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- The leading cause of dyspareunia for women under age 50 is vulvar vestibulitis; for women over age 50, it is vulvovaginal atrophy.
- The skin conditions dermatitis, lichen sclerosus, and lichen planus are a significant cause of dyspareunia complaints.
- Candida can be difficult to diagnose; the fissuring experienced by patients with this infection is often attributed to other causes.
- Desquamative inflammatory vaginitis leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis.
- Generalized vulvar dysesthesia involves constant or episodic unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva. In contrast, localized vulvar dysesthesia is provoked pain in the vestibule.
Due in part to underreporting of the condition, the incidence and prevalence of dyspareunia—defined as genital pain experienced just before, during, or after sexual intercourse1—is uncertain.2
Because it is easy to miss subtle physical findings such as small fissures, periclitoral scarring, or a focus of tender vestibulitis under a hymenal remnant, getting to the root of dyspareunia can present a significant challenge to clinicians. Adding to the difficulty is the fact that intermittent conditions such as cyclical Candida albicans are hard to diagnose.
This review of 5 common but often overlooked causes describes what is known about dyspareunia and how to conduct a complete evaluation, including physical examination, diagnostic tests, and questions to ask the patient.
CAUSE 1Inadequate estrogenization
Vulvovaginal atrophy is the leading cause of sexual dysfunction, affecting up to 50% of women over age 50. It contributes to a lack of vaginal lubrication with sexual arousal and, consequently, dyspareunia and postcoital bleeding.3 Even when a woman is taking oral hormone replacement therapy, the vagina can lack sufficient estrogen.
Younger women also may experience atrophy and lowered estrogen levels. For example, a 34-year-old woman with premature ovarian failure may experience slight burning, dryness, and pain on penetration.
Tamoxifen can be a source of dyspareunia: It can cause vaginal atrophy in the premenopausal woman or estrogenization with Candidal invasion in postmenopausal patients.
Atrophy also can occur:
- with hypothalamic amenorrhea caused by excessive exercise or marked weight loss
- during the postpartum period and breast-feeding
- with the use of some low-estrogen (20 μg) contraceptives and medroxyprogesterone acetate
- after radiation or chemotherapy
Fortunately, atrophy is easily reversed with local estrogen in the form of cream, tablets, or the vaginal ring. Because the latter does not elevate circulating estradiol levels after the first 24 hours of use, many oncologists are willing to allow this therapy for breast cancer patients.4
When dyspareunia persists despite local estrogen use, we must seek out other causes.
CAUSE 2A skin disease
Dermatitis. There are 2 types of dermatitis: eczematous, in which the irritant is essentially unknown, and contactant, which arises from known irritants or allergens. In some cases, the exposure to an irritant may be fairly recent. In others, the continuing combination of irritants and tight clothing or abrasive activity eventually leads to symptoms.
Physical findings of dermatitis include erythema (with or without scaling) and fissuring—especially of the perineum. A biopsy is diagnostic.
Recommended treatment includes meticulous vulvar hygiene and the use of 2.5% hydrocortisone cream twice daily for 14 to 30 days, followed by twice-weekly “maintenance” applications. For moderate or severe cases, a medium-potency steroid (betamethasone valerate 0.1%) or an ultrapotent steroid (clobetasol 0.05%) may be used in the same manner. In addition, physicians should educate patients with dermatitis about the chronicity of the condition and the importance of eliminating the cause, if possible.
Poorly treated eczema leads to lichen simplex chronicus. One clue to this condition is a history of atopy or eczema elsewhere on the body.
Lichen sclerosus and lichen planus. These dermatoses cause changes in the color and texture of the epithelium.
Because lichen planus can produce erosion of the vestibule, it often is mistaken for vestibulitis. With this condition, erosions are intensely erythematous and vary from small areas to involvement of the entire vestibule. You will also note a serpiginous white border or subtle white reticules adjacent to erosions.
Both lichen sclerosus and lichen planus can produce intense itching or progress without clinical symptoms.
Lichen sclerosus, meanwhile, causes whitened epithelium with the thinned and wrinkled appearance of cigarette paper; areas of hyperkeratosis also may be present. Changes may occur from the periclitoral area to the anus in a keyhole configuration.
Both lichen sclerosus and lichen planus:
- can produce intense itching or progress without clinical symptoms
- can scar extensively and cause bridging synechiae at the fourchette, elimination of the labia minora, and fusion of the prepuce over the glans clitoris
- can produce anal fissuring and painful defecation
While lichen sclerosus never involves the vagina, vaginal lichen planus produces inflammatory vaginitis that can scar and reduce the size of the vagina—even obliterate it entirely.
Treatment for both diseases consists of ultrapotent topical steroids to arrest the inflammatory process. Vaginal lichen planus is treated with hydrocortisone suppositories (25 mg at bedtime), with the length of treatment dependent on severity.5 More potent steroids may be necessary.
CAUSE 3Candida
This infection can be extremely difficult to diagnose for a variety of reasons. Patients come in partially treated with over-the-counter antifungals. Many have taken a fluconazole tablet with a long half-life of action. Others have a cyclical candidiasis that is seen only in the luteal phase of the cycle. In these cases, fissuring is often attributed to other causes.
Complicating matters further, a wet mount will be negative in the presence of Candida approximately 50% of the time.6 For these reasons, a culture is essential when there is an index of clinical suspicion and white blood cells are present on the wet mount.
Uncomplicated Candida is treated by topical -azole creams for 3 or 7 days or a single fluconazole 150-mg tablet.
Complicated Candida (that is, more than 3 infections in a year or infection in a pregnant or immune-compromised host) will require longer courses of therapy.7
CAUSE 4Desquamative inflammatory vaginitis
Because the intense inflammation produced by the 2 diseases are similar, some people believe desquamative inflammatory vaginitis is a form of lichen planus8—in fact, it is sometimes called lichenoid vaginitis. However, desquamative inflammatory vaginitis does not scar the vagina, suggesting a different cause. Its profusely irritative discharge—microscopically characterized by sheets of white blood cells—resembles Trichomonas and Candida. Sheets of white blood cells and parabasal cells also resemble Trichomonas, Candida, or severe atrophy.
Questions such as “Are you sexually active?” and “Do you have any concerns about your sex life?” can begin a discussion of dyspareunia. Other vital questions include the following:
When did the pain begin? Primary complete dys-pareunia may result from a congenital anomaly or psychosocial issues, but the leading cause is vulvar vestibulitis.2 Acquired dyspareunia has many causes.
When and where does the pain or discomfort occur? Ask the patient to describe its severity, character, duration, location, and time during the menstrual cycle. Superficial dyspareunia usually is due to vestibulitis, inadequate lubrication, or an anatomic abnormality of the introitus.3 Other causes include vulvar atrophy, infection, urethral disorders, and vulvar dermatitis or dermatosis. Pain associated with deep penetration or thrusting may be related to a retroverted uterus or to impaired mobility of the pelvic organs due to scarring from endometriosis or pelvic inflammatory disease.4 Cystitis and interstitial cystitis may cause deep midline dyspareunia, as well as dysuria and other urinary tract symptoms. Deep dyspareunia can also be due to vaginal dryness or atrophy. Consider adnexal or bowel pathology when the pain occurs laterally.
Are there other sexual problems? Pain during intercourse often causes sexual dysfunction, which needs to be addressed before the pain can resolve.
What have you tried to treat or prevent the pain? Successful aids can offer diagnostic clues.
Is there any vaginal discharge, itching, burning, odor, or bleeding? These may be present with vaginitis or a neoplasm. Increased discharge may be due to vestibulitis.
Do you have any gynecologic problems, such as endometriosis, fibroids, or chronic pelvic pain? These conditions have well-known associations with deep dyspareunia. Endometriosis and vulvar vestibulitis occur together.
Have you had vulvovaginal or pelvic infections, such as candidiasis, herpes, gonorrhea, or chlamydia?Recurrent herpes or Candidal infection can be painful and difficult to diagnose; pelvic inflammatory disease can cause scarring and decreased mobility of pelvic organs.
What gynecologic surgery or other procedures have you undergone? Childbirth, radiation or chemotherapy, or incontinence procedures may lead to dyspareunia. Female circumcision is practiced in some cultures and should be considered when appropriate. Scarring and fibrosis can distort anatomy, narrow the vagina/introitus, and decrease tissue mobility, thereby causing pain during thrusting. Chemotherapy and radiation may result in premature ovarian failure (hypoestrogenism). Radiation vulvitis contributes to superficial pain.
What is your natural lubrication like? If it is low, have you tried commercially available lubricants? Natural lubrication may be reduced from hypoestrogenism, certain drugs, or difficulty with arousal.
What do you use for contraception? Latex allergy from condoms or a diaphragm, or an irritant reaction to spermicides may be at the root of the pain. Lowestrogen oral contraceptives or depot medroxyprogesterone acetate contribute to poor lubrication. The intrauterine device is a risk factor for recurrent Candida.
What medical or psychiatric problems are you currently being treated for? Skin disorders such as eczema and lichen planus may be associated with vulvar dermatitis. Inflammatory bowel disease may be related to pelvic adhesions. Interstitial cystitis can cause both dyspareunia and dysuria.
What drugs are you taking? Many medications are associated with dyspareunia due to side effects such as decreased sexual arousal, vaginal lubrication, or serum estrogen levels.
Have you ever been sexually abused or had a traumatic injury involving your genitals? Did you receive counseling or help for this? Many women have worked through their trauma, but unresolved issues can contribute to ongoing pain. Sexual abuse is a risk factor for chronic pelvic pain but is not associated with vestibulitis.5
What do you think may be causing this problem? Often, the patient will provide the answer.
REFERENCES
1. Stewart EG. Approach to the woman with dyspareunia. UpToDate. Available at: www.uptodate.com. In press.
2. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90:583-589.
3. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
4. Steege JF, Ling FW. Dyspareunia: A special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
5. Edwards L, Mason M, Phillip M, et al. Childhood sexual and physical abuse: incidence in patients with vulvodynia. J Reprod Med. 1997;42:135-139.
The inflammation leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis (though bacterial vaginosis never causes such inflammation).
Vulvodynia consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva and can be constant or episodic.
Though antibiotics may yield transient improvement,9 management most often consists of 25-mg hydrocortisone suppositories (or compounded as 100 mg for severe cases) at bedtime for 14 days, then every other day for 14 days. After this course of therapy has been completed, clinicians must reevaluate the patient to determine whether she needs extended therapy (in severe cases) or can begin maintenance with a weekly suppository (for cases that are mild but chronic).
If dyspareunia does not resolve after the inflammation abates, superimposed neuroinflammatory pain (vestibulitis) will need treatment.
CAUSE 5Vulvodynia or vulvar vestibulitis
Vulvodynia (generalized vulvar dysesthesia). This condition—which consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva—may be constant or episodic. Dyspareunia in these cases may involve postcoital exacerbation of symptoms.
The cause is unknown, but some suspect a lesion of the pudendal nerve in its long course from the spine to the vulva.
There may be virtually no physical findings, or there may be areas of tenderness, hyperesthesia, or hypoesthesia. A biopsy will be nonspecific. Vulvodynia is therefore diagnosed by ruling out infectious, dermatologic, or other causes of genital pain.
The following treatments are usually successful:
- tricyclic antidepressants such as nortriptyline, starting with a bedtime dose of 10 mg and working up to 50 mg to 150 mg
- the antiepileptic agent gabapentin, starting with a bedtime dose of 100 mg and working up to as much as 1,000 mg (this is usually substituted for the tricyclic antidepressant if that therapy alone is ineffective)
This condition may be either primary or secondary. With primary vestibulitis, a woman experiences pain with her first use of a tampon, her first exposure to a speculum, and the initiation of sexual relations. For those with secondary vestibulitis, pain on contact results after a period of comfortable sexual relations.
This pain is thought to stem from inflammation or trauma that initially sensitizes nociceptors in the vestibular mucosa, leading to prolonged neuronal firing. This in turn sensitizes the wide-dynamic-range neurons in the dorsal horn to respond abnormally, converting the sensation of touch into pain (allodynia).11 There often is a history of an unresolved irritative event such as Candidal infection, repeated genital infection,12 topical treatments,13 and early and sustained use of oral contraceptives.14 All are suspected causes.
Diagnosis is made once other pathology has been ruled out and a Q-tip test has demonstrated that contact elicits pain in the vestibule.
Numerous treatment protocols have been described, but current interest focuses on addressing neuroinflammatory pain. This can be done at the peripheral afferents by reducing inflammation and hyperexcitability with topical xylocaine 5% in a compounded sterol-lanolin base 5 times daily; centrally, this is accomplished using tricyclics in doses of 50 mg to 150 mg.
Note that primary vestibulitis is extremely difficult to treat; vestibulectomy and perineoplasty improve the condition by 60% to 90% when medical management fails.15
- Vaginismus, an involuntary spasm of the perineal and levator muscles, may occur in patients with vestibulitis. While primary vaginismus is psychologic in origin, secondary vaginismus represents a conditioned response to pain,16 usually vestibulitis. In patients with secondary disease, pelvic-floor motor instability has been well-demonstrated; these women have a reduced ability to contract or relax the pelvic floor and increased muscular instability at rest.17
Recent studies of the vestibule and vagina provide new insights into an organic explanation of dyspareunia in women who are otherwise healthy.
Clinicians have long known that the vulva and vestibule are innervated by the pudendal nerve, composed of both somatic motor efferents and sensory afferents. But autonomic nerve fibers from the inferior hypogastric plexus and caudal sympathetic chain ganglia also provide genital sensation and may contribute to the perpetuation of neuroinflammatory pain.1 Although the vulvar vestibule is by definition visceral tissue, it is considered to havenonvisceral innervation.2 Thus, sensations to touch, temperature, and pain are similar to sensations evoked in the skin and can be exquisitely painful.
The traditional view that the vagina has a paucity of nerve endings was contradicted with demonstration of profound innervation, with greater numbers of nerve fibers in the distal areas than in more proximal parts.3 The vagina itself can hurt.
In addition, the presence of luteinizing hormone and human chorionic gonadotropin receptors on the bladder trigone supports the complaint of cyclic worsening of pelvic dyspareunia.4 Circumvaginal motor spasm from hypertonicity of the levator plate5 is an evolving area of study.
Shifting views. Nineteenth-century gynecologists approached dyspareunia primarily from a surgical perspective, using a wide variety of operative interventions. In time, the surgical approach was replaced by an emphasis on psychosocial issues: Women who complained of dyspareunia were frequently classified as “frigid,” while physiological correlates were largely ignored.6 Still later, “deep-thrust” dyspareunia was considered suggestive of an organic source, whereas superficial or entrance dyspareunia was thought to derive from emotional or psychological issues.7
Gradually, an integrated and pain-model approach has evolved. It is now theorized that an instigating pain event is perpetuated by other factors.8
REFERENCES
1. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
2. Cervero F. Sensory innervation of the viscera: peripheral basis of visceral pain. Physiol Rev. 1994;74:95-138.
3. Hilliges M, Falconer C, Ekman-Ordeberg G, Johansson O. Innervation of the human vaginal mucosa as revealed by PGP 9.5 immunohistochemistry. Acta Anat. 1995;13:119-126.
4. Tao YX, Heit M, Lei ZM, et al. The urinary bladder of a woman is a novel site of luteinizing hormone-human chorionic gonadotropin receptor gene expression. Am J Obstet Gynecol. 1998;179:1026-1031.
5. Glazer HI, Jantos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
6. Levine SB, Rosenthal M. Marital sexual dysfunction: female dysfunctions. Ann Intern Med. 1977;86:588-597.
7. Steege JF, Ling FW. Dyspareunia: a special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
8. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
Vaginismus is diagnosed by eliciting muscle spasms in the pelvic floor by depressing the levators. If a woman has primary vaginismus of psychogenic origin, there is no tenderness in the vestibule; note, however, that the exam may be so difficult for her to endure that evaluating the vestibule is not possible.
Pelvic-floor motor instability is treated with physical therapy and biofeedback. In secondary disease, vestibulitis must also be concomitantly addressed. Primary disease, meanwhile, is treated by desensitization techniques that help the patient control the relaxation of her musculature.
The fine points of examination
Asking the right questions. Before you begin the physical exam, it is crucial to get as much information as possible about the patient’s condition. The dyspareunia history includes the following:
- a complete description of the pain problem and any concomitant sexual dysfunction
- exploration of potential gynecologic causes
- exploration of potential medical causes
- psychosocial information18
The physical exam. Although guided by the history, the physical examination needs to be as comprehensive as possible. It should include:
- systematic, meticulous inspection of every structure to confirm normal color, texture and architecture, and the presence or absence of lesions.
- gentle palpation of all tissues for the source of the discomfort. This should include a Q-tip test of the vestibule for tender foci.
- a speculum exam with inspection for mucosal integrity without fissure, erosion, or ulceration, as well as a check for the presence or absence of rugae and discharge. (Testing for pH is done with a reactive cardboard strip while the speculum is in place; then samples for wet mount and cultures are collected.)
- gentle single-digit exam of the vestibule to confirm the Q-tip test, as well as single-digit palpation of the pelvic-floor musculature, anterior vaginal wall, urethra, and bladder to confirm superficial pain and avoid confusion with pelvic sources.
- bimanual examination to evaluate for any nodularity or masses in the vagina, rectovaginal septum, or pelvis, as well as for mobility and tenderness of the pelvic organs.
Note that with generalized dysesthesia (vulvodynia), there may be no physical findings.
- Take steps to navigate the pain. Some women cannot tolerate a vulvar or vaginal examination; asking about previous experience will make it easier to tailor the exam appropriately. The following techniques also may be appropriate:
- use of premedication
- presence of a support person
- an agreement to stop the exam if the patient so requests
- use of a pediatric speculum
It may not be possible to complete all components of an examination at a single visit. For example, a patient may have to return for a vaginal examination and wet mount if menses are present at the initial appointment.
Cultures for Candida and Trichomonas are important when microscopy is negative.
Essential laboratory studies.
- Vaginal pH. A normal level (3.5 to 4.5) rules out bacterial infection and atrophy. Candida grows at any pH. Elevated pH is nonspecific and can represent recent intercourse or a small amount of blood. However, it also can suggest such causes of dyspareunia as atrophy, vaginal lichen planus, desquamative vaginitis, and Trichomonas.
- Wet mount reveals 4 important features:
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Pathogens.Candida or Trichomonas may be identified. Microscopy for Candida lacks sensitivity; a negative examination in a symptomatic woman mandates a culture for Candida.19
- Background flora. As mentioned earlier, lactobacillus dominates the normal vagina; when this predominance is seen on microscopy, there is no bacterial infection. A vaginal culture may grow Escherichia coli, group B streptococcus, Gardnerella, and a variety of normal commensals, but these are not the cause of dyspareunia when pH is normal and lactobacilli dominate the slide.
- White blood cells. Large numbers suggest Candida, lichen planus, Trichomonas, gonorrhea, chlamydia, or desquamative inflammatory vaginitis.
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Cultures for Candida and Trichomonas are important when microscopy is negative. Routine vaginal culture is not recommended. Cultures for herpes, gonorrhea, or chlamydia may be necessary.
- Biopsy and blood tests offer data on hormonal levels or type-specific antibodies for herpes. Biopsy of the vulva or vagina is indicated whenever there is a visible lesion that needs identification.
- Urine culture, colposcopy, or imaging such as ultrasonography and spine films may be indicated.
- Specialty referrals may be helpful for evaluation of the gastrointestinal or genitourinary tract, or for diagnostic laparoscopy for endometriosis.
Dr. Stewart reports no financial relationship with any companies whose products are mentioned in this article.
1. American College of Obstetricians and Gynecologists. Technical Bulletin #211: Sexual dysfunction. Washington, DC: ACOG; 1995.
2. Jamieson DJ, Steege JR. The prevalence of dysmenorrhea, pelvic pain and irritable bowel syndrome in primary care practices. Obstet Gynecol. 1996;87:55-58.
3. Jalbuena JR. Atrophic vaginitis in Filipino women. Climacteric. 2001;4:75.-
4. Johnston A. Estrogens–pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulation–Estring. Acta Obstetrica Gynecol Scand. 1996;163(suppl):16-25.
5. Anderson M, Kulzner S, Kaufman RH. Treatment of vulvovaginal lichen planus with vaginal hydrocortisone suppositories. Obstet Gynecol. 2002;100:359-362.
6. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
7. Sobel JD, Faro SF, Force RW, et al. Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol. 1998;178:203-211.
8. Edwards L, Friedrich EG. Desquamative vaginitis: lichen planus in disguise. Obstet Gynecol. 1988;71:832-836.
9. Sobel JD. Desquamative inflammatory vaginitis: A new subgroup of purulent vaginitis responsive to topical 2% clindamycin therapy. Obstet Gynecol. 1994;171:1215-1220.
10. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90(4 pt 1):583-589.
11. Bohm-Starke N, Hilliges M, Brodda-Jansen G, Rylander E, Torebjork E. Psychophysical evidence of nociceptor sensitization in vulvar vestibulitis syndrome. Pain. 2001;94:177-183.
12. Baggish MS, Miklos JR. Vulvar pain syndrome: A review. Obstet Gynecol Surv. 1995;50:401-411.
13. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome. Dermatol Clin. 1992;10:435-444.
14. Bouchard C, Brisson J, Fortier M, Morin C, Blanchette C. Use of oral contraceptive pills and vulvar vestibulitis: A case control study. Am J Epidemiol. 2002;156:254-261.
15. Bornstein J, Zarfati D, Abramovici H. Perineoplasty compared with vestibuloplasty for severe vulvar vestibulitis. Obstet Gynecol. 1997;89:695-698.
16. Meana M, Binik YM. Painful coitus: A review of female dyspareunia. J Nerv Ment Dis. 1994;182:264-272.
17. Glazer HI, Janos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
18. Phillips NA. The clinical evaluation of dyspareunia. Int J Impotence Research. 1998;10(suppl 2):S117-S120.
19. Nyirjesy P, Seeney SM, Grody MHT, et al. Chronic fungal vaginitis: the value of cultures. Am J Obstet Gynecol. 1995;173:820-823.
- The leading cause of dyspareunia for women under age 50 is vulvar vestibulitis; for women over age 50, it is vulvovaginal atrophy.
- The skin conditions dermatitis, lichen sclerosus, and lichen planus are a significant cause of dyspareunia complaints.
- Candida can be difficult to diagnose; the fissuring experienced by patients with this infection is often attributed to other causes.
- Desquamative inflammatory vaginitis leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis.
- Generalized vulvar dysesthesia involves constant or episodic unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva. In contrast, localized vulvar dysesthesia is provoked pain in the vestibule.
Due in part to underreporting of the condition, the incidence and prevalence of dyspareunia—defined as genital pain experienced just before, during, or after sexual intercourse1—is uncertain.2
Because it is easy to miss subtle physical findings such as small fissures, periclitoral scarring, or a focus of tender vestibulitis under a hymenal remnant, getting to the root of dyspareunia can present a significant challenge to clinicians. Adding to the difficulty is the fact that intermittent conditions such as cyclical Candida albicans are hard to diagnose.
This review of 5 common but often overlooked causes describes what is known about dyspareunia and how to conduct a complete evaluation, including physical examination, diagnostic tests, and questions to ask the patient.
CAUSE 1Inadequate estrogenization
Vulvovaginal atrophy is the leading cause of sexual dysfunction, affecting up to 50% of women over age 50. It contributes to a lack of vaginal lubrication with sexual arousal and, consequently, dyspareunia and postcoital bleeding.3 Even when a woman is taking oral hormone replacement therapy, the vagina can lack sufficient estrogen.
Younger women also may experience atrophy and lowered estrogen levels. For example, a 34-year-old woman with premature ovarian failure may experience slight burning, dryness, and pain on penetration.
Tamoxifen can be a source of dyspareunia: It can cause vaginal atrophy in the premenopausal woman or estrogenization with Candidal invasion in postmenopausal patients.
Atrophy also can occur:
- with hypothalamic amenorrhea caused by excessive exercise or marked weight loss
- during the postpartum period and breast-feeding
- with the use of some low-estrogen (20 μg) contraceptives and medroxyprogesterone acetate
- after radiation or chemotherapy
Fortunately, atrophy is easily reversed with local estrogen in the form of cream, tablets, or the vaginal ring. Because the latter does not elevate circulating estradiol levels after the first 24 hours of use, many oncologists are willing to allow this therapy for breast cancer patients.4
When dyspareunia persists despite local estrogen use, we must seek out other causes.
CAUSE 2A skin disease
Dermatitis. There are 2 types of dermatitis: eczematous, in which the irritant is essentially unknown, and contactant, which arises from known irritants or allergens. In some cases, the exposure to an irritant may be fairly recent. In others, the continuing combination of irritants and tight clothing or abrasive activity eventually leads to symptoms.
Physical findings of dermatitis include erythema (with or without scaling) and fissuring—especially of the perineum. A biopsy is diagnostic.
Recommended treatment includes meticulous vulvar hygiene and the use of 2.5% hydrocortisone cream twice daily for 14 to 30 days, followed by twice-weekly “maintenance” applications. For moderate or severe cases, a medium-potency steroid (betamethasone valerate 0.1%) or an ultrapotent steroid (clobetasol 0.05%) may be used in the same manner. In addition, physicians should educate patients with dermatitis about the chronicity of the condition and the importance of eliminating the cause, if possible.
Poorly treated eczema leads to lichen simplex chronicus. One clue to this condition is a history of atopy or eczema elsewhere on the body.
Lichen sclerosus and lichen planus. These dermatoses cause changes in the color and texture of the epithelium.
Because lichen planus can produce erosion of the vestibule, it often is mistaken for vestibulitis. With this condition, erosions are intensely erythematous and vary from small areas to involvement of the entire vestibule. You will also note a serpiginous white border or subtle white reticules adjacent to erosions.
Both lichen sclerosus and lichen planus can produce intense itching or progress without clinical symptoms.
Lichen sclerosus, meanwhile, causes whitened epithelium with the thinned and wrinkled appearance of cigarette paper; areas of hyperkeratosis also may be present. Changes may occur from the periclitoral area to the anus in a keyhole configuration.
Both lichen sclerosus and lichen planus:
- can produce intense itching or progress without clinical symptoms
- can scar extensively and cause bridging synechiae at the fourchette, elimination of the labia minora, and fusion of the prepuce over the glans clitoris
- can produce anal fissuring and painful defecation
While lichen sclerosus never involves the vagina, vaginal lichen planus produces inflammatory vaginitis that can scar and reduce the size of the vagina—even obliterate it entirely.
Treatment for both diseases consists of ultrapotent topical steroids to arrest the inflammatory process. Vaginal lichen planus is treated with hydrocortisone suppositories (25 mg at bedtime), with the length of treatment dependent on severity.5 More potent steroids may be necessary.
CAUSE 3Candida
This infection can be extremely difficult to diagnose for a variety of reasons. Patients come in partially treated with over-the-counter antifungals. Many have taken a fluconazole tablet with a long half-life of action. Others have a cyclical candidiasis that is seen only in the luteal phase of the cycle. In these cases, fissuring is often attributed to other causes.
Complicating matters further, a wet mount will be negative in the presence of Candida approximately 50% of the time.6 For these reasons, a culture is essential when there is an index of clinical suspicion and white blood cells are present on the wet mount.
Uncomplicated Candida is treated by topical -azole creams for 3 or 7 days or a single fluconazole 150-mg tablet.
Complicated Candida (that is, more than 3 infections in a year or infection in a pregnant or immune-compromised host) will require longer courses of therapy.7
CAUSE 4Desquamative inflammatory vaginitis
Because the intense inflammation produced by the 2 diseases are similar, some people believe desquamative inflammatory vaginitis is a form of lichen planus8—in fact, it is sometimes called lichenoid vaginitis. However, desquamative inflammatory vaginitis does not scar the vagina, suggesting a different cause. Its profusely irritative discharge—microscopically characterized by sheets of white blood cells—resembles Trichomonas and Candida. Sheets of white blood cells and parabasal cells also resemble Trichomonas, Candida, or severe atrophy.
Questions such as “Are you sexually active?” and “Do you have any concerns about your sex life?” can begin a discussion of dyspareunia. Other vital questions include the following:
When did the pain begin? Primary complete dys-pareunia may result from a congenital anomaly or psychosocial issues, but the leading cause is vulvar vestibulitis.2 Acquired dyspareunia has many causes.
When and where does the pain or discomfort occur? Ask the patient to describe its severity, character, duration, location, and time during the menstrual cycle. Superficial dyspareunia usually is due to vestibulitis, inadequate lubrication, or an anatomic abnormality of the introitus.3 Other causes include vulvar atrophy, infection, urethral disorders, and vulvar dermatitis or dermatosis. Pain associated with deep penetration or thrusting may be related to a retroverted uterus or to impaired mobility of the pelvic organs due to scarring from endometriosis or pelvic inflammatory disease.4 Cystitis and interstitial cystitis may cause deep midline dyspareunia, as well as dysuria and other urinary tract symptoms. Deep dyspareunia can also be due to vaginal dryness or atrophy. Consider adnexal or bowel pathology when the pain occurs laterally.
Are there other sexual problems? Pain during intercourse often causes sexual dysfunction, which needs to be addressed before the pain can resolve.
What have you tried to treat or prevent the pain? Successful aids can offer diagnostic clues.
Is there any vaginal discharge, itching, burning, odor, or bleeding? These may be present with vaginitis or a neoplasm. Increased discharge may be due to vestibulitis.
Do you have any gynecologic problems, such as endometriosis, fibroids, or chronic pelvic pain? These conditions have well-known associations with deep dyspareunia. Endometriosis and vulvar vestibulitis occur together.
Have you had vulvovaginal or pelvic infections, such as candidiasis, herpes, gonorrhea, or chlamydia?Recurrent herpes or Candidal infection can be painful and difficult to diagnose; pelvic inflammatory disease can cause scarring and decreased mobility of pelvic organs.
What gynecologic surgery or other procedures have you undergone? Childbirth, radiation or chemotherapy, or incontinence procedures may lead to dyspareunia. Female circumcision is practiced in some cultures and should be considered when appropriate. Scarring and fibrosis can distort anatomy, narrow the vagina/introitus, and decrease tissue mobility, thereby causing pain during thrusting. Chemotherapy and radiation may result in premature ovarian failure (hypoestrogenism). Radiation vulvitis contributes to superficial pain.
What is your natural lubrication like? If it is low, have you tried commercially available lubricants? Natural lubrication may be reduced from hypoestrogenism, certain drugs, or difficulty with arousal.
What do you use for contraception? Latex allergy from condoms or a diaphragm, or an irritant reaction to spermicides may be at the root of the pain. Lowestrogen oral contraceptives or depot medroxyprogesterone acetate contribute to poor lubrication. The intrauterine device is a risk factor for recurrent Candida.
What medical or psychiatric problems are you currently being treated for? Skin disorders such as eczema and lichen planus may be associated with vulvar dermatitis. Inflammatory bowel disease may be related to pelvic adhesions. Interstitial cystitis can cause both dyspareunia and dysuria.
What drugs are you taking? Many medications are associated with dyspareunia due to side effects such as decreased sexual arousal, vaginal lubrication, or serum estrogen levels.
Have you ever been sexually abused or had a traumatic injury involving your genitals? Did you receive counseling or help for this? Many women have worked through their trauma, but unresolved issues can contribute to ongoing pain. Sexual abuse is a risk factor for chronic pelvic pain but is not associated with vestibulitis.5
What do you think may be causing this problem? Often, the patient will provide the answer.
REFERENCES
1. Stewart EG. Approach to the woman with dyspareunia. UpToDate. Available at: www.uptodate.com. In press.
2. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90:583-589.
3. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
4. Steege JF, Ling FW. Dyspareunia: A special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
5. Edwards L, Mason M, Phillip M, et al. Childhood sexual and physical abuse: incidence in patients with vulvodynia. J Reprod Med. 1997;42:135-139.
The inflammation leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis (though bacterial vaginosis never causes such inflammation).
Vulvodynia consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva and can be constant or episodic.
Though antibiotics may yield transient improvement,9 management most often consists of 25-mg hydrocortisone suppositories (or compounded as 100 mg for severe cases) at bedtime for 14 days, then every other day for 14 days. After this course of therapy has been completed, clinicians must reevaluate the patient to determine whether she needs extended therapy (in severe cases) or can begin maintenance with a weekly suppository (for cases that are mild but chronic).
If dyspareunia does not resolve after the inflammation abates, superimposed neuroinflammatory pain (vestibulitis) will need treatment.
CAUSE 5Vulvodynia or vulvar vestibulitis
Vulvodynia (generalized vulvar dysesthesia). This condition—which consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva—may be constant or episodic. Dyspareunia in these cases may involve postcoital exacerbation of symptoms.
The cause is unknown, but some suspect a lesion of the pudendal nerve in its long course from the spine to the vulva.
There may be virtually no physical findings, or there may be areas of tenderness, hyperesthesia, or hypoesthesia. A biopsy will be nonspecific. Vulvodynia is therefore diagnosed by ruling out infectious, dermatologic, or other causes of genital pain.
The following treatments are usually successful:
- tricyclic antidepressants such as nortriptyline, starting with a bedtime dose of 10 mg and working up to 50 mg to 150 mg
- the antiepileptic agent gabapentin, starting with a bedtime dose of 100 mg and working up to as much as 1,000 mg (this is usually substituted for the tricyclic antidepressant if that therapy alone is ineffective)
This condition may be either primary or secondary. With primary vestibulitis, a woman experiences pain with her first use of a tampon, her first exposure to a speculum, and the initiation of sexual relations. For those with secondary vestibulitis, pain on contact results after a period of comfortable sexual relations.
This pain is thought to stem from inflammation or trauma that initially sensitizes nociceptors in the vestibular mucosa, leading to prolonged neuronal firing. This in turn sensitizes the wide-dynamic-range neurons in the dorsal horn to respond abnormally, converting the sensation of touch into pain (allodynia).11 There often is a history of an unresolved irritative event such as Candidal infection, repeated genital infection,12 topical treatments,13 and early and sustained use of oral contraceptives.14 All are suspected causes.
Diagnosis is made once other pathology has been ruled out and a Q-tip test has demonstrated that contact elicits pain in the vestibule.
Numerous treatment protocols have been described, but current interest focuses on addressing neuroinflammatory pain. This can be done at the peripheral afferents by reducing inflammation and hyperexcitability with topical xylocaine 5% in a compounded sterol-lanolin base 5 times daily; centrally, this is accomplished using tricyclics in doses of 50 mg to 150 mg.
Note that primary vestibulitis is extremely difficult to treat; vestibulectomy and perineoplasty improve the condition by 60% to 90% when medical management fails.15
- Vaginismus, an involuntary spasm of the perineal and levator muscles, may occur in patients with vestibulitis. While primary vaginismus is psychologic in origin, secondary vaginismus represents a conditioned response to pain,16 usually vestibulitis. In patients with secondary disease, pelvic-floor motor instability has been well-demonstrated; these women have a reduced ability to contract or relax the pelvic floor and increased muscular instability at rest.17
Recent studies of the vestibule and vagina provide new insights into an organic explanation of dyspareunia in women who are otherwise healthy.
Clinicians have long known that the vulva and vestibule are innervated by the pudendal nerve, composed of both somatic motor efferents and sensory afferents. But autonomic nerve fibers from the inferior hypogastric plexus and caudal sympathetic chain ganglia also provide genital sensation and may contribute to the perpetuation of neuroinflammatory pain.1 Although the vulvar vestibule is by definition visceral tissue, it is considered to havenonvisceral innervation.2 Thus, sensations to touch, temperature, and pain are similar to sensations evoked in the skin and can be exquisitely painful.
The traditional view that the vagina has a paucity of nerve endings was contradicted with demonstration of profound innervation, with greater numbers of nerve fibers in the distal areas than in more proximal parts.3 The vagina itself can hurt.
In addition, the presence of luteinizing hormone and human chorionic gonadotropin receptors on the bladder trigone supports the complaint of cyclic worsening of pelvic dyspareunia.4 Circumvaginal motor spasm from hypertonicity of the levator plate5 is an evolving area of study.
Shifting views. Nineteenth-century gynecologists approached dyspareunia primarily from a surgical perspective, using a wide variety of operative interventions. In time, the surgical approach was replaced by an emphasis on psychosocial issues: Women who complained of dyspareunia were frequently classified as “frigid,” while physiological correlates were largely ignored.6 Still later, “deep-thrust” dyspareunia was considered suggestive of an organic source, whereas superficial or entrance dyspareunia was thought to derive from emotional or psychological issues.7
Gradually, an integrated and pain-model approach has evolved. It is now theorized that an instigating pain event is perpetuated by other factors.8
REFERENCES
1. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
2. Cervero F. Sensory innervation of the viscera: peripheral basis of visceral pain. Physiol Rev. 1994;74:95-138.
3. Hilliges M, Falconer C, Ekman-Ordeberg G, Johansson O. Innervation of the human vaginal mucosa as revealed by PGP 9.5 immunohistochemistry. Acta Anat. 1995;13:119-126.
4. Tao YX, Heit M, Lei ZM, et al. The urinary bladder of a woman is a novel site of luteinizing hormone-human chorionic gonadotropin receptor gene expression. Am J Obstet Gynecol. 1998;179:1026-1031.
5. Glazer HI, Jantos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
6. Levine SB, Rosenthal M. Marital sexual dysfunction: female dysfunctions. Ann Intern Med. 1977;86:588-597.
7. Steege JF, Ling FW. Dyspareunia: a special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
8. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
Vaginismus is diagnosed by eliciting muscle spasms in the pelvic floor by depressing the levators. If a woman has primary vaginismus of psychogenic origin, there is no tenderness in the vestibule; note, however, that the exam may be so difficult for her to endure that evaluating the vestibule is not possible.
Pelvic-floor motor instability is treated with physical therapy and biofeedback. In secondary disease, vestibulitis must also be concomitantly addressed. Primary disease, meanwhile, is treated by desensitization techniques that help the patient control the relaxation of her musculature.
The fine points of examination
Asking the right questions. Before you begin the physical exam, it is crucial to get as much information as possible about the patient’s condition. The dyspareunia history includes the following:
- a complete description of the pain problem and any concomitant sexual dysfunction
- exploration of potential gynecologic causes
- exploration of potential medical causes
- psychosocial information18
The physical exam. Although guided by the history, the physical examination needs to be as comprehensive as possible. It should include:
- systematic, meticulous inspection of every structure to confirm normal color, texture and architecture, and the presence or absence of lesions.
- gentle palpation of all tissues for the source of the discomfort. This should include a Q-tip test of the vestibule for tender foci.
- a speculum exam with inspection for mucosal integrity without fissure, erosion, or ulceration, as well as a check for the presence or absence of rugae and discharge. (Testing for pH is done with a reactive cardboard strip while the speculum is in place; then samples for wet mount and cultures are collected.)
- gentle single-digit exam of the vestibule to confirm the Q-tip test, as well as single-digit palpation of the pelvic-floor musculature, anterior vaginal wall, urethra, and bladder to confirm superficial pain and avoid confusion with pelvic sources.
- bimanual examination to evaluate for any nodularity or masses in the vagina, rectovaginal septum, or pelvis, as well as for mobility and tenderness of the pelvic organs.
Note that with generalized dysesthesia (vulvodynia), there may be no physical findings.
- Take steps to navigate the pain. Some women cannot tolerate a vulvar or vaginal examination; asking about previous experience will make it easier to tailor the exam appropriately. The following techniques also may be appropriate:
- use of premedication
- presence of a support person
- an agreement to stop the exam if the patient so requests
- use of a pediatric speculum
It may not be possible to complete all components of an examination at a single visit. For example, a patient may have to return for a vaginal examination and wet mount if menses are present at the initial appointment.
Cultures for Candida and Trichomonas are important when microscopy is negative.
Essential laboratory studies.
- Vaginal pH. A normal level (3.5 to 4.5) rules out bacterial infection and atrophy. Candida grows at any pH. Elevated pH is nonspecific and can represent recent intercourse or a small amount of blood. However, it also can suggest such causes of dyspareunia as atrophy, vaginal lichen planus, desquamative vaginitis, and Trichomonas.
- Wet mount reveals 4 important features:
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Pathogens.Candida or Trichomonas may be identified. Microscopy for Candida lacks sensitivity; a negative examination in a symptomatic woman mandates a culture for Candida.19
- Background flora. As mentioned earlier, lactobacillus dominates the normal vagina; when this predominance is seen on microscopy, there is no bacterial infection. A vaginal culture may grow Escherichia coli, group B streptococcus, Gardnerella, and a variety of normal commensals, but these are not the cause of dyspareunia when pH is normal and lactobacilli dominate the slide.
- White blood cells. Large numbers suggest Candida, lichen planus, Trichomonas, gonorrhea, chlamydia, or desquamative inflammatory vaginitis.
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Cultures for Candida and Trichomonas are important when microscopy is negative. Routine vaginal culture is not recommended. Cultures for herpes, gonorrhea, or chlamydia may be necessary.
- Biopsy and blood tests offer data on hormonal levels or type-specific antibodies for herpes. Biopsy of the vulva or vagina is indicated whenever there is a visible lesion that needs identification.
- Urine culture, colposcopy, or imaging such as ultrasonography and spine films may be indicated.
- Specialty referrals may be helpful for evaluation of the gastrointestinal or genitourinary tract, or for diagnostic laparoscopy for endometriosis.
Dr. Stewart reports no financial relationship with any companies whose products are mentioned in this article.
- The leading cause of dyspareunia for women under age 50 is vulvar vestibulitis; for women over age 50, it is vulvovaginal atrophy.
- The skin conditions dermatitis, lichen sclerosus, and lichen planus are a significant cause of dyspareunia complaints.
- Candida can be difficult to diagnose; the fissuring experienced by patients with this infection is often attributed to other causes.
- Desquamative inflammatory vaginitis leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis.
- Generalized vulvar dysesthesia involves constant or episodic unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva. In contrast, localized vulvar dysesthesia is provoked pain in the vestibule.
Due in part to underreporting of the condition, the incidence and prevalence of dyspareunia—defined as genital pain experienced just before, during, or after sexual intercourse1—is uncertain.2
Because it is easy to miss subtle physical findings such as small fissures, periclitoral scarring, or a focus of tender vestibulitis under a hymenal remnant, getting to the root of dyspareunia can present a significant challenge to clinicians. Adding to the difficulty is the fact that intermittent conditions such as cyclical Candida albicans are hard to diagnose.
This review of 5 common but often overlooked causes describes what is known about dyspareunia and how to conduct a complete evaluation, including physical examination, diagnostic tests, and questions to ask the patient.
CAUSE 1Inadequate estrogenization
Vulvovaginal atrophy is the leading cause of sexual dysfunction, affecting up to 50% of women over age 50. It contributes to a lack of vaginal lubrication with sexual arousal and, consequently, dyspareunia and postcoital bleeding.3 Even when a woman is taking oral hormone replacement therapy, the vagina can lack sufficient estrogen.
Younger women also may experience atrophy and lowered estrogen levels. For example, a 34-year-old woman with premature ovarian failure may experience slight burning, dryness, and pain on penetration.
Tamoxifen can be a source of dyspareunia: It can cause vaginal atrophy in the premenopausal woman or estrogenization with Candidal invasion in postmenopausal patients.
Atrophy also can occur:
- with hypothalamic amenorrhea caused by excessive exercise or marked weight loss
- during the postpartum period and breast-feeding
- with the use of some low-estrogen (20 μg) contraceptives and medroxyprogesterone acetate
- after radiation or chemotherapy
Fortunately, atrophy is easily reversed with local estrogen in the form of cream, tablets, or the vaginal ring. Because the latter does not elevate circulating estradiol levels after the first 24 hours of use, many oncologists are willing to allow this therapy for breast cancer patients.4
When dyspareunia persists despite local estrogen use, we must seek out other causes.
CAUSE 2A skin disease
Dermatitis. There are 2 types of dermatitis: eczematous, in which the irritant is essentially unknown, and contactant, which arises from known irritants or allergens. In some cases, the exposure to an irritant may be fairly recent. In others, the continuing combination of irritants and tight clothing or abrasive activity eventually leads to symptoms.
Physical findings of dermatitis include erythema (with or without scaling) and fissuring—especially of the perineum. A biopsy is diagnostic.
Recommended treatment includes meticulous vulvar hygiene and the use of 2.5% hydrocortisone cream twice daily for 14 to 30 days, followed by twice-weekly “maintenance” applications. For moderate or severe cases, a medium-potency steroid (betamethasone valerate 0.1%) or an ultrapotent steroid (clobetasol 0.05%) may be used in the same manner. In addition, physicians should educate patients with dermatitis about the chronicity of the condition and the importance of eliminating the cause, if possible.
Poorly treated eczema leads to lichen simplex chronicus. One clue to this condition is a history of atopy or eczema elsewhere on the body.
Lichen sclerosus and lichen planus. These dermatoses cause changes in the color and texture of the epithelium.
Because lichen planus can produce erosion of the vestibule, it often is mistaken for vestibulitis. With this condition, erosions are intensely erythematous and vary from small areas to involvement of the entire vestibule. You will also note a serpiginous white border or subtle white reticules adjacent to erosions.
Both lichen sclerosus and lichen planus can produce intense itching or progress without clinical symptoms.
Lichen sclerosus, meanwhile, causes whitened epithelium with the thinned and wrinkled appearance of cigarette paper; areas of hyperkeratosis also may be present. Changes may occur from the periclitoral area to the anus in a keyhole configuration.
Both lichen sclerosus and lichen planus:
- can produce intense itching or progress without clinical symptoms
- can scar extensively and cause bridging synechiae at the fourchette, elimination of the labia minora, and fusion of the prepuce over the glans clitoris
- can produce anal fissuring and painful defecation
While lichen sclerosus never involves the vagina, vaginal lichen planus produces inflammatory vaginitis that can scar and reduce the size of the vagina—even obliterate it entirely.
Treatment for both diseases consists of ultrapotent topical steroids to arrest the inflammatory process. Vaginal lichen planus is treated with hydrocortisone suppositories (25 mg at bedtime), with the length of treatment dependent on severity.5 More potent steroids may be necessary.
CAUSE 3Candida
This infection can be extremely difficult to diagnose for a variety of reasons. Patients come in partially treated with over-the-counter antifungals. Many have taken a fluconazole tablet with a long half-life of action. Others have a cyclical candidiasis that is seen only in the luteal phase of the cycle. In these cases, fissuring is often attributed to other causes.
Complicating matters further, a wet mount will be negative in the presence of Candida approximately 50% of the time.6 For these reasons, a culture is essential when there is an index of clinical suspicion and white blood cells are present on the wet mount.
Uncomplicated Candida is treated by topical -azole creams for 3 or 7 days or a single fluconazole 150-mg tablet.
Complicated Candida (that is, more than 3 infections in a year or infection in a pregnant or immune-compromised host) will require longer courses of therapy.7
CAUSE 4Desquamative inflammatory vaginitis
Because the intense inflammation produced by the 2 diseases are similar, some people believe desquamative inflammatory vaginitis is a form of lichen planus8—in fact, it is sometimes called lichenoid vaginitis. However, desquamative inflammatory vaginitis does not scar the vagina, suggesting a different cause. Its profusely irritative discharge—microscopically characterized by sheets of white blood cells—resembles Trichomonas and Candida. Sheets of white blood cells and parabasal cells also resemble Trichomonas, Candida, or severe atrophy.
Questions such as “Are you sexually active?” and “Do you have any concerns about your sex life?” can begin a discussion of dyspareunia. Other vital questions include the following:
When did the pain begin? Primary complete dys-pareunia may result from a congenital anomaly or psychosocial issues, but the leading cause is vulvar vestibulitis.2 Acquired dyspareunia has many causes.
When and where does the pain or discomfort occur? Ask the patient to describe its severity, character, duration, location, and time during the menstrual cycle. Superficial dyspareunia usually is due to vestibulitis, inadequate lubrication, or an anatomic abnormality of the introitus.3 Other causes include vulvar atrophy, infection, urethral disorders, and vulvar dermatitis or dermatosis. Pain associated with deep penetration or thrusting may be related to a retroverted uterus or to impaired mobility of the pelvic organs due to scarring from endometriosis or pelvic inflammatory disease.4 Cystitis and interstitial cystitis may cause deep midline dyspareunia, as well as dysuria and other urinary tract symptoms. Deep dyspareunia can also be due to vaginal dryness or atrophy. Consider adnexal or bowel pathology when the pain occurs laterally.
Are there other sexual problems? Pain during intercourse often causes sexual dysfunction, which needs to be addressed before the pain can resolve.
What have you tried to treat or prevent the pain? Successful aids can offer diagnostic clues.
Is there any vaginal discharge, itching, burning, odor, or bleeding? These may be present with vaginitis or a neoplasm. Increased discharge may be due to vestibulitis.
Do you have any gynecologic problems, such as endometriosis, fibroids, or chronic pelvic pain? These conditions have well-known associations with deep dyspareunia. Endometriosis and vulvar vestibulitis occur together.
Have you had vulvovaginal or pelvic infections, such as candidiasis, herpes, gonorrhea, or chlamydia?Recurrent herpes or Candidal infection can be painful and difficult to diagnose; pelvic inflammatory disease can cause scarring and decreased mobility of pelvic organs.
What gynecologic surgery or other procedures have you undergone? Childbirth, radiation or chemotherapy, or incontinence procedures may lead to dyspareunia. Female circumcision is practiced in some cultures and should be considered when appropriate. Scarring and fibrosis can distort anatomy, narrow the vagina/introitus, and decrease tissue mobility, thereby causing pain during thrusting. Chemotherapy and radiation may result in premature ovarian failure (hypoestrogenism). Radiation vulvitis contributes to superficial pain.
What is your natural lubrication like? If it is low, have you tried commercially available lubricants? Natural lubrication may be reduced from hypoestrogenism, certain drugs, or difficulty with arousal.
What do you use for contraception? Latex allergy from condoms or a diaphragm, or an irritant reaction to spermicides may be at the root of the pain. Lowestrogen oral contraceptives or depot medroxyprogesterone acetate contribute to poor lubrication. The intrauterine device is a risk factor for recurrent Candida.
What medical or psychiatric problems are you currently being treated for? Skin disorders such as eczema and lichen planus may be associated with vulvar dermatitis. Inflammatory bowel disease may be related to pelvic adhesions. Interstitial cystitis can cause both dyspareunia and dysuria.
What drugs are you taking? Many medications are associated with dyspareunia due to side effects such as decreased sexual arousal, vaginal lubrication, or serum estrogen levels.
Have you ever been sexually abused or had a traumatic injury involving your genitals? Did you receive counseling or help for this? Many women have worked through their trauma, but unresolved issues can contribute to ongoing pain. Sexual abuse is a risk factor for chronic pelvic pain but is not associated with vestibulitis.5
What do you think may be causing this problem? Often, the patient will provide the answer.
REFERENCES
1. Stewart EG. Approach to the woman with dyspareunia. UpToDate. Available at: www.uptodate.com. In press.
2. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90:583-589.
3. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
4. Steege JF, Ling FW. Dyspareunia: A special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
5. Edwards L, Mason M, Phillip M, et al. Childhood sexual and physical abuse: incidence in patients with vulvodynia. J Reprod Med. 1997;42:135-139.
The inflammation leads to the loss of the lactobacillus, with bacterial overgrowth and clue cells similar to bacterial vaginosis (though bacterial vaginosis never causes such inflammation).
Vulvodynia consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva and can be constant or episodic.
Though antibiotics may yield transient improvement,9 management most often consists of 25-mg hydrocortisone suppositories (or compounded as 100 mg for severe cases) at bedtime for 14 days, then every other day for 14 days. After this course of therapy has been completed, clinicians must reevaluate the patient to determine whether she needs extended therapy (in severe cases) or can begin maintenance with a weekly suppository (for cases that are mild but chronic).
If dyspareunia does not resolve after the inflammation abates, superimposed neuroinflammatory pain (vestibulitis) will need treatment.
CAUSE 5Vulvodynia or vulvar vestibulitis
Vulvodynia (generalized vulvar dysesthesia). This condition—which consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva—may be constant or episodic. Dyspareunia in these cases may involve postcoital exacerbation of symptoms.
The cause is unknown, but some suspect a lesion of the pudendal nerve in its long course from the spine to the vulva.
There may be virtually no physical findings, or there may be areas of tenderness, hyperesthesia, or hypoesthesia. A biopsy will be nonspecific. Vulvodynia is therefore diagnosed by ruling out infectious, dermatologic, or other causes of genital pain.
The following treatments are usually successful:
- tricyclic antidepressants such as nortriptyline, starting with a bedtime dose of 10 mg and working up to 50 mg to 150 mg
- the antiepileptic agent gabapentin, starting with a bedtime dose of 100 mg and working up to as much as 1,000 mg (this is usually substituted for the tricyclic antidepressant if that therapy alone is ineffective)
This condition may be either primary or secondary. With primary vestibulitis, a woman experiences pain with her first use of a tampon, her first exposure to a speculum, and the initiation of sexual relations. For those with secondary vestibulitis, pain on contact results after a period of comfortable sexual relations.
This pain is thought to stem from inflammation or trauma that initially sensitizes nociceptors in the vestibular mucosa, leading to prolonged neuronal firing. This in turn sensitizes the wide-dynamic-range neurons in the dorsal horn to respond abnormally, converting the sensation of touch into pain (allodynia).11 There often is a history of an unresolved irritative event such as Candidal infection, repeated genital infection,12 topical treatments,13 and early and sustained use of oral contraceptives.14 All are suspected causes.
Diagnosis is made once other pathology has been ruled out and a Q-tip test has demonstrated that contact elicits pain in the vestibule.
Numerous treatment protocols have been described, but current interest focuses on addressing neuroinflammatory pain. This can be done at the peripheral afferents by reducing inflammation and hyperexcitability with topical xylocaine 5% in a compounded sterol-lanolin base 5 times daily; centrally, this is accomplished using tricyclics in doses of 50 mg to 150 mg.
Note that primary vestibulitis is extremely difficult to treat; vestibulectomy and perineoplasty improve the condition by 60% to 90% when medical management fails.15
- Vaginismus, an involuntary spasm of the perineal and levator muscles, may occur in patients with vestibulitis. While primary vaginismus is psychologic in origin, secondary vaginismus represents a conditioned response to pain,16 usually vestibulitis. In patients with secondary disease, pelvic-floor motor instability has been well-demonstrated; these women have a reduced ability to contract or relax the pelvic floor and increased muscular instability at rest.17
Recent studies of the vestibule and vagina provide new insights into an organic explanation of dyspareunia in women who are otherwise healthy.
Clinicians have long known that the vulva and vestibule are innervated by the pudendal nerve, composed of both somatic motor efferents and sensory afferents. But autonomic nerve fibers from the inferior hypogastric plexus and caudal sympathetic chain ganglia also provide genital sensation and may contribute to the perpetuation of neuroinflammatory pain.1 Although the vulvar vestibule is by definition visceral tissue, it is considered to havenonvisceral innervation.2 Thus, sensations to touch, temperature, and pain are similar to sensations evoked in the skin and can be exquisitely painful.
The traditional view that the vagina has a paucity of nerve endings was contradicted with demonstration of profound innervation, with greater numbers of nerve fibers in the distal areas than in more proximal parts.3 The vagina itself can hurt.
In addition, the presence of luteinizing hormone and human chorionic gonadotropin receptors on the bladder trigone supports the complaint of cyclic worsening of pelvic dyspareunia.4 Circumvaginal motor spasm from hypertonicity of the levator plate5 is an evolving area of study.
Shifting views. Nineteenth-century gynecologists approached dyspareunia primarily from a surgical perspective, using a wide variety of operative interventions. In time, the surgical approach was replaced by an emphasis on psychosocial issues: Women who complained of dyspareunia were frequently classified as “frigid,” while physiological correlates were largely ignored.6 Still later, “deep-thrust” dyspareunia was considered suggestive of an organic source, whereas superficial or entrance dyspareunia was thought to derive from emotional or psychological issues.7
Gradually, an integrated and pain-model approach has evolved. It is now theorized that an instigating pain event is perpetuated by other factors.8
REFERENCES
1. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
2. Cervero F. Sensory innervation of the viscera: peripheral basis of visceral pain. Physiol Rev. 1994;74:95-138.
3. Hilliges M, Falconer C, Ekman-Ordeberg G, Johansson O. Innervation of the human vaginal mucosa as revealed by PGP 9.5 immunohistochemistry. Acta Anat. 1995;13:119-126.
4. Tao YX, Heit M, Lei ZM, et al. The urinary bladder of a woman is a novel site of luteinizing hormone-human chorionic gonadotropin receptor gene expression. Am J Obstet Gynecol. 1998;179:1026-1031.
5. Glazer HI, Jantos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
6. Levine SB, Rosenthal M. Marital sexual dysfunction: female dysfunctions. Ann Intern Med. 1977;86:588-597.
7. Steege JF, Ling FW. Dyspareunia: a special type of chronic pelvic pain. Obstet Gynecol Clin North Am. 1993;20:779-793.
8. Heim LJ. Evaluation and differential diagnosis of dyspareunia. Am Fam Physician. 2001;63:1535-1544.
Vaginismus is diagnosed by eliciting muscle spasms in the pelvic floor by depressing the levators. If a woman has primary vaginismus of psychogenic origin, there is no tenderness in the vestibule; note, however, that the exam may be so difficult for her to endure that evaluating the vestibule is not possible.
Pelvic-floor motor instability is treated with physical therapy and biofeedback. In secondary disease, vestibulitis must also be concomitantly addressed. Primary disease, meanwhile, is treated by desensitization techniques that help the patient control the relaxation of her musculature.
The fine points of examination
Asking the right questions. Before you begin the physical exam, it is crucial to get as much information as possible about the patient’s condition. The dyspareunia history includes the following:
- a complete description of the pain problem and any concomitant sexual dysfunction
- exploration of potential gynecologic causes
- exploration of potential medical causes
- psychosocial information18
The physical exam. Although guided by the history, the physical examination needs to be as comprehensive as possible. It should include:
- systematic, meticulous inspection of every structure to confirm normal color, texture and architecture, and the presence or absence of lesions.
- gentle palpation of all tissues for the source of the discomfort. This should include a Q-tip test of the vestibule for tender foci.
- a speculum exam with inspection for mucosal integrity without fissure, erosion, or ulceration, as well as a check for the presence or absence of rugae and discharge. (Testing for pH is done with a reactive cardboard strip while the speculum is in place; then samples for wet mount and cultures are collected.)
- gentle single-digit exam of the vestibule to confirm the Q-tip test, as well as single-digit palpation of the pelvic-floor musculature, anterior vaginal wall, urethra, and bladder to confirm superficial pain and avoid confusion with pelvic sources.
- bimanual examination to evaluate for any nodularity or masses in the vagina, rectovaginal septum, or pelvis, as well as for mobility and tenderness of the pelvic organs.
Note that with generalized dysesthesia (vulvodynia), there may be no physical findings.
- Take steps to navigate the pain. Some women cannot tolerate a vulvar or vaginal examination; asking about previous experience will make it easier to tailor the exam appropriately. The following techniques also may be appropriate:
- use of premedication
- presence of a support person
- an agreement to stop the exam if the patient so requests
- use of a pediatric speculum
It may not be possible to complete all components of an examination at a single visit. For example, a patient may have to return for a vaginal examination and wet mount if menses are present at the initial appointment.
Cultures for Candida and Trichomonas are important when microscopy is negative.
Essential laboratory studies.
- Vaginal pH. A normal level (3.5 to 4.5) rules out bacterial infection and atrophy. Candida grows at any pH. Elevated pH is nonspecific and can represent recent intercourse or a small amount of blood. However, it also can suggest such causes of dyspareunia as atrophy, vaginal lichen planus, desquamative vaginitis, and Trichomonas.
- Wet mount reveals 4 important features:
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Pathogens.Candida or Trichomonas may be identified. Microscopy for Candida lacks sensitivity; a negative examination in a symptomatic woman mandates a culture for Candida.19
- Background flora. As mentioned earlier, lactobacillus dominates the normal vagina; when this predominance is seen on microscopy, there is no bacterial infection. A vaginal culture may grow Escherichia coli, group B streptococcus, Gardnerella, and a variety of normal commensals, but these are not the cause of dyspareunia when pH is normal and lactobacilli dominate the slide.
- White blood cells. Large numbers suggest Candida, lichen planus, Trichomonas, gonorrhea, chlamydia, or desquamative inflammatory vaginitis.
- Epithelial cells. These should be superficial or intermediate. The presence of parabasal cells suggests atrophy regardless of the age group. It also may indicate inflammation from Candida, lichen planus, or desquamative inflammatory vaginitis.
- Cultures for Candida and Trichomonas are important when microscopy is negative. Routine vaginal culture is not recommended. Cultures for herpes, gonorrhea, or chlamydia may be necessary.
- Biopsy and blood tests offer data on hormonal levels or type-specific antibodies for herpes. Biopsy of the vulva or vagina is indicated whenever there is a visible lesion that needs identification.
- Urine culture, colposcopy, or imaging such as ultrasonography and spine films may be indicated.
- Specialty referrals may be helpful for evaluation of the gastrointestinal or genitourinary tract, or for diagnostic laparoscopy for endometriosis.
Dr. Stewart reports no financial relationship with any companies whose products are mentioned in this article.
1. American College of Obstetricians and Gynecologists. Technical Bulletin #211: Sexual dysfunction. Washington, DC: ACOG; 1995.
2. Jamieson DJ, Steege JR. The prevalence of dysmenorrhea, pelvic pain and irritable bowel syndrome in primary care practices. Obstet Gynecol. 1996;87:55-58.
3. Jalbuena JR. Atrophic vaginitis in Filipino women. Climacteric. 2001;4:75.-
4. Johnston A. Estrogens–pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulation–Estring. Acta Obstetrica Gynecol Scand. 1996;163(suppl):16-25.
5. Anderson M, Kulzner S, Kaufman RH. Treatment of vulvovaginal lichen planus with vaginal hydrocortisone suppositories. Obstet Gynecol. 2002;100:359-362.
6. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
7. Sobel JD, Faro SF, Force RW, et al. Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol. 1998;178:203-211.
8. Edwards L, Friedrich EG. Desquamative vaginitis: lichen planus in disguise. Obstet Gynecol. 1988;71:832-836.
9. Sobel JD. Desquamative inflammatory vaginitis: A new subgroup of purulent vaginitis responsive to topical 2% clindamycin therapy. Obstet Gynecol. 1994;171:1215-1220.
10. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90(4 pt 1):583-589.
11. Bohm-Starke N, Hilliges M, Brodda-Jansen G, Rylander E, Torebjork E. Psychophysical evidence of nociceptor sensitization in vulvar vestibulitis syndrome. Pain. 2001;94:177-183.
12. Baggish MS, Miklos JR. Vulvar pain syndrome: A review. Obstet Gynecol Surv. 1995;50:401-411.
13. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome. Dermatol Clin. 1992;10:435-444.
14. Bouchard C, Brisson J, Fortier M, Morin C, Blanchette C. Use of oral contraceptive pills and vulvar vestibulitis: A case control study. Am J Epidemiol. 2002;156:254-261.
15. Bornstein J, Zarfati D, Abramovici H. Perineoplasty compared with vestibuloplasty for severe vulvar vestibulitis. Obstet Gynecol. 1997;89:695-698.
16. Meana M, Binik YM. Painful coitus: A review of female dyspareunia. J Nerv Ment Dis. 1994;182:264-272.
17. Glazer HI, Janos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
18. Phillips NA. The clinical evaluation of dyspareunia. Int J Impotence Research. 1998;10(suppl 2):S117-S120.
19. Nyirjesy P, Seeney SM, Grody MHT, et al. Chronic fungal vaginitis: the value of cultures. Am J Obstet Gynecol. 1995;173:820-823.
1. American College of Obstetricians and Gynecologists. Technical Bulletin #211: Sexual dysfunction. Washington, DC: ACOG; 1995.
2. Jamieson DJ, Steege JR. The prevalence of dysmenorrhea, pelvic pain and irritable bowel syndrome in primary care practices. Obstet Gynecol. 1996;87:55-58.
3. Jalbuena JR. Atrophic vaginitis in Filipino women. Climacteric. 2001;4:75.-
4. Johnston A. Estrogens–pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulation–Estring. Acta Obstetrica Gynecol Scand. 1996;163(suppl):16-25.
5. Anderson M, Kulzner S, Kaufman RH. Treatment of vulvovaginal lichen planus with vaginal hydrocortisone suppositories. Obstet Gynecol. 2002;100:359-362.
6. Wesselman U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain. 1997;73:269-294.
7. Sobel JD, Faro SF, Force RW, et al. Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol. 1998;178:203-211.
8. Edwards L, Friedrich EG. Desquamative vaginitis: lichen planus in disguise. Obstet Gynecol. 1988;71:832-836.
9. Sobel JD. Desquamative inflammatory vaginitis: A new subgroup of purulent vaginitis responsive to topical 2% clindamycin therapy. Obstet Gynecol. 1994;171:1215-1220.
10. Meana M, Binik YM, Khalife S, Cohen DR. Biopsychosocial profile of women with dyspareunia. Obstet Gynecol. 1997;90(4 pt 1):583-589.
11. Bohm-Starke N, Hilliges M, Brodda-Jansen G, Rylander E, Torebjork E. Psychophysical evidence of nociceptor sensitization in vulvar vestibulitis syndrome. Pain. 2001;94:177-183.
12. Baggish MS, Miklos JR. Vulvar pain syndrome: A review. Obstet Gynecol Surv. 1995;50:401-411.
13. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome. Dermatol Clin. 1992;10:435-444.
14. Bouchard C, Brisson J, Fortier M, Morin C, Blanchette C. Use of oral contraceptive pills and vulvar vestibulitis: A case control study. Am J Epidemiol. 2002;156:254-261.
15. Bornstein J, Zarfati D, Abramovici H. Perineoplasty compared with vestibuloplasty for severe vulvar vestibulitis. Obstet Gynecol. 1997;89:695-698.
16. Meana M, Binik YM. Painful coitus: A review of female dyspareunia. J Nerv Ment Dis. 1994;182:264-272.
17. Glazer HI, Janos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
18. Phillips NA. The clinical evaluation of dyspareunia. Int J Impotence Research. 1998;10(suppl 2):S117-S120.
19. Nyirjesy P, Seeney SM, Grody MHT, et al. Chronic fungal vaginitis: the value of cultures. Am J Obstet Gynecol. 1995;173:820-823.