As described in the title of an editorial in the journal Pain,¹ female dyspareunia represents more than bad sex. Defined as recurrent acute pain experienced primarily during penile–vaginal intercourse, dyspareunia is a common symptom that can affect a woman's quality of life in many ways. For many women with dyspareunia, it can be a source of frustration, because she may find herself going from gynecologist to family doctor to therapist in a search of answers to the etiology of her symptoms and of possible treatments. For health care providers, patients with chronic dyspareunia may represent a daunting challenge, particularly if easier interventions fail. However, for many women with dyspareunia, effective treatments will often alleviate their symptoms. Particularly with the condition vulvar vestibulitis syndrome (VVS), an increasing number of publications are giving us much greater insights into this disease.

Dyspareunia can be classified in many different ways. Some authors categorize this symptom as being primary, occurring ever since the first attempt at vaginal intercourse, or secondary, beginning spontaneously after previous pain-free and enjoyable intercourse. It may also be characterized as superficial, in which the patient notices pain primarily during vaginal penetration, or deep, in which the pain is worse with deeper penetration or thrusting. This chapter focuses on the evaluation and treatment of women with superficial dyspareunia, with a particular emphasis on what may be its most common cause, VVS.

Although most experts feel that dyspareunia is a common problem, the incidence of this symptom is difficult to estimate. In a study of five primary care practices in North Carolina, Jamieson and Steege² found that 46% of sexually active respondents reported dyspareunia during or after intercourse. Of these women, 17% described pain near the opening of the vagina, 64% reported pain deep inside, and 8% had both. For most of these women, dyspareunia was only occasional, but 10% avoided sex and 3% had tried different sexual positions to avoid the pain. In terms of pelvic pain symptoms, dyspareunia ranked second only to dysmenorrhea in this study population. In another study, Glatt and colleagues found that 51 of 313 women (16%) had chronic dyspareunia, and that most women had not discussed it with their health care provider.³

Classically, much of the discussion of dyspareunia has focused on whether this is a psychological problem or a physical one.⁴ As discussed by Meana and colleagues, dyspareunia is one of the few pain syndromes to be classified as a psychiatric illness in DSM-IV, and the psychiatric view has been that dyspareunia is primarily a sexual dysfunction. It is my personal observation that this perception of dyspareunia as a sexual dysfunction makes many women too embarrassed to mention this problem to their health care provider, and that many health care providers may give such symptoms, if voiced, scant attention. However, detailed studies of women with dyspareunia show that such attitudes are unwarranted. In a study of 105 women with dyspareunia and 105 matched controls, Meana and colleagues⁵ performed an extensive standardized gynecological and psychological evaluation. Women with dyspareunia had higher frequencies of VVS and vulvovaginal atrophy. In terms of psychological symptoms, patients with no physical findings reported more symptoms such as obsessive–compulsive sensitivities, interpersonal sensitivity, depression, and phobic anxiety. However, women with VVS were similar to controls in terms of psychopathology. These women, however, reported lower frequencies of intercourse, lower levels of desire and arousal, less success at achieving orgasm, and more erotophobia; these findings could almost be expected to be a result of having chronic pain with intercourse. It is worth emphasizing that only 27% of the women in this study had no abnormalities on a gynecological examination.

As mentioned previously, many women with dyspareunia are reluctant to volunteer their concerns about the symptoms. As described by Bachmann,⁶ simply asking “Are you sexually active?” and “Are you having any sexual difficulties or problems at this time?” is an effective way of identifying sexual problems. In a patient presenting with vulvovaginal problems, I routinely will ask about dyspareunia as part of the symptom complex that brings a patient to the office. Frequently, women with dyspareunia will attribute it to a vaginal infection and will not discuss this as a specific presenting symptom. Surprisingly, in some of these women, dyspareunia turns out to be the primary and only symptom.

Before performing a detailed history and physical examination on a patient reporting dyspareunia, it is important to realize that any of the organs in the pelvis, if affected with a problem, can lead to this symptom. Furthermore, as summarized in Table 1, a broad array of pathological conditions can cause pain. Thus, when evaluating a patient with dyspareunia, the clinician should perform a very detailed history and physical examination, along with appropriate laboratory evaluation, to obtain as specific of a diagnosis as possible. Once a specific diagnosis is ascertained, a treatment plan can be established. In turn, this plan should be constantly reevaluated as the patient returns for follow-up visits to ensure adequate progress and also to treat intervening conditions in a timely manner. For example, a patient with lichen sclerosus may initially find that her pain with intercourse resolves with ultrapotent topical corticosteroid therapy but then returns a few months later when she has an episode of vulvovaginal candidiasis.

Table 1. Etiologies of Superficial Dyspareunia

Once an adequate history about the dyspareunia has been taken, attention should be given to other associated vulvovaginal symptoms, such as itching, burning, irritation, or an abnormal discharge; positive answers to these questions suggest the possibility of an infectious or dermatological cause to the pain. Postpartum or postmenopausal women, especially if they note vaginal dryness, may have atrophic vaginitis. Finally, one should keep in mind that dyspareunia may be a symptom attributable to a systemic disorder. In a study of women with systemic sclerosis, Bhadauria and colleagues found that they were more likely to report dyspareunia (56%) or vulvar ulcerations (23%) than a control group with systemic lupus erythematosus or rheumatoid arthritis.⁷ In a prospective study of 11 women with chronic dyspareunia and musculoskeletal symptoms, Raynaud's phenomenon, or symptoms of ocular or oral dryness, Mulherin and colleagues found that they had some form of Sjögren's syndrome.⁸ Thus, a thorough review of systems is important to possibly uncover a more serious underlying disease.

When examining a woman with dyspareunia, one should attempt to evaluate the vulva, vulvar vestibule, hymen, vagina, cervix, bladder, and rectum, because any of these structures, if affected by a pathological condition, can be the source of the patient's pain. Thus, one should begin with a careful inspection of the vulva and vestibule. When evaluating the vulva, the clinician should pay close attention to the structures of the external genitalia and look closely for abnormal areas of erythema or edema. Patches of white epithelium, labial atrophy, phimosis of the clitoris, or other evidence of vulvar scarring may suggest the presence of lichen sclerosus. Palpation of the vulva and the vestibule with a cotton-tipped applicator will serve to localize the symptoms. Evidence of fissures or ulcers should lead the examiner to suspect a herpes simplex virus or yeast infection. Examination of the hymen may reveal a stenotic hymen. In addition to assessing the qualities of the vaginal secretions, inspection of the vagina should include a careful search for areas of erythema, erosions, and atrophy. Similarly, the cervical examination will assess for evidence of edema, erythema, friability, and mucopus. On bimanual examination, the clinician can focus on each separate area and try to reproduce the patient's dyspareunia. Finally, by inserting two fingers deeply into the vagina, one can get a sense of whether there exists any stenosis in either the introital or the deeper vaginal areas, as well as whether there is increased muscle tone in the bulbocavernosus or levator muscles.

Laboratory evaluation depends to some degree on the findings of the examination. A vaginal pH and saline and 10% KOH microscopy are mandatory tests in any woman with dyspareunia. Because the sensitivity of microscopy to detect yeast is only 50% and because VVC is a frequent cause of dyspareunia, I routinely perform yeast cultures. Ancillary tests such as trichomonas cultures ands DNA tests for gonorrhea and chlamydia are helpful in situations in which the history is suggestive of a sexually transmitted disease or the wet mount reveals significant polymorphonuclear leukocytes. Any ulcer in the vulvar or vestibular skin should be evaluated with a herpes simplex virus culture and a rapid plasma reagent (RPR). Furthermore, vulvar or vaginal biopsy may be the appropriate diagnostic test if some sort of dermatological condition or a neoplasm is suspected. In women with bladder pain or other urinary symptoms, a urinalysis and urine culture are indicated. If these are negative, evaluation by a urologist may be helpful. Finally, in patients in whom some type of underlying systemic illness such as Sjögren's syndrome is suspected, referral to a rheumatologist for a more detailed evaluation is in order.

As a final consideration, the clinician may find that in some women with severe dyspareunia, perhaps in part secondary to vaginismus, a full examination may be next to impossible. In this situation, one should have no hesitation to recommend an examination under anesthesia to ensure that no anatomical problems are adding to the patient's pain.

To a great degree, successful treatment of dyspareunia will depend on the establishment of an accurate diagnosis and subsequent therapy. Apart from the treatment of VVS, the reader is referred to other chapters in this textbook for more detailed management of the many causes of dyspareunia.

No matter what the cause, certain adjunctive maneuvers may help alleviate the patient's symptoms. Avoiding soaps and chemical irritants may help to decrease vulvar or vestibular inflammation. I will recommend routine use of a lubricant with intercourse. Because chronic pain may lead to decreased lubrication as a secondary phenomenon, it is easier to have patients use a lubricant rather than have them worry about this issue. In women who use latex condoms and who may be latex-sensitive, use of a polyurethane condom or some other method of birth control may avert a reaction to the condom. Finally, as noted earlier, dyspareunia is a symptom that may have many psychological ramifications, ranging from decreased libido to relationship difficulties to vaginismus. In women with chronic dyspareunia, particularly if she voices concerns of this symptom on other aspects of her life, referral for psychosexual counseling, preferably to an expert in treating this problem, is invaluable. Multimodal sex therapy, consisting of individual and couples therapy and other interventions such as cognitive–behavior techniques, is an important part of the multidisciplinary approach to these disorders.⁹

Vulvodynia is defined as chronic vulvar burning condition of unknown etiology. The nomenclature for this condition is currently in flux. Under the umbrella of the term “vulvodynia” are two major subgroups, most recently known as dysesthetic vulvodynia and VVS. The International Society for the Study of Vulvovaginal Disorders (ISSVD) has proposed renaming these respective conditions as generalized vulvar dysesthesia and vulvar dysesthesia localized to the vestibule,¹⁰ but this chapter will use the older more widely accepted terminology and will focus on VVS, a common cause of dyspareunia.

Although there are descriptions of VVS dating back to more than a century ago,¹¹ VVS became more clearly described in the early 1980s in articles by Woodruff, Parmley, and Friedrich.^12,13 In their articles, they described a condition in which women reported a burning pain on contact with the vestibule and in which examination revealed foci of tender inflamed areas in the vestibule. Twenty years later, despite hundreds of articles on the subject, this remains a condition in which there remains a wide spectrum of opinion about possible causes, accuracy of diagnosis, and optimal treatment approach.

VVS is a condition whose primary hallmark symptom is dyspareunia with intromission. Although exact data on the prevalence of VVS in the general population remain scarce, certain studies suggest that this is a common condition. In a mail and telephone survey of 4915 Boston area women, Harlow and colleagues found that 16% of surveyed women reported a history of chronic knife-like or excessive pain on contact with the genital area lasting for at least 3 months or longer, and 7% were experiencing it at the time of the survey.¹⁴ In a prospective study of 210 women seen in a private practice gynecological practice over a 6-month period of time, Goetsh found that 15% fulfilled the diagnostic criteria for VVS.¹⁵ Similarly, Nyirjesy and colleagues found that up to 15% of patients referred to a tertiary care center for the evaluation of chronic vaginal and vulvar symptoms had VVS.¹⁶ These studies suggest that VVS is a fairly common cause of vulvar pain.

Women with VVS present with a primary report of dyspareunia, particularly with intromission. Most of the time, these symptoms occur in women who have previously had comfortable, pain-free intercourse and then gradually or acutely noticed this problem. Other activities that involve contact with the introital area, such as tampon insertion, wearing tight clothes, or bike riding, may cause pain. Patients also note variable amounts of burning, irritation, and itching in their daily activities. Symptoms are almost completely localized to the vulvar vestibule.

A clinical diagnosis is made by fulfilling Friedreich's criteria, which consist of a history of vulvar pain with attempted intromission during intercourse, finding focal areas of erythema confined to the vulvar vestibule, and eliciting tenderness on palpation of these areas with a cotton-tipped applicator. In most cases, patients are required to have duration of symptoms of more than 6 months before their symptoms are diagnosed as VVS. Although most clinicians agree on Friedreich's criteria, fulfilling these criteria may not always be straightforward. For example, vestibular erythema is relatively common in many women and of itself may be a normal finding. Furthermore, tenderness to pressure on examination may depend on the technique of the examiners and their ability to elicit the appropriate response. Finally, although the diagnosis of VVS entails an exclusion of other conditions that can cause vulvar inflammation and pain, such as candidiasis or vulvar nonneoplastic epithelial disorders, the role of ancillary tests such as vaginal evaluations for causes of vaginitis, fungal cultures, or even vulvar biopsies varies tremendously within the published literature. Nevertheless, Bergeron and colleagues, in trying to assess the reliability of diagnosing VVS when performed by two independent gynecologic examinations, did find substantial interrater agreement, particularly when it came to the criterion of tenderness.¹⁷

In carefully performed controlled studies, investigators have successfully demonstrated that there are measurable physical differences between women with VVS and healthy women. Laser Doppler perfusion imaging to map the superficial blood flow in the vestibular mucosa has shown significant increases in perfusion values, particularly at the posterior fourchette.¹⁸ Bohm-Starke and colleagues were able to demonstrate increased tenderness to punctate mechanical, thermal, distension but not vibrational stimuli in the vestibules of VVS patients.¹⁹ The finding that these women may have increased pain perception elsewhere (i.e., the forearm) raises the possibility that VVS may represent some sort of systemic pain condition.²⁰

Epidemiology of VVS

In their 1986 study of 67 women with VVS, Peckham and colleagues²¹ found that this condition predominantly occurs in white women. Although the age range of affected women was broad (14–67 years), most women were in their 20s and 30s, with a median age of 25 years. Eighty percent described an acute onset of symptoms; however, once they acquired the condition, the duration of symptoms extended months to years. An “in-depth” evaluation of nine women for intercurrent conditions, allergies, or extragenital physical findings did not find any notable findings.

Danielsson and colleagues,²² in a case-control study of Swedish women with VVS, sought to focus on differences in medical, psychosexual, and psychological aspects of this disease. Women with VVS were more likely to report back, neck, and shoulder pain, gastrointestinal symptoms, headaches, urinary tract infections, and other skin problems. In terms of gynecological history, they were more likely to report dysmenorrhea, a history of vulvovaginal candidiasis, and human papillomavirus (HPV) infection; the study could not ascertain the accuracy of diagnoses of infectious factors. Women with VVS had not experienced abuse more often than controls. Before their condition, these women had similar satisfaction scores regarding their sexual relationship; not surprisingly, they reported lower satisfaction scores after VVS, less frequency of vaginal intercourse, and more instances of participating in sexual activity without really wanting to. There were no significant differences between cases and controls in terms of social network and psychological factors. Other studies comparing women with VVS to control women and those with chronic pelvic pain have yielded fairly similar results.^23,24 Compared with controls, women with VVS were more likely to be using oral contraceptives and to have been using them for a longer time;²⁵ the association was strongest for those women who were using pills with high-progestogenic, high-androgenic, and low-estrogenic potency.

Studies of VVS patients have attempted to further our understanding of this syndrome by approaching it from a number of different aspects. Patient histories suggest that an infectious process may play a role in the development of VVS. As noted earlier 80% of women with VVS describe an acute onset that then leads to the more chronic pain. However, the multiple treatments that the typical VVS patient has received before the establishment of a proper diagnosis make it difficult to identify the precipitating cause in these women.

When efforts began to identify an infectious cause for VVS, attention rapidly turned to HPV. In 1988, Turner and Marinoff described seven women with VVS who all had HPV DNA in tissue specimens.²⁶ Subsequent studies also found HPV DNA in 30% to 100% of patients with VVS.²⁷ However, more recent studies, which used PCR as the tool for detecting HPV, have led to a reevaluation of the link between VVS and HPV. Wilkinson and colleagues²⁸ found HPV types 6, 11, 16, and 18 in only 3 of 31 biopsy specimens of women with VVS. Marks and colleagues found that VVS patients with HPV DNA by PCR were clinically identical to women with VVS who tested negative for HPV DNA;²⁹ their findings suggest that HPV, if present, may be an innocent bystander. A study from Israel found HPV in 54% of VVS and only 4% of control women,³⁰ but the control group consisted of women undergoing vaginal operations for various benign causes or undergoing repair of an episiotomy. Hybridization tests for HPV types 6, 11, 16, 18, and 33 were negative in 39% of women, and no one HPV type was consistently found in the other positive samples. It is not clear that the control group was appropriately matched for potential confounding factors. However, a Canadian study comparing women with VVS to controls found similar rates of HPV in cases (29.6%) and controls (23.9%).³¹ Finally, in a study meant to evaluate clinical symptoms and signs associated with detection of HPV, no association was found between HPV and symptoms of vulvovaginal burning or pain.³²

Studies that have sought other infectious etiologies for VVS have generally found microbes present at an expected prevalence, although control groups were not always used. For example, although no controls were included, culture identified an expected prevalence of microbes in 57 cases of VVS that included Ureaplasma urealyticum (18%), Gardnerella vaginalis (14%), and Candida species (9%); Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, and Mycoplasma hominis were not detected.³³In situ stains for Candida,^34,35 Gram-positive bacteria,³⁴ and Mycobacterium³⁴ have uniformly been negative, although these techniques are relatively insensitive.

In 1989, Ashman and Ott noted that Candida albicans antigens cross-react with certain antigens in vulvovaginal tissue.³⁶ As proposed by these authors, they suggested that an effective immune response against C. albicans is aborted by this cross-reactivity and that, after repeated infections, susceptible patients become hyperreactive to the cross-reactive antigens, and the patient has VVS in the absence of active Candida infection. Candida, a commensal microorganism known to cause the most common clinical infections of the vulva and vagina, is certainly a likely candidate as a possible cause of VVS.

Epidemiological studies of the relationship between VVS and VVC have yielded conflicting results. Most studies of VVS patients have not bothered to look for the presence of Candida by microscopy or culture and have not explored the issue at all. While Candida species were found in 9% of women in one report, ³³ Nyirjesy and Halpern found Candida species by culture in 24% of women with VVS.³⁷ In two case-control studies,^38,39 VVS was strongly associated with a history of physician-diagnosed VVC with an odds ratio of approximately 5, as well as physician-diagnosed bacterial vaginosis (BV). The discrepancies in findings may be related to the small number of patients in all three studies, but are also caused by the methods used to detect Candida. For example, Candida was diagnosed by a culture performed only once,³³ multiple times,³⁷ and by a patient history of physician-diagnosed VVC.^38,39 Finally, in a prospective cohort study of 996 Swedish women, more women with vulvar pain had VVC (22.8%) than those without pain (12.4%).⁴⁰

Other studies of women with vulvar vestibulitis have sought to further delineate some of the histological changes that occur with this condition. Preliminary studies have suggested that women with VVS have a local elevation of inflammatory cells⁴¹ and proinflammatory cytokines,⁴² suggestive of a hyperimmune response. The histopathology from the vestibular area of women with VVS has demonstrated a chronic, predominantly lymphocytic, inflammatory infiltrate.^34,43 A moderate to severe level of inflammation is present in 60% to100% of women with VVS. The degree of inflammation seems to be greater beneath the squamous epithelium than beneath the vestibular glands.⁴³ From two studies that examined controls without VVS, it is less clear whether such inflammation may also occur in normal women.^35,44 Although Pyka and colleagues observed mast cells in only 21% of patients with VVS,³⁴ others have noted increased numbers of mast cells in VVS compared with controls.⁴¹ However, other findings consistent with allergic reactions, such as increased numbers of eosinophils, are not usually present.⁴¹ In terms of local cytokine production, Foster and Hasday⁴² found that vulvar and vestibular tissue obtained from women with vulvar vestibulitis contained twice the tissue concentrations of IL-1β (p =.02) and TNF-α (p = .07) as compared with tissue from women undergoing rectocele repair. Of interest, both the degree of inflammation found on histology and the concentration of IL-1β and of TNF-α in the tissue were higher in the vulvar area than the vestibular area of both patients with VVS and controls. The authors felt that the higher levels of these two cytokines are responsible for the localized pain and tenderness that VVS patients exhibit.

Taken in aggregate, these findings of a hyperimmune response are consistent with some sort of infectious or postinfectious process. It is possible that some of this response occurs because of genetic factors. VVS seems to occur predominantly in a white population.^21,38 Additionally. women with VVS are more likely to have a homozygous form of allele 2 of the gene encoding for the IL-1 receptor antagonist than control women.⁴⁵ This allele is associated with greater biological activity of IL-1β, a proinflammatory cytokine.⁴⁶ In vitro, these women may also demonstrate an inability to produce interferon-α, a cytokine that may limit chronic inflammation.⁴⁷

Given the preceding studies, one could speculate that VVS represents a multistep process. Some initial injury, such as a localized infection, may trigger inflammation in the vestibule. In the susceptible woman, once this inflammation develops, there are qualitative differences to her inflammatory pattern, differences that might be genetically predetermined, that prevent adequate resolution of the inflammation. These localized changes could over time also lead to damage to peripheral nerve fibers, which in turn exert a positive feedback mechanism on the entire process. Such changes were observed by Bohm-Starke and colleagues,⁴⁸ who noted increased numbers of intraepithelial nerve endings in women with VVS compared with healthy controls.

As can be expected when the cause is unknown and has been attributed to such a wide variety of diseases, many treatment options have been proposed for VVS. In brief, these options can be classified as either medical or surgical. With medical therapy, attention is initially focused on eliminating factors that may contribute to vulvovaginal irritation. At our center, patients receive extensive counseling about soaps and laundry detergents, choice of pads or panty liners, and the use of lubricants with intercourse. Much of this counseling is geared toward having the patient minimize the number of interventions that she is using in the area. For example, it is not uncommon for patients with VVS to engage in overzealous hygiene to “keep the area clean,” which in turn exacerbates her symptoms. If an infection such as VVC is encountered, we will often choose to prolong courses of therapy in an effort to prevent relapse and gain better insight into the amount of symptoms that can be attributed to the infection.

In those women whose symptoms remain, as outlined in Table 2, there is an extensive list of potential treatments. In some women, use of topical lidocaine before coitus may successfully control symptoms. Topical corticosteroids or some other antiinflammatory therapy seems a logical step to treat the local inflammation regardless of etiology. Although conversations with health care providers who regularly treat VVS reveal that many will empirically attempt a trial of corticosteroid therapy before more aggressive attempts at therapy, published data with regard to outcomes after corticosteroid therapy are sparse. Nyirjesy and Halpern³⁷ reported a positive response, defined as a response in which the patient felt that her symptoms had diminished to an acceptable or nonexistent level, in 34% of 68 patients treated with 0.25% desoximetasone cream used topically twice daily for 4 weeks. Murina and colleagues,⁴⁹ using three weekly methylprednisolone and lidocaine injections in 22 women, found that 32% had complete resolution of their symptoms and 36% showed marked improvement. In a pilot study of 11 patients treated with 4% cromolyn cream applied three times daily, 10 had marked improvement. However, in a prospective double-blind placebo-controlled study, there was a similar response rate between cromolyn and placebo groups.⁵⁰ The finding that 42% of patients experienced a 50% or greater reduction in symptoms highlights the need for more placebo-controlled study and a better understanding of this disease.

Table 2. Possible Therapies for VVS

Because tricyclic antidepressants block the reuptake of norepinephrine and serotonin, neurotransmitters that are involved in pain pathways, they are used extensively in women with VVS. However, few studies have evaluated this therapy. Nyirjesy and Halpern³⁷ reported that 20 of 35 (57%) VVS patients had significant improvement with amitriptyline in doses up to 100 mg daily. In a larger study of 148 women who received 75 mg amitriptyline daily, Pagano reported a response rate of 60%.⁵¹

When it was thought that VVS was caused by HPV infection, intralesional injections of α-interferon were suggested as a possible therapy for VVS. A total of 12 one-million-unit injections are administered in the vestibule (three times per week for 4 weeks) in such a way as to inject the entire vestibule. Apart from the pain of the local injection, patients may report flu-like symptoms such as headache, myalgia, and fever. Initially, cure rates of almost 90% were reported.⁵² However, other studies of α-interferon have shown a success rate as low as 0%³⁷ to 49%.⁵³ Intralesional interferon may also be helpful in patients with recurrent disease after vestibulectomy.⁵⁴

In the past decade, a treatment that has assumed more prominence in the medical management of VVS is electromyographic biofeedback of the pelvic floor musculature. As suggested by Glazer and colleagues,⁵⁵ hyperirritability of the pelvic floor muscles is often noted in women with VVS. They hypothesized that this hyperirritability destabilizes the pelvic floor muscles and thus perpetuates the vulvar skin disturbance. Pelvic floor muscle electromyographic biofeedback therapy, which consists of a series of exercises to strengthen the pelvic floor muscles with biofeedback assistance, allowed up to 79% of 28 women with VVS to resume comfortable coitus. Other studies of biofeedback therapy have had similar results.^56,57

Surgical treatment for VVS has been well described as a viable approach to women with this disorder. The surgery that has been best described is a partial vestibulectomy with vaginal advancement (also known as perineoplasty).¹² With this procedure, the entire posterior vestibule, along with the posterior hymen, is excised. Then, after mobilization of the vagina by dissecting it free from its underlying attachments, a flap of vagina is brought out over the denuded area and sutured into place. Although most procedures can be performed in an outpatient setting, it can take up to 3 months to get a sense of whether the disorder is cured. With this procedure, success rates of 63% to 100% have been described.^12,54,58,59 It is encouraging to note that even with a mean of 3.3 years of follow-up, Bergeron and colleagues still found a “positive” outcome in 63% of patients. Although complications such as hemorrhage, infection, and poor healing are of theoretical concern, they seem to occur surprisingly seldom. The development of postoperative Bartholin cysts also seems to be fairly rare.

In an effort to find a less extensive procedure, alternative surgeries for VVS have been proposed. In a prospective randomized trial, vestibuloplasty, consisting of a simple undermining of the affected areas, then closure, was ineffective in 10 patients, in comparison with nine of 11 women whose VVS was cured with vestibulectomy.⁶⁰ Local surgical excision of the inflamed vestibular areas may be effective as a more limited procedure, but it has only been described in a small series of 12 patients.⁶¹ Finally, flashlamp-excited dye laser therapy yielded a complete and partial response rate of 62% and 30%, respectively, in a series of 175 women with VVS.⁶²

Faced with many different options in the treatment of VVS, it can be difficult to decide how to treat each individual patient. Whereas some experts advocate a limited role for surgery,⁶³ others use it extensively.⁶⁴ In a randomized trial of group cognitive behavioral therapy, biofeedback, and vestibulectomy, all groups improved significantly, although the best response was seen in those women randomized to surgery.⁵⁷ Finally, even in those patients whose VVS fail medical therapy, surgery is effective in up to 90% of women with persistent VVS.⁵¹ However, these preceding statements are tempered by the observation that most of the data with regard to treatment of VVS is based on retrospective case series. Given the fact that no treatment has been shown to be clearly superior to others, it makes sense to try to tailor the therapy to the individual patient. For a woman hoping for a quick effective approach, surgery early on may be the best choice. For another woman who is averse to any type of surgery, a stepwise approach to medical therapy, such as described by Nyirjesy and Halpern,³⁷ may be an appropriate way to begin, but the patient may need to understand that it may take quite a bit of time until she experiences an adequate level of symptomatic relief. It is encouraging to note that, with all treatment modalities, there is a substantial chance of adequate improvement. It is my personal feeling that for women with VVS who are often frustrated with the previous lack of an adequate diagnosis and therapy, a message of hope and reassurance is clearly warranted.

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