Female sexual dysfunction (FSD) is a common health problem that may affect up to 43% of women.1 Over past decades the definition of FSD has evolved. The World Health Organization’s International Classification of Diseases (ICD-10, 1980) emphasized physical factors that influence the sexual response, in contrast with the focus on psychological ones by the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM). More recently, the American Foundation for Urologic Disease (AFUD) defined FSD as disorders of libido, arousal, orgasm, and sexual pain that lead to personal distress or interpersonal difficulties.2
While the DSM-V due in 2012 is expected to make further adjustments to the current classification system, the most recent revision of the definition was generated at the Third International Consultation on Sexual Medicine (ICSM), published in 2010,3 and is a modification of the AFUD classification system. The ICSM definitions were formulated by an international panel of 21 experts in the field of female sexual medicine (Tables 18-1 and 18-2).3,4
||Download (.pdf) Table 18-1
|Disorder ||Definition |
|Sexual desire/interest disorder ||Diminished or absent feelings of sexual interest or desire, absent sexual thoughts or fantasies, and a lack of responsive desire. Motivation (here defined as reasons/incentives) for attempting to become sexually aroused is scarce or absent. The lack of interest is considered to be beyond the normative lessening with lifecycle and relationship duration. |
Arousal disorder Subjective sexual arousal disorder
Genital sexual arousal disorder
Combined genital and subjective arousal disorder Persistent genital arousal disorder
|Sexual arousal disorders are divided into 4 subtypes: |
Absence of or markedly diminished feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of sexual stimulation. Vaginal lubrication or other signs of physical response still occur.
Complaints of impaired genital sexual arousal; self-report may include minimal vulvar swelling or vaginal lubrication from any type of sexual stimulation and reduced sexual sensation from caressing genitalia. Subjective sexual excitement still occurs from nongenital sexual stimuli.
Absence of or markedly diminished feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of sexual stimulation as well as complaints of absent or impaired genital sexual arousal (vulvar swelling, lubrication).
Spontaneous, intrusive, and unwanted genital arousal (ie, tingling, throbbing, pulsating) in the absence of sexual interest and desire. Any awareness of subjective arousal is typically but not invariably unpleasant. The arousal is unrelieved by one or more orgasms and the feeling or arousal persists for hours or days.
|Women’s orgasmic disorder ||Despite the self-report of high sexual arousal/excitement, there is a lack of orgasm, markedly diminished intensity of orgasmic sensations, or marked delay of orgasm from any kind of stimulation |
|Dyspareunia ||Persistent or recurrent pain with attempted or complete vaginal entry and/or penile vaginal intercourse. |
|Vaginismus ||Persistent or recurrent difficulties of the woman to allow vaginal entry of a penis, a finger, and/or any object, despite the woman’s expressed wish to do so. Often associated (phobic) avoidance, involuntary pelvic muscle contraction, and anticipation/fear of pain. Structural or other physical abnormalities must be ruled out/addressed. |
||Download (.pdf) Table 18-2
|Disorder ||Definition |
|Hypoactive sexual desire disorder (HSDD) ||Persistent or recurrently deficient (or absent) sexual fantasies and desire for sexual activity. The judgment of deficiency or absence is made by the clinician, taking into account factors that affect sexual functioning, such as age and the context of the person’s life. |
|Female sexual arousal disorder (FSAD) ||Persistent or recurrent inability to attain, or to maintain until completion of sexual activity, an adequate lubrication–swelling response of sexual excitement. |
|Female orgasmic disorder (FOD) ||Persistent or recurrent delay in, or absence of, orgasm following a normal sexual excitement phase. Women exhibit wide variability in the type or intensity of stimulation that triggers orgasm. The diagnosis of female orgasmic disorder should be on the clinician’s judgment that the women’s orgasmic capacity is less than would be reasonable for her age, sexual experience, and the adequacy of sexual stimulation she receives. |
|Sexual Pain Disorders Dyspareunia Vaginismus ||Recurrent or persistent genital pain associated with sexual intercourse Recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with sexual intercourse. |
Although the ICSM classification system does not comment on personal distress or interpersonal difficulties, these are mandated in the definition by the DSM-IV-TR and AFUD. For example, if a woman has low sexual desire, but is not bothered by it, then it is not considered dysfunctional, and does not require treatment.
Normal sexual function in women is made possible by an interaction between mental and physical well-being; the etiology of FSD lies in physiological or psychological roots or both.
A large prevalence study of 1,749 women aged 18 to 59 published in JAMA in 1999 demonstrated sexual dysfunction to be more prevalent in women (43%) than in men (31%). Younger age, poor educational status (less than high school education), and physical and emotional health were important risk factors for FSD. Race had a variable influence with black women having the highest rates of hypoactive desire and Hispanic women having the lowest rates of FSD. Moreover, sexual dysfunction was highly associated with negative experiences in sexual relationships and overall well-being.1 However, this study was limited by excluding women over the age of 59. Later, Lindau et al. conducted a prevalence study on the sexual problems of women aged 57 to 85 years old.5 They reported the most prevalent sexual problem for women in this age group was low desire (43%), followed by difficulty with vaginal lubrication (34%), inability to climax (34%), and pain during intercourse (17%). Of note, women who rated their health as poor were less likely to be sexually active. While these reports were instrumental in our understanding of the prevalence of sexual complaints, they did not assess for sexual distress.
The PRESIDE study, published in 2008, reported that the age-specific point prevalence of any sexual problem was 43% in women aged 18 and older, similar to the earlier reports. However, only 12% of women reported that sexual problems were associated with personal distress.6 Distress was more common in women aged 45 to 64 years old than in younger or older women. Risk factors for distressing sexual problems included poor self-assessed health, low education level, depression, anxiety, thyroid conditions, and urinary incontinence. The prevalence of FSD included desire problems (39%), arousal disorder (26%), and orgasmic dysfunction (21%). Sexual pain disorders were not reported.
In the 1950s, Drs William Masters and Virginia Johnson were pioneers in the study of the female sexual response. They described a linearly progressive model moving through four phases: excitement (arousal), plateau, orgasm, and resolution (Figure 18-1).7 Dr Helen Singer Kaplan modified the Masters and Johnson model by starting with desire, and then excitement (arousal) and finally orgasm. The plateau and resolution phases were felt to be clinically relevant in men, but less relevant in women and thus were eliminated. Except for the pain component, the Kaplan model addresses the other three pertinent disorders of FSD: desire, arousal, and orgasm. Most recently, Dr Rosemary Basson described a circular model for female sexual response, with intimacy being the emotional motivator for sexual encounters (Figure 18-2).8
Masters and Johnson sexual response cycle. Three examples of the sexual response in women with the possibility of single or multiple orgasms (#1), no orgasm (#2), and rapid progression through each phase (#3). (From ref.7)
Basson model. Circular sexual response cycle of overlapping phases may be experienced many times during any one sexual encounter. Desire may or may not be present initially: it is triggered by the arousal to sexual stimuli. The sexual and nonsexual outcomes influence future sexual motivation. (From ref.8)
Recent research has suggested that no one model may be appropriate for all women. In a study of 133 nurses, equal proportions of women endorsed the Masters and Johnson, Kaplan, and Basson models emphasizing the heterogeneity of women’s sexual response.9 Particularly noteworthy in this study, the Basson model was chosen most frequently by women with sexual problems as demonstrated by lower Female Sexual Function Index (FSFI) domain scores in that group. This suggests that the nature of the sexual response in women may be dictated by individualized sexual function.
Female sexual anatomy is composed of the genital organs: vagina and vulva, as well as higher processing levels in the brain. Intact sexual function occurs via an interaction between physical and emotional factors. A woman’s perception of her anatomy or body image may also play a role in her sexuality.
The vulva is composed of the labia majora, labia minora, vestibule, and clitoris. The labia majora are the external “lips” of the vulva and are homologous to the scrotum of the male. Normal labial size varies widely, particularly with respect to the labia minora. Labia majora range from 7 to 12 cm (average 9 cm) in length, whereas labia minora are 2 to 10 cm (average 6 cm) in length and 0.7 to 5 cm (average 2 cm) in width (Figure 18-3).10 The labia minora may be very long or asymmetric, which could result in physical symptoms. The vestibule is the involution of the urogenital membrane, at the terminal end of the urogenital sinus (Figure 18-4). Congenital neuronal hyperplasia in the primitive urogenital endoderm may be due to increased density of C-afferent nociceptors in the vestibular mucosa, resulting in vestibulodynia.11 This condition may also develop in other women over time, with potential triggers including vulvovaginal infections, such as candidiasis or desquammative inflammatory vaginitis or hormonal alterations including oral contraceptive pills, menopause, oophorectomy, or infertility treatments.11
Variations of normal labia minora. Note the prominence or relative absence of labia majora and minora in each photograph. (From ref.10)
Vestibule. (Figure owned by Division of Urogynecology, Good Samaritan Hospital, Cincinnati, OH.)
The vagina is a fibromuscular tube with a squamous, nonkeratinizing epithelium. While average vaginal length is 9.6 cm, there is considerable variation in both length and caliber of the vagina. During genital arousal, the proximal vagina distends and the vessels of the vaginal subepithelium become engorged, allowing a transudative fluid to diffuse across the vaginal epithelium. Hormonal influences, particularly estrogens, are felt to be critical to the blood supply and engorgement of the vagina. Often, postmenopausal women experience vaginal dryness due to loss of estrogen. Other conditions may cause alterations in the length and caliber of the vagina, which could interfere with sexual satisfaction. Certain pelvic reconstructive surgeries may result in a shortened vaginal length, or narrowed vaginal introitus, and could lead to dyspareunia. Vaginal delivery may be associated with laxity of the vaginal muscles or tissues and lead to less sensation with sexual intercourse. Indeed, while the vagina may be regarded as a female sexual organ, studies have confirmed that nerves occur regularly throughout the proximal, distal, anterior, and posterior vagina and cervix without any area of increased nerve density12 or “g-spot,” which is in sharp contrast to the nearby clitoris that consists mostly of dense nerve tissue.
Strategically placed within the vulva and distal vagina lies the clitoris, which is the predominant sexual end organ of the female. The clitoral complex is a term referring to the distal vagina, urethra, and clitoris13 and this complex is the embryonic homologue to the male penis (Figure 18-5),14,15 although it differs from the male version most notably in its size. On closer examination, the clitoris is in essence a smaller, more compact version of its male counterpart with the major difference that the sole function of the clitoris is to provide sexual pleasure. Clitoral anatomy has been well described using MRI and cadaver studies (Figures 18-6 and 18-7).13,16 The only visual external component of the clitoris is the glans with its accompanying hood or “prepuce.” Due to its external nature, it is considered a part of the vulva. The nonvisual portions of the clitoris lie deep to the vulva and include the erectile tissues of the paired body (corpora), crura, and bulbs that connect at the root. The clitoral root is of great importance to female sexuality and is highly responsive to direct stimulation. The majority of the neurovascular supply to the vulva, distal vagina, and clitoris is supplied by the pudendal nerve and artery.
Embryologic homologues. Color-coded homologues demonstrating tissue composition of the corresponding male and female genital anatomy. Note the penile and clitoral glans are homologous structures. (Reproduced from Ref.15 Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)
Coronal MRI demonstrating the clitoral glans and body. Note similar morphology to male penis.
Sagittal MRI demonstrating the clitoral glans and body. The clitoral glans and body create a boomerang- like structure beneath the pubic symphysis. (Figure owned by Division of Urogynecology, Good Samaritan Hospital, Cincinnati, OH).
Some consider the brain to be the ultimate sexual organ; thus, several recent studies have used functional MRI (fMRI) to illustrate the brain regions associated with love including passionate, companionate, maternal, and unconditional love types. For this review, we will focus on passionate love, although all forms of love have a common subcortical dopaminergic reward-related brain system involving dopamine and oxytocin receptors.17 Passionate love specifically recruits the ventral tegmental area, which is the central platform for pleasurable feelings and pair-bonding, rich in dopamine, oxytocin, and vasopressin receptors and caudate nucleus associated with representation of goals, reward detection, expectation, and the preparation for action.17 Thus, passionate love is a complex emotion that is reward-based and goal-directed, usually toward a specific partner.
Other research has utilized fMRI to illustrate regions of the brain associated with sexual desire. In a recent fMRI study comparing women with hypoactive sexual desire disorder (HSDD) with normal females, there was a greater activation of the frontal gyri (Brodmann areas 10 and 47) suggesting that women with HSDD allocated significantly more attention to monitoring and/or evaluating their sexual responses/performance compared with the normal participants who had the majority of the activation in the midbrain regions (Figure 18-8).18 Mindfulness is an eastern practice with roots in Buddhist meditation that focuses on present moment and nonjudgmental awareness. Mindfulness or “being in the moment” may be decreased or lacking in women with FSD where the frontal cortex is activated when it should be quiescent. In other words, normal sexual response requires deactivation of the higher thought processes and executive function of the frontal lobe and activation of the instinctual limbic system of the midbrain. Our current understanding of the female sexual response in relation to brain activation patterns suggests differences between women with and without sexual dysfunction in encoding arousing stimuli and/or retrieval of past erotic experiences.18
fMRI imaging. Normal women (green) and women with HSDD (red) during erotic stimuli. Overlap areas appear yellow. (From ref.18)
Hormones and neurotransmitters modulate sexual function and, in general, dopamine, estrogen, progesterone, and testosterone play an excitatory role in sexual desire, while serotonin, opioids, and prolactin play an inhibitory role.19 It is hypothesized that FSD may be due to a reduced level of excitatory activity, an increased level of inhibition, or both. Receptors for hormones are expressed in both the brain and genital tissues suggesting a central (desire) as well as peripheral (arousal) component. During genital arousal, many neurotransmitters are involved in the sexual response. The most important neurotransmitters are nitric oxide (NO) and vasoactive intestinal peptide (VIP), and both are enhanced by estrogen.20
The major androgens in women, listed in descending order of serum concentration, are dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione, testosterone, and dihydrotestosterone (DHT). DHEA and androstenedione are produced by the ovaries and adrenals, whereas DHEAS is mostly produced by the adrenal glands. DHEAS, DHEA, and androstenedione are pro-androgens and require conversion to testosterone to exert androgenic effects. Testosterone appears to be the primary sex steroid influencing desire, while progesterone may mediate receptivity to partner approach. The production rate of testosterone in the normal female is 0.2 to 0.3 mg per day with 25% secreted by the ovary, 25% secreted by the adrenal, and 50% from peripheral conversion.21 Circulating levels are in the range 0.2 to 0.7 ng/mL (0.6–2.5 nmol/L)22 (Figure 18-9).23
Steroidogenesis and peripheral conversion of sex steroids. DHEA and androstenedione are produced by the ovaries and adrenals, whereas DHEAS is mostly produced by the adrenals. The majority of testosterone production is via peripheral conversion. (From Ref.23 Copyright The Medical Journal of Australia 1999.)
Normative ranges of androgen levels in women have not been established due to poor sensitivity and reliability of assays. Symptoms of androgen insufficiency may include diminished well-being, fatigue, diminished desire, reduced sexual receptivity, and diminished sexual pleasure.24 These symptoms may resemble depression and environmental stressors, making diagnosis difficult. Although an androgen insufficiency syndrome (AIS) in women was initially proposed in 2001, it remains controversial and ill-defined. Etiologies for AIS include:
Ovarian (chemotherapy, radiation therapy, oophorectomy)
Adrenal (adrenal insufficiency, adrenalectomy)
Drug related (corticosteroids, antiandrogenic agents, oral contraceptives, oral estrogen replacement therapies)
Testosterone levels gradually begin to decline in the third decade in females. By menopause the levels may be half of their peak, leading to greater likelihood of symptoms at this time.25 However, it is important to note that the ovarian stroma continues to secrete androgens throughout a woman’s lifetime. Androgens are converted into estrone, the dominant form of estrogen in menopause, by aromatase in the peripheral tissues. Premenopausal and postmenopausal women undergoing oophorectomy will have androgen and estrogen deficiencies, with an abrupt decrease in testosterone levels by approximately 50%.26
Estrogen deficiency results in a myriad of symptoms including mood changes, memory loss, sleep disturbances, decreased libido, decreased intensity of arousal/orgasm, decreased vaginal lubrication, and decreased sense of well-being. Estrogens have vasodilatory and vasoprotective effects that increase vaginal, clitoral, and urethral arterial flow.27 Estradiol is produced at the rate of 100 to 300 mg per day21 prior to menopause and then falls precipitously causing reduced overall blood flow to the hormonally responsive urogenital system and resultant vulvovaginal atrophy. Estradiol levels less than 50 pg/mL are associated with vaginal dryness, increased frequency and intensity of dyspareunia, pain with penetration, and burning.28 Vaginal dryness with associated dyspareunia is the most common sexual problem related to low estrogen in menopausal women.
As stated previously, dopamine is the key neurotransmitter that modulates sexual desire. Increasing levels of serotonin (eg, reuptake inhibition, as with the selective serotonin reuptake inhibitors [SSRIs]) can diminish dopaminergic effects on sexual function. Additionally, endogenous opioids may reduce pleasure-seeking and thus orgasmic experience, resulting in an inhibitory effect on sexual desire (Figure 18-10).19
Neurotransmitters. Positive and negative influences of hormones and neurotransmitters on sexual desire. (Redrawn with permission from Ref.19)
Although sexual pain is considered a domain of FSD, it also may be part of the physiology of further sexual dysfunction. A potential cascade of responses stem from an initial pain experience including anticipation of subsequent pain, pelvic floor hypertonicity/levator myalgia/vaginismus that may lead to worsening pain, low desire, sexual avoidance, poor arousal and/or orgasmic capacity, and development of subsequent untoward relationship effects. This may lead to a downward spiral of repetitive pain that in its most severe form may lead to apareunia. The location of the pain, with either entry or deep penetration, provides information of the etiology. Entry pain is associated with vestibulodynia, vaginal dryness or atrophy, levator hypertonicity, or vaginal stenosis while deep pain may be secondary to endometriosis, pelvic inflammatory disease, painful bladder syndrome/interstitial cystitis, levator hypertonicity, and other causes.
With the widespread use of synthetic polypropylene mesh for the treatment of stress urinary incontinence and/or pelvic organ prolapse, mesh exposures and mesh contractures may occur and have been associated with dyspareunia. A recent multicenter randomized controlled trial evaluating vaginal mesh for the treatment of pelvic organ prolapse reported a 15.6% mesh erosion (or exposure) rate within three months of placement, although some mesh exposures were asymptomatic.29 Others have suggested that scar tissue incorporation of the synthetic materials may lead to a 50% or greater contraction of the implanted size, with subsequent dyspareunia and tension on the lateral pelvic attachments.30
Relationship problems (marital discord, lack of intimacy, etc) and potential stressors (financial, job, health) contribute to FSD. Concurrent Axis I psychiatric diagnoses should be delineated during the workup of FSD including depression, anxiety, and anorexia. Often, a history of a sexual trauma may be elucidated, as 17.6% of US women report a history of prior sexual assault.31 Women with the highest risk of sexual violence (82%) are female veterans with a history of posttraumatic stress disorder.32 Recently, normal variations in personality, such as introversion, emotional instability, and not being open to new experiences, have been identified as risk factors for FSD, specifically orgasmic dysfunction.33
Female sexual function is a complex entity composed of physiological, psychological, cultural, and environmental factors. Any alterations may lead to increased or decreased sexual satisfaction. Despite the common nature of sexual complaints, dealing with these problems in the office setting may be challenging. Provider comfort, bias, and degree of training can impact patients being screened for this information.34 In addition, patients are often unlikely to volunteer intimate and sensitive information without being asked.
Providers can start the conversation by commenting on the frequency of sexual problems in the population. Questions should be open ended and nondirective. Appropriate pauses and time for the patient to elaborate are important.35 Later in the interview, direct questions may elucidate more detailed information about the complaint. Another technique is to use a standardized intake form and questionnaires to identify patients with concerns related to FSD. Following identification of a problem, a comprehensive evaluation should be performed.
The evaluation for FSD should include a medical, sexual, and psychosocial history, physical examination, and laboratory testing. If necessary, the patient may need to schedule a second appointment, as the process can be time consuming.
The medical history should include medical, surgical, obstetrical, and gynecological information. Cardiovascular disease has been linked to female arousal disorders, due to concurrent atherosclerosis of the vessels supplying the vagina and clitoris. This phenomenon has been documented in studies of men showing erectile dysfunction to be a precursor of coronary artery disease.36 Neurologic disease such as multiple sclerosis, spinal cord injury, or diabetes can affect sexual function by impairing both arousal and orgasm.37 Additionally, general medical health is directly correlated with sexual health.
Previous surgery should be ascertained. In many cases, sexual function improves or is unchanged after pelvic surgery. Many studies have documented positive impact of hysterectomy on sexual function, with no significant differences based on removal or preservation of the cervix.38,39 However, certain patients have reported diminished sensation, impaired lubrication, and vaginal changes following such procedures. Additionally, removal of the ovaries may lead to FSD secondary to estrogen and/or androgen depletion. Other surgical repairs such as Burch bladder suspension with posterior colporrhaphy may be associated with increased rates of dyspareunia postoperatively.40 Postoperative vaginal stenosis, while rare, can result from levatorplasty at the time of posterior colporrhaphy and/or aggressive trimming of the vaginal mucosa at the time of colporrhaphy, leading to dyspareunia or apareunia.41 With the widespread use of synthetic mesh for the treatment of stress incontinence and/or pelvic organ prolapse, mesh exposures and contractures may be a potential cause of postoperative pain.
Obstetrical history, specifically related to previous operative delivery, tears, or episiotomy, may outline sites for potential denervation or dyspareunia. Gynecological conditions such as endometriosis, recurrent vaginal infections, recurrent urinary tract infections, pelvic organ prolapse, or urinary/fecal incontinence should be addressed. A history of pelvic trauma or injury including motor vehicle collisions may be an important etiology for diminished sensation or pain.
Several medications may impact libido, arousal, and orgasm, although most have been identified through studies of male sexual dysfunction42-45 (Table 18-3).46 The most common medications reported to cause FSD are the SSRIs with 30% to 70% of patients reporting decreased desire, arousal, or orgasm.47 In women using SSRIs, the proposed physiological mechanism of SSRI-induced sexual side effects is enhanced serotonin activity inhibiting dopaminergic, alpha-adrenergic, and cholinergic systems in the genitourinary tract and decreased levels of NO production.48
Medications with Sexual Side Effects46
||Download (.pdf) Table 18-3
Medications with Sexual Side Effects46
|Medication ||Mechanism of Action ||Sexual Side Effects |
|Antihypertensives: || || |
|1. Beta-blockers ||Effects on sympathetic and vascular system, dose dependant ||Diminished libido, ejaculatory dysfunction |
|2. Alpha-blockers ||Uncertain ||Sexual dysfunction unspecified, ejaculatory dysfunction |
|3. Diuretics ||Uncertain, may be effect on vascular smooth muscle ||Impotence, impaired ejaculation, decreased libido |
|Psychotherapeutic agents: || || |
|1. TCA ||Anticholinergic side effects ||Impotence |
|2. SSRIs ||Serotonergic effects ||Diminished desire, arousal, orgasm |
|3. Lithium ||In conjunction with benzodiazepines ||Erectile dysfunction |
|4. Neuroleptics ||Increased prolactin levels and testosterone antagonism ||Erectile dysfunction, priapism |
|Anticonvulsants: carbamazepine, phenytoin, phenobarbital, primidone ||Affect cytochrome P450 pathway and increase metabolism of androgens ||Sexual dysfunction unspecified |
|Hormonally active agents: oral contraceptives, antiestrogens, antiandrogens, estrogens ||Effects on estrogen, androgen, and sex hormone–binding globulin levels ||Decreased libido, sexual dysfunction unspecified |
|Chemotherapeutic agents ||Presumed due to gonadal suppression ||Sexual dysfunction unspecified |
|Gastrointestinal agents: cimetidine, ranitidine, famotidine, omeprazole ||Possibly due to antiandrogen effect ||Impotence and painful erections |
|Cardiovascular agents || || |
|1. Lipid-lowering agents ||Uncertain ||Diminished libido, erectile dysfunction |
|2. Digoxin ||Decreased testosterone levels, increased estrogen levels, related to sex hormone–like structure ||Erectile dysfunction |
The sexual history is a key aspect of this evaluation. Important factors in sexual function include frequency of sexual encounters, last satisfying sexual encounter, and current level of function in domains of desire, arousal, and orgasm. It is often useful to determine the previous highest level of sexual function and activity to document any inciting factors or lifelong conditions such as primary anorgasmia. Other important issues are intimacy and relationship health, past sexual experiences and number of partners, level of knowledge regarding sexual anatomy and self-stimulation, and a woman’s attitude toward her own sexuality and body image as well as the sexual functioning of her partner including erectile dysfunction, premature ejaculation, or poor general health. The associated degree of personal distress and emotional bother should be quantified. Sexual orientation should be addressed if contributory.
Several validated instruments are available for assessment of sexual function, including the female sexual function index (FSFI), the Female Sexual Distress Scale-R (FSDS-R), the Pelvic Organ Prolapse/Urinary Incontinence Sexual Function Questionnaire (PISQ), Body Exposure during Sexual Activity Questionnaire (BESAQ), and the Brief Index of Sexual Function for Women (BISF-W).49-53 Domain and total scores may be calculated and assist in delineating the source of the problem with questions that address desire, arousal, orgasm, pain, and relationship factors. The results also provide a baseline to follow response to intervention. The PISQ is the only condition-specific measure of sexual function for women with pelvic floor disorders. The FSFI is the most widely used due to ease of completion and validation based on the DSM-IV. Additionally, general health may be addressed with the 12-item Short Form Health Survey (SF-12),54 as women with poor health have higher likelihood of sexual dysfunction.
The physician must establish the nature of the FSD as primarily physiological in origin, primarily psychological in origin, or mixed. Psychiatric diseases such as depression, anxiety, and other common conditions are part of the differential diagnosis of sexual dysfunction, and are important comorbidities in treatment. Use of tobacco, alcohol, and/or illicit drugs is critical to ascertain in the social history as substance abuse will negatively influence sexual function.
Lastly, it is important to screen patients for need of psychotherapy in conjunction with medical treatment. Relationship problems and potential stressors, if identified, should be outlined in detail. A history of sexual assault or trauma may be a potential contributor to the current sexual dysfunction. Patients with these features should undergo assessment by a therapist to address role for future treatment.
On physical examination attention should be given to assessing the external and internal genitalia. Gentle inspection of the vulva and vestibule should be performed with a cotton swab to assess for pain, abnormal sensation (hyperparasthesia), and/or erythema, suggestive of vestibulodynia (Figure 18-11). Vulvar tissues should be evaluated for presence of vulvovaginal atrophy or vulvar dystrophy that may result in fusion of the clitoral hood and labia. In severe cases, identification of the clitoris may not be possible. A general neurologic screening of S2–4 can be performed by testing perineal sensation. Often, use of a mirror to show the patient her anatomy during the examination may be helpful.
Cotton swab test for vestibulodynia. (Figure owned by Division of Urogynecology, Good Samaritan Hospital, Cincinnati, OH.)
The urethra should also be inspected for signs of atrophy such as urethral prolapse, diverticulum, or infection. Urethral cultures may be sent if there is a history of entry dyspareunia or if urethral pain or discharge is noted by milking the urethra. A cystoscopy, ultrasound or pelvic MRI may be necessary if a urethral diverticulum is suspected. Symptoms of urinary incontinence or painful bladder syndrome should be evaluated with a simple filling cystometrogram.
Pain mapping of the vagina with digital palpation should include the bladder base, evaluating for painful bladder syndrome and posterior introitus, as well as evaluation of the levator and coccygeus muscles. Levator hypertonicity/myalgia or vaginismus, termed proctalgia fugax when pain is referred to the anus, is a common disorder caused by repetitive painful stimuli resulting in hypertrophy of the levator muscle fibers including the puborectalis and pubococcygeus muscles. The levator muscles are located in the outer third of the vagina, and the tone may be severe enough to preclude speculum or penile insertion. The strength of the pelvic muscles can be graded on a scale of zero to five using a modified Oxford scale during the digital pelvic examination. Coordinated versus uncoordinated contraction and relaxation should also be noted. Episiotomy scars and previous surgical incisions may be sites of tenderness due to vaginal narrowing, scarring, or nerve entrapment.
Pelvic floor support should be assessed, focusing on symptomatic pelvic organ prolapse, significant shortening of the vagina (vaginal length <6 cm) precluding full penile insertion, or introital laxity that may cause decreased sexual sensation by both partners. In women with a history of synthetic mesh placement, palpate the vaginal canal in its entirety and use a split speculum to ensure a mesh exposure is not present. Infectious conditions such as bacterial vaginosis, candidiasis, or other sexually transmitted infections should be screened for and treated. Rare conditions, such as extreme angulation of the vagina after abdominal perineal resection (APR), should not be overlooked in women with a history of rectal or anal cancer.
Certain patients may need further attention during the physical examination. Women with a history of female genital cutting (FGC), also known as female genital mutilation, female circumcision, or infibulation, may have altered anatomy of the vulva that could affect their sexual function. Types I and II FGC involve partial or complete excision of the clitoral hood or glans and partial or complete removal of the labia, while Type III—the most severe form of FGC—is associated with partial or complete removal of the external genitalia and a stenotic neo-introitus (Figure 18-12).55 In these subjects, despite the altered external appearance, an intact clitoris may be present and palpable underneath the scar. Tapping on the clitoris or its presumed location may provoke a reflex contraction of the levator ani.
Female genital cutting (FGC). FGC is a tradition practiced in parts of Africa, Middle East, and Asia. Type III FGC, also called infibulation, involves removing part or all of the external genitalia (prepuce, clitoral glans, labia minora, and majora). (From ref.55)
Finally, a bimanual examination is necessary to evaluate the cervix, uterus, and adnexa for pain or other pathology such as an adnexal mass or tubo-ovarian abscess/pelvic inflammatory disease.
Laboratory studies may be performed if a hormonal deficiency is suspected. If menopausal status is uncertain, estradiol, follicle-stimulating hormone, and luteinizing hormone may be obtained. Although there is no precise cutoff value to determine whether estrogen deficiency is the cause of sexual dysfunction or simply a contributor, estradiol levels less than 50 pg/mL are associated with vaginal dryness and dyspareunia.28 Testing DHEAS levels will reflect adrenal androgen secretion and may highlight an adrenal insufficiency. Thyroid-stimulating hormone may identify a thyroid dysfunction. Assessment of androgen production can be obtained by measuring free testosterone (bioactive) or by calculating a free androgen index (FAI), or more accurately the free testosterone index (FTI).56 Only the free (or unbound) testosterone can exert its effects on the target tissue and ideally is measured by equilibrium dialysis assay; however, most labs do not offer this test; thus, the FTI is used as a surrogate:
The FTI is inversely related to sex hormone–binding globulin (SHBG), which may be increased in women taking exogenous hormones, such as OCPs or oral hormone replacement.57 Additionally, the FTI makes assumptions about albumin levels, as testosterone binds not only to SHBG but also to albumin. Because of the paucity of research on normal levels of androgens in women, levels in the lowest tertile or quartile are thought to require treatment in patients with clinical signs of AIS and without estrogen deficiency.58,59 Testosterone levels should be measured in the morning of days 8 to 18 of the menstrual cycle, as the levels are at their highest during this time. In addition, a complete blood count, liver function tests, and lipid profile may be helpful, especially if treatment with medications is anticipated.60 Consider a prolactin level only if clinical symptoms of galactorrhea or infertility are present or if the patient is on medications that may alter prolactin.
Specialized diagnostics such as duplex Doppler ultrasonography or vaginal plethysmography are used to measure blood flow in the vagina, although these investigations are most often used in conjunction with a clinical trial. Vaginal/clitoral sensory perception thresholds to temperature and vibration have also been reported. These specialized tests require expensive equipment and are not widely available, nor necessary for clinical practice. More common imaging studies such as pelvic ultrasound and pelvic MRI should be performed for appropriate anatomical indications including urethral diverticulum, pelvic masses, abnormal pelvic anatomy, or possibly in severe FGC cases, although are not usually indicated in most FSD evaluations.
Once the history, physical, psychological interview, and diagnostic testing are complete, the patient should return to the office for discussion with or without her partner. Using either the ICSM or DSM-IV-TR classification system, she may fall into one or more categories including desire, arousal, orgasm, or pain disorders. It is important to ascertain the most distressing symptom as complaints often overlap. At this visit, therapeutic options may be addressed.
An open conversation should take place with the patient and her partner. Discussion about the diagnosis, and its potential physiological basis, is important and goals and expectations of treatment should be established. Intimacy is a powerful motivator in the female sexual response and may need to be addressed as a contributor to FSD. Women often initiate sexuality to enhance emotional closeness, and this impetus may drive libido. Further willingness to experience arousal arises from the need to increase intimacy.61 If any marital discord or interpersonal issues are present, these should be evaluated, with appropriate follow-up to a therapist. Certified sex therapists undergo special training in this area and have a variety of backgrounds, including psychiatry, counseling, psychology, or social work.
Patient education is also paramount. Do not assume that your patient, regardless of age, knows her own anatomy or how it functions. Be sensitive to certain cultural and religious issues, such as self-stimulation or self-exploration being forbidden. Patients should be taught, for example, that not having an orgasm with each sexual encounter does not mean that the experience was a failure, and that clitoral stimulation may be more likely to lead to orgasm than coital intercourse.62 A brief discussion of foreplay may be beneficial. In many patients recommendation of topical lubricants, vaginal moisturizers, or local vaginal estrogen may aid with dyspareunia related to vaginal dryness.
Patients may begin by informing themselves about their situation. Reading books or articles about sexual function can establish that others have had similar experiences, and may validate patient’s feelings about her perceived sexual dysfunction. Experimentation with different sexual positions and encouraging women to familiarize themselves with their sexual response, to include the use of vibrator therapy, may be helpful in the right patient.62 Lifestyle changes are also important. Modification of known risk factors such as hypertension, hyperlipidemia, diabetes, cigarette smoking, or drug and alcohol abuse is part of the treatment process. Exercise, a healthy diet, and adequate sleep will promote physical and sexual well-being. Behavioral modification and nonpharmacologic therapies are first-line treatment.
Medication adjustments may be helpful. Antidepressants, specifically SSRIs, are a common medication that may have a negative impact on sexual function. Strategies to manage antidepressant-induced sexual dysfunction include reducing the drug to the minimally effective dose, waiting for adaptation, drug holidays, pharmacologic antidotes, and switching to another antidepressant with a more favorable profile, such as the selective norepinephrine reuptake inhibitors (SNRIs: venlafaxine, desvenlafaxine, duloxetine, and nefazodone) or other antidepressants (eg, bupropion).63 However, one must be aware that switching antidepressants to one with a favorable side effect profile may result in a reduced antidepressant response. Another option is to add an antidepressant with a favorable profile to their current regimen, such as bupropion.64,65 Bupropion is a potent and selective dopamine reuptake inhibitor with no clinically significant affinity for the serotonergic transporter or serotonergic, cholinergic, adrenergic, or histaminergic receptors.66 There has also been some reported success with sildenafil treatment of SSRI-associated sexual dysfunction.67
Another class of medications potentially associated with sexual dysfunction is hormonal contraception, such as OCPs. Decreased libido in subjects taking OCPs has been reported, likely due to elevation of SHBG and subsequent reduction in bioavailable testosterone.57 Thus, switching to nonhormonal contraceptive methods, including barrier methods, copper intrauterine devices, or permanent sterilization, or nonsystemic methods such as levonorgestrel intrauterine device may have a positive effect on libido.
Although many clinicians believe first-line treatment of FSD in postmenopausal patients should involve estrogen replacement,59,68 studies have documented that systemic estrogen alone is often insufficient to cure symptoms of sexual dysfunction in this group.68,69 Additionally, oral estrogen treatment increases SHBG levels and depletes levels of bioavailable testosterone, potentially exacerbating androgen insufficiency. Recent shifts in attitude regarding estrogen replacement have led to reluctance of patients to start hormonal treatment unnecessarily. Therefore, for complaints of dyspareunia due to vulvovaginal atrophy, treat with a local vaginal estrogen preparation with low systemic absorption. Several studies have shown reduction in irritative symptoms and improvement in vaginal maturity with local vaginal creams, tablets, and rings. Transdermal systemic estrogen replacement does not increase SHBG, thus is more appropriate in patients with vasomotor symptoms and FSD. Appropriate counseling regarding risks and benefits of hormonal treatment is prerequisite to initiating therapy.
Sexual Desire/Interest Disorder or HSDD
After other psychological and physiological conditions, such as marital discord or dyspareunia, have been ruled out, HSDD may be the primary diagnosis. As stated earlier, androgens are the predominant hormone responsible for sexual desire. Nevertheless, androgen replacement in women is controversial. Although studies have documented an association between androgen replacement and improvement in sexual desire, long-term follow-up is lacking, leading to concerns about safety in this population. Currently the only commercially available testosterone preparation for women is methyltestosterone combined with esterified estrogen, FDA approved for postmenopausal patients with refractory vasomotor symptoms.
Lobo et al. evaluated the effects of oral estrogen 0.625 mg with or without methyltestosterone 1.25 mg on hypoactive sexual desire in postmenopausal women. At 16 weeks follow-up, therapy with methyltestosterone increased bioavailable testosterone and improved sexual interest/desire, and frequency of sexual interest/desire, in most subjects.70 Shifrin et al. demonstrated that women who underwent surgical menopause with hysterectomy and oophorectomy on systemic estrogen had improved sexual function and psychological well-being following treatment with 300 μg transdermal testosterone patch.69 However, there was a strong placebo response in this study, and many subjects had evidence of borderline high androgen levels. Similarly, Davis et al. reported that in postmenopausal women not on estrogen replacement, a significant increase in sexually satisfying episodes in a 300 μg transdermal testosterone patch group (an increase of 2.1 episodes vs 0.7, P <.001) was demonstrated when compared with placebo.71 This study provides further evidence that in postmenopausal women, testosterone therapy may be initiated without replacement of estrogen. Other studies have shown a correlation with low androgen levels and decreased libido in both premenopausal and postmenopausal subjects.72
Patients who have symptoms of androgen insufficiency with documented low testosterone by laboratory testing may be candidates for replacement. It is important to inform patients that use of all androgen replacement therapy for low sexual desire is “off-label,” and not FDA approved in women. Several methods for providing androgen replacement exist, including pellets, compounded creams, topical gels, patches, and oral supplementation. Often treatments are compounded and thus not subject to the same rigors as FDA-approved prescriptions. Topical testosterone 1% gel preparations are FDA approved for men with hypogonadism, and are sometimes used off-label for women with low libido. Although these preparations are more predictable in their formulation, amounts necessary to treat women are a fraction of those for males, leading to difficulty in dispensing. All testosterone preparations must be carefully dosed and monitored to avoid supratherapeutic levels and negative side effects. At present time, a topical 300 μg testosterone gel (LibiGel™, Biosante, Lincolnshire, IL) specifically designed for women is currently in Phase III clinical trials and has shown promising results.73
Relatively strong contraindications to androgen therapy include androgenic alopecia, moderate to severe acne, clinical hirsutism, history of polycystic ovarian syndrome, hyperlipidemia, or liver dysfunction, while absolute contraindications include pregnancy, lactation, and suspected androgen-dependent neoplasia.74 Most of the available data are based on short-term studies and long-term safety and efficacy are unknown. Therapy should be performed under close physician supervision, after thorough patient counseling. As stated earlier, patients with levels in the lowest tertile to quartile may be candidates for treatment, due to insensitivity of the assays at lower ranges and paucity of research on normal levels of androgens in women. Early effects of androgen therapy include acne and hirsutism, with a recent study reporting a 2.9% increased rate of acne in the testosterone therapy group.70 Long-term side effects such as male pattern baldness, voice changes, and hypertrophy of the clitoris are infrequent within normal androgen ranges. Androgen therapy may adversely affect the lipid profile, especially with oral preparations that are metabolized in the liver.74 Peripheral conversion to estrogens does occur and potential risk for breast cancer and endometrial stimulation exists with use. Benefits of androgens include increased muscle mass and stimulation of bone formation as well as reduction of vasomotor symptoms.75 Prior to therapy with testosterone replacement, lipids, liver function tests, and hemoglobin should be evaluated. At one to two months following onset of therapy, laboratory tests should be repeated to avoid supraphysiological dosing and/or liver dysfunction or dyslipidemia.58
DHEA is an intermediate in the biosynthesis of androgens. It is available as a nutritional supplement. DHEA is also not FDA regulated and quality of formulations varies; hence, follow-up androgen levels are required approximately one to two months after medication adjustment. Reported improvements in libido, arousal, and orgasm have been found in patients with low androgen levels prior to treatment; however, these are small studies and not placebo controlled.77,78 Thus, long-term risks and benefits are unknown. Appropriate patient counseling about the experimental nature of the therapy is essential prior to initiating treatment.
Given the documented inhibitory influence of serotonin on female libido, there has been interest in development of a serotonin agonist/antagonist for therapy of low desire.76 However, concern for side effects and lack of FDA support has led to the latest of these treatments to be abandoned. Bupropion is currently the only nonhormonal medication commercially available in an off-label use for women with HSDD who have contraindications to hormone therapy. It targets the dopaminergic reward-related brain system, as it is a potent and selective dopamine reuptake inhibitor. In a randomized, double-blind, placebo-controlled study of 232 women, bupropion improved BISF-W scores from 15.8 to 33.9 (P =.001).66
Treatments for FSAD have received much attention and various formulations are available without a prescription that have undocumented safety and efficacy for FSD. Therapies that report benefits often base their claims on small studies with short-term follow-up. Similar to therapies used in males for erectile dysfunction, many of these focus on increasing blood flow as a mechanism for improving sexual arousal. However, in women subjects, improved blood flow, lubrication, and engorgement do not necessarily correlate with improved subjective arousal.79
L-Arginine is a precursor in the formation of NO, a mediator of vaginal and clitoral smooth muscle relaxation. ArginMax (Daily Wellness Company, Sunnyvale, CA) is a daily nutritional supplement containing L-arginine and other vitamins. A small study evaluated 77 women, of which 34 women were treated with ArginMax and 43 with placebo. Findings were improved sexual desire, satisfaction, frequency of orgasm, and clitoral sensation in four weeks in the ArginMax group,80 although systemic long-term side effects are unknown. Topical L-arginine is marketed widely for treatment of arousal disorder with several over-the-counter preparations available. These agents are designed to be applied to the vulva prior to sexual activity (heighteners/sensitizers). Often such products contain menthol, which may be irritating to the patient. There are no published studies on the effectiveness of these treatments and side effects are unknown.
Another topical agent is Zestra (Semprae Laboratories, Inc, Charleston, SC), a botanical feminine massage oil. The product is marketed as being “all natural,” and available at many pharmacies without a prescription. A small amount is applied to the vulva prior to activity. In a recent large study of 256 women aged 21 to 65 years old over a 12-week period, Zestra provided a significant increase in arousal, although 15% of women complained of mild to moderate genital burning.81
Sildenafil is a selective Type 5 phosphodiesterase inhibitor, which decreases the metabolism of cGMP, the second messenger in NO-mediated relaxation of clitoral and vaginal smooth muscle. Currently it is only approved for use in males; results of studies in women have been conflicting.82,83 Most recently, a large randomized controlled trial of 781 women showed no significant effect on subjective assessment of lubrication, sensation, or sexual enjoyment with sildenafil in women with sexual arousal disorder.83 These data suggest that sildenafil does not clearly benefit women with FSAD, likely due to a lack of awareness in some women of genital changes. Thus, the women who may benefit from off-label use of sildenafil include those with a diagnosis of genital sexual arousal disorder, rather than subjective sexual arousal disorder.
Tibolone is a synthetic steroid with estrogenic, progestagenic, and androgenic properties. It is not currently available in the United States, but has been utilized in Europe for 20 years. Randomized controlled trials have demonstrated that tibolone produces improvements in sexual function, including desire and arousal, more effectively than transdermal estradiol/progestin84,85; however, there are concerns about increased risk of breast cancer and stroke.86
The Eros Therapy (NuGyn, Inc, Spring Lake Park, MN) is the first FDA-approved nonpharmacologic device for treatment of FSD. It is a battery-operated handheld device, which is placed over the clitoris (Figure 18-13). The device provides a gentle adjustable vacuum suction and a low-level vibratory sensation. It is designed to be used three or more times a week for approximately five minutes at a time. Use of the Eros Therapy has been shown to increase blood flow to the clitoral area as well as to the vagina and pelvis.87 Small nonblinded studies have shown it may significantly improve arousal, orgasm, and overall satisfaction in patients with sexual arousal disorder.88,89 This may include women with a history of pelvic radiation who have a poor vasculature system.90 The treatment provides an alternative for patients who wish to avoid use of pharmacologic agents or hormonal therapy.
Eros Therapy. Device provides suction and vibration to the clitoris. (photograph owned by Division of Urogynecology, Good Samaritan Hospital, Cincinnati, OH).
Therapy for orgasmic disorder may be the most challenging for the physician. It is important to document whether the disorder is primary, secondary, or situational. Primary or lifetime anorgasmia is the most difficult to treat, and often requires referral for sex therapy. Patients should be encouraged to explore self-stimulation if not already done so, with or without a vibrator. Secondary anorgasmia may be due to pelvic floor changes from vaginal delivery, aging, or hormonal deficiencies. Pelvic floor physical therapy with biofeedback may improve orgasmic disorders related to weak musculature. Hormonal replacement with estrogens or androgens can improve orgasmic dysfunction in patients with deficiency. Patients may also benefit from the Eros Therapy. Overall, however, there is a paucity of research in this area.
Cognitive behavioral therapy and couples therapy play a role in treatment. If possible, any etiology for pain, such as vulvovaginal atrophy or vestibulodynia, should be addressed first. Proper perineal hygiene should be emphasized. This includes keeping the area clean and dry, wearing breathable underwear (eg, cotton), and avoidance of harsh detergent soaps, bubble baths, douching, and depilatories. For vestibulodynia, medical therapies include off-label use of antidepressants, including amitryptyline, nortriptyline, or duloxetine, or nerve-modulating agents such as gabapentin or pregabalin, although sedation is a common reason for discontinuation of these medications.
Treatment of levator hypertonicity involves physical therapy, often with dilators for desensitization. Other poorly studied remedies include trigger point injections, compounded diazepam, and/or botulinum toxin injections. Overall, diagnosis and therapy of vulvar and pelvic pain is complex and involves multiple modalities, which are beyond the scope of this review.
Although surgical treatment is usually not indicated for FSD, there are some situations in which surgery is appropriate. These may include refractory vulvar vestibulodynia, labial hypertrophy, vaginal laxity, and severe vaginal stenosis due to FGC, vulvar dystrophy, or iatrogenic causes. Surgical treatment of pelvic floor disorders, such as pelvic organ prolapse, urinary incontinence, or fecal incontinence, may also improve sexual function.
In cases of vulvar vestibulodynia that fail to respond to conservative therapies with diet, salt soaks, mineral baths, and/or oral medication, surgical management with removal of the vestibule is an option (Figure 18-14).91 This can be accomplished sharply or by laser, with either localized excision or complete excision of the vestibule. Generally, the vaginal epithelium is undermined and the distal vagina advanced to provide a more generous platform for penetrative intercourse. The minor vestibular glands including Skene glands or periurethral glands should be excised if they were painful during cotton swab testing. In a recent report of 104 women who underwent vestibulectomy, 93% of women reported satisfaction with the procedure and 89% were able to have intercourse.92
Vestibulectomy. (From ref.91 © Elsevier 2011.)
In rare cases, women with extremes in width of the labia minora may experience physical symptoms such as discomfort in clothing, discomfort during exercise, and entry dyspareunia. In such subjects, a labial reduction procedure may be warranted. In a retrospective study of 163 simple labial reductions, no significant complications were noted and 93% had a successful functional outcome (Figure 18-15).93 More complex labial reduction procedures have been described, such as the z-plasty (Figure 18-16).94 It is important to differentiate surgical correction for physical symptoms from cosmetic correction.
Simple labial reduction. Kocher clamps delineate the borders for excision of redundant tissue (A). The remaining anterior flaps will become the labia minora of desired size (B). (From ref.93 © Elsevier 2000.)
Labial reduction “z-plasty.” Excision of central portions of labia minor with reapproximation in a z-closure fashion with interrupted delayed absorbable suture. (From ref.94 © Wolters Kluwer.)
In some situations, vaginal looseness or laxity may occur following childbirth, and lead to alterations in sexual function. A small pilot study has reported on the tolerability and success of nonsurgical tightening with radio-frequency thermal therapy,95 but surgical correction with a perineoplasty is the mainstay of treatment. The goal of surgical correction of laxity is to reduce the genital hiatus to improve penetrative sensation. This is accomplished by excising a diamond-shaped portion of the distal vaginal epithelium and perineal skin, sharply mobilizing the posterior vaginal epithelium, plicating the fibromuscular tissues of the perineum, and trimming any redundant vaginal epithelium. In a report of 53 patients, 94% felt that the vagina was tighter,96 although long-term outcomes and psychosocial and safety data are lacking.
In cases of Type III FGC, a defibulation procedure allows the vagina to be patent and may reveal the intact buried clitoral glans in approximately half of the cases97 (Figure 18-17).55 Defibulation releases the vulvar scar tissue in the midline, exposing the introitus, urethral meatus, and possible clitoral glans, as well as creating a new labia majora. Care should be taken not to injure any clitoral tissue in the process. Experts recommend general or regional anesthesia to avoid posttraumatic stress disorder that may be experienced with local anesthesia.55 A recent study reported on 40 women with a history of Type III FGC who underwent defibulation; 100% were satisfied with their results and no intraoperative or postoperative complications occurred.97
Defibulation. A Kelly clamp is placed in the neo-introitus to delineate the length of the scar. Two allis clamps are placed at 2 and 10 o’clock and a vertical incision is made with Mayo scissors to expose the vagina and urethral meatus. Care should be taken to palpate the clitoral region prior to incision to avoid additional injury, if present. Edges of the labia are then reapproximated with a subcuticular suture. (From ref.55)
For patients with postsurgical vaginal narrowing or severe vulvar dystrophy, surgical management can be performed to increase introital caliber by reverse perineoplasty with vaginal advancement. After excision of a triangular portion of perineal skin, the posterior vaginal epithelium is mobilized sharply and advanced to cover the perineal skin defect. A retrospective review of 64 patients who underwent perineoplasty for the treatment of introital stenosis related to vulvar lichen sclerosus found that quality of intercourse improved in 86% of patients.98
If pelvic organ prolapse and/or urinary incontinence are contributing to FSD, then surgery to repair the pelvic floor disorder may restore quality of life and sexual function. Widespread use of synthetic mesh for pelvic floor disorders has led to particular complications such as mesh exposure/erosion, as well as pain along mesh attachments during intercourse. Removing mesh that produces uncomfortable sensations during intercourse, such as tugging or pulling, may be necessary if conservative therapies have failed.99
Female sexual dysfunction is a multifactorial and highly prevalent and distressing disease, affecting a large number of women.
A collaborative and comprehensive evaluation, patient and partner education, and behavior modification, followed by individualized pharmacotherapy and/or surgical management in select patients, should be the standard management of women with sexual dysfunction.
FSD is a multifactorial and highly prevalent and distressing disease, affecting a large number of women. Recent media attention to male sexual dysfunction has led to increasing female patient awareness and a desire to seek help from their physician. Despite this, many physicians fail to acknowledge FSD as part of the medical history, possibly due to lack of time or insufficient training. It is necessary to have a framework for diagnosis and treatment. A collaborative and comprehensive evaluation, patient and partner education, and behavior modification, followed by individualized pharmacotherapy and/or surgical management in select patients, should be the standard management of women with sexual dysfunction. Ultimately, as research in the field progresses, a better understanding of the physiology and pharmacotherapy of FSD will be attained.
et al. Report of the international consensus development conference on female sexual dysfunction: definitions and classifications. J Urol
M, Van Lankveld
L. Summary of the recommendations on sexual dysfunctions in women. J Sex Med
American Psychiatric Association, Task Force on DSM-IV. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text revision. Washington, DC: R.R. Donnelly & Sons Company; 2000:535–558.
et al. A study of sexuality and health among older adults in the United States. N Engl J Med
et al. Sexual problems and distress in United States women: prevalence and correlates. Obstet Gynecol
VE. The sexual response cycle. In: Human Sexual Response. New York: Ishi Press; 2010:5.
R. Female sexual response: the role of drugs in the management of sexual dysfunction. Obstet Gynecol
. 2001; 98(2):350–352.CrossRef
WA. Women’s endorsement of models of female sexual response: the nurses’ sexuality study. J Sex Med
SM. Female genital appearance: ‘normality’ unfolds. BJOG
. 2005; 112:643–646.CrossRef
et al. Umbilical hypersensitivity in women with primary vestibulodynia. J Reprod Med
et al. A prospective study examining the anatomic distribution of nerve density in the human vagina. J Sex Med
J. The anatomy of the distal vagina: towards unity. J Sex Med
. 2008; 5:1883–1891.CrossRef
FH. Atlas of Human Anatomy. 5th ed. Philadelphia: Saunders; 2011:368.
KR. Magnetic resonance imaging anatomy of the female genitalia in premenopausal and postmenopausal women. J Urol
. 2003;170: 138–144.CrossRef
JW. Neuroimaging of love: fMRI meta-analysis evidence toward new perspectives in sexual medicine. J Sex Med
. 2010; 7:3541–3552.CrossRef
et al. Women with hypoactive sexual desire disorder compared to normal females: a functional magnetic resonance imaging study. Neuroscience
A. The pathophysiology of hypoactive sexual desire disorders in women. Int J Obstet Gynecol
RN. Female Sexuality and “Normal” Sexual Function in Urogynecology and Reconstructive Pelvic Surgery—Just the Facts. New York: McGraw-Hill; 2006:316.
MA. Hormone biosynthesis, metabolism, and mechanism of action. In: Speroff
MA, eds. Clinical Gynecological Endocrinology and Infertility. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:42.
SR. Androgen treatment in women. Med J Aust
. 1999; 170:545–549.
et al. Female androgen insufficiency: the Princeton consensus statement on definition, classification, and assessment. Fertil Steril
. 2002;77(4) :660–665.CrossRef
S. Biological and psychosocial pathophysiology of female sexual dysfunction during the menopausal transition. J Sex Med
WT. Reproductive hormone levels in gynecologic oncology patients undergoing surgical castration after spontaneous menopause. Gynecol Oncol
PM. Ovarian hormones and vaginal blood flow: using laser Doppler velocimetry to measure effects in a clinical trial of post-menopausal women. Int J Impot Res
. 1998;10(suppl 2): S91–S93.
PM. Sexuality and menopause. Obstet Gynecol
. 1990;75(suppl 4):26S–30S.
et al. Vaginal mesh for prolapse: a randomized controlled trial. Obstet Gynecol
. 2010; 116:293–303.CrossRef
DR. Polypropylene vaginal mesh grafts in gynecology. Obstet Gynecol
United States Department of Justice. Full Report of the Prevalence, Incidence and Consequences of Violence against Women. Findings from the National Violence Against Women Survey
. Washington, DC: Centers for Disease Control and Prevention; 2000. Available at: http://www.ncjrs.gov/pdffiles1/nij/183781.pdf
et al. Distress and pain during pelvic examinations: effects of sexual violence. Obstet Gynecol
TD. Normal variations in personality are associated with coital orgasmic infrequency in heterosexual women: a population-based study. J Sex Med
et al. Practice patterns of physician members of the American Urogynecologic Society regarding female sexual function: results of a national survey. Int Urogynecol J Pelvic Floor Dysfunct
R. Resident education and training in female sexuality: results of a national survey. J Sex Med
I. Female sexual dysfunction: incidence, pathophysiology, evaluation and treatment options. Urology
RC. Sexual response in women with spinal cord injuries: implications for our understanding of the able-bodied. J Sex Marital Ther
et al. Sexual functioning after total compared with supracervical hysterectomy: a randomized trial. Obstet Gynecol
MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol
MM. Management of iatrogenic vaginal constriction. Obstet Gynecol
F. Incidence of sexual dysfunction associated with antidepressant agents: a prospective multicenter study of 1022 outpatients. J Clin Psychiatry
. 2001;62(suppl 3):10–21.
JR. Clinical evaluation of female sexual dysfunction: new diagnostic and treatment strategies. Prim Psychiatry. 2001;8(4):54–59.
M. Sexual dysfunction with psychotropic drugs. Expert Opin Pharmacother
MM. Female sexual dysfunction: principles of diagnosis and therapy. Obstet Gynecol Surv
et al. Prevalence of sexual dysfunction among newer antidepressants. J Clin Psychiatry
B. An open-label series using loratadine
for the treatment of sexual dysfunction associated with selective serotonin reuptake inhibitors. Prog Neuropsychopharmacol Biol Psychiatry
RC. The female sexual function index (FSFI): cross-validation and development of clinical cutoff scores. J Sex Marital Ther
Y. Validation of the female sexual distress scale-revised for assessing distress in women with hypoactive sexual desire disorder. J Sex Med
C. A short form of the pelvic organ prolapse/urinary incontinence sexual questionnaire (PISQ-12). Int Urogynecol J Pelvic Floor Dysfunct
Y. Baring the body in the bedroom: body image, sexual self-schemas, and sexual functioning among college women and men. Electron J Hum Sex
. 2004;7. Available at: http://www.ejhs.org/volume7/bodyimage.html
SR. Self-report assessment of female sexual function: psychometric evaluation of the Brief Index of Sexual Functioning for Women. Arch Sex Behav
SD. A 12-item short-form health survey: construction of scales and preliminary tests of reliability and validity. Med Care
NM. Surgical techniques: defibulation of type III female genital cutting. J Sex Med
. 2007;4: 1544–1547.CrossRef
JM. A critical evaluation of simple methods for the estimation of free testosterone
in serum. J Clin Endocrinol Metab
FC. Comparison of androgens in women with hypoactive sexual desire disorder: those on combined oral contraceptives (COCs) vs. those not on COCs. J Sex Med
GD. Androgen insufficiency in women: summary of critical issues. Fertil Steril
. 2002;77(suppl 4):s94–s99.CrossRef
S. Androgens and female sexuality. J Gend Specif Med
AT. Screening for androgen deficiency in women: methodological and interpretive issues. Fertil Steril
. 2002; 77(4):S83–S87.CrossRef
R. Women’s sexual desire—disordered or misunderstood? J Sex Marital Ther
T. Female sexual dysfunction. Curr Womens Health Rep
J. Strategies for the treatment of antidepressant-related sexual dysfunction. J Clin Psychiatry. 2001;62(suppl 3):34–43.
EL. A placebo-controlled trial of bupropion
SR as an antidote for selective serotonin reuptake inhibitor-induced sexual dysfunction. J Clin Psychiatry
MR. Reversal of SSRI-induced female sexual dysfunction by adjunctive bupropion
in menstruating women: a double-blind, placebo-controlled and randomized study. J Psychopharmacol
A. A randomized, double-blind, placebo-controlled study of the efficacy and safety of bupropion
for treating hypoactive sexual desire disorder in ovulating women. BJU Int
JK. Hormonal aspects of sexual function in women: treatment advantages with hormone replacement therapy. Prim Psychiatry. 2001;8(4):60–64.
et al. Transdermal testosterone
treatment in women with impaired sexual function after oophorectomy. N Engl J Med
B, van der Hoop
RG. Comparative effects of oral esterified estrogens
with and without methyltestosterone
on endocrine profiles and dimensions of sexual function in postmenopausal women with hypoactive sexual desire. Fertil Steril
J. Decreased free testosterone
and dehydroepandrosterone-sulfate (DHEA-S) levels in women with decreased libido. J Sex Marital Ther
gel (LibiGel™) significantly improves sexual function in surgically menopausal women in phase II study. Presented at: Annual Meeting of the International Society of Women’s Sexual Health; October 30 , 2004; Atlanta, GA.
et al. Endocrine aspects of female sexual dysfunction. J Sex Med
et al. Androgen replacement therapy with dehydroepiandrosterone for androgen insufficiency and female sexual dysfunction: androgen and questionnaire results. J Sex Marital Ther
. 2002;28(suppl): 165–173.CrossRef
RF. Dehydroepiandrosterone: a springboard hormone for female sexuality. Fertil Steril
. 2002;77(4) :S19–S25.CrossRef
N. Efficacy and safety of sildenafil
citrate in women with sexual dysfunction associated with female sexual arousal disorder. J Womens Health Gend Based Med
ML. A double-blind placebo-controlled study of ArginMax, a nutritional supplement for enhancement of female sexual function. J Sex Marital Ther
J. Randomized, placebo-controlled, double-blind, parallel design trial of the efficacy and safety of Zestra in women with mixed desire/interest/arousal/orgasm disorders. J Sex Marital Ther
C. Premenopausal women affected by sexual arousal disorder treated with sildenafil
: a double-blind, cross-over, placebo-controlled study. BJOG
EA, Weijmar Schultz
et al. Tibolone and transdermal E2/NETA for the treatment of female sexual dysfunction in naturally menopausal women: results of a randomized active-controlled trial. J Sex Med
et al. Tibolone versus conjugated estrogens
and sequential progestogen in the treatment of climacteric complaints. Maturitas
. 1996;23(1) :55–62.CrossRef
V. Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet
KL. The role of mechanical devices in treating female sexual dysfunction and enhancing the female sexual response. World J Urol
I. A new non-pharmacological vacuum therapy for female sexual dysfunction. J Sex Marital Ther
KL. Treating symptoms of female sexual arousal disorder with the Eros-clitoral therapy device. J Gend Specif Med. 2001;4(2):1–6.
et al. Clitoral therapy device for treatment of sexual dysfunction in irradiated cervical cancer patients. Int J Radiat Oncol Biol Phys
. 2005;61(4) :1078–1086.CrossRef
MM. Atlas of Pelvic Anatomy and Gynecologic Surgery. 3rd ed. St. Louis: Elsevier; 2011:888.
SC. Surgical treatment of vulvar vestibulitis syndrome: outcome assessment derived from a postoperative questionnaire. J Sex Med
B. Hypertrophy of the labia minora: experience with 163 reductions. Am J Obstet Gynecol
GJ. Central wedge nymphectomy with a 90-degree Z-plasty for aesthetic reduction of the labia minora. Plast Reconstr Surg
BH. Radiofrequency treatment of vaginal laxity after vaginal delivery: nonsurgical vaginal tightening. J Sex Med
OK. Colpoperineoplasty in women with a sensation of a wide vagina. Acta Obstet Gynecol Scand
AE. Defibulation to treat female genital cutting: effect on symptoms and sexual function. Obstet Gynecol
et al. Perineoplasty for the treatment of introital stenosis related to vulvar lichen sclerosus. Am J Obstet Gynecol
R. Dyspareunia and mesh erosion after vaginal mesh placement with a kit procedure. Obstet Gynecol