CHAPTER 4: Benign Disorders of the Lower Genital Tract

The lower reproductive tract, comprising the vulva, vagina, and cervix, exhibits a wide spectrum of benign and neoplastic diseases. Disorder characteristics often overlap, and thus differentiating normal variants, benign disease, and potentially serious lesions can be challenging. Lower reproductive tract infection is a frequent cause and discussed in Chapter 3, whereas congenital anomalies and preinvasive neoplasia are infrequent and described in Chapters 18 and 29. The benign lesions highlighted in this chapter are common, and mastery of their identification and treatment is essential.

Vulvar skin is more permeable than surrounding tissues because of differences in structure, hydration, occlusion, and friction susceptibility (Farage, 2004). Accordingly, pathology can develop in this area, although frequency estimates are difficult because of patient underreporting and clinician misdiagnosis. Lesions may result from allergen or irritant exposure, infection, trauma, or neoplasia. As a result, symptoms may be acute or chronic and include pain, pruritus, dyspareunia, bleeding, and discharge. Effective therapies are available for most disorders, yet embarrassment and fear may prove significant roadblocks to care for many women.

General Approach to Vulvar Complaints

The initial encounter includes reassurance that the patient’s complaints will be investigated thoroughly. Women often minimize and may be uncomfortable with describing their symptoms. They may relate protracted histories of assorted diagnoses and treatments by numerous providers and may voice frustration and doubt that relief is possible. Patients are not promised a cure but rather that every effort will be made to alleviate their symptoms. This can require multiple visits, tissue sampling, treatment attempts, and even a multidisciplinary plan. A patient-provider partnership approach to management enhances compliance and care satisfaction.

During counseling, the suspected diagnosis, current treatment plan, and recommended vulvar skin care are outlined. Printed materials that explain common conditions, medication use, and skin care are helpful. Patients are often relieved to learn that their complaints and conditions are not unique. Thus, referral to national websites and support groups is usually welcomed.

Diagnosis

History

Scheduling adequate time for the initial evaluation is a wise investment, as detailed information is essential. Symptom characterization includes descriptions of abnormal sensations, duration, precise location, and associated vaginal pruritus or discharge. Patients often refer to vulvar pruritus as vaginal, and symptom location should be clarified. A thorough medical history addresses systemic illnesses, medications, and known allergies. Obstetric, sexual, and psychosocial histories and any potentially provocative events around the time of symptom onset often suggest etiologies. Hygiene and sexual practices should be investigated in detail.

Of symptoms, vulvar pruritus is frequent with many dermatoses. Patients may have been previously diagnosed with psoriasis, eczema, or dermatitis at other body sites. Isolated vulvar pruritus may be associated with a new medication. Patients may identify foods that provoke or intensify symptoms, and in such cases, a food diary may be helpful. Most often, vulvar pruritus is due to a contact or allergic dermatitis. Common offenders include strongly scented body soaps and laundry products. Excessive washing and use of wash cloths can result in skin drying and mechanical trauma. Washing often becomes more aggressive with pruritus as patients assume their hygiene is lacking. Any of these practices can create an escalating itch-scratch cycle or exacerbate the symptoms of other preexisting dermatoses. Last, patients frequently use nonprescription remedies for relief of vulvovaginal itching or perceived odor. These products commonly contain multiple known contact allergens, and their use is discouraged (Table 4-1).

Physical Examination

Examination of the vulva and surrounding skin is completed using adequate lighting, optimal patient positioning, and a magnifying lens or colposcope. Both focal and generalized skin changes are carefully noted, as neoplasia may arise within a field of generalized dermatosis. Abnormal pigmentation, skin texture, nodularity, or vascularity is evaluated. Touch with a small probe such as a cotton swab defines the anatomic boundaries of generalized symptoms and precisely locates focal complaints (Fig. 4-1). A medical record diagram noting vulvar findings and symptoms aids treatment assessment over time.

Vaginal complaints or vulvar conditions without obvious etiology typically prompt vaginal examination. Careful inspection may reveal generalized inflammation or atrophy, abnormal discharge, or focal mucosal lesions such as ulcers. In these cases, saline preparation of secretions for microscopic evaluation (“wet prep”), vaginal pH testing, and aerobic culture to detect yeast overgrowth are collected. A general skin examination, including the oral mucosa and axillae, may suggest the cause of some vulvar conditions. A focused neurologic examination to evaluate lower extremity sensation and strength as well as perineal sensation and tone may help evaluate vulvar dysesthesias.

Vulvar Biopsy

Vulvar skin changes are frequently nonspecific and typically require biopsy for accurate diagnosis. Biopsy is strongly considered if the cause of symptoms is not obvious; if initial empiric treatment fails; if the cause of symptoms is not obvious; or if focal, exophytic, or hyper-/hypopigmented lesions are present. During biopsy, ulcerative lesions are sampled at their edges, and hyper- or hypopigmented areas at their thickest region (Mirowski, 2004). Conditions with variable histologic appearance may require multiple biopsies for correct disorder classification.

The steps for vulvar biopsy are shown in Figure 4-2. First, the biopsy site is cleaned with an antimicrobial agent and infiltrated with a 1- or 2-percent lidocaine solution. Biopsy is performed most easily with a Keyes skin punch. The open, circular blade is designed to remove a shallow disc of tissue when gently pressed against the skin and rotated. Keyes punches are available in various diameters, ranging from 2 to 6 mm, and size selection is based on lesion dimensions and on whether sampling or excision is the goal. Vulvar skin and lesion thicknesses are variable, and over-rotation of or undue pressure on the Keyes punch is avoided. Too deep a biopsy will leave a depressed scar. Rotation and pressure should stop when decreased resistance is felt, signaling the dermis has been reached. The tissue disc core is then freed at its base with fine scissors. Larger punch biopsies (4 to 6 mm) may require closure with an absorbable suture.

For raised or pedunculated lesions, fine scissors may be used. Occasionally, a No. 15 blade scalpel is selected for larger focal lesions. Tissue is excised parallel to the natural vulvar skin folds, and the defect is sutured to aid healing and minimize scarring. Larger lesions, for which simple closure would create significant incision tension, are best excised by clinicians experienced in more advanced plastic surgery techniques.

Following biopsy, bleeding may be controlled with direct pressure, silver nitrate stick, or Monsel paste. Silver nitrate may permanently discolor the skin, which may upset the patient and confuse subsequent examinations. If needed, simple interrupted stitches using a fine, rapidly absorbable suture provide hemostasis and edge approximation. Nonnarcotic oral analgesics usually suffice to relieve postbiopsy discomfort.

The International Society for the Study of Vulvovaginal Disease (ISSVD) provides classification systems for vulvar abnormalities. Their 2006 Classification of Vulvar Dermatoses specifically focuses on dermatoses and divides these based on biopsy-obtained histology. Their more recent terminology and organization system does not supplant the 2006 system. Instead, it classifies a broader group of dermatologic disorders that includes dermatoses, infections, and neoplasias by their similar clinical presentations to aid identification and management (Lynch, 2007, 2012). The next sections describe the more frequently encountered conditions.

Lichen Simplex Chronicus

An itch-scratch cycle typically leads to chronic trauma from rubbing and scratching (Lynch, 2004). Early examination reveals excoriations within a background of erythema. With chronic trauma, the skin responds by thickening, termed lichenification. Thus, in long-standing cases, vulvar skin is thick with exaggerated skin markings causing a leathery, gray appearance. Skin changes are usually bilateral and symmetric and may extend beyond the labia majora. Intense vulvar pruritus causes functional and psychologic distress, and sleep is often disrupted. Potential pruritus triggers include irritation from clothing, heat, or sweating; chemicals contained within hygiene products and topical medications; laundry products; and even food sensitivities (Virgili, 2003). A detailed history typically leads to the diagnosis.

Treatment involves halting the itch-scratch cycle. First, provocative stimuli are eliminated, and topical corticosteroid ointments help to reduce inflammation. In addition, lubricants, such as plain petrolatum or vegetable oil, and cool sitz baths help to restore the skin’s barrier function. Oral antihistamine use, trimmed fingernails, and cotton gloves worn at night can help decrease scratching during sleep. If symptoms fail to resolve within 1 to 3 weeks, biopsy is indicated to exclude other pathology. Histology classically shows thickening of both the epidermis (acanthosis) and the stratum corneum (hyperkeratosis). In these refractory cases, a trial of higher-potency corticosteroid may improve symptoms.

Lichen Sclerosus

This classically presents in postmenopausal women, although cases are less often found in premenopausal women, children, and men (Fig. 14-8). In a referral dermatologic clinic, lichen sclerosus was found in 1:300 to 1:1000 patients with a tendency toward whites (Wallace, 1971). Others estimate an incidence of childhood lichen sclerosus to be 1 in 900 (Powell, 2001).

The cause of lichen sclerosus remains unknown, although infectious, hormonal, genetic, and autoimmune etiologies have been suggested. Approximately 20 to 30 percent of patients with lichen sclerosus have other autoimmune disorders, such as Graves disease, types 1 and 2 diabetes mellitus, systemic lupus erythematosus, and achlorhydria, with or without pernicious anemia (Bor, 1969; Kahana, 1985; Poskitt, 1993). Accordingly, concurrent testing for these is indicated if other suggestive findings are present.

Diagnosis

Although sometimes asymptomatic, most individuals with lichen sclerosus complain of anogenital symptoms that often worsen at night. Inflammation of local terminal nerve fibers is suspected. Pruritus-induced scratching creates a vicious cycle that may lead to excoriations and vulvar skin thickening. Late symptoms can include burning and dyspareunia due to vulvar skin fragility and structural changes.

Perianal involvement is frequently seen. The typical white, atrophic papules may coalesce into porcelain-white plaques that distort normal vulvar anatomy. As a result, labia minora regression, clitoral concealment, urethral obstruction, and introital stenosis can develop. The skin generally appears thinned and crinkled. Over time, involvement may extend to the perineum and anus to form a “figure-eight” or “hourglass” shape (Fig. 4-3) (Clark, 1967). Thickened white plaques, areas of erythema, or nodularity should prompt biopsy to exclude preinvasive and malignant lesions. This characteristic clinical picture and histologic findings typically confirm the diagnosis. In long-standing cases, histologic findings may be nonspecific, and clinical suspicion will guide treatment.

Treatment and Surveillance

Curative therapies are not available for lichen sclerosus. Thus, treatment goals are symptom control and prevention of anatomic distortion. Despite its classification as a nonneoplastic dermatosis, patients with lichen sclerosus demonstrate an increased risk of vulvar malignancy. Malignant transformation within lichen sclerosus develops in 5 percent of patients. Histologic cellular atypia may precede a diagnosis of invasive squamous cell carcinoma (Scurry, 1997). Accordingly, lifetime surveillance of women with lichen sclerosus every 12 months is prudent (Neill, 2010). Persistently symptomatic, new, or changing lesions should be biopsied (American College of Obstetricians and Gynecologists, 2010).

As with all vulvar disorders, hygiene recommendations focus on minimizing chemical and mechanical skin irritation (Table 4-2). The chronicity of lichen sclerosus and lack of cure elicits an array of emotions. Support groups dedicated to this condition, such as that found at www.lichensclerosus.org, offer needed psychologic support.

Corticosteroids

First-line therapy for lichen sclerosus is an ultrapotent topical corticosteroid preparation such as 0.05-percent clobetasol propionate (Temovate) or 0.05-percent halobetasol propionate (Ultravate). Ointment formulations are preferred by some providers over creams due to their protective and less irritating properties (Table 4-3). Clobetasol propionate offers effective antiinflammatory, antipruritic, and vasoconstrictive properties. Theoretic adrenocorticosuppression and iatrogenic Cushing syndrome may be risks if it is used in large doses for extended periods.

Treatment initiation within 2 years of symptom onset usually prevents significant scarring, but no treatment scheme is universally accepted for topical corticosteroid use. The currently recommended dosing schedule of the British Association of Dermatologists is 0.05-percent clobetasol propionate once nightly for 4 weeks, followed by alternating nights for 4 weeks, and finally tapering to twice weekly for 4 weeks (Neill, 2010). After this initial therapy, recommendations for maintenance therapy vary and range from tapering corticosteroids to “as needed” use to ongoing once- or twice-weekly applications. During initial treatment, some patients may also require oral antihistamines or topical 2-percent lidocaine jelly particularly at night to control itching.

Corticosteroids can also be injected into affected areas, a treatment offered by specialty clinics familiar with techniques and potential complications. One study of eight patients evaluated the efficacy of once-monthly intralesional infiltration of 25 to 30 mg of triamcinolone hexacetonide for a total of 3 months. Severity scores decreased in all categories including symptoms, gross appearance, and histopathologic findings (Mazdisnian, 1999).

Other Topical Treatments

Estrogen cream is not a primary therapy for lichen sclerosus. However, its addition is indicated for menopausal atrophy, labial fusion, and dyspareunia. Testosterone ointment has failed to show efficacy in trials and is no longer recommended (Bornstein, 1998; Sideri, 1994).

Retinoids are reserved for severe, nonresponsive cases of lichen sclerosus or for patients intolerant of ultrapotent corticosteroids. Topical tretinoin reduces hyperkeratosis, improves dysplastic changes, stimulates collagen and glycosaminoglycan synthesis, and induces local angiogenesis (Eichner, 1992; Kligman, 1986a,b; Varani, 1989). Virgili and colleagues (1995) evaluated the effects of topical 0.025-percent tretinoin (Retin-A, Renova) applied once daily, 5 days a week for 1 year. Complete remission of symptoms was seen in more than 75 percent of women. However, more than one quarter of patients experienced skin irritation, which is common with retinoids.

Topical calcineurin inhibitors such as tacrolimus (Protopic) and pimecrolimus (Elidel) have antiinflammatory and immunomodulating effects. These are indicated for moderate to severe eczema and have been evaluated for lichen sclerosus (Goldstein, 2011; Hengge, 2006). Moreover, these agents, compared with topical corticosteroids, theoretically lower the risk of skin atrophy, since collagen synthesis is unaffected (Assmann, 2003; Kunstfeld, 2003). However, from a double-blind, randomized, prospective study, Funaro and associates (2014) concluded that topical clobetasol propionate was more effective in treating vulvar lichen sclerosus than topical tacrolimus. In the face of recent Food and Drug Administration (FDA) concerns regarding its link to various cancers, clinicians should exercise caution when prescribing tacrolimus for extended periods (Food and Drug Administration, 2010).

Last, phototherapy after pretreatment using 5-aminolevulinic acid was investigated in one small series of 12 postmenopausal women with advanced lichen sclerosus. Significant reductions in patient symptoms and short-term improvement for up to 9 months were noted (Hillemanns, 1999).

Surgery

Surgical intervention should be reserved for significant sequelae and not for primary treatment of uncomplicated lichen sclerosus. For introital stenosis, Rouzier and coworkers (2002) described marked improvements in dyspareunia and quality of sexual intercourse if perineoplasty was performed (Section 43-22). Vaginal dilation and corticosteroids are recommended following most surgical corrections of introital stenosis. For clitoral adhesions, surgical dissection can be used to free the hood from the glans. Reagglutination can be averted using initial nightly application of ultrapotent topical corticosteroid ointment (Goldstein, 2007).

Inflammatory Dermatoses

Contact Dermatitis

A primary irritant or allergen creates vulvar skin inflammation, termed contact dermatitis (Fig. 4-4). This condition is common, and in unexplained cases of vulvar pruritus and inflammation, irritant contact dermatitis is diagnosed in up to 54 percent of patients (Fischer, 1996).

Irritant contact dermatitis classically presents as immediate burning and stinging upon exposure to an offending agent. In contrast, patients with allergic contact dermatitis experience a delayed onset and an intermittent course of pruritus and localized erythema, edema, and vesicles or bullae (Margesson, 2004). A detailed history will help distinguish between the two, and an inquiry for potential offending agents can help identify the irritant (see Table 4-1).

With allergic contact dermatitis, patch testing may aid in identifying responsible allergen(s). Alternative conditions, such as candidiasis, psoriasis, seborrheic dermatitis, and squamous cell carcinoma, can be excluded through appropriate use of cultures and biopsy.

Treatments for both entities involve elimination of the offending agent(s), restoration of the natural protective skin barrier, inflammation reduction, and scratch cessation (Table 4-4) (Farage, 2004; Margesson, 2004).

Intertrigo

Friction between moist skin surfaces produces this chronic condition. Found most often in genitocrural folds, intertrigo can also develop in the inguinal and intergluteal regions. Superimposed bacterial and fungal infections may complicate the condition.

The initial erythematous phase, if untreated, can progress to intense inflammation with erosions, exudate, fissuring, maceration, and crusting (Mistiaen, 2004). Symptoms typically include burning and itching. With long-standing intertrigo, hyperpigmentation and verrucous changes can develop.

Treatment entails the use of drying agents such as cornstarch and application of mild topical corticosteroids for inflammation. If skin changes do not respond, then seborrheic dermatitis, psoriasis, atopic dermatitis, pemphigus vegetans, or even scabies are considered. If the area is superinfected with bacteria or yeast, appropriate therapy is warranted.

To prevent recurrent outbreaks, obese patients are encouraged to lose weight. Other preventions include light-weight, loose-fitting clothing made of natural fibers, improved ventilation, and thorough drying between skin folds after bathing (Janniger, 2005).

Atopic Eczema

Classically presenting in the first 5 years of life, atopic dermatitis is a severe pruritic dermatitis that follows a chronic, relapsing course. Scaly patches with fissuring are evident. Individuals with atopic eczema may later develop allergic rhinitis and asthma (Spergel, 2003).

Topical corticosteroids and immunomodulators, such as tacrolimus, can control flares (Leung, 2004). For dry skin, moisturizing with emollients can offer relief.

Psoriasis

Approximately 1 to 2 percent of the United States’ population is affected by psoriasis (Gelfand, 2005). Psoriasis is a T-cell—mediated autoimmune process in which proinflammatory cytokines induce keratinocyte and endothelial cell proliferation. Thick, red plaques covered with silvery scales are generally found on extensor limb surfaces. Occasionally, lesions involve the mons pubis or labia (Fig. 4-5). Psoriasis can be exacerbated by nervous stress and menses, with remissions experienced during summer months and pregnancy. Pruritus may be minimal or absent, and this condition is often diagnosed by skin findings alone.

Several treatments are available, and topical corticosteroids are widely used because of their rapid efficacy. High-potency corticosteroids are applied to affected areas twice daily for 2 to 4 weeks and then reduced to weekly applications. Diminishing response and skin atrophy are potential disadvantages of long-term corticosteroid use, and recalcitrant cases are best managed by a dermatologist. Vitamin D analogues, such as calcipotriene (Dovonex), although similar in efficacy to potent corticosteroids, are frequently associated with local irritation but avoid skin atrophy (Smith, 2006). Phototherapy offers short-term relief, but long-term treatment plans require a multidisciplinary team (Griffiths, 2000). For moderate to severe psoriasis, several FDA-approved immunomodulating biologic agents are available and include infliximab, adalimumab, etanercept, and ustekinumab (Smith, 2009).

Lichen Planus

This uncommon disease involves both cutaneous and mucosal surfaces and affects genders equally between ages 30 and 60 years (Mann, 1991). Although not completely understood, T-cell autoimmunity directed against basal keratinocytes is thought to underlie its pathogenesis (Goldstein, 2005). Vulvar lichen planus can present as one of three variants: (1) erosive, (2) papulosquamous, or (3) hypertrophic. Of these, erosive lichen planus is the most common vulvovaginal form and the most difficult variant to treat. Lichen planus may be drug-induced, and nonsteroidal antiinflammatory drugs, β-blocking agents, methyldopa, penicillamine, and quinine drugs have been implicated.

Diagnosis

Table 4-5 summarizes the most common imitators of lichen planus. Women typically complain of chronic vaginal discharge with intense vulvovaginal pruritus, burning pain, dyspareunia, and postcoital bleeding. On inspection, papules classically are brightly erythematous or violaceous, flat-topped, shiny polygons most commonly found on the trunk, buccal mucosa, or flexor surfaces of the extremities (Goldstein, 2005; Zellis, 1996). Lacy, white striations (Wickham striae) are frequently found in conjunction with the papules and may also be present on the buccal mucosa (Fig. 4-6). Deep, painful erosions in the posterior vestibule can extend to the labia, resulting in agglutination. With speculum insertion, vulvar skin and vaginal mucosa bleed easily. Vaginal erosions can produce adhesions and synechiae, which may lead to vaginal obliteration.

Women with suspected lichen planus require a thorough dermatologic survey looking for extragenital lesions. Nearly one quarter of women with oral lesions will have vulvovaginal involvement, and most with erosive vulvovaginal lichen planus will have oral involvement (Pelisse, 1989). Diagnosis is confirmed by biopsy.

Vulvar Lichen Planus Treatment

Pharmacotherapy remains the first-line treatment for this condition. Additionally, vulvar care measures, discontinuing any medications associated with lichenoid changes, and psychologic support should be instituted.

Erosive vulvar lichen planus is treated initially with ultrapotent topical corticosteroid ointments, such as 0.05-percent clobetasol propionate applied daily for up to 3 months, and then slowly tapered. Refractory cases are common and may respond to a preparation containing 0.05-percent clobetasol butyrate, 3-percent oxytetracycline, and 100,000 U/g nystatin (Trimovate) (Cooper, 2006). Used in small case series, other beneficial agents include systemic corticosteroids, topical tacrolimus ointment, topical cyclosporine, and oral retinoids (Byrd, 2004; Eisen, 1990; Hersle, 1982; Morrison, 2002).

Vaginal Lichen Planus Treatment

Commonly prescribed to treat hemorrhoids, corticosteroid suppositories containing 25 mg of hydrocorti­sone used vaginally are helpful—specifically, if used twice daily and then tapered to maintain symptom remission (Anderson, 2002). For poorly responding patients, compounding pharmacies can provide a 100-mg hydrocortisone suppository. Potent corticosteroids are prescribed judiciously, as systemic absorption may lead to adrenocorticosuppression (Moyal-Barracco, 2004a). Combining local corticosteroid therapy with vaginal dilator use may help restore coital function in patients with moderate vaginal synechiae.

If topical medications fail, systemic treatment with prednisone 40 to 60 mg daily for up to 4 weeks may modulate symptoms (Moyal-Barracco, 2004a). Although no alternative systemic medications have been fully studied, methotrexate, hydroxychloroquine, and mycophenolate mofetil administered by providers familiar with their use are effective within a multidisciplinary approach (Eisen, 1993; Frieling, 2003; Lundqvist, 2002). Surgical adhesiolysis is a last resort. In general, vulvovaginal lichen planus is a chronic, recurrent disease for which symptomatic improvement is possible, but complete control is unlikely.

Hidradenitis Suppurativa

This chronic disease is manifested by recurrent papular lesions that may lead to abscess, fistula formation, and scarring predominantly in apocrine gland-bearing skin (Fig. 4-7). In order of frequency, affected areas include the axillae; inguinal, perianal, and perineal skin; inframammary regions; and retroauricular skin. Chronic inflammation obstructs skin follicles, with subsequent subcutaneous abscess formation, skin thickening, and deformity. Abscesses typically form sinus tracts, and the resulting disfigurement and chronic purulent drainage can be devastating physically, emotionally, and sexually.

The etiology of hidradenitis suppurativa is unknown. More than one quarter of patients will report a family history of the disease, and an autosomal dominant inheritance pattern has been hypothesized (der Werth, 2000). Although Mortimer and colleagues (1986) found higher plasma concentrations of androgens in women with hidradenitis suppurativa, others have been unable to replicate this finding (Barth, 1996).

Treatment of early cases includes local hygiene and weight reduction in patients who are obese along with topical or oral antibiotics and warm compresses. Used individually, appropriate long-term oral antibiotics and their dosages include: tetracycline, 500 mg twice daily; erythromycin, 500 mg twice daily; doxycycline, 100 mg twice daily; or minocycline, 100 mg twice daily. Topical 1-percent clindamycin solution applied twice daily may also be effective (Jemec, 1998). Additionally, a 10-week course of oral clindamycin, 300 mg twice daily, plus rifampicin, 600 mg twice daily, has shown efficacy (Gener, 2009).

As reviewed by Rhode and associates (2008), an arsenal of other treatment modalities has been reported with varying efficacies. These include cyproterone acetate (an antiandrogen available in Europe), corticosteroids, isotretinoin, cyclosporine, and infliximab. An evidence-based review of pharmacologic interventions provided by Alhusayen (2012) suggests antibacterials and anti-tumor necrosis factor therapy are effective for hidradenitis. In late 2015, the FDA approved Humira (adalimumab) for the treatment of moderate to severe hidradenitis. Nonmedical therapies include laser and phototherapy. Severe, refractory cases may require surgical excision that often involves extensive resection of the vulva and surrounding areas. Plastic surgery techniques are often needed to close these large defects. Unfortunately, postoperative local recurrences can develop.

Aphthous Ulcers

Nearly 25 percent of women in the second and third decade of life will experience these self-limited mucosal lesions. Classically found on nonkeratinized oral mucosa, aphthous ulcers may also develop on vulvovaginal surfaces. Lesions are painful and can recur every few months. Distinguishing an aphthous ulcer from genital herpes may require appropriate cultures, serologies, and/or biopsies. Histologically, aphthous ulcers are composed of a mononuclear infiltrate with a fibrin coating. Although the etiology is unknown, some theorize the origin to be immune-mediated epithelial cell damage (Rogers, 1997). Other described triggers include stress, trauma, infection, hormonal fluctuation, and nutritional deficiencies of vitamin B₁₂, folate, iron, or zinc (Torgerson, 2006). Despite the normally self-limited nature of these ulcers, persistent lesions can lead to painful scarring (Rogers, 2003). Clinicians should consider human immunodeficiency virus testing when aphthae are large and slow to heal.

High-potency topical corticosteroids can be used at the onset of ulceration. Oral corticosteroids may be used to decrease inflammation in cases resistant to topical corticosteroids. Finally, colchicine, dapsone, and thalidomide have been shown to be effective, although they are rarely used.

Systemic illnesses may initially manifest on the vulvar or vaginal mucosa as bullous, solid, or ulcerative lesions. Examples include systemic lupus erythematosus, erythema multiforme (Stevens-Johnson syndrome), pemphigus, pemphigoid, and sarcoidosis. A thorough history and physical examination usually suffice to link genital lesions with preexisting conditions. However, biopsy of vulvovaginal lesions may provide a new and unexpected diagnosis if the disorder has not yet become evident elsewhere.

Acanthosis Nigricans

This condition is characterized by velvety to warty, brown to black, poorly marginated plaques. These changes are typically found at skin flexures, especially on the neck, axillae, and genitocrural folds (Fig. 17-6).

Acanthosis nigricans is commonly associated with obesity, diabetes mellitus, and polycystic ovarian syndrome. Thus, if signs or symptoms of these are present, appropriate evaluation is warranted. Common to these conditions, insulin resistance with compensatory hyperinsulinemia is thought to promote the skin thickening of acanthosis nigricans. Insulin binds to insulin-like growth factor (IGF) receptors and leads to keratinocyte and dermal fibroblast proliferation (Hermanns-Le, 2004). Less commonly, acanthosis nigricans is caused by other insulin-resistance or fibroblast growth-factor disorders, as reviewed by Saraiya (2013).

Treatment of acanthosis nigricans has not been evaluated in randomized trials. However, weight loss can ameliorate insulin resistance, which may lead to plaque improvement. In those prescribed metformin for glucose control, improved acanthosis nigricans has been demonstrated (Romo, 2008). Topical keratinolytics and exfoliants may have benefit (Levy, 2012).

Crohn Disease

Up to one third of women with Crohn disease suffer from anogenital involvement, which may precede gastrointestinal (GI) symptoms and a Crohn disease diagnosis. Vulvar lesions are commonly “metastatic” in that they show typical Crohn disease granulomatous inflammation but are not contiguous with the GI involvement (Sides, 2013). However, vulvar and perianal abscesses and fistulae may extend directly from GI tract lesions. Four manifestation types are vulvar edema (usually asymmetrical), ulceration, hypertrophic lesions, and chronic abscesses (Barret, 2014). Linear “knife-cut” ulcerations and other lesions often affect inguinal, genitocrural, and interlabial folds (Fig. 4-8). All can be asymptomatic but may cause burning or pruritus.

Therapy for gastrointestinal Crohn disease generally benefits external Crohn lesions. Vulvar lesions unrelated to GI disease activity often respond to prolonged courses of oral metronidazole and corticosteroids. Anti-tumor necrosis factor alpha treatments have shown promising efficacy (Barret, 2014). Surgery often can be avoided or delayed with appropriate vulvar care, nutrition, and close collaboration with a gastroenterologist. Used as last resorts, excision of fistulous tracts or other refractory lesions and vulvectomy can be complicated by poor healing and scarring (Sides, 2013). Regardless of management, recurrence is common.

Behçet Disease

This rare, chronic, autoinflammatory, systemic vasculitis most commonly affects patients in their twenties and thirties and those of Asian or Middle Eastern descent. Behçet disease is characterized by mucocutaneous lesions (ocular, oral, and genital) and associated systemic vasculitis. Oral and genital ulcers appear similar to aphthous ulcers and generally heal within 7 to 10 days. Nevertheless, associated pain can be debilitating. Treatment for these lesions mirrors that for aphthous ulcers.

The exact etiology of Behçet disease remains unknown, although genetic and autoimmune etiologies are suspected. Vasculitis dominates the disease process, which may involve the brain, GI tract, joints, lungs, and great vessels. Accordingly, for those suspected of Behçet disease, referral to a rheumatologist for additional testing and treatment is recommended.

Benign variations of vulvar, perineal, and perianal skin pigmentation are commonly encountered, especially in women with darker skin. Diffuse areas of increased pigmentation are usually encountered on the labia minora and fourchette. Areas tend to be bilateral and symmetric and have an even tone and normal texture. With gentle stretching, the color attenuates evenly. This is also seen with pigment variation of chronic inflammatory dermatoses.

Various benign vulvar lesions may appear pigmented. These include benign melanosis, lentigenes, cherry hemangiomas, angiokeratomas, and seborrheic keratosis (Heller, 2013). Focal vulvar abnormalities raise concern for premalignant or malignant conditions, and prompt biopsy avoids diagnostic delay. As discussed in Chapter 29, high-grade intraepithelial neoplasia or invasive cancer can appear white (hyperkeratotic) or hyperpigmented and can present with or without symptoms. Melanoma is discussed in Chapter 31.

Nevus

Discrete, rounded, pigmented lesions, known as nevi or moles, are easily overlooked on the vulva. These warrant close surveillance as more than half of all melanomas arise from preexisting nevi (Kaufman, 2005). Congenital and dysplastic nevi have the most malignant potential.

Common nevi are classified into three groups: junctional, compound, and dermal, depending on whether the melanotic nevus cells are located at the epidermis-dermis junction, extend into the dermis, or evolve over time to reside entirely within the dermis. Dermal nevi may appear bluish or have normal skin coloration depending on the depth of the nevus cells and may be raised, papillary, or pedunculated.

Recommendations vary regarding biopsy of pigmented vulvar lesions. The American College of Obstetricians and Gynecologists (2008) recommends biopsy of all such lesions. Others suggest nevus-sampling criteria used elsewhere on the body in which asymmetry, uneven pigmentation, irregular borders, diameter >5 mm, and erosion or fissuring should prompt biopsy (Edwards, 2010). Burning or itching also raises concern. Histologic atypia requires full lesion excision with adequate margins. Anatomically challenging biopsies, as with periclitoral lesions, and physical or histologic atypia may prompt referral to clinicians with specialized knowledge and experience with such lesions. Small, bland nevi that are not biopsied warrant a careful descriptive or photographic entry in the medical record and surveillance at least annually until the lesion is deemed stable. Self-examination is encouraged, and changes in lesion or symptoms are important.

Vitiligo

Loss of epidermal melanocytes can result in depigmented skin, termed vitiligo (Fig. 4-9). No race or ethnicity has greater risks for vitiligo, but the disease may be more disfiguring and distressing for darker-skinned individuals (Grimes, 2005).

Although etiology remains unknown, genetic factors are the most likely cause (Zhang, 2005). Approximately 20 percent of patients have at least one affected first-degree relative. Vitiligo may be mediated by an autoimmune process that destroys melanocytes. Autoimmune diseases such as Hashimoto thyroiditis, Graves disease, diabetes mellitus, rheumatoid arthritis, psoriasis, and vulvar lichen sclerosus are associated with vitiligo (Boissy, 1997; Vrijman, 2012).

Most commonly, depigmentation is symmetric and generalized, although distribution may be acral (limbs, ears) or localized. Depigmentation progression over time is variable. Sometimes confused with the epithelial changes seen with lichen sclerosus, vitiligo preserves normal skin texture and contour and is otherwise asymptomatic. There is no cure for vitiligo, and spontaneous repigmentation is rare. Several treatments for vitiligo include narrowband ultraviolet (UV) B phototherapy, excimer laser therapy, and topical immunomodulators (Baciqalupi, 2012). Most cases are self-limited and explanation of the condition alone is often sufficient.

Most solid vulvar tumors are benign and arise from local tissue. Less commonly, malignant lesions arise on the vulva and are typically of squamous cell epithelial origin. Rarely, solid vulvar tumors develop as metastatic lesions. Accordingly, many growths warrant biopsy if not confidently diagnosed visually.

Epidermal and Dermal Lesions

Acrochordons, commonly known as skin tags, are benign, soft fibroepithelial lesions. Most often seen on the neck, axilla, or groin, these skin-colored polypoid masses are usually devoid of hair and generally measure 1 to 6 mm in diameter but can grow larger (Fig. 4-10). They are often mistaken for vulvar condylomata, and lack of therapeutic response should prompt removal for histologic analysis. Surgical removal is likewise recommended for chronic irritation or cosmetic concerns. Small lesions are easily removed under local anesthesia in an office setting. Acrochordons have been linked to diabetes mellitus, and insulin-mediated fibroblast proliferation may explain this relationship (Demir, 2002).

Seborrheic keratosis may be observed in women with concurrent lesions on the neck, face, or trunk. Sharply circumscribed, slightly raised lesions containing waxy material are typical. The malignant potential of these slow-growing lesions is minimal. Therefore, excision is offered only in cases of discomfort, disfigurement, or unclear diagnosis.

Keratoacanthoma is a rapidly growing keratinocyte proliferation originating in a pilosebaceous gland. Rarely developing on the vulva, lesions begin as firm, round papules that progress to a dome-shaped nodule with a central crater. Untreated, the lesion usually spontaneously regresses within 4 to 6 months and leaves only a slightly depressed scar. Controversy surrounds its malignant potential (Ko, 2010; Savage, 2014). Some consider keratoacanthoma benign, whereas others classify it as a well-differentiated squamous cell carcinoma. Nevertheless, its histologic resemblance to this cancer merits surgical excision in most cases with a 4- to 5-mm margin.

Syringoma is a benign eccrine (sweat gland) tumor found most frequently on the lower eyelid, neck, and face. Rarely, the vulva may be involved bilaterally with multiple 1- to 4-mm firm papules (Fig. 4-11). The clinical appearance of vulvar syringoma is not pathognomonic. Thus, vulvar punch biopsy will establish the diagnosis and exclude malignancy. Treatment is not required. However, for those with pruritus, mild-potency topical corticosteroids and antihistamines may be helpful. In those with refractory pruritus, surgical excision or lesion ablation may be offered.

Subcutaneous Masses

Leiomyoma of the vulva is a rare tumor felt to arise either from smooth muscle within the vulva’s erectile tissue or from transmigration through the round ligament. Surgical excision to exclude leiomyosarcoma is warranted (Nielsen, 1996).

Fibroma is a benign tumor rarely arising from deep vulvar connective tissue by fibroblast proliferation. Lesions are primarily found on the labia majora and range from 0.6 to 8 cm in diameter. Larger lesions often become pedunculated with a long stalk and may cause pain or dyspareunia. Surgical excision is indicated for symptomatic lesions or if the diagnosis is unclear.

Lipoma is a soft sessile or pedunculated mass composed of mature adipose cells. Similar to fibromas, observation is reasonable in the absence of patient complaints, although symptoms may prompt surgical excision. These lesions lack a fibrous connective tissue capsule. Thus, complete dissection may be complicated by bleeding and require a larger incision.

Ectopic breast tissue may develop along the theoretical milk lines, which extend bilaterally from the axilla through the breast and ventrally to the mons pubis. Uncommonly found in the vulva, extramammary breast tissue is hormonally sensitive and may enlarge in response to pregnancy or exogenous hormones. Uncommonly, these typically soft masses may also develop breast pathologies including fibroadenoma, Phyllodes tumor, Paget disease, and invasive adenocarcinoma.

Bartholin Gland Duct Cyst and Abscess

Mucus produced to lubricate the vulva originates in part from the Bartholin glands. Obstruction of this gland’s duct is common and may follow infection, trauma, mucus changes, or congenitally narrowed ducts. However, the underlying cause is often unclear.

In some cases, cyst contents may become infected and lead to abscess formation. These tend to develop in populations with demographic profiles similar to those at high risk for sexually transmitted infections (Aghajanian, 1994). However, a wide spectrum of organisms has been cultured. Escherichia coli is the most common isolate, but various other gram-positive and gram-negative aerobes and anaerobes are found (Kessous, 2013; Mattila 1994; Tanaka, 2005). Infrequently, Neisseria gonorrhoeae or Chlamydia trachomatis is identified.

Diagnosis and Treatment

Most Bartholin gland cysts are small and asymptomatic except for minor discomfort during sexual contact (Fig. 4-12). With larger or infected cysts, however, patients may complain of severe vulvar pain that precludes walking, sitting, or sexual activity (Fig. 3-18).

On physical examination, cysts typically are unilateral, round or ovoid, and fluctuant or tense. If infected, they display surrounding erythema and are tender. The mass is usually located in the inferior labia majora or lower vestibule. Whereas most cysts and abscesses lead to labial asymmetry, smaller cysts may be detected only by palpation. Bartholin abscesses on the verge of spontaneous decompression will exhibit an area of softening, where rupture will most likely occur.

Small, asymptomatic Bartholin gland duct cysts require no intervention except exclusion of neoplasia in women older than 40 years. However, a symptomatic cyst may be managed with one of several techniques. These include incision and drainage (I&D), marsupialization, and Bartholin gland excision, which are described and illustrated in Sections 43-6 through 43-8. Abscesses are treated with I&D or marsupialization.

Malignancy

After menopause, Bartholin gland duct cysts and abscesses are uncommon and should raise concern for neoplasia. However, carcinoma of the Bartholin gland is rare, and its incidence approximates 0.1 per 100,000 women (Visco, 1996). Most are squamous carcinomas or adenocarcinomas (Heller, 2014). Given the rarity of these cancers, Bartholin gland excision is typically not indicated. Alternatively, in women older than 40 years, drainage of the cyst and biopsy of cyst wall sites adequately excludes malignancy (Visco, 1996).

Urethral Diverticulum and Skene Gland

Ductal occlusion of the Skene gland or paraurethral glands may lead to paraurethral cystic enlargement and possible abscess formation. Their symptoms and treatment are described in Chapter 26.

Epidermoid Cysts

These cysts, also known as epidermal inclusion or sebaceous cysts, are commonly found on the vulva, and less so in the vagina. Although histologically similar and lined by squamous epithelium, it is unclear if they represent separate entities. Vulvar epidermoid cysts typically form from plugged pilosebaceous units (Fig. 4-13). However, epidermoid cysts can also follow traumatic implantation of epidermal cells into deeper tissues. These cysts are variable in size, typically round or ovoid, and skin colored, yellow, or white. Generally, cysts are filled with viscous, gritty, or caseous foul-smelling material. Epidermoid cysts are generally asymptomatic and require no further evaluation. If symptomatic or secondarily infected, incision and drainage is recommended.

In 2003, the ISSVD defined vulvodynia as “vulvar discomfort, most often described as burning pain, occurring in the absence of relevant visible findings or a specific, clinically identifiable, neurologic disorder” (Table 4-6)(Moyal-Barracco, 2004b). The term vestibulitis was eliminated from ISSVD terminology since inflammatory changes have not been consistently documented. Vulvar pain is described as spontaneous (unprovoked), triggered by physical pressure (provoked), or mixed. Vulvar pain described by most patients as burning, stinging, or a raw irritation is further categorized as localized or generalized.

Limited studies indicate a prevalence of vulvodynia in the general population of 3 to 11 percent (Lavy, 2007; Reed, 2004, 2014). Women from all ethnicities and a wide age range are affected. One study estimated that each year approximately 1 in 50 women will develop vulvodynia (Reed, 2008).

Vulvodynia’s underlying cause is likely multifactorial and variable among individuals (Stockdale, 2014). Suspected risk factors, such as oral contraceptive pill use, genetic or immune factors, or infection (chronic yeast or human papillomavirus), remain unsupported by evidence. Whether predominantly physical or psychosocial factors trigger the pain is controversial, with strong arguments on both sides (Gunter, 2007; Lynch, 2008). Most theories propose that some local injury or noxious stimulus results in maladaptive local and/or central nervous system responses leading to a neuropathic pain syndrome (Chap. 11). Interestingly, patients with vulvodynia have an increased prevalence of other chronic pain disorders, including interstitial cystitis, irritable bowel syndrome, fibromyalgia, and temporomandibular pain (Kennedy, 2005; Reed, 2012).

Diagnosis

Typically, evaluation and management attempts are delayed for years due to patient embarrassment, attempts at self-treatment, and lack of knowledge that it is a medical condition. Diagnosis and treatment delays, often by multiple providers, are common (Harlow, 2003, 2014).

An evidence-based algorithm for the diagnosis of vulvodynia is provided in Figure 4-14 (Haefner, 2005). Given that vulvodynia is a diagnosis of exclusion, an extensive history is critical to securing the correct diagnosis (Table 4-7) (American College of Obstetricians and Gynecologists, 2008).

Vulvodynia refers to vulvar discomfort of at least 3 to 6 months duration without an identifiable cause. Generalized or localized vulvodynia is described variably as burning, rawness, itching, or cutting pain within affected areas (Bergeron, 2001). Pain may follow a touch stimulus (allodynia) such as tight clothing, undergarments, sexual contact, or pelvic examination. Sensations may be constant, intermittent, or episodic with exacerbations noted premenstrually (Arnold, 2006).

Questioning seeks to identify frequently associated comorbid conditions or other risk factors. These may include irritable bowel syndrome, interstitial cystitis, psychologic disorders (anxiety, depression, or posttraumatic stress disorder), or a history of infectious diseases such as herpes simplex or zoster. Documentation of past surgical procedures may help identify pudendal nerve injury. A sexual history may reveal clues of past or current abuse, unfavorable coital patterns, and contraceptive modalities that could provoke vulvodynia. Additionally, clinicians inquire about recurrent candidiasis; prior genital trauma, including childbirth-related injuries; and current hygiene practices. Specifically, questions regarding use of feminine hygiene products, panty liners, laundry and body soaps, bath additives, shaving, and type of undergarment fabric worn can be helpful. Prior therapies are documented to avoid unnecessary treatment repetition.

By definition, vulvodynia lacks specific diagnostic physical signs. Therefore, a thorough examination excludes other possible pathologies. Inspection of the external vulva for lesions or irritation is followed by examination of the vestibule looking for focal, usually mild, erythema at vestibular gland openings. Use of a magnifying lens or colposcope and directed biopsies may be helpful. Of note, Bowen and colleagues (2008) found clinically relevant dermatoses in 61 percent of refractory vulvodynia patients referred to their tertiary care vulvovaginal clinic.

Systematic pain mapping of the vestibule, perineum, and inner thigh is completed, and documentation serves as a reference to assess treatment success (see Fig. 4-1). A cotton swab is used to check for allodynia and hyperesthesia. The swab end can first be unwound to form a cotton-fiber wisp. Subsequently, the wooden stick is broken to form a sharp point to retest the same areas. Pain scale scores are recorded and followed over time.

As a diagnosis of exclusion, no specific laboratory test can confirm vulvodynia, although a saline “wet prep” of vaginal secretions, vaginal pH testing, and appropriate cultures as clinically indicated for yeast and herpes virus help exclude underlying vulvovaginitis. Focal abnormalities typically prompt biopsy.

Treatment

Like other chronic pain conditions, vulvodynia is challenging to treat. Approximately one in 10 women with vulvodynia will experience spontaneous remission (Reed, 2008). Due to few well-designed, randomized clinical trials, no specific therapy for vulvodynia has demonstrated superiority. Often, a combination of several therapeutic approaches is required to stabilize and alleviate symptoms (Haefner, 2005; Landry, 2008). Without improvement, surgical excision is a final option. Treatment approaches to vulvodynia are described further by Haefner and associates (2005) and reviewed by Landry and colleagues (2008).

Behavioral Therapy

The first step in managing all vulvar disorders includes vulvar care as summarized in Table 4-2. Also, accurate medical information can help resolve some of the fears and questions associated with vulvodynia. The National Vulvodynia Association provides patient information and support and can be accessed online at www.nva.org.

Vulvodynia is currently seen as more complex than a simple psychosexual problem. Compared with the general population, no differences in marital contentment or psychologic distress are found (Bornstein, 1999). Nevertheless, early counseling includes a basic assessment of the intimate partner relationship and of sexual functioning. Education regarding foreplay, sexual positions, lubrication, and alternatives to vaginal intercourse is offered if potentially helpful.

Back pain, pelvic floor muscle spasm, or vaginismus may coexist with vulvodynia, and pelvic floor muscle examination is described and illustrated in Chapter 11. If coexistent, a physical therapist familiar with treating these concerns may provide internal and external massage, myofascial release techniques, acupressure, joint manipulation, electrical stimulation, therapeutic ultrasonography, and pelvic floor muscle retraining to improve symptoms (Bergeron, 2002).

Medications

Agents for vulvodynia treatment may be administered topically, orally, or intralesionally. Of topical agents, 5-percent lidocaine ointment applied sparingly to the vestibule 30 minutes prior to sexual intercourse can significantly decrease dyspareunia, and long-term use may promote healing by minimizing feedback pain amplification (Zolnoun, 2003). Numerous other topical anesthetic preparations are reported to have variable success. However, caution is exercised with benzocaine, which is associated with increased rates of contact dermatitis.

Eva and colleagues (2003) found decreased estrogen-receptor expression in women with vulvodynia. However, topical or intravaginal estrogen therapy has yielded mixed results.

As reported by Boardman and coworkers (2008), topical gabapentin cream is well-tolerated, effective, and avoids the potential side effects of systemic gabapentin therapy. In their study, 0.5 mL of a compounded 2-, 4-, or 6-percent gabapentin-containing cream was applied three times daily for at least 8 weeks to affected vulvar areas.

The two major classes of oral medications reported to help vulvodynia are antidepressants and anticonvulsants. However, polypharmacy is avoided by clinicians prescribing one drug at a time, and contraception use is required for reproductive- aged patients. Tricyclic antidepressants (TCAs) have become a first-line agent in the treatment of vulvodynia, and reported response rates may reach 47 percent (Munday, 2001). In our experience, amitriptyline started at doses between 5 and 25 mg orally nightly and increased as needed by 10 to 25 mg weekly yields the best results. Final daily doses do not exceed 150 to 200 mg. Importantly, compliance is encouraged during the nearly 4-week lag required to achieve significant pain relief.

Cases resistant to TCAs may be treated with the anticonvulsants gabapentin or carbamazepine (Table 11-5) (Ben David, 1999). Oral gabapentin is initiated at a dosage of 100 mg three times daily and gradually increased over 6 to 8 weeks to a maximal daily dose of 3600 mg. Pain is reassessed every 1 to 2 weeks (Haefner, 2005).

Although topical corticosteroids generally do not help patients with vulvodynia, injections using a combination of corticosteroids and local anesthetics have been used for localized vulvodynia (Mandal, 2010; Murina, 2001). Alternatively, botulinum toxin A injections into the levator ani muscles have been reported effective for vulvodynia-related vaginismus (Bertolasi, 2009).

Surgery

Women with vulvodynia who fail to improve despite aggressive medical therapy are candidates for surgery. Options include local excision of a precise pain locus, complete resection of the vestibule (vestibulectomy), or resection of the vestibule and perineum (perineoplasty) (Section 43-22). Traas and associates (2006) reported high success rates with vestibulectomy among women younger than 30 years. Perineoplasty is the most extensive of the three procedures. Its incision extends from just below the urethra to the perineal body, usually terminating above the anal orifice. This procedure may be selected if significant perineal scarring is suspected to contribute to dyspareunia. Overall, improvement rates for appropriately selected patients are high following vulvar excision procedures. However, surgery is reserved for those with severe, localized, long-standing vestibular pain who have failed significant attempts at conservative management.

Hematoma

This may develop in the relatively vascular vulva following straddle injury, trauma from coitus or assault, or vulvovaginal procedures. Hematomas may develop within subcutaneous tissues or within the superficial perineal pouch of the anterior perineal triangle (Fig. 38-26). Within the latter, laceration of the vestibular bulb, clitoral crus, or branches of the internal pudendal vessels may create a sizable mass (Fig. 4-15). Given the protected anatomic location and adipose padding of the labia majora, traumatic vulvar and vaginal injuries are rare in adults. These are much more frequent in children who lack such padding, and differentiating straddle injury and sexual abuse in children is often challenging, as injury patterns are not reliably discriminating.

Often requiring a general anesthetic, thorough examination of the vulva and vagina will estimate hematoma stability and the integrity of the surrounding bowel, bladder, urethra, and rectum. If there is no associated organ injury, the venous nature of most vulvar hematomas makes them candidates for conservative management with cool packs followed by sitz baths, pain control, and Foley catheter bladder drainage as needed. In general, vaginal hematomas measuring >4 cm or rapidly expanding are surgically explored to secure bleeding vessels. However, following incision and clot evacuation, a cavity is often seen without an identifiable bleeding vessel. To prevent reaccumulation, the cavity is closed in layers with absorbable or delayed-absorbable suture using a running or interrupted stitch closure.

Laceration

Penetrating trauma accounts for most vaginal injuries. Common causes include pelvic fracture, forced inanimate objects, coitus, and hydraulic forces such as those experienced with water skiing. Atrophic vaginal changes can predispose to injury.

With extensive laceration, examination under anesthesia is usually necessary to perform a thorough assessment and to exclude intraperitoneal damage. Moreover, if the peritoneal cavity has been breached, abdominal cavity exploration by laparotomy or laparoscopy is warranted to exclude visceral injury and supralevator or retroperitoneal hematoma.

Treatment goals include hemostasis and restoration of normal anatomy. Irrigation, debridement, and primary repair are key steps during initial management. The vaginal mucosa is typically reapproximated with running or interrupted stitches with absorbable or delayed-absorbable suture. Uncommonly, infection warrants laceration healing by secondary intention. Nonexpanding hematomas may be managed conservatively, whereas expanding masses often require evacuation and isolation of bleeding vessels. With laceration or hematoma, postoperatively, a vaginal pack can help tamponade any continued bleeding.

Foreign Body

Trauma or chronic irritation from a foreign body placed into the vagina can affect all ages. Objects vary by age group, and small objects may become lodged in a child’s vagina during play. An adolescent may be unable to retrieve or may be unaware of a vaginal tampon or piece of a broken condom. In adults, sexual misadventure or abuse can usually explain most objects found.

Three notable items include a retained tampon or contraceptive sponge and the vaginal pessary. Women with a retained tampon or sponge typically complain of foul-smelling vaginal discharge with some associated pruritus, discomfort, or unscheduled bleeding. A history of multiple unsuccessful retrieval attempts may be elicited. In the absence of a leukocytosis, fever, or evidence of endometritis or salpingitis, simple removal is sufficient treatment. Vaginal lavage to cleanse the vagina is not indicated and may actually increase the ascending infection risk. Toxic shock syndrome has been described with both tampons and contraceptive sponges, and its management is outlined in Chapter 3. Vaginal pessaries are frequently selected to conservatively treat pelvic organ prolapse or incontinence. Associated complications with these devices and their management are described fully in Chapter 24.

Desquamative Inflammatory Vaginitis

This uncommon, severe form of inflammatory vaginitis develops primarily in perimenopausal women, and white women appear most often affected. Although its etiology is unknown, it may represent a variant of erosive vaginal lichen planus (Edwards, 1988). Possible triggers include diarrhea or antibiotic use (Bradford, 2010). Patients typically complain of copious vaginal discharge, introital burning, and dyspareunia, all of which are refractory to common therapies. On examination, a diffuse, exudative, purulent yellow or green discharge is present on the vaginal walls and varying degrees of vestibular-vaginal erythema are noted. Microscopy reveals many polymorphonuclear and parabasal cells, but pathogens such as trichomonads or yeast forms are absent. The vaginal pH is elevated, and exclusionary test results for gonorrhea and chlamydial infection are negative. The profuse leukorrhea may lead to an erroneous diagnosis of pelvic inflammatory disease or cervicitis, but pelvic tenderness is absent. Although no randomized clinical trials are available, Sobel (2011) reports favorable outcomes with 2-percent intravaginal clindamycin cream or intravaginal hydrocortisone cream or suppositories for 4 to 6 weeks. Whether the efficacy of clindamycin is due to its antibacterial or its antiinflammatory properties is unknown (Bradford, 2010). Patients and clinicians should view this as a chronic condition with expectation of prolonged treatment courses, relapse, and need for retreatment.

Diethylstilbestrol-induced Reproductive Tract Abnormalities

In the mid-1900s, diethylstilbestrol (DES), a synthetic nonsteroidal estrogen, was prescribed to women in the United States for several pregnancy-related problems. Daughters exposed in utero to DES had congenital reproductive tract anomalies and demonstrated increased rates of vaginal clear cell adenocarcinoma (Herbst, 1971). More commonly, vaginal adenosis, areas of columnar epithelium within the vaginal squamous mucosa, are found in these women. Vaginal adenosis typically appears as red, granular patches. Symptoms include vaginal irritation, discharge, intermenstrual bleeding, and postcoital bleeding. A fuller discussion of DES-related defects is found in Chapter 18.

Gartner Duct Cyst

Most vaginal cysts are epidermoid cysts, urethral diverticula, or Gartner duct cysts. The last are uncommon vaginal cysts developing from mesonephric (wolffian) duct remnants (Chap. 18). They are typically asymptomatic and found within the lateral vaginal wall during routine examination. Symptoms, if present, include dyspareunia, vaginal pain, and difficulty inserting tampons. Examination reveals a tense cyst that is palpable or seen to bulge from beneath the vaginal wall. Observation is reasonable in most cases, although marsupialization or excision may be appropriate for symptomatic Gartner duct cysts.

Eversion

The squamocolumnar junction (SCJ) borders between the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix. As described and illustrated in Chapter 29, endocervical tissue in some women may migrate outward from the endocervical canal in a process termed eversion, thought to be hormonally mediated. As a result, the SCJ lies further distally from the external cervical os. Although eversion is a normal finding, asymmetry of the columnar epithelium surrounding the cervical os can mimic an erosive lesion, and cervical biopsy can aid clarification.

Nabothian Cyst

Mucus-secreting columnar cells line the endocervical canal. During squamous metaplasia, squamous epithelium may cover functional glandular cells and secretions may accumulate. As this benign process continues, smooth, clear, white or yellow, rounded elevations may form and are visible during routine examination (Fig. 4-16). They also are frequently seen as well-defined anechoic sonolucency along the endocervical canal (Fig. 2-14).

Nabothian cysts typically do not warrant therapy. However, if they grow large enough to make Pap testing or cervical examination difficult or cause symptoms, they can be opened with a biopsy forceps and drained. Moreover, if the diagnosis of a cervical mass is uncertain, biopsy for histologic confirmation is obtained.

Endocervical Polyp

One of the most common benign neoplasms of the cervix is a hyperplastic projection of endocervical tissue known as an endocervical polyp (Fig. 8-8). Lesions are usually found during routine pelvic examination. They are generally asymptomatic but may be associated with leukorrhea or postcoital spotting. Additional discussion and treatment options are found in Chapter 8.

Cervical Stenosis

This narrowing of the cervical canal or opening may be congenital or acquired. Congenital stenosis is rare and likely due to segmental müllerian hypoplasia (Chap. 18). In contrast, acquired stenosis is usually iatrogenic due to scarring after cervical excisional procedures such as cold-knife conization and loop electrosurgical excision. This complication is estimated to follow 1 to 2 percent of such procedures. Infection, neoplasia, severe atrophy, and radiation changes are rarer causes.

Diagnosis is based on symptoms and physical findings, as a precise and universally accepted definition is lacking. Symptoms of stenosis in menstruating women include dysmenorrhea, amenorrhea, and infertility. Postmenopausal women are usually asymptomatic until fluid, exudates, or blood accumulates behind the obstruction. The terms hydrometra (fluid), pyometra (pus), or hematometra (blood) are used to describe these conditions and are discussed additionally in Chapter 9. An inability to introduce a dilator into the endocervical canal is generally considered diagnostic. If obstruction is complete, a soft, enlarged uterus from trapped intracavitary fluid is sometimes palpable.

Cervical stenosis is relieved by introduction of dilators of progressively increasing diameter, which may require anesthesia. Preprocedural misoprostol may aid by softening the cervix (Chap. 41). In postmenopausal women, pretreatment for several weeks with vaginal estrogen cream may also assist dilatation. Moreover, sonographic guidance can help avert uterine perforation, especially in postmenopausal women (Christianson, 2008). If cervical stenosis is suspected as contributory to infertility, assisted reproduction techniques may be indicated as described in Chapter 20.