Vulvovaginal pain may be caused by a variety of disorders. Pain may be constant or intermittent, provoked by touch or spontaneous, and may be classified in various ways. The most common classification system was developed by the International Society for the Study of Vulvovaginal Disease (ISSVD) [3]. It divides possible causes of vulvar pain into four categories : infectious, inflammatory, neoplastic, and neurologic [3]. In addition, it defines the term vulvodynia as “vulvar discomfort, most often described as burning pain , occurring in the absence of relevant and visible findings, or specific, clinically identifiable, neurologic disorder.” This classification distinguishes between generalized and localized pain, and each of these subgroups is further subdivided into provoked, unprovoked, or mixed (continuous pain, exacerbated by touch). The term vulvodynia is reserved for these cases of vulvar pain occurring in the absence of physical findings [4] and therefore can be used only after specific, recognized disorders are ruled out (Table 4.1).

In the presence of inflammatory conditions, pain and dyspareunia may result from friction and damage of irritated tissues, tears, fissures, and irritation of sensitized and inflamed nerve fibers. It is beyond the scope of this chapter to review in detail the various vulvovaginal disorders. Therefore the discussion will be limited only to common conditions that may cause pain and must be ruled out prior to establishing a diagnosis of vulvodynia.

Yeast Infection is a common cause for vulvovaginitis and 80–90 % of cases are caused by Candida albicans [5]. Symptoms vary from slight vaginal discharge and discomfort to a severe form of vulvovaginitis including itching, pain, burning, and dyspareunia. In such cases, vulvar swelling, fissures, and erythema are commonly present (Fig. 4.2a). Most vulvovaginal yeast infections do not present with specific findings on vaginal examination, including the classic curdy cheese-like discharge often associated with Candida infections. As symptoms and signs of vulvovaginal candidiasis are often nonspecific, a laboratory diagnosis is often essential. Microscopic examination may aid with the diagnosis (Fig. 4.2b), but the precise species cannot be recognized; therefore, a culture is needed to identify the specific organism and confirm the diagnosis.

A single episode of yeast vulvovaginitis can cause a short duration of pain. However, 5–8 % of adult women suffer from intractable or recurrent candidal vulvovaginitis (RVVC), which is defined as four or more symptomatic episodes of infection in 12 months. Evaluation of patients for RVVC usually fails to reveal the precipitating cause such as uncontrolled diabetes, immunosuppression, excess of estrogen, or antibiotic usage [6]. The recurrence is believed to result from reinfection or relapse, implying incomplete clearance of candida from the vagina. In such a situation, treatment is directed at control rather than cure, and requires long-term maintenance therapy with a suppressive prophylactic agent [7]. Because of the chronic nature of therapy for RVVC, oral treatments are most useful. The recommended regimen is a weekly oral dose of fluconazole 150 mg. Alternatively, topical prophylactic treatment consists of weekly 500 mg clotrimazole suppositories [8].

Trichomoniasis , a sexually transmitted disease, is caused by the protozoan Trichomonas vaginalis. Severity ranges from an asymptomatic carrier state to severe inflammatory vaginitis. Patients may complain of malodorous, yellow-green discharge with vulvar irritation, itch, and dyspareunia. However, many women are asymptomatic [9]. Findings may be absent but are typically characterized by diffuse vaginal erythema and profuse purulent vaginal discharge.

None of the clinical features of trichomonas vaginitis is sufficiently specific to allow for a diagnosis based on signs and symptoms alone; therefore, the definitive diagnosis requires isolation of the organism (Fig. 4.2c). The sensitivity for diagnosing vaginal trichomoniasis by microscopy is low (60–70 %) but for optimal results it is recommended to immediately evaluate a fresh sample of vaginal discharge using a microscope. Other available laboratory methods used for diagnosis include culture, PCR assays, immunochromatographic capillary flow dipstick technology (the OSOM Trichomonas Rapid Test), and more. The recommended treatment is oral metronidazole or tinidazole.

Vulvoaginal atrophy results from inadequate estrogen levels in the vagina. While dyspareunia may affect 10–15 % of fertile women, it affects up to 39 % of postmenopausal women [10]. In this age group, dyspareunia is attributed mainly to vaginal atrophy. Vulvovaginal atrophy occurs most commonly with menopause but can occur due to lactation, medicines, and occasionally, due to usage of extra-low dose contraceptive pills [11]. Estrogen plays a major role in maintaining the normal vaginal environment. Estrogen withdrawal induces significant changes in the vagina causing it to become pale, thin, and less flexible [12]. As a result, blood flow diminishes, secretions decrease, vaginal flora changes, and pH increases. These changes predispose menopausal women to potential dyspareunia through several mechanisms. Vaginal dryness causes increased friction during intercourse. The thin vaginal walls are friable and prone to mechanical damage and formation of petechiae, ulcerations, and tears occurring with sexual activity. With long-standing estrogen deficiency, the vagina may become shorter, narrower, and less elastic. All of these changes increase the likelihood of trauma, infection, and pain. Furthermore, changes occurring with aging, such as subcutaneous fat loss and decreased skin lipid production, can result in slower healing after injury. Age dependent hypotonia and hypertonia of the pelvic floor muscles can also contribute to dyspareunia [13]. Patients with atrophy may complain of dryness, itching, discharge, pain, dyspareunia, and irritative urinary symptoms [12]. Symptoms are usually progressive and do not resolve spontaneously. Diagnosis is made by identifying characteristics changes on physical examination, noting an elevated vaginal pH and the presence of parabasal cells on microscopy (Fig. 4.2d) [14].

The primary goal of treating symptomatic vaginal atrophy is to alleviate symptoms. First-line therapies include nonhormonal, long-acting vaginal moisturizers and low-dose vaginal estrogen. For women with symptomatic vulvovaginal atrophy who prefer a nonvaginal therapy, transdermal and oral hormone therapy as well as the selective estrogen-receptor modulator, ospemifene, are options [15]. Because the overall dose of estrogen is low and is associated with less absorption, topical estrogen is generally considered safer and is less worrisome to patients. Atrophic changes, including those observed with microscopy, are rapidly and markedly reversed with topical estrogen therapies. Intravaginal estrogen preparations may be insufficient if vestibular symptoms are predominant. This results from preferential distribution of the absorbed hormones to the uterus. The hormonal preparation should be placed in the outer third of the vagina for best clinical results [16].

Desquamative inflammatory vaginitis [14] (DIV) is a rare cause of noninfectious, purulent vaginitis. Its diagnosis is based on symptoms, signs, and laboratory findings that are nonspecific. DIV is a chronic condition , as most patients will have complaints for more than a year before being diagnosed. The most common manifestation of DIV is copious, purulent vaginal discharge. However, 90 % of sexually active patients complain of dyspareunia [17]. As DIV is primarily a vaginal condition, the pain is mainly with thrusting. However, when DIV causes vestibular inflammation or erosions, patients may have pain with intromission as well. Some patients may not know they have dyspareunia because they have ceased having intercourse due to the abnormal discharge. Other symptoms include vulvovaginal burning and irritation [17].

On physical examination , patients may exhibit findings of vulvar erythema and introital ecchymotic spots. A vaginal examination typically reveals diffuse erythema and a purulent yellow or green vaginal discharge (Fig. 4.3b), occasional ecchymotic spots (usually located in the inner third of the vagina), and colpitis macularis. Similar to vaginal atrophy, the pH is elevated and microscopy shows parabasal cells, but there is a marked increase in inflammatory cells (a ratio of inflammatory cells to epithelial cells >1:1), as well as vaginal flora abnormality with the loss of dominant lactobacillus morphotype (Fig. 4.2e) [18].

The differential diagnosis for DIV includes other disorders causing purulent vaginitis. These include infectious vaginitis such as trichomoniasis and Group A Streptococcal vaginitis, dermatologic disorders such as erosive lichen planus and mucosal blistering disorders and usage of chemical irritants. It is therefore essential to exclude other etiologies before confirming diagnosis.

Because of the similarities between vaginal atrophy and DIV, it may be difficult to distinguish them from each another. With atrophy, the epithelial surface remains intact, and response to local estrogen therapy is usually rapid. Thus, failure to reverse the abnormal appearance of the vulvar vestibule or vagina and consequent symptoms with topical estrogen therapy constitutes a diagnostic test.

Little is known regarding etiology, treatment options and long-term follow-up. Both topical vaginal clindamycin and vaginal corticosteroids have anti-inflammatory affect and are useful for treating DIV; the choice of treatment should consider the availability and cost of these medications [18]. The treatment , either topical clindamycin or corticosteroids, is administered daily for 2–4 weeks. Initial therapeutic response is extremely encouraging, with 86 % of patients experiencing dramatic improvement; however, relapse and chronic manifestations frequently require long-term topical therapy [18].

Contact dermatitis is an inflammation of the skin due to exposure to an exogenous agent acting as primary irritant or an allergen. As vulvar tissue is more susceptible to irritants than other tissues, contact dermatitis is common and can complicate all other vulvovaginal conditions. Common vulvar irritants include soaps, panty liners, wet wipes, menstrual hygiene products (pads and tampons), toilet paper, laundry detergents, fabric softeners, cosmetics, spermicides, condoms, lubricants, urine, sweat, and topical medications.

Symptoms are of nonspecific inflammation, and include burning, itching, pain, and fissuring of vulvar tissue. Diagnosis is based on detailed history, exclusion of infectious causes, and high level of suspicion. Physical findings may range from mild erythema (Fig. 4.3c) to severe inflammation (erythema, edema, and fissures), sometimes with a secondary infection. Finalizing the diagnosis may require a biopsy to rule out coexisting conditions. Patch testing may be helpful in cases of allergic contact dermatitis.

Lichen sclerosus (LS) is a chronic, inflammatory skin disorder affecting 0.1–1.7 % of women [19] with a distinct predilection for the anogenital region. The mean age at onset of symptoms is 45.5 years, but LS may appear at any age, with 9 % of women experiencing onset of LS in prepuberty, 41 % in the reproductive years, and 50 % postmenopausal [20]. The etiology of LS has not yet been adequately explained, but there is increasing evidence that autoimmune mechanisms play a pathogenic role, with a possible genetic susceptibility.

LS is usually a scarring, chronic progressive or relapsing and remitting, lifelong condition. The characteristic sites involved are the interlabial sulci, labia minora, labia majora, clitoris, clitoral hood, perineum, and perianal area, giving rise to the characteristic “figure-of-eight” appearance. Alternatively, it may involve only small areas of skin. Typically, there is no vaginal involvement.

The typical lesions are porcelain-white papules and plaques with hyperkeratosis. The area evolves into a dry, hypopigmented, sclerotic, and later atrophic lesion. LS causes scarring of vulvar tissue, with loss of normal architecture including disappearance and fusion of labia minora, clitoral adhesions, sealing of the clitoral hood, burying of the clitoris, and narrowing of the introital opening (Fig. 4.3d). Otherwise, it can appear as nonspecific erythema, edema, erosions, fissuring, purpura, and ecchymoses. Tearing during sexual intercourse or physical examination is common.

Clinically, while 10–20 % of patients are asymptomatic, most patients present with itch, chronic scratching, pain, soreness, and dysuria. A high proportion of women report significant sexual difficulties including dyspareunia and apareunia due to continuing inflammatory disease as well as due to anatomic changes and scarring from long-standing active disease.

The diagnosis of LS is usually clinical, and when features are typical, histologic examination is not always essential. However, in the early stages of the disease the diagnosis can be difficult and a biopsy is required.