Anne E. Burke
Linda C. Rogers
Vulvovaginal symptoms constitute a significant proportion of problems seen by primary care providers. The diagnosis and treatment of these disorders can be both satisfying and exasperating. Most diagnoses are readily made in one office visit. Treatment is usually easily rendered. However, the patient with recurrent or persistent symptoms presents special problems. Appropriate evaluation and treatment of both the easily treated patient and the patient with persistent symptoms require knowledge of the anatomy, physiology, and pathology of the vulva and vagina.
Anatomy and Physiology
Vulva
The external genitalia of the female human is called the vulva (Fig. 102.1). The vulva consists of the labia majora, labia minora, vestibule, clitoris, prepuce, and mons pubis.
The mons pubis (mons veneris) is a cushion of fat covered by stratified squamous skin and its appendages (hair follicles, sebaceous and apocrine sweat glands). The mons is located superior to the clitoris and encompasses the triangular-shaped hair-bearing tissue situated in front of the symphysis pubis. The labia majora are composed of
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longitudinal folds of fat and connective tissue. When the labia majora are parted, the vaginal vestibule is seen. The vestibule begins at the hymenal ring and extends outward to the labia minora, upward to the frenulum of the clitoris, and downward to include the posterior fourchette. The vaginal orifice (introitus) and urethral meatus open in the midline of the vestibule. Ducts of the Skene glands (paraurethral glands), the Bartholin glands (major vestibular glands), and the minor vestibular glands also open in the vestibule. The hymen, a firm, often crescent-shaped membrane consisting of a double plate of stratified squamous epithelium, partially obscures the vaginal orifice (introitus) in virgins. Residual tags of the hymen, the carunculae hymenalis, are often noted at the inferior edges of the introitus. The fourchette, the most posterior boundary of the vestibule, is formed by the fusion of the inferior aspects of the labia majora. The clitoris is located in the midline at the most superior aspect of the vestibule.
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FIGURE 102.1. Anatomy of the vulva. |
Vulvar Glands
The major vestibular glands, or Bartholin glands, are paired glands whose ducts exit at the introitus, above the fourchette at the 4 and 8 o’clock positions. The minor vestibular glands are numerous small glands whose ducts exit laterally to the hymenal ring. These small glands may extend superiorly to the region of the urethra. Ducts from the Skene glands (paraurethral glands) open in the vesti-bule immediately beneath the urethral meatus.
Vagina
The vaginal wall consists of an outer fibrous layer, a middle muscular layer, and an inner epithelial layer composed of nonkeratinizing, stratified squamous cells. No glands are present in the normal vagina.
Compared with the neural supply of the vulva, the vagina has few nerve endings. For this reason, vaginal infections are often asymptomatic until pathologic discharge comes in contact with the vulva. Normal vaginal discharge is composed of transudation through the vaginal wall, secretions of Bartholin and Skene glands, desquamated vaginal epithelial cells, cervical mucus, endometrial fluid, tubal fluid, and leukocytes. The squamous epithelium of the vagina is hormone dependent. In the absence of estrogen, the vaginal epithelium is thin and fragile and consists of undifferentiated basal and parabasal cells. Progesterone leads to a decrease in superficial cells and a relative increase in intermediate cells. Pregnancy, lactation, and oral contraceptives produce the progesterone-dominant state.
Bacteria normally present in the vagina include Lactobacillus, Staphylococcus epidermidis, Corynebacterium species, nonhemolytic streptococci, diphtheroids, Peptostreptococcus, Bacteroides species, and Mycoplasma species (1). Yeast are normal inhabitants of the vagina. The presence of Gardnerella vaginalis, also a normal inhabitant of many women's vaginas, is not itself diagnostic of vaginal pathology (2,3). The composition of vaginal flora may vary over the course of the menstrual cycle (3).
Physiologic vaginal discharge (pH, 3.8 to 4.5) is not malodorous or associated with pruritus. It varies in amount (usually about 1 to 4 milliliters per day), is white or mucoid in color, and typically is thick in consistency and odorless. The amount and consistency of the discharge depend on several factors: hormonal profile, presence of menstrual flow, frequency of coitus, use of antibiotics, and even stress (4). The saline wet slide preparation of normal discharge shows rare leukocytes, variable numbers of mononuclear cells, large gram-positive rods, and vaginal epithelial cells with distinct borders (Table 102.1).
Vulvovaginitis
Abnormal vaginal discharge with associated vulvar irritation is the hallmark of vulvovaginitis. The most common vulvovaginal problems are vulvovaginal candidiasis, bacterial vaginosis (BV), and trichomonas infections. This triad accounts for about 90% of all cases of vaginitis (5). Atrophic vaginitis is a common problem among older women. Foreign bodies are a rare cause of vulvovaginitis in adults. Although they are not a cause of adult vaginitis, gonorrhea and chlamydial infections of the cervix (see Chapter 37) may initially manifest as an abnormal discharge and therefore may be misinterpreted as a vulvovaginitis.
Candida
Vulvovaginal candidiasis (VVC) (Table 102.1) is an extremely common cause of adult vulvovaginitis, accounting for almost 30% of infections in symptomatic women (6). Candida albicans, is believed to cause over 90% of VVC (7). Other species, such as C. glabrata and C. tropicalis, are responsible for the remainder (8,9,10). The Centers for Disease Control and Prevention (CDC) classifies nonalbicans VVC as “complicated” (11). The presence of Candida within the vagina is not sufficient for the diagnosis of vulvovaginitis; the point prevalence ofCandida colonization is 20% to 30% in nonpregnant women of reproductive age (4,6,11,12). Therefore, one should prescribe treatment only if the woman is symptomatic; the presence of yeast in a Papanicolaou (Pap) smear or other examination is not in itself an indication for treatment.
The change in Candida from normal flora to a pathogen occurs when the organisms proliferate to the point that the normal microbiologic balance of the vagina is upset. Predisposing factors to infection include pregnancy, diabetes mellitus (DM), immunosuppression, antibiotic or corticosteroid therapy, iron deficiency anemia, vaginal surgery,
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hormonal or barrier contraceptives, and infection with human immunodeficiency virus (HIV) (8,12,13,14). Candida may also proliferate in the setting of persistently moist and macerated skin, as can occur with the use of occlusive synthetic clothing. In many cases there is no identifiable predisposing factor.
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TABLE 102.1 Vaginal Discharge |
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Patients usually present with intense vulvar itching or burning associated with a thick, curd-like vaginal discharge. The vulva and vagina are typically inflamed. The vaginal mucosa may exhibit adherent white patches of exudate. Vulvar erosions with satellite pustules may be seen. Microscopic evaluation of an admixture of vaginal secretions with a 10% potassium hydroxide (KOH) solution typically supports the diagnosis. The KOH causes lysis of epithelial cells, leukocytes, and red blood cells, facilitating viewing of budding filaments, pseudohyphae, or spores. The presence of pseudohyphae and a normal vaginal pH in a woman with symptoms of vaginitis is suggestive of candidiasis. However, the sensitivity of the KOH slide for yeast may be as low as 61% (15). Failure to identify yeast on microscopic examination should therefore not preclude treatment in a woman with classic symptoms, although repeatedly negative wet smears should prompt further evaluation.
Treatment
Candida vulvovaginitis may be treated either topically or orally (Table 102.2). Antifungal medications include imidazole derivatives, the triazole derivative gentian violet, and the antifungal polyene macrolide antibiotic nystatin. The imidazole derivatives, triazoles, and nystatin increase the permeability of the cell membrane of fungi. This alteration of permeability results in the loss of the selective barrier function of the cell membrane so that potassium and other cellular constituents are lost.
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TABLE 102.2 Regimens for Treatment of Vulvovaginal Candidiasis (VVC) |
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The U.S. Food and Drug Administration (FDA)-approved prescription treatment of Candida vulvovaginitis includes oral and topical regimens. Terconazole is a topical triazole effective against a broad spectrum of candidal strains, including C. albicans, C. glabrata, and C. tropicalis(16). An oral treatment, fluconazole 150 mg in one dose, maintains therapeutic concentrations in vaginal secretions for 72 hours and appears to be as effective as topical therapy (14,17). Fluconazole may interact with other medications, including cimetidine, hydrochlorothiazide, isoniazid, phenytoin, rifampin, theophylline, warfarin, and zidovudine. Although it is unlikely that one 150-mg dose will cause a serious adverse reaction, there is potential for arrhythmia when fluconazole is taken with a nonsedating antihistamine, or for idiosyncratic liver dysfunction, which could be more serious when it occurs in a patient with existing liver disease. The advantages of fluconazole include patient preference and compliance. Fluconazole is a Category C drug in pregnancy. There have been case reports of teratogenicity with higher or prolonged dosing, but none with the single-dose regimen (18).
A number of imidazoles are now available over the counter, although some regimens are still available by prescription. Topical miconazole, clotrimazole, butoconazole, and tioconazole are available as nonprescription medications. Over-the-counter (OTC) imidazoles are effective primarily against C. albicans vulvovaginitis. Therefore, it is prudent to prescribe a broad-spectrum antifungal agent when treating complicated cases of VVC. Of particular note are studies that show enhanced in vitro or in vivo activity against Candida species with terconazole, butoconazole, and tioconazole (2,16).
Many women seek advice about an abnormal discharge via telephone, often after attempting self-medication. However, because the reliability of self-diagnosis is poor (19), self-medication with OTC antifungals is recommended only if the following is indicated:
If a pelvic examination is scheduled based on the telephone discussion, then certain precautions are necessary. Before being seen for pelvic examination, the woman should not have used any intravaginal medication for at least 48 hours, because intravaginal medication may mask the correct diagnosis.
With any effective antifungal regimen, symptoms typically diminish in 1 to 2 days. If a multiday regimen is prescribed, the physician should encourage patients to complete the treatment course. The 7-day regimen described previously is recommended during pregnancy (11), and has also been shown to be more effective than oral fluconazole in severe infections (8).
All patients should be encouraged to wear cotton underwear that is nonconstricting. Excess vaginal moisture and heat associated with nylon or other synthetic materials and with tight-fitting pants may increase susceptibility to candidiasis.
Resistant or Recurrent Candidiasis
Candida infections of the vagina may persist or recur. Persistent vulvovaginal candidiasis is a consequence of inadequate treatment. Recurrent infections, defined as four or more symptomatic episodes annually, are caused by reintroduction of the organism and affect fewer than 5% of women with candidiasis (11). The only way to distinguish persistent from recurrent infection is by documenting eradication of the infection after a treatment course. This documentation, in practice, is not done commonly after an initial episode. However, if a second episode of Candida vulvovaginitis is experienced soon after the first, the caregiver should see the patient in followup within 1 to 2 weeks to re-examine the patient and determine whether the organism has been eradicated. Culture should be performed to identify the causative organism. Persistent infection should be treated with a 7- to 14-day course of a broad-spectrum antifungal agent. In cases of treatment failure, consideration can be given to alternative therapies such as gentian violet, boric acid, or flucytosine.
Recurrent infection requires more intensive treatment: 10 to 14 days of topical therapy, or additional doses of oral fluconazole (8). The diagnosis must also be confirmed, because contact dermatitis or infection with other organisms may cause similar symptoms. Suppressive therapy should be initiated only after culture confirmation of the diagnosis. Suppressive (maintenance) regimens include: clotrimazole (500-mg dose vaginal suppositories once weekly), ketoconazole (100-mg dose once daily), fluconazole (100- to 150-mg dose once weekly), and itraconazole (400-mg dose once monthly or 100-mg dose once daily) (11,20). Maintenance therapy should be continued for 6 months. Patients using ketoconazole should be monitored for hepatotoxicity.
Behavioral modifications may also play a role in management of recurrent infection. Perineal hygiene should be encouraged, and wearing of nonocclusive underwear and avoidance of pantyhose may be helpful. If recurrences continue, a gynecologist should be consulted.
The role of treatment of the sexual partner in vulvovaginal candidiasis is controversial. Although one study suggested a benefit from routine treatment of male sexual partners (14), other studies have failed to demonstrate a
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reduction in recurrences, and so routine treatment of male partners is not recommended (11,14).
If recurrences are related predictably to specific events, such as menses, a prophylactic topical or oral antimycotic used for several days before onset of menses may be preventive. Sometimes recurrences are related to coitus, and for women in whom coital events can be predicted, prophylactic therapy is helpful.
Patients who continue to have recurrent infections despite the institution of these measures should be evaluated for DM (see Chapter 79) and HIV infection (see Chapter 39). Many patients experience recurrent vulvovaginal candidiasis in the absence of recognized predisposing factors.
Bacterial Vaginosis
Bacterial vaginosis (Table 102.1) is the most prevalent cause of vaginal symptoms among reproductive-age women. Because many women with BV are asymptomatic (21), the infection is probably even more prevalent than is recognized (4). Multiple species have been implicated as the cause of BV, including Gardnerella vaginalis, Mycoplasma hominis, anaerobic bacteria such as Bacteroides, and Peptostreptococcus. (1,22,23). Like C. albicans, most of these organisms are found in low concentrations in the vaginas of normal, asymptomatic women (2,3,4). Associated symptoms are caused by overgrowth of these bacteria and a decrease in the proportion of Lacto-bacillus (24).
Patients with symptomatic BV usually complain of thin, creamy, malodorous vaginal discharge with accompanying vulvar itching or burning. The odor of this infection is usually described as fishy or musty and is commonly noted after coitus, when the alkaline seminal fluid has caused the release of volatile fatty acids and amines.
The diagnosis is confirmed through examination of the saline wet slide preparation, production of the characteristic odor, and determination of the vaginal pH. With the use of Nitrazine paper, vaginal pH can be determined easily. Vaginal discharge of women with BV typically has a pH between 5.0 and 6.0. The saline wet slide preparation is significant for vaginal squamous cells covered with G. vaginalis and other bacteria (“clue cells”) (Fig. 102.2). Clue cells are the most reliable predictor of BV (24). Leukocytes usually are not abundant unless a mixed infection is present. The addition of a 10% KOH solution to the discharge causes the release of amines and volatile fatty acids that produce the fishy odor (whiff test).
The diagnosis of bacterial vaginosis is made when at least three of the following four criteria (criteria of Amsel) are met (25):
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FIGURE 102.2. “Clue” cells. |
Gram staining may also be useful, as may some commercially available diagnostic cards. Culture is not helpful.
Treatment
The treatment of choice for BV vaginitis is metronidazole 500 mg orally two times a day for 7 days, or 0.75% metronidazole gel intravaginally two times a day for 5 days, or 2% clindamycin phosphate cream, 5 g intravaginally for 7 nights (11). (Patients should be advised that the mineral oil in clindamycin cream can weaken condoms, diaphragms, and cervical caps.) Topical treatment is associated with a lower incidence of systemic side effects. These regimens are associated with cure rates of 70% to 80% (26), with the oral metronidazole regimen having the highest associated cure rates (greater than 90% short-term) (27,28). Oral metronidazole may also be given as a single 2-g dose, although this may be somewhat less effective, and recurrence rates may be higher than with the longer regimen (4). Additionally, the higher oral dose is more likely to be associated with gastrointestinal (GI) side effects. Because of the side effects that develop when the drug is taken with alcohol (disulfiram reaction), its use should be avoided in anyone using alcohol or anyone suspected of having severe hepatic disease. Alternative clindamycin regimens may also be administered. Acceptable regimens are clindamycin 300 mg orally two times a day for 7 days, or clindamycin phosphate ovules, 100 mg intravaginally for 3 days. A single-dose intravaginal clindamycin cream (Clindesse) regimen was recently approved.
The role of sexual transmission in the acquisition of BV has not been resolved completely. G. vaginalis can be recovered from most male contacts of infected women, yet Gardnerella also can be isolated from up to one third of
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women who have never been sexually active. Additionally, recurrence rates for the infection are the same for women whose partners do or do not harbor G. vaginalis (29). Because of the possible role of sexual transmission, condoms should be used during therapy. However, because there is no clear evidence that treatment of the partner improves recurrence rates, routine treatment of male partners is not currently recommended (11,30).
BV has been associated with preterm birth, and treatment of BV may reduce the risk of preterm complications in high-risk women (31,32,33). However, treatment of asymptomatic BV in all pregnant women has not been shown to affect pregnancy outcome (34). Because of the association between BV and posthysterectomy vaginal cuff cellulitis, preoperative treatment should be given to affected women (35).
Trichomonas
Trichomonas infection (Table 102.1) is the third most common cause of vaginitis, with a prevalence of 4% to 35% (36). It is a sexually transmitted disease (STD) caused by the motile, flagellated protozoan, Trichomonas vaginalis. Symptomatic patients classically have a copious, malodorous vaginal discharge accompanied by vulvar pruritus. Additional symptoms include vaginal burning, vaginal spotting, dysuria, frequency, and urgency. Pelvic discomfort may be experienced by some patients. Dyspareunia is common. On physical examination, variable amounts of vulvovaginal erythema may be seen. The vaginal mucosa or cervix may exhibit a characteristic strawberry appearance (reddish color with punctate hemorrhages).
The diagnosis is established by assessing vaginal pH and examining the saline wet slide preparation (see earlier discussion). The vaginal pH is greater than 4.5. On the saline preparation (Fig. 102.3), a multitude of polymorphonuclear leukocytes are seen. Among the white blood cells, trichomonads can be identified by the movement of their flagellae. Sensitivity of the wet mount for the trichomonads is relatively low, at 50% to 70% (37). Culture on a Diamond medium, which has a sensitivity and specificity greater than 95%, can be considered.
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FIGURE 102.3. Saline preparation showing trichomonads. |
Liquid-based Pap smears are more sensitive than conventional Pap smears in the diagnosis of trichomoniasis, with sensitivity and specificity of 61% and 99%, respectively (38). Conventional Pap smears, by contrast, have a high false-positive rate (37).
Treatment
Treatment consists of a single 2-g dose of oral metronidazole (11). An alternative regimen is metronidazole 500 mg, twice a day for 7 days. Patients who do not respond to initial therapy may be treated with metronidazole 500 mg, two times per day for 7 days, or tinidazole 500 mg three times daily for 7 days. If treatment failure occurs again, the patient should be treated with a single, 2-g dose of metronidazole once a day for 3 to 5 days (11). Metronidazole should be used cautiously in patients with severe hepatic disease. Some practitioners hesitate to administer metronidazole in the first trimester of pregnancy, although studies have failed to show adverse pregnancy outcomes (39,40). Therefore, current recommendations are that use of metronidazole to treat symptomatic patients is acceptable, even in the first trimester of preg-nancy (11).
When taken within 24 hours of alcohol consumption, metronidazole causes severe reactions similar to those that occur when alcohol and disulfiram are consumed together. In these situations or when there is an intolerance to systemic metronidazole, metronidazole gel twice a day for 7 days may be tried as an alternative, although this regimen is less effective (41). Sexual partners should be treated, and there is no need to attempt to recover the organism from the partner. Intercourse should be avoided or a condom used during treatment.
Vaginal Atrophy and Atrophic Vaginitis
Vaginal atrophy occurs in to some degree in nearly all menopausal women, and more than half become symptomatic with vaginal dryness, irritation, and dyspareunia. Women who are breast-feeding or perimenopausal may also be sufficiently estrogen deficient to become symptomatic. Estrogen deficiency results in thinning and fragility of the vaginal and vulvar epithelium, which comes to be comprised primarily of parabasal and intermediate cells. This altered vaginal environment is associated with an elevation of pH to as high as 7.0. In this milieu, pathogenic bacteria may flourish, causing atrophic vaginitis, which affects 10% to 40% of postmenopausal women (42). Because symptoms may appear 10 years or longer after menopause, the condition is often underdiagnosed
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and undertreated (42). Rarely, atrophic vaginitis develops in girls who are premenarchal (i.e., have unestrogenized tissues) when an additional precipitant, such as wearing of occlusive clothing made of synthetic materials, is encountered.
Atrophy without superimposed infection can cause significant discomfort, especially during coitus, because the atrophic vagina does not lubricate well and is more easily injured. Visual examination of the normal atrophic vagina reveals a pale vaginal mucosa with decreased or absent rugal folds. Vulvar examination demonstrates thin, often shiny skin with decreased subcutaneous tissue and variable loss of hair. In atrophic vaginitis, erythema and petechial hemorrhages may be superimposed on these findings. The patient may complain of a thin, blood-tinged vaginal discharge and vulvar and vaginal dryness.
Examination of a saline wet slide preparation of the discharge of women with atrophic vaginitis typically shows numerous leukocytes mixed with immature, intermediate, and parabasal epithelial cells. Microorganisms seen on the slide are usually secondary invaders of the inflamed mucosa. Often, in the past, diagnosis was made by taking a smear of the vaginal wall and determining the maturation index; however, this test is no longer recommended because it has not proved to be reliable.
Both symptomatic vaginal atrophy and atrophic vaginitis are treated most effectively with vaginally applied estrogen. Vaginal symptoms are relieved in only 55% of women using the estrogen patch, and in 73% of women on oral estrogen, but in 80% to 95% of women on vaginal estrogens (43). Many women on oral or transdermal estrogens may need the addition of vaginally applied estrogen to fully relieve symptoms.
Options for vaginally applied estrogens include creams, tablets, and rings. Creams are most commonly used, and allow for considerable dosing flexibility. As an example, one-half to one applicator of estrogen cream every night for 1 to 2 weeks can be followed by application every other night for 1 to 2 weeks. The medication can then generally be discontinued, and most patients have only infrequent symptoms (e.g., every 1 to 2 months), for which an applicator full on 1 or 2 days when there are symptoms usually provides adequate control. Some patients, however, require up to 24 months of therapy, and the response may still be incomplete (44).
Rings and tablets have been shown to be better accepted by patients, and there is data to support greater safety because of significantly less systemic absorption (45). Most studies find that the low-dose ring and estradiol tablets relieve vaginal dryness and dyspareunia as well as estrogen creams. A reduced risk for urinary tract infections (UTIs) has been demonstrated with vaginal estrogens and some studies have found a decrease in urge incontinence (45). However, recent large studies have demonstrated worsening incontinence of all types with any estrogen therapy (46,47).
The estradiol ring releases 7.5 µgs of estradiol daily. It can remain in the vagina for up to 3 months (48,49). The vaginal tablet contains 25 µg of estradiol and is usually inserted twice a week, but also may be used once a week. Studies have shown an initial increase in serum estradiol levels in the first 2 weeks of therapy because estrogen is well absorbed by an atrophic mucosa. After 2 weeks however, there is no significant effect on serum levels (45). Women with high intake of alcohol or impaired liver function may have higher serum levels of estradiol. Most women maintain an atrophic endometrium with low-dose preparations, but some women do have endometrial effects. There is some evidence that there may be a uterine “first-pass” effect with vaginal estrogen, causing higher uterine levels of estrogen than with the equivalent dose of oral or transdermal estrogen (50). There are currently no evidence-based guidelines on management of unopposed low-dose vaginal estrogen for women with a uterus, but one suggested approach is to do a “progestin challenge” either after 3 months of therapy, or yearly, to assess the amount of endometrial stimulation. Those with any significant bleeding would merit closer monitoring of their endometrium (51).
The clinician should be certain that none of the contraindications for estrogens (e.g., breast cancer) is present and that the same precautionary surveillance (e.g., for hypertension) is provided to the patient using long-term topical estrogen preparations.
Some patients cannot or will not use topical vaginal preparations and prefer to avoid long-term systemic hormonal replacement therapy. In this instance, oral conjugated estrogen 0.625 mg/day may be prescribed for 1 month. Occasionally a repeated course is necessary if symptoms persist. If retreatment courses become frequent, it is necessary to provide close surveillance for the complications of estrogen therapy (see Chapter 106). Generally a gynecologist should be consulted to participate in the care of the patient with frequently recurrent attacks of atrophic vaginitis.
Water soluble vaginal lubricants have also been shown to have some efficacy in relieving vaginal dryness, pruritus, and dyspareunia. These can be recommended to women who cannot or do not want to use estrogens (52). They can also be informed that sexual activity will help them maintain vaginal health. Women who are sexually active have lower vaginal pH and better cell maturation (51).
Cytolytic Vaginosis and Desquamative Inflammatory Vaginitis
Cytolytic vaginosis and desquamative inflammatory vaginitis are uncommonly recognized vulvovaginitides
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that are often confused with other vaginal inflammatory conditions. Cytolytic vaginosis is caused by an overgrowth of lactobacilli, which results in an acidic environment and causes shedding and cytolysis of vaginal epithelial cells. The vaginal discharge of cytolytic vaginosis usually increases during the luteal phase of the menstrual cycle and grossly resembles a candidal discharge; the discharge is thick and white, with an acidic pH. The patient usually experiences severe vulvar burning, dysuria, and dyspareunia (53). KOH preparation reveals an absence of fungi. The saline wet slide preparation reveals an abundance of lactobacilli, fragmented epithelial cells, and naked nuclei. Therapy has not been well established. Currently an intravaginal douche two to three times a week of 30 to 60 mg sodium bicarbonate in 1 L of warm water is recommended. Alternatively, the patient can take amoxicillin clavulanate 500 mg, three times a day for 7 days (53,54).
Desquamative inflammatory vaginitis is a disorder of unknown cause that usually is characterized by copious sterile vaginal discharge and epithelial cell exfoliation (55). Patients experience intense vulvar pain and burning, severe dyspareunia, and dysuria. Conditions such as lichen planus and pemphigus vulgaris have been associated with desquamative inflammatory vaginitis (56,57). The vulva and vagina are usually very inflamed, with various stages of denudation. The discharge is seropurulent, with a pH as high as 7.4 (57). The characteristic violaceous papules and gingival and buccal mucosal lesions of lichen planus may be seen if the patient has the form of desquamative inflammatory vaginitis that is associated with lichen planus (58). Saline wet slide preparation reveals parabasal cells, an absence of lactobacilli, a predominance of inflammatory cells, and fragmented epithelial cells. This entity is distinguished from atrophic vaginitis by the lack of response to topical estrogen, and by a clinical history consistent with normal ovarian function (58). A biopsy of the affected area of the vagina should be taken in order to rule out another cause. Treatment options for desquamative inflammatory vaginitis are not well-established. One study found a 95% improvement rate with use of 2% clindamycin suppositories, although the relapse rate was as high as 30% (55). There may also be a role for topical corticosteroids, with or without clindamycin (57). One half of a 25-mg rectal steroid suppository or one applicator of rectal hydrocortisone foam intravaginally should be used twice daily for 1 to 2 months; the dosage can then be reduced to once a day for an additional 2 months, followed by one- to three-times-a-week maintenance therapy. Estrogen therapy may also help in women with estrogen deficiency (57). If there is no response, a gynecologist or dermatologist should be consulted for confirmation of the diagnosis and consideration of additional treatments, including systemic corticosteroids or antibiotics.
Foreign Body
An occasional cause of vaginal discharge in adults is a foreign body. Lost tampons, forgotten diaphragms, and other smaller objects are easily found by examination. Symptoms improve after removal of the foreign body. Because secondary bacterial infection is also present, use of metronidazole, or clindamycin as prescribed for BV, or a povidone douche once daily for 3 to 4 days may accelerate healing.
Gonococcal and Chlamydial Infections
In the United States, gonococcal and chlamydial infections are the most common STDs of the upper genital tract. These infections may initially manifest as an abnormal discharge that is the result of an associated cervicitis. However, the patient usually considers the discharge a sign of vaginal infection. Although a purulent discharge is classically associated with gonorrhea, a mucopurulent discharge is also seen with chlamydia. Both infections may be asymptomatic. Chapter 37 presents a full discussion of diagnosis and treatment of gonococcal and chlamydial infections.
Pelvic Inflammatory Disease
PID is a clinical diagnosis. It refers to upper genital tract inflammation caused by ascending pelvic infection and can include endometritis, salpingitis, tubo-ovarian abscess, and/or peritonitis. Most cases are believed to be attributable to initial infection with gonorrhea or chlamydia, but vaginal flora (e.g. G. vaginalis, Haemophilus influenzae, anaerobes, and enteric gram-negative rods) have also been implicated. Mycoplasma hominis and Ureaplasma urealyticum are also recent suspects (11). The sequelae of PID can be severe: a single episode of acute salpingitis causes infertility in approximately 8% of patients, and this complication rate can increase to 40% after three or more bouts with PID (59).
PID usually begins shortly after a menstrual period, and is typically characterized by fever, nausea, abdominal pain, and marked pelvic tenderness. Nonspecific symptoms such as dyspareunia, abnormal vaginal bleeding, and discharge may also be indicative of PID. The mildness and lack of specificity of symptoms in many cases may delay diagnosis (11). One recent study suggested that one fourth of women presenting to an ambulatory clinic with either gonorrhea or chlamydia actually had subclinical PID (60). The CDC recommends empiric treatment for PID if the following minimum diagnostic criteria are met (11):
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Additional criteria that increase the specificity of the diagnosis include
The majority of affected women will have either mucopurulent discharge or WBCs noted on saline wet preparation.
There are additional, highly specific criteria for the diagnosis of PID. While not necessary to confirm in all cases, they may sometimes be useful. These include
Treatment
Because PID is usually polymicrobial, broad-spectrum antibiotic coverage must be effective against chlamydia, gonorrhea, and anaerobes, the common organisms involved. Because the male sexual partner is often infected as well, he should be treated (see Chapter 37). Women receiving treatment for PID should either abstain from intercourse or ensure that their partners use condoms until completion of therapy.
Table 102.3 includes indications for hospitalization are included with treatment recommendations. PID during pregnancy is rare. An obstetrician-gynecologist should be consulted promptly if this diagnosis is entertained during pregnancy. Erythromycin, amoxicillin, or azithromycin should be used in pregnant patients.
The presence of a pelvic or tubo-ovarian abscess, poor compliance, immunocompromise, severe illness with nausea, vomiting, or high fever; or failure of outpatient treatment should also prompt hospital admission (11,61). The switch from intravenous to oral antimicrobial therapy should be based on clinical assessment and can be done 24 hours after the patient has shown clinical improvement.
All regimens used to treat PID should cover gonorrhea and chlamydia even if cultures are negative. Anaerobic coverage is also currently recommended. Table 102.3 shows intravenous treatment regimens. A review of the literature suggests that these regimens have clinical cure rates greater than 90% (61). After patients have demonstrated significant clinical improvement, oral therapy should be continued with doxycycline 100 mg orally twice daily or clindamycin 450 mg four times a day to complete a 14-day course. Adequate anaerobic coverage is likely of greater importance in patients with tubo-ovarian abscesses, concurrent BV, or HIV infection (61). If tubo-ovarian abscess is present, the use of clindamycin, clindamycin with doxycycline, or metronidazole with doxycycline should be considered.
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TABLE 102.3 Management of Pelvic Inflammatory Disease |
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Outpatient cefoxitin- and ofloxacin-based regimens, listed in Table 102.3, have cure rates of at least 89%. Outpatient therapy should incorporate followup within 72 hours to assess response to treatment, and to expedite admission, intravenous therapy, and further evaluation if no significant improvement has occurred.
Any sexual partners of the patient within the 60 days preceding the diagnosis of PID should be
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treated empirically for gonorrhea and chlamydia even if the patient's cultures are negative. Some experts also recommend rescreening women for gonorrhea and chlamydia 4 to 6 weeks after diagnosis and treatment of PID (11). Future use of condoms should be recommended: consistent condom use following an episode of PID has been associated with significantly reduced risks of recurrence and inferti-lity (62).
Vulvar Ulcerations
Herpes Simplex Virus
Herpes simplex virus is a common cause of painful vulvar ulcerations. Chapter 37 discusses HSV and the evaluation of genital ulcers.
Syphilis
Syphilis is an STD caused by the spirochete Treponema pallidum. Vulvar ulcerations can be seen in all stages of syphilis. Chapter 37discusses diagnosis and treatment of syphilis.
Chancroid
Chapter 1 discusses chancroid.
Tampon-Related Ulceration and Toxic Shock Syndrome
Repetitive tampon use during periods of diminished or absent menstrual flow may result in vaginal ulceration. Typically, patients with this problem develop intermenstrual bleeding or abnormal vaginal discharge. The ulcers are usually located in one of the vaginal fornices. They are superficial, erythematous, and 1 or 2 mm in diameter (often they are mistaken for herpes). The ulcers heal spontaneously in a few days if tampon use is discontinued.
Toxic shock syndrome (TSS) is a multisystem illness associated with fever greater than 102°F (39°C), hypotension, rash, skin desquamation, vomiting, and diarrhea (63). Shock may develop within 48 hours after the onset of the disorder. Other manifestations include palmar erythema, myalgias, and multi-organ system involvement. TSS is caused by strains of Staphylococcus aureus that produce superantigens, which exert toxic systemic effects (64). Increased incidence of TSS in the 1980s was associated with use of higher-absorbency tampons during menstruation (63). Since then, the incidence has decreased, although there has been concern for a recent increase in incidence since 2002 (11,63).
Pelvic examination typically reveals a purulent vaginal discharge. The vaginal walls are usually inflamed and may be ulcerated. Bimanual examination does not usually reveal any abnormal tenderness. If a tampon is present at the time of the examination, it should be removed and cultured. Testing for gonorrhea and chlamydia should be done to rule out either infection, which may occasionally be associated with symptoms that mimic the toxic shock syndrome.
Treatment of TSS consists of hospitalization for aggressive fluid resuscitation and hemodynamic monitoring. The vagina should be swabbed with Betadine, and any visible abscesses drained. Broad-spectrum antibiotics should be initiated, and continued for 10 to 15 days. First-line agents include β-lactamase-resistant antibiotics, nafcillin, oxacillin, or cephalosporins (65). Vancomycin can be used in case of penicillin allergy.
Cases of TSS must be reported to the state health department and to the CDC. The patient should not use tampons for several subsequent menstrual cycles. Generally, all patients using tampons should be encouraged to change them at least every 6 hours, and to avoid tampons made of superabsorbent material.
Other Causes of Vulvar Ulcerations
Less common causes of vulvar ulceration include granuloma inguinale, lymphogranuloma venereum, chancroid, hidradenitis suppurativa (Chapter 37), Behçet disease, Crohn disease, and tuberculosis. Table 102.4 shows a synopsis of common findings, diagnosis, and treatment of vulvar ulcerations. Any patient with an ulcer that is nonhealing, recurrent, or not easily diagnosed should be referred to a gynecologist or dermatologist.
Miscellaneous Lesions
Bartholin Gland Cyst or Abscess
Obstruction of the major duct of the Bartholin gland caused, for example, by inflammation, results in a Bartholin cyst (Fig. 102.1; Table 102.5). Infection of the duct can lead to a Bartholin abscess. Most Bartholin cysts occur because of mechanical blockage of the outflow of normal mucus secreted by the gland. If the cyst causes no symptoms and is only 1 to 3 cm in diameter, no treatment is necessary. Large cyst size, associated pain, or dyspareunia may indicate the need for intervention. Antibiotic therapy is not indicated for an uninfected cyst. If the patient is older than 40 years of age, a biopsy or excision to rule out carcinoma should be considered.
When treatment is indicated for a Bartholin cyst, the goal is to create a pathway from the cyst to the vaginal vestibule. This can be accomplished by incision and drainage, marsupialization, or, rarely, excision (66). These procedures should be done by a gynecologist. Infection of
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the Bartholin gland or duct is referred to as a Bartholin abscess. A Bartholin abscess harbors N. gonorrhoeae in approximately 10% of cases. Therefore, testing for gonorrhea and chlamydia is indicated. Other common causative organisms include E. coli and Bacteroides (67). The infection is often polymicrobial. Adequate drainage may obviate the need for systemic antibiotics. Sitz baths provide temporary symptomatic relief until drainage can be performed.
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TABLE 102.4 Causes of Vulvar Ulcerations |
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TABLE 102.5 Common Nonmalignant Vulvar Lesions |
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To drain a Bartholin abscess, one should perform the following:
Abscesses can also be treated by placement by a gynecologist of a Word catheter or marsupialization. Broad-spectrum antibiotics (which provide coverage for the likely etiologic agents) can be considered. Options include cephalosporins, clindamycin, or azithro-mycin (68).
Condylomata Acuminata (Genital Warts)
Condylomata acuminata are caused by human papillomavirus (HPV) and are transmitted sexually. Chapter 37 discusses these lesions.
Vulvar Papules
Folliculitis
Overgrowth of skin staphylococci and streptococci can result in vulvar folliculitis. Predisposing factors for this disorder include immunosuppressive therapy, local trauma, poor hygiene, and occlusive (synthetic) clothing. Infection of the hair follicle is identified by erythematous papules or pustules with a central hair shaft. Treatment consists of cleansing the area with a germicidal soap. Warm sitz baths or compresses help relieve the discomfort. Gentamicin or bacitracin ointment may be prescribed to accelerate healing. If the lesions do not heal within 1 week, systemic dicloxacillin, cephalexin, or erythromycin should be prescribed. In a diabetic patient, the infection could become worse more rapidly; therefore, a systemic and a topical antimicrobial agent are usually prescribed at the time of diagnosis.
Acrochordon
Acrochordons, commonly known as skin tags, are sessile or pedunculated fibroepithelial polyps. Acrochordons are benign and need be removed only if they are large or annoying to the patient. A gynecologist or dermatologist should be consulted or a biopsy performed if there is doubt regarding the diagnosis.
Molluscum Contagiosum
Molluscum contagiosum (see Chapter 117) is a pox virus that causes a benign, uncommon infection that is transmitted by close contact, including sexual intercourse. The adult patient characteristically sees a physician because of a painless new growth in the vulva, perineal area, or thighs. The lesions have a typical appearance, permitting diagnosis by inspection in most instances (Fig. 102.4). The individual lesions are wart-like papules varying from 1
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to 10 mm in diameter. They have a smooth surface and a central umbilical depression containing keratin. There may be multiple separate lesions or one large, coalesced lesion. If there is any doubt about the diagnosis, the central cheese-like core may be expressed onto a slide and examined under a microscope using the low-power objective. Characteristic large inclusion bodies, which occupy most of the cytoplasm of the cells, are identified. Occasionally, the lesion resembles bacterial infection, such as folliculitis or furunculosis, but in these instances, the expression of pus (rather than a cheesy material) from the lesion permits differentiation. If doubt remains regarding the diagnosis, the patient should be referred to a dermatologist or gynecologist for confirmation.
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FIGURE 102.4. Molluscum contagiosum. |
Most lesions will regress within 9 to 12 months (69). Therapy consists of scraping open the papule (with a scalpel blade), evacuating its contents, and curetting or cauterizing the base. Large lesions may need to be anesthetized with lidocaine injection before they are opened or curetted. The patient should be seen approximately 1 week after the initial treatment for retreatment of any resistant or new lesions. Other treatment options include cryotherapy and imiquimod (69). Also, the patient should be evaluated for the presence of another STD that may have been acquired simultaneously. Tests for chlamydia, gonorrhea, and syphilis should be obtained. The patient's sexual partner should be evaluated for lesions of molluscum contagiosum or evidence of another STD. A condom should be used until the patient's lesions have healed.
Hypopigmented and Hyperpigmented Lesions of the Vulva
Hypopigmented and hyperpigmented lesions of the vulva may range from nonmalignant to malignant disorders. Differentiation of the various processes is difficult by inspection alone. Biopsy must be performed to determine the diagnosis. Referral to a gynecologist or dermatologist is recommended when any such lesion is identified (see Chapter 104).
Lichen Sclerosus
Lichen sclerosus is a progressive and chronic condition marked by inflammation and thinning of the vulvar epithelium (70). It is most commonly seen in the anogenital region (71,72). Premenarchal girls and postmenopausal women are most likely to be affected (73), although women of any age can experience the condition. The etiology is unknown.
The most typical symptoms are itching and pain, although many women are asymptomatic (73). Dyspareunia and dysuria may occur in more advanced cases, in which the labia may become fused and the vulvar architecture is distorted. Classically, lichen sclerosus appears as thin, white skin in the affected area (70). Lesions can appear wrinkled or “parchment-like” (73). Fissuring, excoriations, or petechiae may be seen. The diagnosis must be established with a biopsy.
Vulvar lichen sclerosus carries a risk of malignancy: squamous cell carcinoma of the vulva can occur in approximately 5% of cases (74). Therefore, patients should be examined at least annually.
The mainstay of treatment is a potent topical corticosteroid. Options include clobetasol or halobetasol propionate ointment (0.05%), daily for 6 to 12 weeks, then one to three times weekly for maintenance therapy. Clinical improvement is likely (75). However, symptom recurrence is likely in the absence of maintenance therapy (76). There may also be a role for retinoids or immune system modulators such as pimecrolimus, although these medications should be used with caution, due to potential for skin irritation and unknown long-term effects. There is no role for topical hormones (other than corticosteroids), including testosterone, in the treatment of lichen sclerosus (70,74). Consultations with a dermatologist and a gynecologist may be useful.
Lichen Planus
As with vulvar lichen sclerosus, vulvar lichen planus is a chronic condition. Lichen planus may also involve the skin, oral mucous membranes, scalp, or nails (77). The etiology is unknown, but it is probably immunologically mediated (78).
There are three main subtypes of vulvar lichen planus: papulosquamous, erosive, and hypertrophic (rare). The papulosquamous type is associated with pruritic papules on the vulva or perianal area. The erosive type is associated with erythematous, painful erosions with a white border (Wickham striae) (79). As opposed to lichen sclerosus, vaginal involvement is commonly seen with the erosive form of lichen planus (79). Typical symptoms include vulvar pain or pruritus, vaginal discharge, and dyspareunia. There can be loss or distortion of the vulvar and vaginal architecture. Vaginal narrowing may develop, making intercourse extremely difficult and painful. Diagnosis of lichen planus must be confirmed with a biopsy.
Treatment of lichen planus can be difficult, as genital lesions may not respond well to therapy (80). Ultrapotent topical steroids, such as clobetasol propionate ointment 0.05%, can be applied nightly for 3 to 6 weeks, then twice a week for maintenance. Lower dose topical steroids can also be used for maintenance; regimens may vary. Vaginal suppositories (25 mg hydrocortisone twice a day for 2 months) have been used with success (77). Short courses (up to 4 weeks) of oral steroids may benefit women who have severe cases of lichen planus.
There may also be a role for immune system modulators such as tacrolimus. Some small studies have shown benefit
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(81,82), although there is concern about the effects of long-term use of these medications. Vaginal dilator therapy may be helpful in cases of vaginal narrowing. Surgical options are available for severe or non-responsive cases. Consultations with appropriate specialists—dermatologist, gynecologist, or otolaryngologist—may be indicated.
Psoriasis and Seborrheic Dermatitis
Chapter 116 discusses psoriasis and seborrheic dermatitis. The classic appearance of psoriasis is usually altered on the vulva. Because the vulva is moist, the psoriatic scale often is not present, and psoriasis may appear as a nonspecific dermatitis. It is rare for a patient to have psoriasis only on the vulva, so a general dermatologic examination should be performed. Patients with suspected psoriasis on the vulva should be referred to a dermatologist or gynecologist for confirmation of the diagnosis.
Sebaceous Cyst (Epidermal, Keratinous, or Inclusion Cyst)
Sebaceous cysts present as firm, superficial spherical lesions, fixed in the dermis (Chapter 113). No treatment is necessary unless the cyst is infected (Chapter 32), or otherwise bothersome because of its size. Treatment then is excision.
Intertrigo
Chapter 2 discusses intertrigo.
Contact Dermatitis (Reactive Dermatitis)
Chapter 116 discusses contact dermatitis.
Vulvodynia
Vulvodynia is a syndrome of unexplained vulvar pain. The syndrome is often accompanied by sexual dysfunction and psychological disability. Symptoms must be present for at least three months. The two localized types are clitorodynia and vestibulodynia (83). The most common type of vulvodynia is vestibulodynia. Vulvodynia is still not well understood, and patients often go to many different providers before being diagnosed. A recent population based survey found that 12% of women have had symptoms consistent with vulvodynia at some point in their lives (84).
There are many theories regarding the etiology of vulvodynia, but the most accepted theory is that it is a syndrome of neurologically mediated pain. Many patients identify a history of frequent candidal infections, treatments for condyloma, or other injury that preceded the onset of pain. Tissue injury causes the release of inflammatory neuropeptides, and nociceptors in the region become sensitized, leading to hyperesthesia or allodynia (pain in response to a stimulus that does not ordinarily provoke pain) (85).
Vulvodynia can negatively impact a woman's self esteem and relationship with her partner. Most studies have not found more frequent histories of sexual abuse, but a recent study found there may be higher rates of physical abuse in a subset of patients with vulvodynia (84). Other pain syndromes are also common in patients with vulvodynia, such as irritable bowel syndrome (IBS), interstitial cystitis, and fibromyalgia (86). An increased sensitivity to touch in nongenital sites in the body has also been documented (87). The muscles of the pelvic floor frequently play an important role in the perpetuation of pain in vulvodynia. Muscle hypertonicity may be primary and lead to vulvar pain, or muscle splinting may begin as a response to localized vulvar pain, but then become chronic.
Evaluation
The evaluation of a patient with vulvar pain begins with a careful pelvic examination. Any suspicious areas on the vulva should be biopsied. The vaginal discharge should be assessed, and any vaginitis treated. It is critical to make sure the vagina is well estrogenized. Mild degrees of atrophic vaginitis in perimenopausal women are frequently missed, but can have a large impact on vaginal symptoms. All patients should have vaginal fungal cultures sent because there is significant overlap in symptomatology between fungal infections and vulvodynia. A careful history must be taken to identify potential irritants. Antibacterial and perfumed soaps are frequent culprits, but other possibilities are over-the-counter vaginal products, sanitary pads, fabric softener sheets, and laundry detergents.
Urinary tract symptoms are also common in patients with introital dyspareunia. The presence of interstitial cystitis or urethritis may explain a patient's symptoms, or be an important contributing factor. Any patient with persistent urinary symptoms, especially in the presence of a negative urine culture, should be referred for cystoscopy.
The level of tenderness around the introitus can be assessed at each visit by lightly touching a cotton-tipped swab to various locations around the vulva and recording the patient's rating of the level of pain (Figure 102.5). Assessment of the pelvic floor muscles for hypertonicity or tenderness is equally important.
Treatment
Treatment of vulvodynia is aimed at breaking the cycle of pain, inflammation, sensitization, muscle tension, and maladaptive behaviors. A combination of therapies is usually necessary, frequently requiring a multidisciplinary approach, especially if the pain is long-standing.
Medications that are used to treat neuropathic pain in other areas of the body are used to treat vulvodynia as well (e.g., tricyclic antidepressants, anticonvulsants).
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Table 102.6 summarizes some of these medications (88, 89, 90, 91, 92, 93). It may be helpful to explain to the patient that these drugs are used for their effects on the pain pathways rather than for depression.
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FIGURE 102.5. Vulvar examination for vulvodynia. (From Haefner HK. Critique of new gynecologic surgical procedures: surgery for vulvar vestibulitis. Clin Obstet Gynecol 2000;43:689 .) |
There are also many topical medications that have been used in the treatment of vulvodynia (Table 102.6) (88,90). Evidence for the efficacy of most is either anecdotal or based on limited evidence. Many of the medications can be prepared by a compounding pharmacist. Many patients receive topical steroids, but there is no evidence of efficacy, and care must be taken to avoid steroid rebound dermatitis and genital atrophy. One small trial supports the use of submucosal infiltrations into the vulva of methylprednisolone and lidocaine (92). Many patients prefer to use a topical medication to avoid the risks and side effects associated with centrally acting drugs. A combination of a peripherally acting and a centrally acting medication is often beneficial.
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TABLE 102.6 Medications Used for the Treatment of Vulvodynia |
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Physical therapists with specialized training in pelvic floor therapy are invaluable in the treatment of vulvodynia, and should be consulted whenever there is tightness, weakness, or tenderness in the pelvic floor muscles. Biofeedback may be effective for some patients with vulvodynia (93).
Finally, the patient can be referred to a gynecologist for a surgical procedure, such as local excision, vestibulectomy, or perineoplasty, if more conservative techniques are ineffective. Most patients prefer to avoid an invasive procedure if possible, but success rates of 80% or greater are usually reported for surgical treatments. One randomized study comparing cognitive behavioral therapy, biofeedback, and surgical vestibulectomy found that all treatments significantly reduced pain, but that vestibulectomy was the most effective (94).
It is important to treat any muscle hypertonicity prior to surgery to maximize chances of a good outcome. Patients with primary vulvodynia, or pain beginning with their partner's first attempt at vaginal penetration, have poorer responses to surgery (95).
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Chronic Pelvic Pain
Chronic pelvic pain is a common clinical problem, with an estimated prevalence of 15% in women age 18 to 50 years (96). It is frustrating to patient and clinician alike: the symptoms are often poorly defined, diagnosis can take time, and often no cause is found. Further, there is no treatment that effects an easy cure. Despite these frustrations, however, chronic pelvic pain is treatable, and improvement is likely for many patients.
There is no single definition for chronic pelvic pain. One suggested definition is noncyclic pain of 6 or more months’ duration that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks, and is of sufficient severity to cause functional disability or lead to medical care (97). Diagnosis alone can require several visits and, once a treatment plan is established, frequent followup may be necessary to monitor improvement and provide continued support for the patient. Both the clinician and the patient must understand that a clear cause may not emerge and that complete resolution of symptoms may not occur (98).
Causes of Pelvic Pain
Chronic pelvic pain is a complex, multifactorial entity that can result from any number of causes. It should not be assumed that all pelvic pain is gynecologic in origin: GI, genitourinary, and musculoskeletal conditions are often implicated. The list of potential causes is long and diverse. One common gynecologic cause is endometriosis, although not all patients with endometriosis suffer from pelvic pain. Other gynecologic associations include pelvic adhesions and pelvic inflammatory disease (99). Bowel dysmotility disorders, especially irritable bowel syndrome, may be present in a majority of women with chronic pain complaints. Musculoskeletal and urologic disorders (e.g., interstitial cystitis) also account for a significant proportion of diagnoses of chronic pelvic pain (100,101).
Evaluation of the Patient with Chronic Pelvic Pain
The most important components of the evaluation of the patient with chronic pelvic pain are a thorough history and physical examination. Imaging techniques and laboratory studies should be used judiciously, because their role in diagnosis is limited (98).
History
The goal of the history is to elucidate the nature of the pain. Questions must be asked regarding the character, intensity, and distribution of the pain, as well as the duration of symptoms. The woman should also be asked whether the pain demonstrates a cyclic variation, specifically in relation to the menstrual cycle, and whether the symptoms themselves have changed over the course of time. Asking the woman to maintain a pain diary can be extremely helpful and is recommended for all patients who present for evaluation of pain. The clinician should also explore the impact that the pain has had on the patient's life and relationships, as well as the possible effects these may have had on the pain. A comprehensive review of systems is useful in determining related GI, urologic, or affective complaints. Mood disorders or depressive symptoms in particular may compound pain symptoms, and vice versa.
Direct inquiries should be made regarding a history of sexual abuse. Studies indicate that such a history is more common in patients with chronic pelvic pain (98,102). However, many patients with chronic pelvic pain do not have a history of sexual abuse, so it should not merely be assumed.
Physical Examination
A general physical and neurologic examination is indicated for any woman presenting for evaluation of chronic pelvic pain. At the start of the physical examination, the patient should be asked to point to the site of the pain: if one finger is sufficient, the pain is more likely to emanate from a specific source than if she uses her whole hand (100). The abdominal and pelvic examinations are important components of the evaluation, as is a thorough musculoskeletal examination. With the woman's permission, the clinician should attempt to reproduce her pain during the course of the examination.
Abdominal examination should begin with visual inspection for surface irregularities or scars. Palpation should include the back and inguinal region as well as the abdomen. Point tenderness (“trigger points”) (see Chapter 74), which may be localizable by palpation with a single examining finger, should be noted, as should any deeper or more diffuse tenderness. Much of the musculoskeletal examination, including flexion and extension of the abdominal musculature and lower extremities, can also be incorporated into the abdominal examination. The pelvic examination should be comprehensive, including speculum examination, bimanual examination, and examination of the external genitalia and should also focus (with the woman's permission) on symptom reproduction (98).
Diagnostic Studies
Some investigators recommend that a complete blood count, urinalysis, and cervical cultures be performed in all patients, with the decision to perform additional tests individualized for each woman (100). Endoscopic studies, including laparoscopy, can be valuable if endometriosis or adhesions are suggested by the results of the history and
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physical examination (103). A pelvic ultrasound may be useful to rule out a pelvic mass as cause of the pain (97). Questionable ultrasound findings can be followed up using magnetic resonance imaging or computed tomography.
Treatment
One should make an effort to treat any identifiable symptoms and to improve the woman's quality of life. Given the complex nature of chronic pelvic pain, this may involve a multidisciplinary approach. Mainstays of medical therapy (96) include oral analgesics, specifically nonsteroidal anti-inflammatory drugs (NSAIDs), which are most effective if used on a round-the-clock basis. Some patients benefit from the use of antidepressants, specifically tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). While evidence is limited for the efficacy of such medications in the treatment of chronic pelvic pain, they may be useful in treating associated depression (97). Narcotics should be used with caution: risk of addiction appears to be low, but there are no published data to confirm efficacy (97,102).
Treatment should also be targeted to the particular source of the patient's pain. Pain related to the menstrual cycle, for instance, can be treated with a trial of hormonal therapy, such as a monophasic oral contraceptive or a continuous progestin (oral or injectable). Pain from endometriosis may respond to hormonal manipulation as well, although the evidence for some hormonal medications is somewhat limited (97). Bowel disorders may respond to medical treatment or dietary alteration, including fiber supplementation. Alternative modalities, such as injection with local anesthetics or acupuncture, may also be considered. Physical therapy has been associated with improvement in pain in some observational studies (104). Psychotherapy can be a useful adjunct to medical treatment. For women who do not respond to treatment, referral to a specialist may be indicated.
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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