Vulvovaginitis

INTRODUCTION

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Background

Vulvovaginitis is the most common gynecologic condition seen by practitioners rendering primary care to women. The term vulvovaginitis is a semantic compromise that categorizes many vaginal infections as vulvovaginitis because the 2 are interrelated. Discharge, burning, and pruritus are the most common symptoms, accompanied by signs of vulvar irritation such as erythema and excoriation of the vulvar skin.

Traditionally, the 3 classic entities of vaginitis include bacterial vaginosis, Trichomonas infection, and candidiasis. However, this article focuses on topics that are primarily inflammatory disorders and affect the vulvar region.

Pathophysiology

The vulva, the external genitalia of the female, includes the labia majora and minora, the clitoris, and the vestibule of the vagina. During the reproductive years of a healthy woman's life, the vagina maintains a moist environment that is in constant fluctuation. The secretion of an alkaline transudate from the vaginal epithelium and cervical glands maintains this moist environment with a pH ranging from 3.8-4.5. In addition, the vagina and its microflora form a unique balanced environment that can change under pressure from external stimuli but returns to normal with removal of the stimuli. It can vary in degree during the menstrual cycle, pregnancy, and sexual activity.

The vaginal epithelium consists of 3 cell layers: superficial, intermediate, and basal. These cells are capable of storing glycogen under the influence of estrogen. Glycogen is available in the fully mature cells in the superficial layer of the epithelium. With elevated levels of either exogenous or endogenous estrogen, all levels of the epithelium thicken as a result of glycogen storage. With diminishing levels of estrogen, the layers become thin and atrophic.

In an adult woman's reproductive years, the bacterial flora of the healthy vagina contains numerous microorganisms, including aerobic and anaerobic gram-positive and gram-negative bacteria. Lactobacillus and Corynebacterium predominate over other bacteria such as Streptococcus, Bacteroides, Staphylococcus, and Peptostreptococcus. Both Lactobacillus and Corynebacterium produce lactic and acetic acid from glycogen, thus maintaining the low vaginal pH. Additional bacteria are kept in check by the acid-producing bacteria and are rarely pathogenic, but they may become pathogenic if the environmental balance is affected.

DIFFERENTIAL DIAGNOSIS

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The focus of this article includes Candida vulvovaginitis, atrophic vaginitis, contact dermatitis, pediatric vulvovaginitis, and vulvar vestibulitis.

The complete differential includes the following:

• Allergic reaction
• Physiologic leukorrhea
• Atopic dermatitis
• Lichen simplex chronicus
• Lichen sclerosus
• Paget disease
• Psoriasis
• Vulvodynia

In prepubertal girls with vaginal discharge, the following should be considered:

• Anatomic abnormality
• Foreign bodies
• Neoplasm
• Sexual abuse
• Hygiene

VULVOVAGINAL CANDIDIASIS

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In the United States, estimates indicate that approximately 50% of college-aged women will have an episode of vulvovaginal candidiasis. At some point in their lifetime, nearly 75% of all women experience an attack of Candida vulvovaginitis. Approximately half of these women have more than 1 episode, and a few have frequent relapses.

Etiology

Vulvovaginal candidiasis can be an acute, chronic, recurrent, or persistent condition that can involve the vulva, vagina, and adjacent crural areas. The specific causative agent belongs to the genus Candida. These organisms are found in almost all humans and many animals. An estimated 10-50% of reproductive-aged American women are considered opportunistic carriers. Candida albicans is identified approximately 85-90% of the time. Recently, an increased frequency of other Candida species, such as Candida glabrata, Candida tropicalis, and Candida krusei, has been reported.

Predisposing agents

Any host factor that affects the vaginal environment or vaginal secretions can play a role in the initiation of Candida vulvovaginitis. Pregnancy is one of the most common predisposing factors. Studies have demonstrated that up to one third of pregnant women worldwide on any day can be affected. The high levels of reproductive hormones and an increase in the glycogen content in the vaginal environment create a favorable environment for Candida species. In combination, these 2 changes provide an abundant source of carbon for candidal growth, germination, and adherence. Furthermore, the acidity of the pregnant vaginal flora can suppress the growth of other microorganisms that are naturally inhibitory to Candida. Although the initial attachment of the organism occurs more readily at high pH values (6-7), the germ tube formation and the development of mycelia are favored by a low vaginal pH (<5).

Older studies of women using high-dose estrogens in oral contraceptives found an increase in vaginal colonization by Candida. The mechanism is believed to be similar to that found in pregnancy. However, the newer oral contraceptives with a lower estrogen dose do not seem to predispose the patient to Candida vulvovaginitis.

Disorders associated with an altered immune response, such as acquired immunodeficiency syndrome (AIDS) and diabetes mellitus, also predispose to Candida vulvovaginitis.

Antimicrobials are thought to predispose a patient to Candida by reducing the number of protective resident vaginal bacteria. The most common offenders are broad-spectrum agents such as tetracycline, cephalosporins, and ampicillinlike agents.

A study by Horowitz et al in 1987 demonstrated Candida species in ejaculate fluid of partners of patients with recurrent Candida infections. They suggested that the carrier rate might be low. Traditionally, vulvovaginal candidiasis is not considered a sexually transmitted disease because it occurs in celibate women, and Candida itself is considered part of the normal vaginal flora.

Clinical

In acute vulvovaginal candidiasis, vulvar pruritus and burning are the main symptoms. Patients commonly complain of both symptoms after intercourse or upon urination. Dyspareunia may develop and become severe enough to lead to intolerance of intercourse. Physical findings include erythema and edema of the vestibule and labia majora and minora. The rash may extend to the thighs and to the perineum. Thrush patches usually are found loosely adherent to the vulva. A thick, white, curdlike vaginal discharge usually is present.

The clinical picture of chronic persistent candidiasis differs in that it includes marked edema and lichenification of the vulva with poorly defined margins. Often, a grayish sheen made up of epithelial cells and organism covers the area. Symptoms include severe pruritus, burning, irritation, and pain. This patient group usually is older, obese, and often has long-standing diabetes mellitus.

Diagnosis

The diagnosis depends both on the demonstration of a species of Candida and the presence of clinical symptoms. Diagnostic tests include a positive wet-mount test or potassium hydroxide preparation. Vaginal pH usually remains normal in vulvovaginal candidiasis.

The wet-mount test involves microscopic examination of vaginal discharge or scrapings from vulvar lesions mixed with physiological saline under both low-power and high-power magnifications. Under microscopic viewing, the spores and conidia are visible. The presence of yeast blastospores or pseudohyphae can be detected in approximately 30-50% of patients with symptomatic vulvovaginal candidiasis. Adding 10% potassium hydroxide to the solution lyses white blood cells, red blood cells, and vaginal epithelial cells, making the alkali-resistant branching budding hyphae of Candida easier to see. This method may increase the sensitivity; however, at least one third of patients with symptomatic candidiasis have negative findings with this method. Nevertheless, positive results from these 2 tests, in combination with a normal vaginal pH, are helpful in confirming the diagnosis.

Most studies demonstrate that 85-90% of vaginal isolates are C albicans. As a result, fungal cultures have not been used by most clinicians as part of the initial evaluation. The rationale is thought to be that using fungal cultures will be too sensitive and will detect yeast that may be colonizing the patient but not causing the symptoms.

Treatment

The cell wall of the organism is a complex glycoprotein that depends on the biosynthesis of ergosterol. Azole compounds found in antimycotic drugs are believed to block this step in biosynthesis. Topical antimycotic drugs can achieve cure rates in excess of 80%. The only oral azole agent approved for this indication by the US Food and Drug Administration (FDA) is fluconazole, which also achieves a high rate of cure. It achieves therapeutic concentrations in vaginal secretions for at least 72 hours after the ingestion of a single 150-mg tablet.

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Most women with vulvovaginal candidiasis usually respond quickly to one of the therapies described above. Despite therapy, recurrent vulvovaginal candidiasis, defined as 4 or more episodes of infection per year, can occur in less than 5% of healthy women. Recurrences may be caused by other species of Candida that are not equally susceptible to the usual first-line treatments. Appropriate fungal cultures may be taken to identify the species. Treatment entails longer courses of antimycotic therapy (10-14 d) regardless of the route of administration.

Several studies have shown the effectiveness of antifungal maintenance suppressive therapy for several months. Although an optimal regimen has not yet been established, regimens include ketoconazole (400 mg/d), itraconazole (50-100 mg/d), fluconazole (100 mg/wk) for 6 weeks, and clotrimazole (500-mg vaginal suppositories once per wk). These regimens have been used for up to 6 months.

Topical boric acid has been used for decades as a treatment for vulvovaginal candidiasis. Although it often is effective, it is classified as a poison and may be absorbed systematically through the vaginal mucosa. For protection, it is encapsulated in a gelatinous capsule and administered as a suppository. Treatment includes 600 mg in size 0 gelatin capsule intravaginally daily for 2 weeks.

ATROPHIC VAGINITIS

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Etiology

Extremely low estrogen production, as found after menopause or bilateral oophorectomy, can lead to atrophy of the vaginal and vulvar epithelium. Vulvovaginal atrophy is considered a natural process after estrogen withdrawal; atrophic vaginitis, however, is not.

During the perimenopausal period, estrogen secretion, primarily estradiol, remains at approximately 120 ng/L. After menopause, it decreases to approximately 18 ng/L. The reduction of endogenous estrogen causes thinning of the epithelium and a diminished glycogen content. Glycogen is necessary for rapid multiplication and maintenance of lactobacilli. The lack of glycogen contributes to a reduction in lactic acid production and an increase in vaginal pH, thus leading to the overgrowth of nonacidophilic species and the disappearance of Lactobacillus. In some patients, this new flora may include the introduction of bacteria that can incite a superficial infection in denuded regions and alter vaginal secretions.

In addition, during estrogen withdrawal, the papillae of the vagina flatten and the rugae nearly disappear, leaving the vagina relatively smooth. The mucosa becomes progressively thinner and eventually may become only a few cell layers thick. A moderately thick layer of intermediate cells may be present in some areas, with only a row of basal cells in others. Eventually, the vagina becomes denuded of epithelium.

Clinical

Clinical symptoms include vaginal soreness, postcoital burning, dyspareunia, burning leukorrhea, and occasional spotting. The most common symptom is vaginal spotting, which usually results from a break in the thin vaginal mucosa. Dyspareunia may result from ulceration of the vulvovaginal epithelium. The vagina is noted to be thin, with occasional petechia and diffuse redness with few or no vaginal folds. A serosanguinous discharge may be present, with a pH of 5-7. A wet mount often shows white blood cells and a paucity of Lactobacillus.

Treatment

Accumulating evidence indicates that the vaginal symptoms readily respond to estrogen treatment. With treatment, mucosal thickening with glandular function can be maintained well into the postmenopausal period. Estrogenic effect on vaginal cytology is quantified by using the maturation index by using vaginal smears from the lateral walls of the upper one third of the vagina.

Treatment usually entails the use of topical vaginal estrogen for 1-2 weeks to alleviate symptoms. An increase in superficial cells and vaginal maturation index occurs at levels of plasma estrogen that are barely above those of treatment. Once symptoms improve, continuation of treatment at decreased intervals is necessary for maintenance. An oral estrogen regimen also can be used.

Studies demonstrate that vaginal creams produce serum estradiol levels one-fourth that of oral estrogen but are 4-times more potent than oral estrogen on the vagina. However, data on the safety of vaginal estrogens and resulting plasma levels are limited.

Numerous studies have used different treatment regimens; treatment usually is selected based on clinician preference. The manufacturers of Premarin vaginal conjugated estrogen cream suggest 0.5-2 g applied 3-7 times per week for 3 weeks, followed by 1 week without, for 3-6 months.

The advantages of vaginal estrogen cream include lower plasma levels and that it is more efficacious than oral treatment. However, disadvantages include compliance issues due to the application process itself and its messiness. For this reason, the silastic vaginal ring (Estring) and vaginal tablets (Vagifem) were developed.

The vaginal ring is placed into the vagina to release controlled small doses of estrogen daily (7.5 mcg of estradiol). Serum estrogen is slightly increased but usually remains in the menopausal range. The ring has noted to be at least of equal efficacy to vaginal estrogen cream in regards to tissue integrity and patient acceptance. It is intended to be used continuously for 90 days and can be used during sexual intercourse.

Vagifem is a vaginal tablet that contains 25 g of 17-beta estradiol and has been demonstrated to be well tolerated and effective. In a 12-week, double-blind, randomized, placebo-controlled study by Eriksen et al, Vagifem was found to improve symptoms compared to placebo. Again, treatment is clinician-based, with a common regimen being 1 tablet daily followed by a twice-weekly maintenance application.

In regards to the risk of unopposed estrogen and risk of endometrial proliferation and possible subsequent endometrial carcinoma, studies, although short-term, have not demonstrated a risk. Estradiol levels in the range of less than 70 pmol/L have been shown to be associated with atrophy of the endometrium. These forms of estrogen all maintain plasma levels well below 30 pmol/L during steady state. Thus, the risk of endometrial carcinoma is considered minimal. However, one must note that these studies all have been short-term. Some authors recommend that either the course should be of short duration, or, if long, then a progesterone challenge test or biopsy may be indicated periodically.

Hormone replacement therapy is not the only option for postmenopausal women. Women who cannot or do not want to take hormones may decide to take nonpharmacological therapies, such as herbal treatments. Herbal treatments are used widely by women; however, they remain largely unstudied by the scientific community. A survey by the North American Menopause Society indicated that up to 10% of women use herbal therapies for menopausal symptoms.

Three agents that have been under study include dong quai, black cohosh, and isoflavones.

Many women in both Europe and the United States have used dong quai, a traditional Chinese herb extracted from the Angelica sinensis root, for menopausal symptoms. In a small study of 71 women with hot flashes, patients were given either dong quai daily (4.5 g) or placebo for 6 months. The study did not find a difference in endometrial thickness or in the vaginal maturation index between the 2 groups. Although women in both Europe and the United States use this herb alone, Chinese practitioners prescribe it in conjunction other herbs. Dermatitis secondary to photosensitization is a common adverse effect of this drug.

Black cohosh (Cimicifuga racemosa) is marketed as a precursor of progesterone that has estrogenlike effects. It is a phytoestrogen that contains triterpene, a flavonoid, and has been used in Germany for decades to treat menopausal symptoms. It has been found to reduce levels of luteinizing hormone, but not follicle-stimulating hormone, in menopausal women. According to a few studies, extract doses of either 2 tablets or 40 drops twice daily can safely reduce menopausal symptoms. Data are limited, and no data are available on toxicity. In rare cases, it can cause stomach upset. It has an additive hypotensive effect when combined with antihypertensives. The recommended dosage is for a maximum duration of 6 months.

Phytoestrogens are naturally occurring plant sterols that have both estrogenic and antiestrogenic effects in humans. They include isoflavones (found in soybeans), coumestans (found in red clover and alfalfa sprouts), and lignans (found in oil seeds such as flaxseed).

Phytoestrogens are absorbed and converted by the intestinal flora into compounds that resemble estrogen. They then bind with and activate human estrogen receptors. If endogenous estrogen levels are high, they exhibit antiestrogenic effects; however, in postmenopausal women in whom levels are diminished, they are found to exhibit estrogenic properties.

Interest in isoflavones escalated after observation that Asian women, who consume much more isoflavones than Western women, experience fewer menopausal symptoms. A small study of menopausal Thai women demonstrated that only 27% reported menopausal vasomotor symptoms as opposed to 85% of Western women.

Studies, although limited, have demonstrated small increases in vaginal superficial cells with the ingestion of isoflavone. However, no significant increase in follicle-stimulating hormone or luteinizing hormone has been demonstrated.

VULVAR VESTIBULITIS

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Etiology

The vestibule consists of nonpigmented and nonkeratinized squamous epithelium devoid of skin. It contains mucus-secreting minor vestibular glands, ductal orifices of the Bartholin glands, Skene glands, and the urethral meatus. It is within this region that the inflammatory entity vulvar vestibulitis arises.

Vulvar vestibulitis is a condition that was first recognized over a century ago. Skene described it in 1889 as a condition of "excessive sensitivity" and "hyperesthesia." Although recognized years ago, this condition remains poorly understood.

While many theories have been proposed, the etiology of this condition remains unknown. Vulvar vestibulitis was not widely recognized until Woodruff and Parmley reported it in the 1980s. They thought that the etiology was an infection of the vestibular glands that was best treated by perineoplasty. In 1988, Pyka et al studied surgically excised specimens of the vulvar vestibule of 41 patients diagnosed with vulvar vestibulitis. Pyka identified it in 66% of the specimens?minor vestibular glands. All of these glands demonstrated some degree of squamous metaplasia forming the vestibular clefts.

Freidrich coined the name vulvar vestibulitis in 1987. Other names noted in the literature include focal vulvitis, minor vestibulitis gland syndrome, periglandular vestibulitis, and erythematous vulvitis en plaques. Despite several different names, the classic definition according to Freidrich’s criteria includes the following signs and symptoms confined to the vulvar vestibule: (1) severe pain upon touching the vestibule or attempted vaginal entry, (2) tenderness to pressure localized within the vulvar vestibule, and (3) physical findings confined to vestibular erythema of various degrees.

Several theories have attempted to discover an etiology for this entity. Histopathological studies have not been helpful in that they have demonstrated a nonspecific inflammation of the vestibular region affecting mostly the superficial stroma and occasionally the epithelium. Marinoff and Pyka proposed that Candida may be a causative organism; however, the presence of yeast in these patients with vulvar vestibulitis has not been confirmed by other reports. Some authors believe that it may be secondary to the use of several types of topical medication that may have produced an allergic sensitization within the vulvar vestibule while being used for the treatment of vulvovaginal candidiasis.

More recent studies have investigated the role of human papilloma virus (HPV) infection; however, the evidence has been controversial. Turner and Marinoff reported a 100% rate of HPV positivity in vulvar biopsies in 7 patients with vestibulitis, while Bergeron reported negative viral findings in all 11 of his biopsies. Further studies are needed to elucidate the relationship, if any, between HPV and vulvar vestibulitis.

Several other agents have been implicated in the etiology of vulvar vestibulitis. Therapeutic agents used in the treatment of clinical and subclinical HPV, such as cryosurgery, trichloracetic acid, podophyllin, and laser treatment, also have been implicated. Several cases have been reported after the use of 5-fluorouracil cream. Chemical irritants, such as those found in feminine hygiene products, also have been investigated as possible initiating agents.

Alkaline vaginal pH has been demonstrated to cause irritation to the vestibule. Any etiological cause that alters the vaginal pH can lead to overgrowth of anaerobic and/or disappearance of the normal flora, ie, Lactobacillus. Hypotheses suggest that the constant bathing of the vestibule by an alkaline vaginal discharge may lead to chronic irritation and inflammation. Finally, some authors have associated vulvar vestibulitis with a history of sexual abuse, elective abortions, severe marital conflicts, depression, and anxiety.

Recent studies have begun to focus on specific pain receptors found in the vulvar tissue. As a brief overview, the sensory innervation of the inferior portion of the vulva is primarily from the branches of the pudendal nerve. The ilioinguinal and branches of the genitofemoral nerve innervate the superior portion of the vulva. These nerve fibers are of 2 types: (1) those responsible for touch and (2) others responsible for nociception (perception of a noxious stimuli). The mechanism hypothesized is that the nociception fibers are innervated first instead of the touch fibers. This is followed by a prolonged innervational response of the nociception fibers, leading to an abnormal neurological response from the dorsal horn of the medulla.

Westrom and Willen tested this theory by obtaining vulvar biopsies of 47 women with clinical vestibulitis. In 44 specimens, they noted that not only were regions of marked increase of vestibular nerve formation present, but a significant correlation was found between inflammation and nerve-bundle density. The authors concluded that a chronic inflammatory reaction in the vestibule might lead to proliferation of nerve fibers. Thus, treatment entails surgical removal of these nerve fibers.

Clinical

Women who are first affected usually are young, sexually active, and of Caucasian origin. Most patients have endured their symptoms for several months and have empirically tried various remedies with no improvement. Usual symptoms include pain, soreness, burning, and a feeling of rawness that is aggravated by stress, exercise, tight clothing, coitus, and tampon use. The pain usually is not considered constant; it is elicited by any attempt to enter the vagina. Many patients complain of an irritating vaginal discharge and a vulvar burning sensation. Examination may reveal small spots of erythema around the vestibular glands, with rare ulceration. Lesions predominantly are found in the lower portion of the vestibule. Unfortunately, standard pelvic examination typically reveals no physical findings. Gentle pressure with a cotton-tipped applicator around the base of the hymenal ring and posterior fourchette usually elicits the pain.

Treatment

Considerable controversy exists regarding the optimum mode of treatment. Many therapeutic regimens have been used with varying success. Of the treatments listed, most have not been evaluated prospectively and are based on clinical experiences reported in the literature.

Generally, no specific cure is available, but spontaneous resolution has been reported; thus, treatment should focus on alleviation of symptoms. Pain management has consisted of modalities such as sex therapy, behavioral modifications, biofeedback, and acupuncture.

Remedies that have been used with some success include topical application of anesthetics such as 5% Xylocaine ointment applied 15-30 minutes prior to intercourse. Other treatments include the use of a protective coating, such as from petroleum jelly or A&D ointment, to minimize contact with any irritating vaginal discharges; topical corticosteroids; wet compresses with aluminum acetate; and anti-inflammatory agents.

A case report by Solomons in 1993 demonstrated the use of oral calcium citrate combined with a low oxalate diet. He noted that calcium oxalate crystals released in urine might act as an irritant in the development of vulvar vestibulitis. He recommends a low oxalate diet with the ingestion of calcium citrate (200 mg calcium and 950 mg citrate) to theoretically inhibit the formation of calcium oxalate crystals. Many authors recommend this trial of treatment; however, studies are lacking with regard to benefit.

A number of trials have used alpha interferon and noted to have some success. The idea was initiated after noting the success of this agent with condylomata acuminata. Horowitz et al treated 17 women with severe vulvar vestibulitis with intravestibular injections of alpha interferon, one million units 3 times per week for a period of 1 month. His findings noted that 15 of the 17 women demonstrated considerable improvement. Favorable response was gauged by improvement of clinical symptoms such as dyspareunia. However, recommendations at this time indicate that alpha interferon should be used as a mode of treatment for women who present with concomitant HPV infections.

As a last resort, surgical excision may be considered. Woodruff and Parmley developed the original surgical mode of treatment. They described a U-shaped excision of the posterior hymenal ring 0.5 cm on each side of the hymen starting 0.5 cm below the urethra on each side. In their study, they reported that women who fulfilled the criteria of vulvar vestibulitis who underwent surgery demonstrated a success rate of 80%. Most studies have reported success rates of 60%. Postoperative complications are uncommon but include dehiscence, hematoma, infection, uneven healing, or nodular excrescences along the suture line.

PEDIATRIC VULVOVAGINITIS

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Etiology

Vulvovaginitis is considered to be the most common gynecologic problem in premenarchal girls, although the actual incidence has not been cited. Anatomically, prepubertal girls are at risk for developing nonspecific vulvovaginitis due to the absence of labial fat pads and pubic hair, diminishing the protection of the introitus by the labia majora. Children also are noted to have small labia minora that tend to open and lead to exposure when the child squats. In addition, the proximity of the vagina to the anus compounded by poor hygiene can contribute.

Physiologically, prepubertal girls have diminished estrogen concentration, leaving the mucosa susceptible to irritation and inflammation. As opposed to adult women, children lack colonization by lactobacilli. Lactobacilli contribute to an acidic environment in the vagina. Without their presence, the vagina is more neutral-to-alkaline in its pH. This leads to an environment that is an appropriate medium for microbial growth once inoculated.

The vulvar skin is susceptible to irritation and is easily traumatized by chemicals, soaps, and medications. Articles of clothing, such as nonabsorbent items, nylon tights, nylon bathing suits, and close-fitting clothes may cause maceration and infection, particularly in hot weather, leading to inflammation.

Although noninfectious etiologies are more common, specific infections that can occur often are respiratory or enteric pathogens. Respiratory pathogens include Streptococcus pyogenes, group A streptococci, Haemophilus influenzae, and Staphylococcus aureus. S pyogenes infections can occur secondary to inoculation from nasopharyngeal infections, fecal carriage, or skin infections. Streptococci infections result when the bacteria overwhelm the protective vaginal lactobacilli. This type of vaginosis frequently is iatrogenic and occurs as an overgrowth condition following treatment of bacterial vaginosis with metronidazole (which is ineffective against streptococci). Bacterial vaginosis, which occurs from the synergistic interaction of Gardnerella vaginalis, anaerobes, and Mycoplasma hominis, also must be considered. Parasitic etiologies include pinworm infestation.

An additional factor that must be considered is the possibility of sexual abuse. Trauma from forced insertion of a penis or foreign objects can lead to inflammation and bleeding. Sexually transmitted diseases such as chlamydia or gonorrhea may exacerbate the condition.

Clinical

Symptoms include diffuse vulvovaginal pain, burning, pruritus, dysuria, and possible seropurulent discharge. The vulvovaginal region usually has a markedly mottled erythematous appearance. In cases with an infectious cause, the vaginal discharge may be more purulent and malodorous.

Diagnosis

The challenge in diagnosing vulvovaginitis in this age group is differentiating between infectious and noninfectious causes. Making the diagnosis is difficult due to the overlap between normal flora and potential pathogens in the pediatric population. The presence of an organism is not necessarily deemed to be the etiological cause. A nonspecific etiology is found in 33-85% of cases of prepubertal girls in clinical practice. This diagnosis should be made if vaginal cultures grow normal flora and no other etiology is known for the vulvovaginitis.

Most authors conclude that a microbiological investigation is indicated if visible vaginal discharge with moderate-to-severe inflammation is present upon examination. Diagnostic tests include a wet prep, smear for Gram stain, pinworm test, and culture. Wet preps may include normal squamous cells, absence of lactobacilli, and white blood cells in adult streptococci vaginosis. Other exclusion methods may be used, such as a pinworm test or chlamydia/gonorrhea probe, if sexual abuse is suspected.

Treatment

Evaluation should include a vaginal culture. If a specific overgrowth of bacteria is noted, antibiotics should be initiated. An adequate response can be achieved with a course of oral penicillin, cephalosporins, or erythromycin.

Nevertheless, most episodes do not have a specific cause. In those cases, treatment should focus on improved hygiene, hand washing, and sitz baths. Patients should be instructed to sit in warm water for 10-15 minutes once or twice a day. Bland soap can be used; however, the vulva should not be scrubbed. Afterwards, the patient should gently pat dry the vulvar region or allow it to air-dry. Clothes should be washed in a mild detergent with no rinse or dryer additives.

CONTACT DERMATITIS

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Etiology

The vulvar skin is a frequent site of contact dermatitis. The cutaneous response may be allergic or irritant-induced. An allergic reaction implies previous exposure to an allergen and sensitization. It is a cell-mediated (type IV) immunologic response that can occur in sensitized individuals. Irritant-induced contact dermatitis can be acute or chronic. It may occur from acute exposure to a potent irritant or upon repeated exposure to a weak irritant.

Predisposing agents

Irritants include moisture, urine, vaginal discharge, topical medications, anticandidal agents, latex, spermicide agents, cosmetics, douching, fragrances, cleansing products, and underwear.

Clinical

Clinical symptoms consist of varying degrees of tenderness, pain, burning, and pruritus. Urinary retention may occur in severe cases.

Pruritus is the cardinal symptom. However, an acute reaction may develop as a result of exposure to a potent irritant that involves the mucosa, leading to burning, rawness, and pain. This initially presents as red and edematous skin followed by exudation and weeping, which may lead to secondary infections. The irritant also may be potent enough to cause erosion, ulceration, or necrosis.

Repetitive exposure to weak irritants with an insufficient period of healing and restoration of skin integrity between each exposure characterizes chronic contact dermatitis. Contact dermatitis of long duration may include lichenification, scaling, thickening of the skin, and white plaques.

When the mechanism is an allergen, the symptoms may not be apparent until 24-48 hours after contact, as opposed to immediate symptoms with an irritant.

Diagnosis usually is based on the patient's history and physical examination.

Treatment

Literature is limited on treatment options. Most treatment regimens are empiric and based on clinical experience.

The first step towards treatment is removal of the inciting agent. Patch testing may be necessary for allergen identification. Avoidance of sexual intercourse, douching, detergents, soaps, and perfumes is essential. Mild vulvovaginal reactions usually subside rapidly after the causative agent is withdrawn.

Cleansing can be accomplished by gentle flushing of the area once a day with clear water and patting the area dry. Triamcinolone ointment, 0.1% applied twice a day, can help in irritant contact dermatitis. Severe lesions can be treated with wet compresses of aluminum acetate solution for 30 minutes several times a day. After each application, the vulvar skin must be kept clean and dry.

CONCLUSION

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The differential diagnosis for women with symptoms of vulvovaginitis is complex. Discharge, burning, and pruritus usually are the presenting symptoms, with signs of vulvar irritation that may include erythema and excoriation of the vulvar skin. Primary or secondary infections, skin irritants, or contact dermatitis may produce vulvar irritation. Irritation from bodily fluids such as urine and normal vaginal secretions may cause symptoms when the environment is kept moist as with tight-fitting or occlusive clothing.