Stacie Zelman
EPIDEMIOLOGY
Vulvovaginitis is a common gynecological complaint, affecting females of all ages.
Bacterial vaginosis (BV) is the most common cause of vaginitis. Up to 50% of women with BV are asymptomatic. BV is associated with preterm labor and premature rupture of membranes (PROM).
Candida is the second most common etiology of vulvovaginitis. Factors associated with increased rates of colonization include pregnancy, oral contraceptives, uncontrolled diabetes mellitus, and frequent visits to STD clinics. Infection is rare in premenarcheal girls and decreases in incidence after menopause unless hormone replacement therapy is used.
Trichomonas vaginalis accounts for up to 20% of cases of vaginitis. The risk of infection increases with increasing numbers of sexual partners, early onset of sexual activity, and lower socioeconomic status. It is associated with preterm delivery, low birthrate, PID, and cervical cancer. Trichomonas is also associated with increased transmission of other STDs such as HIV, HSV, and HPV
PATHOPHYSIOLOGY
The pathophysiology of vulvovaginitis is related to inflammation of the vulva and vaginal tissues. Causes include infection, irritants and allergens, foreign bodies, and atrophy.
In females of childbearing age, estrogen causes the development of a thick vaginal epithelium with glyco-gen stores that support the normal flora. The glycogen is converted by lactobacilli and acidogenic coryne-bacteria to lactic acid and acetic acid that forms the acidic environment (pH 3.8–8.4) that discourages the growth of pathogenic bacteria.
Causes of infectious vulvovaginitis include tricho-moniasis, caused by T. vaginalis; bacterial vaginosis, caused by replacement of normal flora by overgrowth of both anaerobes and Gardnerella vaginalis;and candidiasis, usually caused by Candida albicans.
Contact dermatitis results from exposure of vulvar epithelium and vaginal mucosa to chemical irritants or allergens. Secondary infections can occur.
Retained foreign bodies can cause severe localized infections from Escherichia coli, anaerobes, or overgrowth of other vaginal flora.
Atrophic vaginitis during menarche, pregnancy, and lactation, and after menopause, results from the lack of estrogen stimulation on the vaginal mucosa. Decreased estrogen results in loss of normal rugae, atrophy of squamous epithelium, and increase in vaginal pH.
CLINICAL FEATURES
Bacterial vaginosis may present with a malodorous vaginal discharge and pruritus. The associated odor may be described as having a “fishy” smell. Examination findings range from mild vaginal redness to a frothy gray-white discharge.
Candida vaginitis causes vaginal discharge, severe pruritus, dysuria, and dyspareunia. Examination reveals vulvar and vaginal erythema, edema, and thick “cottage cheese” discharge. Odor is an uncommon presenting symptom.
Trichomonas vaginalis causes vaginal discharge, peri-neal irritation, dysuria, spotting, and pelvic pain. Examination reveals vaginal erythema and a frothy, malodorous discharge.
Contact vulvovaginitis causes pruritus and a burning sensation. Examination reveals an edematous, ery-thematous vulvovaginal area.
Vaginal foreign bodies can cause a bloody or foul-smelling discharge. Examination generally reveals the foreign body.
Atrophic vaginitis causes vaginal soreness, dyspareunia, and occasional spotting or discharge. Examination reveals a thin, inflamed, and even ulcerated vaginal mucosa.
DIAGNOSIS AND DIFFERENTIAL
A detailed gynecologic history should be obtained and a gynecologic examination performed.
Microscopic evaluation of vaginal secretions using normal saline (demonstrating clue cells for BV and motile T. vaginalis for trichomoniasis) and 10% potassium hydroxide (KOH) (demonstrating yeast or pseudohyphae for candidiasis and fishy odor for BV) will frequently provide the diagnosis.
Secretions from the sidewall of the vagina should be tested for pH using nitrazine paper. A pH greater than 4.5 is typical of BV or trichomoniasis. A pH less than 4.5 is typical of physiologic discharge or a candidal infection.
Historically, bacterial vaginosis is diagnosed according to the Amsel criteria by three of the following four criteria: (1) thin, homogeneous discharge, (2) pH >4.5, (3) fishy odor when 10% KOH is added to the discharge (positive amine test result), and (4) greater than 20% clue cells, which are epithelial cells with clusters of bacilli stuck to the surface, seen on saline wet prep.
Candida vaginitis is diagnosed microscopically by the presence of yeast buds and pseudohyphae. Using a 10% KOH solution will dissolve the epithelial cells, making the findings easier to see. Sensitivity is 80%.
Trichomoniasis is diagnosed microscopically by the presence of motile, pear-shaped, flagellated tri-chomonads that are slightly larger than leukocytes. A wet prep for trichomonas may be negative in men.
Contact vulvovaginitis is diagnosed by ruling out an infectious cause and identifying the offending agent.
On wet preparation, atrophic vaginitis will show erythrocytes and increased polymorphonuclear leukocytes (PMNs) associated with small, round epithelial cells. These cells are immature squamous cells that have not been exposed to sufficient estrogen.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Bacterial vaginosis is treated with metronidazole 500 milligrams PO twice daily for 7 days or clin-damycin 300 milligrams PO twice daily for 7 days. All symptomatic patients should be treated regardless of pregnancy status. Pregnant women, particularly those at high risk for preterm labor, should be considered for treatment even if asymptomatic. The recommended treatment in pregnancy is metronidazole 250 milligrams PO three times daily for 7 days, but a single 2-gram PO dose is an alternative regimen. No treatment is necessary for male partners or asymptomatic women. Any patient receiving metronidazole should be counseled to abstain from drinking alcohol during treatment and for the 24 hours following completion of treatment.
For trichomoniasis, metronidazole 2 grams PO in a single dose is the treatment of choice (or alternatively 500 milligrams PO twice daily for 7 days). Metronidazole gel is much less effective, and not recommended. Most infected men are asymptomatic; however, male partners need treatment to avoid retransmission of the disease. Patients should also be counseled to abstaining from sexual activity until the treatment regimen is complete. Any patient receiving metronidazole should be counseled to abstain from drinking alcohol during treatment and for the 24 hours following completion of treatment.
Uncomplicated Candida vaginitis is treated with the topical imidazoles, such as butoconazole 2% cream—5 grams daily for 3 days orclotrimazole 100 milligrams—2 tablets/daily for 3 days ormiconazole 200 milligrams vaginal suppository—1 suppository daily for 3 days. Alternative treatment for uncomplicated or complicated Candida is a single dose of fluconazole 150 milligrams PO. Treatment of sexual partners is not necessary unless candidal balanitis is present. Pregnant patients should receive topical treatment only.
Contact vulvovaginitis is treated by removal of the offending agent. Cool sitz baths and wet compresses of dilute boric acid or Burow’s solution may provide some relief. Topical corticosteroids can also be used to relieve symptoms and promote healing. Superinfections with Candida should be treated as previously discussed.
Vaginal foreign bodies require removal of the object. No other therapy is necessary, unless superinfection is present.
Atrophic vaginitis is treated with topical vaginal estrogen cream or tablets. Patients should be warned about possible side effects such as breast or perineal pain, and/or uterine bleeding. Estrogen should not be used if there is a history of cancer of any of the reproductive organs or postmenopausal bleeding. Refer patients to a gynecologist.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 106, “Vulvovaginitis,” by Gloria J. Kuhn and Robert P Wall.