Chapter 40. Female Urology & Female Sexual Dysfunction

Female urology encompasses urinary incontinence as well as pelvic reconstructive medicine for prolapse. It is common for urinary incontinence and pelvic organ prolapse to coexist in the same woman or to develop subsequently. This chapter will concentrate on pelvic organ prolapse as urinary incontinence has been discussed in detail in Chapter 29.

Pelvic organ prolapse is the protrusion of the pelvic organs (uterus, bladder, and bowel) into or past the vaginal introitus. Estimates of prevalence vary widely depending on definition used, whether the patient is symptomatic, the epidemiologic methods used, and the population studied. The U.S. National Center for Health Statistics estimates over 250,000 operations performed for genital prolapse apart from hysterectomy. With aging of the population, these quality of life issues and their treatment assume additional importance.

Bony Pelvis

The maintenance of continence and prevention of pelvic organ prolapse rely on the support mechanisms of the pelvic floor. The bony pelvis is the rigid foundation to which all of the pelvic structures are ultimately anchored. These bones are the ilium, ischium, pubic rami, sacrum, and coccyx. It is important to understand and discuss the bony pelvis from the perspective of a standing woman. In the upright position, the bony arches of the pelvic inlet are oriented in an almost vertical plane (Figure 40–1). This directs the pressure of the intra-abdominal and pelvic contents toward the bones of the pelvis instead of the muscles and fascial attachments of the pelvic floor. This dispersion of forces minimizes the pressure on the pelvic musculature and transmits them to the bones that are better suited to the long-term cumulative stress of daily life.

Musculofascial Support

The muscles of the pelvic floor, particularly the levator ani muscles, have a critical role in supporting the pelvic organs and play an integral role in urinary, defecatory, and sexual function. The levator muscle complex consists of the pubococcygeus, the puborectalis, and the iliococcygeus (Figure 40–2). The pubococcygeus originates on the posterior inferior pubic rami and inserts on the midline organs and the anococcygeal raphe. The puborectalis also originates on the pubic bone, but its fibers pass posteriorly and form a sling around the vagina, rectum, and perineal body, resulting in the anorectal angle and promoting closure of the urogenital hiatus. The iliococcygeus originates from the arcus tendineus levator ani (ATLA) and inserts in the midline onto the anococcygeal raphe.

The ATLA is a linear fascial covering of the obturator internus muscle, and extends from the ischial spine to the posterior area of the superior ramus (Figure 40–2). The levator ani muscle group forms a broad hammock upon which the bladder, proximal vagina, and intrapelvic rectum lie, providing the musculofascial support for a large portion of the anterior pelvis. The space between the levator ani musculature through which the urethra, vagina, and rectum pass is called the urogenital hiatus. The fusion of levator ani where they meet in the midline creates the so-called levator plate.

The pelvic diaphragm has investing connective tissue, which is often referred to as “fascia”; it is, however, less organized and less distinct than traditional fascia (eg, rectus abdominis fascia). This visceropelvic fascia consists of collagen, smooth muscle, and elastin. Microscopic studies suggest that this fascia may be histologically indistinct from the deep vaginal wall, and not a separate “fascia.”

The pelvic fascia consists of two leaves—the endopelvic fascia (abdominal side) and the perivesical fascia (vaginal side). The urethra, bladder, vagina, and uterus are all contained within these two layers of fascia. The two leaves fuse laterally to insert along the arcus tendineus.

There are three important components of the pelvic fasciae. Anteriorly, the pubourethral ligaments attach to the lower portion of the pubis and insert on the proximal third of the urethra. Laterally, the arcus tendineus fascia pelvis extends from the pubourethral ligament (inferior portion of pubic symphysis) to the ischial spine. The arcus tendineus fascia pelvis is a thickening of the fascia overlying the iliococcygeus muscle. It corresponds to the lateral attachment of the anterior bladder wall to the pelvic sidewall (Figure 40–3). Fascia extending medially from this arc carries a variety of names (pubourethral, pubocervical, urethropelvic, vesicopelvic) and provides important support to the urethra and anterior vaginal wall. Posterior to the ischial spine, the fascia fans out to either side of the rectum and attaches to the pelvic sidewall as the strong cardinal and uterosacral ligaments (Figure 40–4). The cardinal and uterosacral ligaments hold the uterus and upper vagina in their proper place over the levator plate.

Innervation

Many anatomic and surgical texts suggest that the levator ani muscles are dually innervated from the pudendal nerve on the perineal surface and direct branches of the sacral nerves on the pelvic surface. However, recent anatomic, neurophysiologic, and experimental evidence indicates that the levator ani muscles are innervated solely by a nerve traveling on the intrapelvic surface of the muscles without contribution of the pudendal nerve. This nerve originates from S3, S4, and/or S5 and innervates both the coccygeus and the levator ani muscle complex. After exiting the sacral foramina, it travels 2–3 cm medial to the ischial spine and ATLA across the coccygeus, iliococcygeus, pubococcygeus, and puborectalis. Given its location, the levator ani nerve is susceptible to injury during parturition and pelvic surgery.

The pudendal nerve innervates the striated urethral and anal sphincters as well as the deep and superficial perineal muscles and provides sensory innervation to the external genitalia. This nerve follows a complex course that originates from S2–S4 and travels behind the sacrospinous ligament just medial to the ischial spine, exiting the pelvis through the greater sciatic foramen. It then enters the ischiorectal fossa through the lesser sciatic foramen and travels through the pudendal canal (Alcock's canal) on the medial aspect of the obturator internus muscles before separating into several terminal branches that terminate within the muscles and skin of the perineum.

Pelvic prolapse is prevented by several mechanisms. The most important support is from the continuous contraction of the levator ani pelvic muscles. The activity of skeletal muscle is a combination of basic tone, reflex contraction or relaxation, and voluntary contraction or relaxation. In patients with multiple deliveries, there is widening and descent of the levator plate. Therefore, the musculature becomes less important, and the “fascial” structures become the more important elements of support as the organs cross the pelvic floor.

Because of the complexity of pelvic organ support, vaginal prolapse is likely multifactorial: myopathic or neuropathic disorders, aging, atrophy, chronic increase in abdominal pressures, multiple deliveries, hysterectomy, and hormonal changes. However, intrinsic collagen abnormalities and other individual predisposing factors, such as genetics, differences in pelvic architecture, inherent quality of the pelvic musculature, and tissue response to injury, might explain why patients with known risk factors do not develop prolapse and many patients without risk factors do.

A number of classification systems have been published to facilitate standardization of clinical findings and enable communication about patients. Until recently, none of the systems have been validated. In 1996, the International Continence Society accepted standardization of the terminology for prolapse, known as the POPQ system for pelvic organ prolapse quantification. Although most clinicians still use the Baden-Walker system (Grades 1–4), the POPQ system is the accepted standard for clinical studies and published data on prolapse (Figure 40–5).

The POPQ system is a site-specific quantitative description of support that locates six defined points around the vagina (two anterior, two posterior, and two apical) with respect to their relationship to the hymenal ring. Negative numbers (in centimeters) are assigned to structures that have not prolapsed and positive numbers to those that protrude, with the plane of the hymen defined as zero. Points Aa and Ap are 3 cm above the hymenal ring. Points Ba and Bp are defined as the lowest points of the prolapse. The apex anteriorly is C (cervix), and posteriorly is D (pouch of Douglas). When the uterus is absent, point C is the vaginal cuff and D is omitted. TVL is total vaginal length at rest. GH is the genital hiatus measured from the middle of the urethral meatus to the posterior hymenal ring. PB is the perineal body measured from the posterior aspect of GH to the midanal opening (Figures 40–6 and 40–7).

The terminology avoids assigning a specific label, such as cystocele or rectocele, to the prolapsing part of the vagina, acknowledging that the actual organ(s) frequently cannot be determined on physical examination. Although it is more difficult to learn than traditional systems, reproducibility studies document interobserver and intraobserver reliability.

Symptoms

Pelvic organ prolapse is often asymptomatic until it is severe. Many women present with symptoms in addition to the vaginal bulge, as a result of the associated organ dysfunction.

The most common complaint due to anterior compartment prolapse (cystocele) is vaginal bulging, with or without suprapubic pressure and pain. Other symptoms include urgency, frequency, urge incontinence, and recurrent urinary tract infections. Obstructive voiding symptoms are due to urethral kinking when the bladder descends beyond the pubic ramus, but the urethra remains fixed. This is commonly seen in the setting with previous surgery (eg, bladder neck suspension, urethropexy, sling). Patients may describe using unusual positions to void, such as pelvic tilting, squatting, or standing. Acute urinary retention and hydronephrosis are rare in patients with pelvic prolapse.

Many women with severe prolapse report that their stress incontinence improved as the prolapse worsened. Reduction of the prolapse during examination can produce stress incontinence in more than 50% of clinically continent patients. This unmasking of occult stress incontinence warrants attention when considering surgical therapy.

Constipation and difficult defecation with distal stool trapping or excessive straining are symptoms commonly attributed to posterior compartment prolapse (rectocele). The patient may report having to manually splint the perineum or vagina to assist evacuation.

Physical Examination

A thorough physical examination should be done with a comfortably full bladder, at rest and with straining, in the supine (lithotomy) position. Depending on the patient's ability to strain, examination in the upright position may be performed to accentuate the degree of prolapse to match that reported by the patient. The goal of examination is to determine the degree of prolapse, the specific anatomic defects, and the presence of concomitant organ prolapse in other compartments or incontinence. In the supine position, the origin of prolapse should be determined. Using a half-speculum blade, the posterior vaginal wall is retracted; the patient is asked to strain while the anterior defect is evaluated. After characterizing the anatomic defects, an attempt can be made to reduce the cystocele in order to elicit occult stress urinary incontinence and hypermobility. Similarly, the anterior vaginal wall is retracted to determine the presence of any posterior defect. A digital rectal exam assesses rectal tone, the presence of impacted stool, attenuation of the prerectal fascia, and perineal laxity. Using both blades of speculum, the vaginal vault or cervix can be examined for uterine descent, vault prolapse, and enterocele.

The basic evaluation for prolapse includes a history, physical examination, measurement of postvoid residual volume, and urinalysis. Additional testing may be needed in the setting of a large introital bulge where it may be difficult to differentiate between a severe cystocele, an enterocele, or high rectocele by physical examination only. Imaging studies can be performed to identify which organs are prolapsing. An ideal study should provide precise information about which structures are prolapsed, the presence of urinary retention and obstruction, urethral hypermobility, and urinary incontinence.

Cystourethrography

The patient is upright with a full bladder. Films are taken in a lateral position during both rest and strain. This exam provides information about bladder position, bladder neck funneling, urethral mobility, stress incontinence, and postvoid residual. The normal position of the base of the bladder should be above the pubococcygeal line (Figure 40–8). The presence of a rectocele can also be inferred when bowel gas is identified below the pubic symphysis. This exam is static and does not provide information about other pelvic organs or soft tissues of the pelvic floor.

Ultrasonography

Ultrasound is an attractive imaging modality because it is easy to perform, minimally invasive, and avoids radiation exposure. Tubo-ovarian and renal disease can also be assessed during examination. There is evidence that ultrasound is useful in evaluating bladder neck hypermobility; however, transvaginal imaging for pelvic prolapse does not provide adequate visualization of the soft tissues. Translabial ultrasound can be used to quantify prolapse, although it appears to be better for the anterior compartment and uterine descent than for the posterior compartment.

Dynamic Magnetic Resonance Imaging

Recently, magnetic resonance imaging (MRI) has been used to evaluate pelvic prolapse. It is performed quickly, without contrast or ionizing radiation, and permits visualization of the soft tissues as well as the upper urinary tract. Gousse and colleagues (2000) have shown that in comparison with findings at surgery, MRI has a 100% sensitivity, 83% specificity, and a positive predictive value of 97% when assessing cystoceles. MRI does not require intravesical catheterization, does not require contrast, is fast, and is noninvasive. The drawback is that it may underestimate the extent of cystocele and enterocele because the exam must be performed in the supine position, which diminishes the downward forces that can be generated with abdominal straining. Standing MRIs will be the ultimate modality in obtaining an even more precise study for prolapse. Cost is the main reason that prohibits the wide use of MRIs currently (Figures 40–9A and B).

Video Urodynamic Study

A urodynamic study can be done with or without video assistance. Both methods provide information about bladder compliance, capacity, sensation of filling, detrusor overactivity, and contractility. An advantage in performing videourodynamics is the capability to watch the position and funneling of the bladder neck during filling and straining. This combines cystourethrography with the urodynamic study. Choosing to use fluoroscopy should be based on cost, availability, and familiarity with this method.

The importance of documenting the presence of urinary incontinence in patients with large cystoceles is controversial. The incidence of occult stress urinary incontinence is felt to be as high as 22–80% among patients with high-stage vaginal prolapse. Due to the known masked urinary incontinence, and the high incidence of postoperative “de novo” stress incontinence, many pelvic reconstruction surgeons routinely perform a concomitant anti-incontinence surgery in all anterior vaginal reconstruction, independent of the continence status. This, however, remains a point of debate.

Determining the presence of bladder overactivity is important in preoperative counseling because it can affect the postoperative result. In the majority of cases (60–80%), urgency may resolve after surgery. However, some patients may have no change in urgency or a worsening of their urgency with sling placement and/or bladder neck elevation. Urodynamic study may also suggest urinary obstruction with elevated voiding pressure, low urinary flow, or radiographic evidence of urethral kinking.

Cystourethroscopy

This exam is performed to rule out concurrent pathology in the bladder and urethra, such as bladder carcinoma, urethral diverticulum, stones, or foreign bodies (ie, suture material) from previous surgery. Cystoscopic illumination can also be used to differentiate an enterocele from a cystocele. A pelvic exam is performed with the cystoscope in the bladder. The bladder transilluminates through the anterior vaginal wall so that the extent of the bladder prolapse is demarcated. It can also be used as a bedside urodynamic exam, assessing filling sensation, postvoid residual, and visual cystometrics for bladder contractions. With a full bladder, a supine Valsalva stress test can be performed, looking for urethral leakage.

Upper Urinary Tract Evaluation

Patients with a high-stage cystocele should have upper-tract imaging because there is a 4–7% incidence of moderate hydroureteronephrosis amongst patients with severe vaginal prolapse. This risk is greater in patients with procidentia, compared with vault prolapse. Ultrasound, excretory urography, computed tomography, or MRI can be used. An advantage of MRI is the ability to simultaneously evaluate the upper urinary tract, tubo-ovarian disease, and pelvic organ prolapse simultaneously.

Laboratory Evaluations

Patients must have sterile urine prior to proceeding with an operative procedure. In preparation for surgery, a complete blood count, basic metabolic panel, coagulation profile, and urine culture should be obtained.

Nonsurgical Therapy

When surgery is contraindicated or must be deferred, a patient can be made comfortable with a vaginal pessary. They are of primarily two types, ring and support. Pessaries should be used with care. Without close monitoring of the patient and frequent examinations, ulcerations of the vaginal mucosa and fistula formation to the bladder can occur. Proper sizing, care, cleansing, and estrogen replacement can minimize complications. Vaginal estrogen cream has been shown to have beneficial effects on vaginal epithelium by improving vascularity and total skin collagen content, especially in preparation for surgical correction.

Other nonsurgical treatments include pelvic floor muscle exercises as well as measures to improve the associated factors such as chronic cough, obesity, and constipation. These may help alleviate symptoms and prevent worsening of the prolapse, but the actual prolapse usually will not spontaneously disappear.

Surgical Repairs

The goal of repair is to restore pelvic anatomical support. This is rarely an independent surgery. Often, surgery entails addressing incontinence as well as prolapse of the other compartments. The end result must restore anatomy and function by restoring normal vaginal axis and depth while preserving urinary, bowel, and sexual function. Because the various forms of organ prolapse are interrelated owing to shared support mechanisms, some recommend that all defects be repaired at the same time because occult weaknesses in other sites may be acquired.

Anterior Compartment

Anterior colporrhaphy was initially introduced in 1914. It is a transvaginal approach that reduces the herniation of the bladder by plicating the redundant tissue, imbricating the detrusor, and approximating the tissue in the midline (Figure 40–10). The long-term results have been disappointing. There have been numerous modifications to the anterior colporrhaphy, including the use of synthetic or allograft materials, variations in suture placement, and anchoring techniques. One method places a piece of mesh into the fold of the imbricated bladder wall. Another places the prosthetic layer over the plication sutures and anchors it in place laterally in the arcus tendineus fasciae pelvis or obturator fascia bilaterally. These repairs supported by a piece of biomaterial appear to be more durable than a simple anterior colporrhaphy.

The vaginal paravaginal repair is another technique with various modifications. It involves reapproximation of the weakened lateral vaginal attachments to the arcus tendineus. Two to three interrupted permanent sutures are placed on each side between the arcus tendineus laterally and the pubocervical fascia medially from the back of the pubis to the ischial spine.

Cystoceles can also be repaired abdominally by suturing the endopelvic fascia and lateral vaginal sulcus to the arcus tendineus with interrupted permanent sutures. As a result of multiple modifications to these techniques and the addition of anti-incontinence procedures that are performed concomitantly, the durability of each procedure is uncertain. However, many pelvic reconstruction surgeons have evolved to repairing anterior compartment defects with a graft material to support the bladder with or without anterior colporrhaphy.

More recent innovative approaches for anterior vaginal wall repair anchor an allograft, xenograft, or polypropylene mesh without tension via strips placed through the obturator foramen with a special device (Perigee, American Medical Systems; Anterior Prolift, Gynecare). These techniques await safety and efficacy studies but are increasing in use.

Apical Compartment

An enterocele has a hernia sac behind vaginal epithelium that lacks musculofascial support of the vaginal vault. Repair involves transvaginal dissection of the peritoneal sac from the vaginal wall laterally, the bladder anteriorly, and the rectum posteriorly. Obliteration and ligation of the sac is performed by the use of purse string sutures. Because an enterocele presents due to weakened vault support, the vaginal vault must also be resuspended.

Vaginal vault suspension can be performed by transvaginal reattachment of the uterosacral ligaments to the vaginal apex. Excellent anatomic outcomes have been described, but ureteral injury is a possible complication, with rates as high as 11%. Therefore, cystoscopy after intravenous indigo carmine is essential.

The vaginal vault can also be elevated to the sacrospinous ligament that extends from the ischial spine to the sacrum. Transvaginal placement of sutures needs to be performed with care as the pudendal nerve, artery, and vein are located immediately deep to the sacrospinous ligament, and damage to these structures can cause significant morbidity.

Fixation of the vaginal apex to the iliococcygeus fascia and/or muscle is another method to resuspend the vaginal vault. One or two sutures are placed into the iliococcygeus just anterior to the ischial spine. If the patient is not sexually active, this can be performed without a vaginal incision by placing a monofilament permanent suture at full thickness through the vaginal wall into the muscle either unilaterally or bilaterally. A potential benefit is the absence of critical structures in the area. Very recently, the use of polypropylene mesh to support vaginal vault suspensions has been reported with good success.

Abdominal sacrocolpopexy is considered by most surgeons to be the gold-standard procedure for vaginal vault prolapse. The procedure entails suspension of the vaginal apex to the sacral promontory with or without using a graft bridge. Autologous, allogenic, and synthetic materials have all been described (Figure 40–11). Although this procedure requires an abdominal incision and there is the risk of bleeding from the sacral promontory and postoperative ileus, the resultant anatomy carries the greatest longevity and least risk of sexual dysfunction and dyspareunia. The laparoscopic approach appears to be just as successful in experienced hands. In addition, abdominal sacrocolpopexy also has the potential to resuspend the bladder in cases of concomitant cystocele.

Posterior Compartment

The aims of posterior colporrhaphy for the repair of rectocele are to plicate the prerectal and pararectal fascia in the midline, narrow the posterior aspect of the levator hiatus, and repair the perineal body. Rectocele repair is indicated only if the patient is symptomatic because increased dyspareunia as well as worsening defecatory symptoms occurs in some patients. There is some evidence and opinion that asymptomatic rectoceles should be repaired at the time of repair of other defects because new defects may be acquired if a weakness exists. Until there is compelling evidence of benefit, the decision to repair asymptomatic rectoceles is left to the surgeon's clinical judgment. There is some clinical support to perform the posterior colporrhaphy using mesh or fascia for augmentation. However, there are no definitive recommendations for the exact procedure to be utilized.

Proper treatment of pelvic organ prolapse entails a thoughtful preoperative evaluation, strong knowledge of pelvic floor anatomy, and restoration of the vagina to its normal position and axis while maintaining normal physiologic and sexual function.

Introduction

Sexual dysfunction is a perturbation of normal sexual function that interferes with an individual's ability to engage in satisfactory sexual activity. Sexual dysfunctions are largely defined and described as disruptions of particular parts of the sexual response cycle.

The traditional view of a sexual response is an orderly progression through discrete phases in sequence (desire, arousal, orgasm, and resolution). This linear model, advocated by Masters and Johnson and later by Kaplan, has recently been challenged principally by Basson, who has advocated a circular model that emphasizes the interrelationships between the psychoemotional aspects of sexuality in women (Figure 40–12). In this model, innate sexual desire may play a variable role in an individual woman's sexual response, influencing a woman's sexual incentives, receptiveness, and response to stimuli. There is continuing controversy regarding the accuracy of these competing models, although data are emerging that the circular model of Basson may be more frequently endorsed by women with sexual dysfunction. This is parsimonious as women who have difficulties with, or reduced interest in, sex may be primarily motivated to engage in sex for emotional and psychosocial reasons.

Disorders of female sexual function are summarized in Table 40–1. Many existing definitions of female sexual dysfunction are based on scant empiric evidence, although distress regarding the situation is an important component of most modern definitions. Traditionally, sexual desire disorders have been diagnosed in the setting of infrequent sexual thoughts and fantasies. However, sexual thoughts are infrequent in many women without apparent sexual dissatisfaction and the frequency of sexual fantasies or sexual thoughts has shown little correlation with sexual satisfaction in women. Most contemporary definitions incorporate an absence of receptive desire, that is, interest in sex initiated by a partner's initiation of a sexual encounter. Arousal disorders may be subdivided into subjective arousal disorders, genital arousal disorders, and combined (mixed) arousal disorder. Of note, the Diagnostic and Statistical Manual of Mental Disorders Volume IV Text Revision (DSM-IV-TR) focuses specifically on lubrication in their definition of sexual arousal disorder, whereas the American Urological Association (AUA) definitions do make a distinction between subjective and genital arousal response. There are no defined cut-off scores (objective or subjective) to establish the diagnosis of arousal disorder and therefore the diagnosis is based purely on patient report for both subjective and genital arousal disorders. At the time of this writing, there is controversy over whether there will be a distinction between sexual desire and sexual arousal disorders in the upcoming DSM-V; currently, there is an impetus to combine these disorders into a unifying diagnosis that incorporates both disorders, consistent with the model of Basson.

The diagnosis of an orgasmic disorder per both American Psychiatric Association (APA) and AUA guidelines necessitates that an acceptable and preferred form of sexual stimulation has occurred and orgasm has not resulted. A substantial proportion of the female population does not climax from coital intercourse and absence of climax from coitus should not be diagnosed as a sexual dysfunction unless it represents a distressing change from a woman's prior state of affairs.

Physiology

The basis of desire and perceived arousal in women is poorly understood, but it involves complex interactions among the central nervous system, sex hormones, and psychoemotional factors. The sexual response cycle incorporates numerous changes throughout the body as well; for the purpose of brevity in this chapter, we will focus on genital responses.

The genital arousal response in women is mediated in large part by activity of the parasympathetic and sympathetic nervous system as well as the vascular endothelium. These systems release nitric oxide and vasointestinal polypeptide. These messengers promote vasodilatation, which in turn leads to genital vasocongestion. In the clitoris, this causes engorgement of the corporal bodies and clitoral erection. In the vagina, increased oncotic pressure leads to production of a transudate fluid that is expressed through the vaginal epithelium, producing lubrication. It is important to note that there is no evidence for a glandular component to vaginal lubrication; vaginal wetness is derived entirely from this transudate.

Genital vasocongestive responses occur in women within seconds after erotic stimulation. Interestingly, the genital arousal response appears to be an automated response to sexual stimulation; indeed, it has been shown in many studies that women may exhibit an arousal response to stimuli that are not of subjective interest. For instance, it has been shown that women often exhibit a genital arousal response (increased blood flow) in response to viewing of erotic videos, irrespective of the subject matter, sexual orientation, and personal interest in the sexual activities depicted. Genital arousal response may also occur in response to depictions of nonpreferred activities, such as threat. The reason for this automatic “priming” of genital response is unclear but may be an evolutionarily protective mechanism to ensure adequate genital lubrication for possible sexual activity.

The effect of estrogen levels on sexual function is complex. Although low estrogen levels and vaginal atrophy are associated with reduced measures of vaginal congestion when the woman is not receiving sexual stimulation, the percent increase in congestion in response to erotic stimuli is similar in the presence of low and high estrogen levels (ie, pre- and postmenopausal women). Similarly, changes in the volume of the vaginal wall and clitoris and the relative volume of regional blood in response to sexual stimulation are similar before and after menopause. Estrogen deficiency does not necessarily preclude adequate lubrication, provided that stimulation is sufficient. It is important to note that a woman who is postmenopausal will generally have less baseline lubrication and therefore the necessity of adequate stimulation to prevent painful intercourse is often more apparent in women who are postmenopausal.

Indirect evidence suggests that testosterone and dopamine play a role in modulating sexual response, since testosterone supplementation or treatment with a dopaminergic agonist can augment sexual response. However, large population studies have failed to find the expected positive correlations between sexual function and baseline serum testosterone levels. One possible explanation is that serum levels do not reflect the intracellular production of testosterone from adrenal and ovarian precursors.

Numerous psychosocial factors have been associated with reduced subjective arousal. These include distractions from other life stressors, expectations of a negative experience (eg, as a result of dyspareunia, the partner's sexual dysfunction, or negative experiences in the past), sexual anxiety, fatigue, and depression. Medications including selective serotonin-reuptake inhibitors and oral contraceptives have also been implicated in decreased sexual arousal. Oral contraceptives increase levels of sex hormone–binding globulin, which in turn reduces free testosterone levels; it is hypothesized that some women are particularly sensitive to these effects and may exhibit symptoms, whereas others would not.

On the basis of survey data, several factors have been closely linked to women's sexual satisfaction and desire. These include stable past and current mental health, positive emotional well-being and self-image, rewarding past sexual experiences, positive feelings for the partner, and positive expectations for the relationship. Certain diseases such as multiple sclerosis, renal failure, and premature menopause induced by chemotherapy are also associated with a high incidence of sexual dysfunction. In women, unlike men, vascular diseases associated with age (diabetes, metabolic syndrome, atherosclerosis) have not been clearly correlated with sexual dissatisfaction and problems in women.

Evaluation

A detailed history is the main tool in the assessment and diagnosis of sexual dysfunction and is best obtained from both partners. Important aspects of the history include the quality of the couple's relationship, the woman's mental and emotional health, the quality of past sexual experiences, specific concerns related to sexual activity (such as insufficient nongenital and nonpenetrative genital stimulation), and the woman's thoughts and emotions during sexual activity. A description of a recent sexual encounter may be instructive as it may reveal details that are not immediately disclosed in the history.

A physical examination, including a pelvic examination, is part of routine care. It is of primary usefulness in cases of dyspareunia to rule out superficial conditions (such as candidiasis, vestibulitis) and pelvic conditions (uterine leiomyomas, ovarian pathology) that may be associated with pain during sexual activity. Table 40–2 details features that are potentially relevant to sexual dysfunction that need to be assessed during an examination.

The possibility that laboratory testing will identify causes of sexual dysfunction is low. Estrogen deficiency, for example, can typically be detected by history and physical examination alone. In addition, serum testosterone has not been shown to clearly correlate with sexual function. Measurement of these hormones is of course warranted if supplementation of some kind is contemplated. Measurement of prolactin or thyrotropin is warranted if other symptoms or signs suggest the presence of abnormal levels.

Treatment

The management of sexual dysfunction in women is guided by the history. Data from randomized trials that support the use of any particular intervention are limited.

Psychological

Cognitive behavioral therapy focuses on identifying and modifying factors that contribute to sexual dysfunction, such as maladaptive thoughts, unreasonable expectations, behaviors that reduce the partner's interest or trust, insufficient erotic stimuli, and insufficient nongenital physical stimulation. Strategies are suggested to improve the couple's emotional closeness and communication and to enhance erotic stimulation. Sex therapy for couples is focused on similar issues but also includes sensate focus techniques, consisting initially of nonsexual physical touch, with gradual progression toward sexual touch; partners are encouraged to alternately touch each other and to provide feedback about what touches are pleasurable. These techniques may help to reduce performance pressure in situations where a “goal-oriented” approach toward sexual activity detracts from sexual enjoyment. Attention should also be directed to life stressors and relationship stress, as these factors are likely to exert an influence on a woman's sexual enjoyment.

Pharmacologic

Other than estrogen therapy for dyspareunia related to genitourinary atrophy, no medications are currently approved by the US Food and Drug Administration (FDA) for the treatment of sexual dysfunction in women. However, a testosterone patch for management of hypoactive sexual desire disorder has been approved for use in several European countries. In the United States, off-label use of several drugs has been reported, although data about effectiveness are sparse.

Nonhormonal

The involvement of nitric oxide in neurogenic vasodilatation suggests that phosphodiesterase type 5 inhibitors (PDE5I, used most commonly for erectile dysfunction in men) may ameliorate genital arousal disorder. In a small, laboratory-based, randomized trial, a single 50-mg dose of sildenafil (Viagra, Pfizer) increased subjective arousal, genital sensations, and ease of orgasm in some women with genital arousal disorder. The benefit was observed only among women who had a marked reduction in the normal vasocongestive response to subjectively arousing visual erotic stimulation. Sildenafil has also been shown to enhance orgasmic response in women with sexual dysfunction related to selective serotonin reuptake inhibitors (SSRIs). However, most large-scale studies of women with sexual dysfunction have not demonstrated meaningful improvements in sexual satisfaction amongst women treated with PDE5I. It is logical to speculate that PDE5I may be useful in women with a physical condition that tends to retard genital response with no or limited subjective component to the arousal disturbance; however, evidence to support this hypothesis is generally scant. Future studies are warranted to determine the potential role of PDE5I in this subset of women.

The prevalence of sexual disorders that are associated with the use of antidepressants in women is estimated at 22–58%, with higher rates reported for selective SSRIs and lower rates reported for bupropion. A recent meta-analysis of strategies to ameliorate dysfunction associated with antidepressants did not recommend any particular drug, although the potential advantages of adding bupropion were noted.

Flibanserin is a centrally acting agent with complex actions (both agonist and antagonist) on serotonergic and dopaminergic receptors. Flibanserin has reported efficacy in the treatment of hypoactive sexual desires disorder in women based on a series of phase III clinical trials in women. Approval for flibanserin was not granted by the FDA and its current status as a potential treatment for sexual problems in women is unclear.

Hormonal

Supraphysiologic androgen therapy has been prescribed for sexual dysfunction since the 1930s. More recently, testosterone at lower doses has been studied in randomized trials. The results of four recent randomized trials of testosterone in women have generally shown increases in sexually satisfying events, sexual desire, and response. Important limitations of these studies include their brevity (which is of particular importance, given the expected long-term use of the drug) and that their results are generalizable only to women in whom menopause was surgically induced and who also receive estrogen therapy. In some women who have undergone natural menopause, the ovaries continue to be an important source of androgens, and thus, the effects of androgen supplementation may differ from those whose ovaries have been surgically removed.

There are ongoing health concerns about the long-term supplementation of either androgens or estrogens. There are scant safety or efficacy data of testosterone supplementation for estrogen-deficient women. A chief concern with long-term androgen use is a potential increase in insulin resistance, which could predispose a woman to the metabolic syndrome or exacerbate the syndrome if it is already present. This is in addition to concerns regarding cosmetic side effects including hirsutism and acne.

The role of systemic estrogen in increasing desire and subjective arousal remains unclear. In the Women's Health Initiative trial, no significant differences were found between the estrogen and placebo groups in reported satisfaction after sexual activity. However, sexual dysfunction was not a primary focus of the trial, and the assessment tool was inadequate.

Recommendations and Conclusions

Recommendation guidelines for the evaluation and management of sexual dysfunction in women advocate attention to mental and physical health. Careful attention must also be directed toward both interpersonal and personal psychological issues. Local estrogen therapy is recommended for dyspareunia that is associated with vulvar atrophy that results in reduced sexual motivation. Testosterone therapy and PDE5I should be viewed as investigational and should be prescribed only by clinicians who are knowledgeable about sexual dysfunction in women.

A better understanding is needed of the endogenous and environmental factors that mediate sexual desire and arousal. Randomized clinical trials are also needed to assess the effects of psychological and pharmacologic therapies alone and in combination. The risks and benefits of long-term testosterone therapy require further study. The search for a nonhormonal medical treatment for female sexual dysfunction continues, although recent setbacks may lessen interest in this line of inquiry.

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