performed to exclude the causes listed. A neurological examination should be performed and the lumbar region examined for stigmata of an underlying spinal disorder. The bladder may be palpable and will characteristically be dull to percussion. Investigations

Urinary tract infection should be excluded as it may predispose to voiding difficulty. The simplest investigations are uroflowmetry and ultrasonography for residual, but cystometry and other investigations may be required to make a more accurate diagnosis.

When catheterization is performed for acute retention the residual volume should be recorded. This will confirm the diagnosis and give a guide to the severity of bladder overdistension, and may be useful in assessing prognosis.

Uroflowmetry

This is the most important initial screening procedure and is simple and non-invasive. Measurements may need to be repeated as a single measurement may be unreliable. Obstructed voiding may occur in the presence of normal uroflowmetry because the detrusor may compensate by increasing the voiding pressure. Subtracted cystometry is required to detect this.

Cystometry

The filling phase of cystometry may indicate a lower or upper motor neuron lesion. The voiding phase will confirm any disorder of bladder emptying. The following may give clues during the procedure:

• difficulty catheterizing in presence of obstruction

• residual urine greater than 50 mL

• delayed first sensation (early first sensation in upper motor neuron lesions)

• increased bladder capacity

• pressure rise during filling and compliance usually normal

• maximum voiding pressure will be raised in the presence of obstruction prior to decompensation (it will be low or non-existent when detrusor failure occurs)

• isometric pressure is usually reduced or non-existent, demonstrating poor detrusor reserve.

Radiology

A plain abdominal radiograph will disclose a full bladder, and lumbosacral film will demonstrate congenital conditions such as spina bifida occulta or acquired conditions such as intervertebral disc prolapse. Video cystourethrography can provide additional information at the time of cystometry. Trabeculation diverticula and ureteric reflux can be detected and distal urethral stenosis identified.

Ultrasonography

Abdominal ultrasonography allows non-invasive measurement of urinary residual and also assessment of the upper urinary tract.

Cystourethroscopy

Difficulty in instrumentation of the urethra will suggest stenosis. Cystoscopy will allow visualization of intravesical pathology such as trabeculation, sacculation, and diverticula.

Electromyography

May help diagnose urethral sphincter hypertrophy and multiple system atrophy. Treatment

Prophylaxis

Prevention or early recognition of retention may avoid long-term voiding difficulty. Pre-emptive bladder drainage at radical pelvic or continence surgery or with epidural will prevent long-term problems. When there is evidence of voiding difficulty prior to continence surgery it is reasonable to counsel appropriately and teach intermittent self-catheterization.

Intermittent self-catheterization

Intermittent self-catheterization is the principal treatment for chronic urinary retention. It allows women to lead independent lives with efficient bladder emptying and low rates of urinary tract infection. There are two forms of intermittent self-catheterization: sterile and clean. The former is usually reserved for patients with neuropathic bladders in a hospital environment to prevent cross-infection.

Pharmacotherapy

Cholinergic agents, prostaglandins have been advocated but there is no real evidence that they are of any clinical benefit. Diazepam used as an anxiolytic may help with postoperative voiding problems.

In women with combined urge incontinence and retention, anticholinergic agents such as tolterodine may be used effectively in conjunction with CISC.

Surgery

If voiding difficulty is due to urethral stenosis, urethral dilatation using Hegar dilators or the Otis urethrotome are appropriate options.

Neuromodulation

This two-stage procedure involves stimulation of the S3 nerve root through the S3 foramen. The first stage is that of percutaneous nerve evaluation using a temporary stimulation wire. If this has a beneficial effect then a permanent stimulator is implanted. Early results are encouraging but the mechanism of action is not understood. Further reading

Dwyer PL, Desmedt E. Impaired bladder emptying in women. Aust N Z J Ostet Gynaecol 1994;34:73–8.

Stanton SL, Ozsoy C, Hilton P. Voiding difficulties in the female: prevalence, clinical and urodynamic review. Ob-stet Gynecol 1983;61:144–7. Patient resources

The Bladder and Bowel Foundation: http://www.bladderandbowelfoundation.org

Urinary tract injury Definition

The close association between the lower urinary tract (LUT) and female reproductive organs predisposes the lower urinary tract to injury during gynaecological and obstetric surgery. Most LUT injuries occur during benign surgery and the majority are not recognized during the procedure. Epidemiology

LUT injury occurs in 1–2% of all obstetric and gynaecological procedures (Dowling 1986). The true incidence is possibly higher when unreported and undiagnosed cases and those that spontaneously resolve are accounted for (Daly 1988). Aetiology

The LUT can be injured by penetrating or blunt injury. The most common penetrating injury tends to be surgical, although external violence such as knife and gunshot or unusual sources such as migrating IUCDs, hip prosthesis surgical drains, swallowed objects and filshie clips have all been incriminated. Diathermy, particularly during laparoscopic surgery for endometriosis, accounts for a significant proportion of the injury. Predisposing factors for urinary tract injury are coexisting pelvic adhesion, an enlarged uterus, endometriosis and other causes of distorted pelvic configuration, history of previous irradiation, previous surgery, haemorrhage during surgery and the extent of surgery.

Sites of injury

LUT injury may involve the ureter, bladder, or urethra. Whereas bladder and ureteric injuries account for the majority of these, urethral injuries are becoming increasingly recognized with tape procedures for incontinence.

Classification of injury

The American Association for the Surgery of Trauma (AAST) has devised a classification for ureteric (Table 13.9.1), bladder (Table 13.9.2), and urethral injuries (Table 13.9.3). This is an anatomical classification but does not have clear prognostic implications. Prevention

The best defence against injury to the urinary tract is knowledge of its anatomic relations and use of the avascular spaces of the pelvis to identify structures during surgery. Preoperatively, a detailed history, physical examination and evaluation of the urinary tract to rule out pre-existing urinary dysfunction should be undertaken. Imaging of the renal tract gives information on the kidneys, evidence of ureteric obstruction, and bladder for urinary residuals. Intravenous urography further defines renal function and identifies ureteral obstruction. Retrograde ureteric stenting preoperatively has not been shown to reduce the incidence of ureteric injury during surgery. When the course of the ureter is difficult to determine during surgery, ureteric catheterization or intravenous injection of methylene blue may help to delineate the ureter.

Table 13.9.1 AAST classification of ureteric injury

Table 13.9.2 Bladder injury

Intraoperatively, proper patient positioning, good lighting, appropriate surgical approach, adequate exposure, an early assessment of pelvic pathology, and seeking urological assistance if problems are anticipated help reduce injury. Peritoneal entry should be as high as possible to avoid a cystotomy. Following abdominal entry an attempt to restore normal anatomy and identify the ureters and bladder should be made. During vaginal surgery, downward traction on the cervix when clamping the uterine vessels and upward traction on the bladder holds the bladder and ureter out of the operative field. Blind clamping of vessels should be avoided as it is the commonest cause of urinary tract injury in obstetric practice (Neuman et al. 1991). When dissecting masses it is important to stay near the pathology and identify structures prior to ligation. The bladder should be mobilized in the downward and outward direction thus avoiding both bladder and ureteric injury. When using diathermy, particularly during laparoscopic surgery, short applications are preferable as the depth of penetration depends on both the duration and power of diathermy. Clinical approach: diagnosis and management

Ureteric injury

Table 13.9.3 Urethral injury

Diagnosis of ureteric injury can be made intraoperatively or postoperatively, with 70% being identified postoperatively (Mann 1988). Intraoperatively, ureteric injury can be recognized by intravenous dye injection and extravasation of urine into the operative field. Alternatively, cystoscopy with evidence of urinary excretion, or ureteric catheterization identifies ureteric integrity.

Postoperative investigations are aimed at establishing renal function, ruling out hydronephrosis and confirming ureteric integrity and include an intravenous urogram, contrast computed tomography, retrograde ureterogram, renal ultrasound, and cystoscopy. With unilateral ureteric injury patients may have a transient rise in serum creatinine, although normal levels do not preclude ureteric injury.

Postoperative symptoms of ureteric injury tend to be variable and are shown in Table 13.9.4.

Management of ureteric injury depends largely on the site and type of injury. The general principles include achieving a tension-free anastomosis by adequate mobilization, preservation of adventitial blood supply, ureteric stenting, and passive drainage of the repair site and minimal use of sutures to avoid necrosis. Although a complete description of all repair techniques is beyond the scope of this chapter, broadly speaking when the injury is below the mid-pelvis, an ureteroneocystostomy, or ureteral reim-plantation, is most commonly used. These injuries usually occur within 4–6 cm of the trigone. To ensure this is tension-free, an additional bridging procedure such as a psoas muscle hitch or Boari flap may need to be used.

When the injury occurs above mid-pelvis, there may not be enough proximal ureter left to reach the bladder for reimplantation. At this point a ureteroureterostomy, or end-to-end anastomosis of the injured ureter, becomes the best option. The ends of the ureter are spatulated to decrease the chances of stenosis occurring at the anastomotic site. An omental fat graft can be helpful to aid healing by providing an additional blood supply.

When an injury occurs such that a short proximal ureter exists, as when a substantial length of ureter has been damaged, it may no longer be possible to re-anastomose the ureter to itself. In such a case, a transureteroureterostomy, or end-to-side anastomosis of the proximal ureter to the contralateral ureter, may be required. This should be avoided if possible because stenosis at this anastomotic site could now jeopardize function in both kidneys. If the above options are not possible or the resources to execute them are not immediately available, a single J stent can be inserted into the proximal end of the cut ureter and can be brought out to the skin into a collecting device. Thus, the short ureter is able to drain but is not dissected until repair is possible. This is a temporizing measure to preserve renal function while the patient awaits definitive repair.

Bladder injury

Intraoperative bladder injury is easily identified by instilling indigo carmine in the bladder and noting for leakage of dye into the operative filed. Alternatively, cystoscopy can be used to identify the injury. Postoperatively a similar approach using a radio-opaque dye in conjunction with imaging can be used for identification of injury. Symptoms of bladder injury depend on whether the injury is intra- or extraperitoneal.

Intraperitoneal injury is associated with abdominal distension, shoulder tip pain, and if diagnosis is delayed with the development of uroascites. Peritoneal signs of tenderness and rebound will develop and if infection ensues there may be features of frank peritonitis. Extraperitoneal injury is associated with pain and an occasional rise in blood pressure. Haematuria is the hallmark of bladder injury and frank haematuria is seen in 95% of cases with the remaining 5% having microscopic haematuria.

Table 13.9.4 Symptoms and signs of ureteric injury

The management of bladder injury depends on the site, and grade of injury as well as the timing of recognition. Over half of all bladder injuries will be recognized intraoperatively and require a two-layer closure with absorbable suture to achieve an excellent result. The commonest mistake made is to miss a second rent having found one. All edges of the cystotomy must be identified and mobilized so that repair can be achieved tension free. If the injury is close to the trigone, care to avoid kinking of ureters must be taken. With intraperitoneal injury and repair, the cystotomy site should be covered by omentum or a layer of peritoneum to cushion the repair by adding bulk followed by continuous bladder drainage for at least 7 days, which promotes healing by preventing bladder distension. Isolated extraperitoneal injury can be treated by 7–10 days of continuous indwelling catheterization and expectant management. This is particularly true of injury occurring due to endoscopic procedures, i.e. laparoscopy and cystoscopy. Although prompt repair is usually desirable, with delayed recognition management may warrant delayed surgical repair after a few months to allow the oedema and inflammation to settle.

Urethral injury

Urethral injury is relatively uncommon with gynaecological surgery, and is seen more frequently with trauma to the perineum and fracture of the bony pelvis. Patients with urethral injury are usually unable to void due to extravasation of urine into the subcutaneous tissue. If they are able to void there is usual gross haematuria with swelling and ecchymosis of the perineum. In suspected urethral trauma no attempt to catheterize the urethra should be made until the site of injury has been delineated, as a partial disruption may be converted into a complete injury. Intraoperatively urethral injury is most often recognized by seeing the catheter through an incision in the wall of the urethra. The imaging of choice with suspected urethral injury is retrograde urethrogram. When undertaking urethroscopy in these patients it is best performed with a 0° scope.

Lacerations of the urethra in women should be repaired as soon as it is identified over a transurethral catheter in layers. This differs to repair in males where a delayed repair has better results. Early repair ensures that the integrity of the continence mechanism can be maintained and avoids the development of a fistula. With involvement of the proximal urethra it is important to buttress the urethrovesical junction to avoid postoperative stress incontinence. A bulbocavernosus fat pad can be used if there is a need for additional tissue depth during the repair. Postoperative care

Following a repair, integrity of the urinary tract should be established with a cystogram or IVP to rule out extravasation or confirm ureteral patency prior to removal of catheters and stents. Prognosis

Early recognition of urinary tract injury is associated with excellent results. Intraoperative detection and correction causes little inconvenience to the patient and is associated with minimal complications or long-term sequel. Postoperatively a high index of suspicion should be maintained and immediate investigations instituted in those with suspected injury to achieve optimal outcomes. Further reading

Daly JW, Higgins KA. Injury to the ureter during gynecologic surgical procedures. Surg Gynecol Obstet 1988;167:19–22.

Dowling RA, Corriere JN Jr, Sandler CM. Iatrogenic ureteral injury. J Urol 1986;135:912–15.

Mann WJ, Arato M, Patsner B, Stone ML. Ureteral injuries in an obstetrics and gynecology training program: etiology and management. Obstet Gynecol 1988;72:82–5.

Neuman M, et al. Iatrogenic injuries to the ureter during gynecologic and obstetric operations. Surg Gynecol Obstet 1991;173:268–72.

Uterovaginal prolapse Definition

The word prolapse is derived from the Latin word prolapsus and means a slipping forth or the falling out of place of a part or viscus. A prolapse occurs when there is a defect in the pelvic floor sufficient to allow one or more of the pelvic viscera to fall through. Epidemiology

The incidence of genital prolapse is difficult to determine as many women do not seek medical advice. Broad estimates suggest that 50% of all parous women lose the support of the pelvic floor and have some degree of prolapse with 10–20% seeking medical aid for their problem. Aetiology

The pathophsyiology of pelvic floor disorders is complex and multifactorial. The factors include a combination of genetic predisposition and acquired dysfunction of the muscular and connective tissue support systems due to parturition or the menopause. Damage to the pelvic diaphragm causes the levator plate to become more oblique, creating a funnel which allows the uterus, vagina, and rectum to herniated, resulting in a prolapse. In women with severe prolapse a 50% loss of motor units of the perineal muscles has been demonstrated (Sharf et al. 1976). There is also evidence of fascial denervation (Parks et al. 1977).

Normal supports of the vagina and adjacent pelvic organs are provided by the interaction between the levator ani muscle and the connective tissue supports. In adult women the pelvic floor is inherently weak, predominantly due to their upright posture. Also on account of this orthograde posture, the fascial layers of the pelvic floor are very well developed to provide support for pelvic organs. The pelvic diaphragm collectively refers to the levator ani muscles and connective tissue attachments to the pelvis (Fig. 13.10.1a). Although the levator ani muscle has two component parts, i.e. the diaphragmatic part (coccygeus and iliococcygeus muscles) and the pubovisceral part (pubococcygeus and puborectalis), it functions as a single unit. The levator ani is a skeletal muscle with a baseline resting tone and can be voluntarily contracted. The type I fibres (slow twitch) provide constant tone and the type II fibres (fast twitch) provide reflex and voluntary contractions.

Fig. 13.10.1 (a) Levator ani complex and (b) DeLancey’s three levels of connective tissue supports of the anterior vagina. This article was published in Am J Obstet Gynecol, Vol 166, 6, DeLancey, J.O, ‘Anatomic aspects of vaginal eversion hysterectomy’, pp. 1717–1724, Copyright Elsevier (1992).

Contrary to previous belief, the connective tissue fibres are just as important as the pelvic muscles in providing support to the pelvic organs, but their role is different. The fascial components consist of two types of fascia: parietal and visceral (endopelvic). Parietal fascia covers the pelvic skeletal muscles and provides attachments of the muscles to the bony pelvis. The visceral fascia exists throughout the pelvis as a meshwork of loosely arranged collagen, elastin, and adipose tissue through which blood vessels, lymphatics, and nerves travel to reach the pelvic organs. DeLancey (1992) described three levels of endopelvic fascia support for the vagina (Fig. 13.10.1b). The upper third of the vagina (level I) is suspended from the pelvic walls by vertical fibres of the paracolpium, which is a continuation of the cardinal ligament. In the middle third of the vagina (level II) the paracolpium attaches the vagina laterally to the arcus tend-ineus and fascia of the levator ani muscles. The vagina’s lower third fuses with the perineal membrane, levator ani muscles, and perineal body (level III). Classification

As vaginal wall prolapse is a protrusion of one or more pelvic organs (such as the bladder or the rectum) through the vaginal fascia and the displacement (‘prolapse’) of the associated vaginal wall from its normal location into or outside the vagina, there are different types of vaginal wall prolapse depending on the organs and sites involved. These include anterior vaginal wall prolapse (such as urethrocele and cystocele), posterior vaginal wall prolapse (such as rectocele and enterocele), and apical vaginal wall prolapse (affecting the uterus or the vault in women who have had a hysterectomy). A woman can also present with prolapse of a combination of these sites.

Many systems for staging prolapse have been described, but due to lack of subjectivity have been fraught with problems. The standard for prolapse assessment for clinical researchers is the system accepted by the International Continence Society, the Pelvic Organ Prolapse Quantification system or the POP-Q (Bump et al. 1996).

The POP-Q system makes measurements in centimetres in nine locations on the vagina and vulva relative to the hymen. Its advantage over previous grading systems which have included a general grading as mild, moderate, and severe to more complex classifications such as the Baden Walker system is that the assessment of prolapse for all sites of the vagina is done as well as a quantitative measurement of prolapse with straining relative to the hymen.

Pelvic organ prolapse quantitative scoring system (POP-Q)

Aa Arbitrary point on the anterior wall, measured 3 cm from the external urethral meatus –3 to +3cm (–3 cm with no prolapse)

Ba The most dependent portion of the anterior vagina Value is –3 with no prolapse.

C Least supported portion of the cervix or vaginal cuff

Ap Arbitrary point on the posterior vaginal wall, measured 3 cm from the hymen –3 to +3cm

Bp The most dependent portion of the posterior vagina. Value is –3 with no prolapse

D Position of the cul-de-sac. Point D ranges in value from positive to negative. It is not measured post hysterectomy.

TVL Total vaginal length from the hymen to the posterior fornix (or vaginal apex after hysterectomy)

GH Genital hiatus from the midpoint of the external urethral meatus to the posterior midline of hymen

PB Perineal body from the posterior midline of hymen (GH site) to the midanal opening Prognosis

A large retrospective cohort study (Olsen et al. 1997) of women undergoing surgical treatment for prolapse and incontinence during 1995 which included 149 554 women age 20 or older demonstrated that the lifetime risk of undergoing a single operation for prolapse or incontinence by age 80 was 11.1%. In women undergoing surgery for prolapse, up to one-third of procedures represented recurrent operations. Clinical approach: diagnosis

History

• Something coming down is almost universal. Women describe a vaginal lump which is usually asymptomatic when they get up in the morning and gradually gets worse as the day progresses.

• A uterine prolapse may cause protrusion of the cervix giving a feeling of pressure, and when the prolapse is protruding outside the introitus, bleeding, ulceration of the protruded lump, and discharge may be present.

• An anterior vaginal wall prolapse (cystocele) often presents with urinary symptoms. Increased frequency related to a large residual or recurrent urinary tract infection may occur. Prolapse does not cause stress incontinence (SI) and in fact the symptoms of SI may be masked by the increasing size of the prolapse. Some women may even complain of having to reduce the bulge digitally in order to pass urine, but more commonly of voiding difficulty with the need to strain, double void, or rock in order to empty their bladders. In the presence of large prolapse and vaginal eversion, back flow resulting in hydroureter and hydronephrosis may occur, although this is reversible following correction of the prolapse.

• A posterior vaginal wall prolapse (rectocele and/or enterocele) by comparison may be asymptomatic until quite large. There may be difficulty with defaecation, with incomplete bowel emptying and passive leakage, or problems with intercourse.

• Other non-specific symptoms which may occur in patients with prolapse include pelvic pain, low back ache, and the consequences of a vaginal protrusion such as difficulty walking. Examination

• Bimanual examination.

• Speculum examination at rest and with straining. This should be performed in the left lateral position using a Sims speculum to permit visualisation of the anterior and posterior vaginal walls separately. Investigations

These depend on the history and examination findings and include

• urine culture

• pelvic ultrasound scan

• urodynamic studies

• proctography. Management

Most women with prolapse are asymptomatic so may need no treatment. Current treatment options for vaginal wall prolapse include pelvic floor muscle training (physiotherapy), use of topical hormone replacement therapy, use of mechanical devices (ring or shelf pessaries), and surgery, with or without mesh reinforcement. A trial of lifestyle modification might be beneficial: weight loss, smoking cessation, treatment of constipation, electrical stimulation, or biofeedback.

Physiotherapy

There is some encouragement from the systematic review by Hagen et al. (2004) that pelvic floor muscle training, delivered by a physiotherapist to symptomatic women in an outpatient setting, may reduce severity of prolapse.

Topical hormone replacement therapy

Although there are no studies looking at the impact of oestrogen therapy in women with prolapse, oestrogen has been shown to be of benefit in women with atrophic vaginitis, thereby reducing prolapse symptoms. Taking oestrogen may also help to limit further weakness of the muscles and other connective tissues that support the uterus.

Mechanical devices

Pessaries are a good option for those who wish to remain fertile or avoid surgery. There are a variety of pessaries available, made of rubber, plastic, or silicone-based material. The commonest pessaries are the rings and shelf, but other types being increasingly used are the inflatable, the doughnut, and the Gellhorn, all of which have slightly different uses and specifications.

Surgery

Surgical correction of prolapse depends largely on the compartment which is affected. For vaginal wall prolapse it may involve an anterior colporrhaphy/anterior vaginal wall repair, posterior colporrhaphy/posterior vaginal wall repair or a vaginal hysterectomy. For a vaginal vault prolapse surgical correction may require a sacrospinous fixation, an abdominal sacrocolpopexy, or an infracoccygeal procedure which involves the use of a mesh (e.g. Apogee, Post I-Stop).

The aims of using mesh in the repair of vaginal wall prolapse are to add additional support and to reduce the risk of recurrence, particularly for women with recurrent prolapse or with congenital connective tissue disorders. The evidence for their use in routine practice and primary repairs is however lacking. Prevention

The development of prolapse may not be completely preventable as there are a large number of factors, including genetic and familial, that contribute. Certain precautionary measures such as antenatal and postnatal exercises and avoidance of factors that increase intra-abdominal pressure (persistent heavy lifting, constipation) may however play a role. Further reading

Bump RC, Mattiasson A, B o K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.

DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717–24.

Hagen S, et al. Conservative management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2004; 2: CD003882.

Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6.

Parks AG, Swash M, Urich H. Sphincter denervation in anorectal incontinence and rectal prolapse. Gut 1977;18:656–65.

Sharf B, Zilberman A, Sharf M. Electromyogram of pelvic floor muscles in genital prolapse. Int J Gynecol Obstet 1976;14:2–14.

Urodynamic investigation

The term ‘urodynamics’ is used to describe a combination of tests that assess bladder filling and emptying.

The aim of urodynamics is to

• reproduce the patient’s symptoms

• demonstrate a physiological explanation for the patient’s symptoms. Assessment of the patient with lower urinary tract dysfunction

Urodynamic assessment of a patient with lower urinary tract dysfunction includes full history, clinical examination, urinalysis, and frequency volume diary prior to embarking on laboratory tests.

History

The International Continence Society has published guidelines on the classification of lower urinary tract symptoms. The urogynaecological assessment includes specific enquiry into symptoms of

• stress urinary incontinence (SUI)

• urge urinary incontinence

• urgency, nocturia, frequency

• voiding and urinary stream

• bowel function

• sexual function and dyspareunia

• prolapse

• recurrent urinary tract infections.

Quality of life assessment

Urinary incontinence has a significant impact on a woman’s quality of life. There are numerous standardized quality of life questionnaires now available.

Examination and dipstick urinalysis

Abdominal and pelvic examinations are essential to exclude a pelvic mass. Vaginal examination will help assess the degree of oestrogenization of the lower genital tract and classify and quantify any prolapse. Prolapse can be classified according to severity (mild moderate or severe) by the Baden Walker system or the International Continence Society Pelvic Organ Prolapse (ICS PoPQ) score. Neurological examination may also be necessary to determine any possible neurological cause for the patient’s symptoms. Dipstick testing of urine will help detect a urinary tract infection and diabetes mellitus. Haematuria on dipstick testing confirmed on microscopy requires urgent cystoscopy to exclude a bladder tumour.

Frequency volume chart

Patients are given a frequency volume chart (FVC) prior to attending the urodynamic clinic. The patient is asked to complete a 3-day diary of the fluid intake and voiding habits. A FVC provides information about the following:

• bladder functional capacity

• daytime and night time frequency

• frequency and severity of incontinence episodes

• nature and volume of fluid intake.

Laboratory tests

Urodynamics usually involve the following:

• Uroflowmetry: plots the flow rate of urine against time. This assesses voiding function. Voiding dysfunction manifests in an interrupted, reduced or incomplete urinary stream. The patient attends with a full bladder and sits in private, on a special commode which measures the rate of micturition.

• Cystometry: once the urine has again had dipstick analysis to exclude a UTI a filling catheter and fluid-filled pressure transducer are inserted under aseptic technique into the bladder to measure the intravesical pressure. A fluid-filled pressure transducer is then inserted into the rectum or vagina. This measures intra-abdominal pressure. The bladder is then filled and provocation manoeuvres are performed by the patient. The detrusor pressure is plotted by subtracting the intra-abdominal pressure from the intravessical pressure. The bladder is filled with saline at room temperature usually at a rate of 50–100 mL/minute. Microtip solid state transducers may also be used.

• The patient is asked to inform the practitioner performing the tests when she feels the first sensation of fullness (first sensation), the first desire to void and strong desire to void. Any feelings of urgency or signs of leakage are noted on the trace.

• Mimicking the patient’s symptoms of urgency with or without urinary leakage associated with a rise in detrusor pressure is called detrusor overactivty (DO). Provocation studies are then performed including coughing, jumping and laughing to provoke an involuntary leakage of urine. Urinary leakage in the absence of a rise in detrusor pressure is called urodynamic stress incontinence. At the end of provocation studies the patient is asked to void. Pressure flow analysis on voiding will again screen for a voiding disorder and differentiates between outflow obstruction (high pressure–low flow) and detrusor failure (low pressure–low flow).

Normal reference ranges:

• Flow rate: >15 mL/second

• First sensation: 150–250 mL

• First desire to void: 350–450 mL

• Strong desire to void: 400–600 mL.

Additional tests may include:

• Urethral pressure tests: urethral closure pressure and urethral leak point pressure assess the ability of the urethra to prevent leakage.

• Videourodynamics: formal cystometry performed under X-ray imaging. The filling medium is radio-opaque rather than saline. This demonstrates abnormalities in the bladder anatomy such as diverticulae. It also allows assessment of bladder anatomy in association with function. For example differentiating incontinence due to bladder neck hypermobility and urethral sphincter deficiency (ISD).

• Ambulatory urodynamics: ambulatory urodynamics are used when conventional cystometry fails to demonstrate the patient’s symptoms of DO. The intravessical and rectal pressure lines are inserted but no filling catheter is used. The bladder is allowed to fill physiologically with urine. During this time the patient keeps a diary of symptoms and this is later compared with the subtracted cystometry. This test is thought to detect DO in up to 30% more women. Further reading

Abrams P. Urodynamics, 2nd edn. Springer 1997.

Abrams P, Cardozo L, Fall M, et al. The standardization of terminology in lower urinary tract function. Neurourol Urodynam 2002;21:167–78.

Bump RC, Mattiasson A, Bo K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.

Radley SC, Jones GL. Measuring quality of life in urogynaecology. Br J Obstet Gynaecol 2004;111:33–6.

Van Waalwijk van Doorn ES, Zwiers W, et al. A comparative study between standard and ambulant urodynamics. Neurourol Urodynam 1987; 6: 156.

Vaginal discharge

Vaginal discharge presents with or without irritation and has various causes. Non-infective

• Physiological

• Cervical ectopy

• Foreign bodies

• Vulval dermatitis. Non sexually transmitted: (caused by disturbance of normal vaginal flora)

• Bacterial vaginosis

• Candidiasis. Sexually transmitted

• Chlamydia trachomatis

• Neisseria gonorrhoeae

• Trichomonas vaginalis. Typical features

• Physiological: usually white, non-offensive, varies with menstrual cycle.

• Cervical ectopy: outgrowth of columnar cells from endocervix over the ectocervix causing a mucoid discharge.

• Vulval dermatitis: irritation often associated with a change in soaps, chemicals, washing powders.

• Foreign bodies: seen in children, history of retained foreign body, usually offensive smelling discharge.

• Bacterial vaginosis: 9% prevalence, profuse fishy smelling discharge, no itching or irritation. Typified by an over-growth of anaerobic bacteria. Vagina and vulva appear normal and not inflamed.

• Candidiasis: 10% prevalence, thick white non-offensive discharge associated with vulval itching and irritation. Vagina and vulva appear red and inflamed on examination.

• Chlamydia trachomatis: prevalence 5–10% of women under 25 years of age. Usually asymptomatic in 80% of women but may present with a purulent vaginal discharge. Infection leads to a significant risk of developing pelvic inflammatory disease.

• Neisseria gonorrhoeae: prevalence is unknown, asymptomatic in 50% of women but may present with purulent vaginal discharge. May coexist in women with chlamydia and cause pelvic inflammatory disease.

• Trichomonas vaginalis: prevalence unknown. May be asymptomatic but often presents with a yellow offensive profuse frothy discharge associated with vaginal and vulval itching and irritation and dysuria. Evaluation of patient with vaginal discharge

History

• Nature of discharge-colour, smell, consistency and presence or absence of vaginal irritation. If patient has pelvic pain and pyrexia, suspect pelvic inflammatory disease. Sexual history including new partners, high-risk partners, numerous partners, unprotected intercourse.

Examination

• A chaperone should be present during intimate examinations. Inspection to look at nature of discharge, vaginal and vulval inflammation. Abdominopelvic examination to elicit pelvic tenderness or mass such as an abscess, cervical excitation indicative of pelvic inflammatory disease. Speculum examination to inspect cervix for an ectopy, cervical inflammation, purulent discharge. Investigations

• Vaginal pH: vaginosis (pH >4.5), candidiasis (pH is unknown. The aetiology may be varied but is usually in the gynaecological population is acquired rather than congenital Obstetric

This is the commonest cause of fistulae in developing countries. These fistulae occur largely due to obstructed labour causing pressure necrosis and sloughing of the bladder, urethra, or bowel, or as a result of traumatic injury to the bladder at the time of delivery. Therefore this can happen at the time of Caesarean section, forceps delivery, craniotomy or symphisiotomy, or Gishiri. The vast majority of women who develop obstructed labour have associated fetal demise. Obstetric anal sphincter injury is associated with a 6% incidence of rectovaginal fistulae. Surgical

The commonest cause for surgical fistulae is hysterectomy, and laparoscopic hysterectomy appears to be associated with a higher incidence than abdominal or vaginal hysterectomy. The more complicated the surgery, for example if there are adhesions, previous Caesarean section, or endometriosis or malignancy, the more likely a fistula is to arise. The experience of the surgeon is probably also a factor. Surgical fistulae may also arise after operations such as anterior or posterior repair (especially with the increasing use of mesh)or after urethral diverticulectomy or closure. Radiation

Preoperative pelvic radiation increases the risk of postoperative fistula development. Radiation itself may be a cause of fistula. Malignancy

Carcinoma of the cervix, vagina and rectum may present with a fistula and obviously treatment with surgery or radiotherapy can predispose to fistula.

Inflammatory bowel disease

This is the most significant cause of the intestinogenital fistulae in the UK. These usually present to the colorectal surgeons, and Crohn’s disease is by far the most common cause. Miscellaneous

This category includes infection, penetrating trauma, coital injury, infected pessary, or other foreign body or catheter-related injury. Prevalence

It was suggested that the post-hysterectomy fistula rate is about 1 per 1300 operations in the UK. It is very difficult to give a true prevalence. In the developing world the estimated prevalence is 1–2 per 1000 deliveries. Fistula may be small or large and it is outside of the context of this article to discuss classifications. Presentation

Fistulae between the urinary tract and the genital tract present with continuous and uncontrollable urinary leakage. This happens day and night. A small fistula may only leak intermittently and a large fistula may leak so much the woman’s bladder will be constantly empty. A woman with vesicocervical or vesicouterine fistula may present with cyclical haematuria at the time of menstruation.

Classically fistulae present between 5 and 10 days after the causative injury and especially after direct surgical injury.

Urethrovaginal fistulae distal to the urethral sphincter mechanism may be asymptomatic and may not require treatment.

Rectovaginal fistulae may present with flatus passing through the vagina or faecal loss through the vagina. Investigations

If the fistula is not obvious on clinical examination either under direct inspection with a Sims speculum, or in the case of rectovaginal on rectal examination then after excluding a urinary infection an intravesical dye test can be used. The author’s preference is to use methylene blue through a catheter and to examine the vagina carefully. It is usually done in the lithotomy position. The author finds it much more useful than a 3 swab test.

IVU can be useful especially if the ureter is thought to be affected. It is also useful to know the position of the vesicovaginal fistula in relation to the ureter.

Careful examination with cystoscopy usually will allow the identification of a fistula. A small sound can be passed from the vaginal side and can be visualized in the bladder. Sometimes a fistula may be complex and have more than one opening. Again the position of the ureter, if it is close to the fistula would be noted and at the time of surgery a stent may need to be inserted.

Sigmoidoscopy and proctoscopy are used to identify fistulae especially if there is inflammatory bowel disease present. Management

At an early stage for a urinary tract fistula not involving the ureter a urethral catheter may be inserted and a small fistula may close. A larger fistula will need time for the edges to slough off and heal before repair is attempted. Immediate repair is only appropriate if trauma is recognised within the first 24–48 hours. If infection is present then antibiotics should be used.

Preoperative care

If a woman has a large fistula, the vulval skin may be infected by ammoniacal dermatitis. Silicon barrier creams may be helpful. In developing countries it is important that the patient has appropriate nutrition to improve healing. Also in obstetric fistula there are associated with lower limb weakness, foot drop and limb contraction and physiotherapy may be useful. Surgical management

In general principle it is best to wait till sloughing of the fistula has occurred and the edges are clean before repairing. This may take a variable length of time. Repairs which affect the urinary tract excluding ureteric fistulae can be performed either vaginally or abdominally. Generally urologists use the abdominal route and may go directly retropubically through the bladder or trans peritoneally. The vaginal approach is associated with a far quicker recovery rate and should be the route of choice. In developing countries with larger fistulae many of the surgeons perform ureteric reimplantations through the vaginal route.

Infiltration with 1% xylocaine with 1:200000 adrenaline helps to separate the layers allowing dissection of the vagina from the underlying organ, whether it be bladder or rectum. The dissection should be such that closure is under no tension. Closure usually is undertaken in two layers with interrupted sutures usually Polyglactin 3 0 Then the vagina is closed over the repair under no tension. If the tissue is particularly poor then grafts can be interpositioned. From the vaginal side one can use either the Martius (labial fat pad) graft or bring a flap of pubococcygeus muscle across. For those using the abdominal route the omentum is often used.

Patients should be well hydrated prior to the procedure but it is the management of the bladder afterwards that is vital. Continuous bladder drainage should be ensured and the catheter should not be allowed to be blocked and therefore the catheter should be checked hourly. In developing countries open drainage is carried out and often the patients are allowed to walk around with a bucket with the catheter draining constantly and given responsibility for their own catheter management. For surgical fistulae the author uses 14 days’ catheterization whereas with obstetric fistulae in developing countries 21–42 days have been reported. Results

For primary closure over 90% success rates are reported; however, the success rate falls if the surgery has to be repeated.

Complications include recurrence and the development of subsequent incontinence. Although this is largely thought to be stress incontinence, sometimes it is due to detrusor overactivity as the bladder has been empty for quite a long time and this may lead to a reduction in compliance and capacity. In most young women a period of bladder retraining with or without anticholinergics will resolve the overactivity and any stress incontinence may need to be treated subsequently. Further reading

Hilton P. Fistulae. In: Shaw R, Soutter WP, Stanton SL (eds) Gynaecology. Elsevier science 2003: 835–56.

Vulval pain and pruritus

The vulva lies within the urogenital triangle extending to overlie the pubic symphysis and pubic bones. Embryologically it is a junctional zone derived from ectoderm, hind-gut endoderm, and mesoderm. The vulva consists of the mons pubis, the labia majora and minora, the vestibule of the vagina, the hymen, the Bartholin glands, the clitoris, and the external urethral orifice. The epidermis is a stratified squamous epithelium. Vulval pain may be acute or chronic. Idiopathic chronic vulval pain, soreness, or burning (but not itching) is called vulvodynia. Pruritus vulvae (itching of the female external genitalia) is a symptom and not a diagnosis, and when acute is often of infective aetiology but lichen sclerosis, a common non-infective condition, is a significant cause of long-term symptoms. Vulval pain

Acute

• Infective: causes of acute pain include infected Bartholin’s glands, infected sebaceous cysts, acute herpes simplex infections, occasionally other sexually transmitted diseases, candida, infected eczema, infected psoriasis, and conditions such as infected intertrigo (non-specific inflamed flexures common in the obese).

• Traumatic: these may be accidental, sexual, gynaecological, or surgical. Pain with sexual intercourse may be a feature of scarring with skin conditions including advanced lichen sclerosis (Fig.13.14.1).

• Non-infective cutaneous conditions of the vulva: several systemic conditions can lead to acute vulval pain including erosive lichen sclerosis, epidermolysis bullosa (Petersen, 1996), acrodermatitis enteropathica (Verburg, 1974), ulcerative colitis, Crohn’s disease (Werlin 1992), lupus erythematosis, lichen planus, Behcet’s syndrome (Wechsler and Piette 1992), fissuring of psoariatic vulval skin and neoplasia (e.g. Paget’s disease and squamous cell carcinoma).

• Other causes include spinal nerve compression.

Fig. 13.14.1 Lichen sclerosis. This figure was published in Gynaecology, RW Shaw, WP Soutter and SL Stanton, Copyright Elsevier (2002) pp. 245–258.

Chronic

• Vulvodynia: the International Society for the Study of Vulvovaginal Disease (ISSVD) has defined vulvodynia as ‘vulvar discomfort, most often described as burning pain, occurring in the absence of relevant visible findings or a specific, clinically identifiable, neurologic disorder’. It is not caused by infection (herpes, etc.), inflammation (lichen planus etc), neoplasia, or neurological disorders. Vulvodynia is therefore an idiopathic process. It is said to affect up to 18% of the female population and is generally regarded as an underdiagnosed difficult to treat gynaecological disorder (Gumus 2008). It is often accompanied by psychosexual problems. This is explained by two hypotheses: the presence of long-standing pain leading to the development of these problems (neuropathic hypothesis), or pre-existing distress leading to chronic vulval pain (somatic hypothesis) (Lynch 2008). It is a chronic pain lasting at least 3–6 months without an identifiable cause, i.e. a diagnosis of exclusion. However, recent work (Bowen 2008) has shown that 61% of women with a diagnosis of vulvodynia have a specific disease of the vulval skin identified by a dermatopathologist. The most common of these were lichen sclerosis, atopic dermatitis, and lichen planus. The 39% remaining had non-specific changes and hence were the true vulvodynias.

• Other causes include chronic forms of acute vulval pains listed above. History and examination: key points

• Identify the duration of pain, past medical and surgical history, previous treatments, allergies, and sexual history, including sexually transmitted diseases.

• Examine all areas of the external genitalia ensuring that both the labia majora and labia minora are separated. Perform a vaginal examination if indicated. As vulval conditions may be manifestations of systemic disease, examine other body surfaces, scalp, nail, and oral mucosa. The diagnosis may be obvious elsewhere, e.g. lichen planus (mouth) and psoriasis (scalp).

• Demarcate the type and areas of pain with a cotton bud.

• Adequate lighting and exposure is crucial. Signs to look for include: erythema, lichenification, loss of architecture, ulceration, whiteness, discharge, and excoriation. Special investigations

• Evaluate any vaginal discharge, e.g. with 10% potassium hydroxide for the bacterial vaginosis ‘whiff test’, take swabs as necessary for sexually transmitted diseases.

• Consider taking a small punch biopsy under local anaesthetic. Treatment

Acute pain

General principles apply to most causes. Make a diagnosis and treat appropriately. Multidisciplinary working may be required with dermatologists.

Chronic pain

• Vulvodynia is a difficult condition to treat and multiple therapies have been tried all with varying degrees of success (Haefner 2005). As with all chronic pains a team of therapists including a gynaecologist, dermatologist, pain management physician, and psychologist is ideal, although expensive.

General measures

Suggestions include wearing cotton underwear during daytime and none at night, avoid vulval irritants (e.g. shampoo), clean the vulva with water alone and pat dry, apply a moisturizing emollient once clean and use adequate lubrication during intercourse.

Topical measures

Local anaesthetic preparations such as lidocaine ointment 5% or Emla cream may be used. Long-term 24-hour treatment may minimize feedback amplification of pain and allow healing. Simple petroleum jelly has been used as has topical oestrogen. One study showed low oestrogen receptor levels in women with vulvodynia (Eva 2003). Topical therapies of no proven benefit include corticosteroids, testosterone, and antifungals.

Oral therapy

Drugs used are often those utilized for any chronic pain syndrome. Oral tricyclic antidepressants are commonly used especially amitryptyline. A dose of 5–25 mg nightly increasing to a dose not exceeding150 mg daily can be used (Munday 2001). The anticonvulsant Gabapentin, starting at 300 mg orally for 3 days then increasing to 3600 mg maximum can be used as can carbamazepine (100 mg nocte increasing to a maximum of 400 mg twice daily) for refractory patients. The full therapeutic effect of oral therapies may not be apparent for weeks or months.

Other therapies

Biofeedback and physical therapy are important in vulvodynia. Physical therapy includes soft tissue mobilisation, myofascial release, trigger point pressure and electrical stimulation to alleviate pain caused by muscle spasm (Glazer 1995).

Surgery

Excision of the vulval vestibule is rarely performed and only in those who have failed other managements. Pruritus vulvae

There are many causes of vulval itching.

• Vulval infections: these include bacterial boils, viral infections such as warts (papillomavirus), herpes simplex, molluscum contagiosum, fungal infections such as candida, tinea cruris (ringworm of the groin), pityriasis versi-color, and other infections including scabies (Sarcoptes scabei), pediculosis (Phthirus pubis, the crab louse).

• Vaginal discharge: including candidiasis, trichonomas vaginalis, and bacterial vaginosis.

• Vulval dystrophies: non-neoplastic includes lichen sclerosis, lichen planus, lichen simplex, eczema, and psoriasis. Neoplastic lesions include vulval intraepithelial neoplasia, Paget’s disease of the vulva and occasional a squamous cell tumour.

• Ammoniacal dermatitis secondary to urinary incontinence

• Irritant dermatitis: reaction to detergents, perfume, bath oils, spermicides. Reactions to drugs.

• Psychological causes.

History and examination are identical to that of vulval pain.

Differential diagnosis

This is often a challenge. One method is to make this on the basis of the vulval appearance (Black 2002).

Red rash

Tinea cruris, intertrigo, psoriasis, irritant dermatitis, allergic contact dermatitis, steroid rebound dermatitis, tinea versi-color.

White plaques

Lichen planus, lichen sclerosis, Paget’s disease, vulval intraepithelial neoplasia (VIN).

Papules

VIN, condylomata acuminate, molluscum contagiosum, scabies.

Vaginitis

Bacterial vaginosis, trichomoniasis, candidiasis.

Treatment will be guided by the diagnosis made. Further reading.

Black M, McKay M. Obstetric and gynecologic dermatology, 2nd edn. 2002: 200.

Bowen AR, Vester A, Marsden L, et al. The role of vulvar skin biopsy in the evaluation of chronic vulvar pain. Am J Obstet Gynecol 2008;199:1–467e. 6.

Eva LJ, MacLean AB, Reid WM, et al. Estrogen receptor expression in vulvar vestibuitis syndrome. Am J Obstet Gynecol 2003;189:458–61.

Glazer HI, Rodke G, Swencionis C, et al. Treatment of vulvar vestibulitis syndrome with electromyographic biofeedback of pelvic floor musculature. J Reprod Med 1995;40:283–90.

Gumus II, Sarifakioglu E. Vulvodynia: case report and review of literature. Gyneco Obstet Invest 2008;65:155–61.

Haefner HK, Collins ME, Davis GD, et al. The vulvodynia guideline. J Lower Genital Tract Dis 2005;9:40–51.

Lynch PJ. Vulvodynia as a somatoform disorder. J Reprod Med 2008 53; 391–6.

Munday PE. Response to treatment in dysaesthetic vulvodynia. J Obstet Gynecol 2001;40:283–90.

Petersen CS, Brooks K, Weissman K, et al. Pretibial epidermolysis bullosa with vulvar involvement. Acta Dermato-venerologica 1996;76:80–1.

Verburg DJ, Burd LI, Hoxtell EO, Merill LK. Acrodermatitis enteropathica in pregnancy. Obstet Gynecol 1974;44:233–7.

Wechsler B, Pietter JC. Behcets disease. BMJ 1992;304:1199–200.

Werlin SL, Esterly NB, et al. Crohns disease presenting as unilateral labial hypertrophy. J Acad Dermatol 1992;27:893–5. Internet resources

International Society for the Study of Vulvovaginal Disease: www.issvd.org. Patient resources

www.vulvalpainsociety.org/