Managing Vulvar Vestibulitis

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Managing Vulvar Vestibulitis

A. Driver

The Nurse Practitioner: The American Journal of Primary Health

Care

July 2002

Volume 27 Number 7

Pages 24 - 35

Abstract

Vulvar vestibulitis, a type of vulvodynia, affects many American

women. Patients typically present with a history of intermittent or

continuous, localized, vulvar pain and frequently can’t tolerate sexual

intercourse. Here, review the etiology, history and physical examination,

and comprehensive treatment of vulvar vestibulitis, including

nonpharmacologic, pharmacologic, psychosocial, and surgical measures.

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Vulvar vestibulitis (VV) refers to a type of vulvodynia, or painful

vulva, that seriously interferes with the quality of life for many women.

This chronic condition is characterized by focal redness and inflammation of

the entire vestibule, the posterior vestibule, or the minor vestibular

glands.

Dyspareunia, or pain during sexual intercourse, represents a major

complaint of women with VV. They typically describe the vulvar pain

experienced with VV as rawness, irritation, burning, or stinging; the pain

occurs during sexual intercourse, after intercourse, or both. 1 , 2 Some

women also complain of pain with vulvar pressure in the absence of vaginal

penetration. Unfortunately, reliable estimates on the prevalence of VV don’t

exist.

Many terms identify VV in the literature, including vulvar adenitis ,

nonpathogenic vaginitis , psychosomatic vulvovaginitis , and burning vulva

syndrome.

The condition was first recognized in 1889, but in 1987 Friedrich

proposed a formal definition: Severe pain on vestibular touch or attempted

vaginal entry, tenderness to pressure localized within the vulvar vestibule,

and physical findings confined to vestibular erythema of various degrees. 3

, 4

VV can affect a woman’s life profoundly, leading to chronic pain,

marital or relational stress, low self-esteem, a radical decrease in or

absence of sexual activity, depression, and other symptoms of psychological

distress.

Etiology:

Researchers haven’t identified the cause of VV. Some women experience

an acute episode of VV related to a specific insult, such as an infection or

irritant. Many other women experience chronic pain lasting 6 months to years

without a causal factor identified.

One outdated psychiatric view holds that dyspareunia isn’t usually

associated with an organic cause, but rather has a psychogenic origin. 5 , 6

Researchers, however, now widely accept that VV has an organic,

multifactorial etiology. Convey this to patients to help lessen the

psychological distress that some women experience from perceived sexual

dysfunction. New findings strongly indicate that VV is a connective tissue

disorder commonly associated with fibromyalgia, interstitial cystitis, and

irritable bowel syndrome.

Other widely discussed possible etiologies include various infectious

processes. Infections implicated in VV include Candida , Trichomonas , and

bacterial vaginosis.

In some patients, an autoimmune response or hypersensitivity reaction

to chronic yeast infections may lead to VV. Cross-reactions between Candida

and antigens occur in the vulva, eventually causing an autoimmune reaction

after repeated infections.

Although many women with VV report a history of yeast infections,

researchers haven’t substantiated this relationship. In addition, it’s

difficult to determine if VV after an infection results from the infection

itself or a hypersensitivity reaction to various, repeated treatments for

the infection. 7

Of note, researchers no longer consider human papillomavirus (HPV) a

cause of VV. They have found no significant prevalence of HPV infection in

women with VV compared with women without VV. 8 , 9

Suspected topical or local causes include irritants (soap and

deodorants) and chemicals such as spermicides and 5-fluorouracil (5-FU).

Thankfully, clinicians no longer use 5-FU to treat vulvar HPV infection.

Other local causes include alkalinity from bacterial vaginosis and acid-base

disturbances such as those caused by estrogen deficiency.

The use of calcium citrate to treat VV is based on the suspicion that

urinary oxalates irritate the vulvar mucosa and mediate a histamine release

in the vulvar tissue, causing inflammation and pain. 10 Calcium citrate

decreases the formation of oxalates and, therefore, decreases the amount of

histamine release, inflammation, and pain in the vulvar tissue.

Possible iatrogenic causes of VV include allergic reactions to drugs,

rebound inflammation after topical steroid withdrawal, and destructive

therapeutic agents such as cryosurgery, trichloroacetic acid, and laser

treatments. Genetics may also play a role, as many women with VV have a

female relative with vulvar discomfort.

Many women with VV suffer from interstitial cystitis, an inflammatory

condition of the bladder epithelium that can cause frequency, nocturia,

dyspareunia, and hypogastric pain. Because the epithelium in the bladder and

vulvar vestibule have the same embryologic origin, the urogenital sinus, the

disorders are possibly related. 11 In fact, they may have a common

autoimmune etiology. VV is associated with more variability in urethral

pressure, further supporting the relationship between the vulva and urinary

structures. 12 Further research into the inflammatory susceptibility of the

urogenital sinus-derived epithelium is needed to clarify the relationship

between VV and interstitial cystitis.

History and Presentation:

Ranging from mild to severe, women may have episodic or continuous

pain from VV. Women may experience pain with intercourse, tampon insertion,

urination, and other activities that place pressure on the vulva, such as

prolonged sitting, speculum insertion, biking, jogging, and wearing

tight-fitting clothes.

Pain at the vaginal introitus, point tenderness, slight or marked

erythema, and the absence of infection or other vulvar disease are the

hallmarks of VV. 4 For some women, the pain associated with VV may

spontaneously resolve in 6 to 12 months. For others, the pain becomes

chronic.

A woman may have postcoital burning for up to 24 hours. Women with VV

may have sexual intercourse infrequently due to pain, and some women can’t

tolerate intercourse at all. Many women have tried over-the-counter and

prescription treatments and have a history of frequent Candida infections.

Affecting women of all ages, VV most frequently occurs in

European-American, middle-class women in their 20s and 30s who are sexually

active. 5 It also occurs more frequently among professional women in

monogamous, stable relationships. Because it affects more whites than

blacks, genetic predisposition represents a valid etiologic factor.

VV can be separated into primary and secondary categories. In primary

VV, a woman experiences vulvar pain with the first attempt at sexual

intercourse or tampon insertion. More common in nulliparous women, primary

VV is associated with more severe pain and a strong family history of

dyspareunia.

Women acquire secondary VV after months or years without vulvar pain

with sexual activity, and its onset may be sudden or increase over time. 13

, 14 Some women also present with mixed VV, where symptoms come and go after

the first attempt at vaginal contact or penetration.

Differential Diagnosis:

Consider many diagnoses when a patient describes entrance dyspareunia.

First, consider skin conditions such as contact and irritant dermatitis,

topical steroid withdrawal, chronic dermatitis and lichen planus, psoriasis,

and tinea. Include infections in the differential diagnosis; for example,

rule out Candida , Trichomonas , herpes simplex virus (HSV), and HPV. Also

consider systemic diseases such as lupus, pellagra, and Reiter’s syndrome.

Also investigate other diagnoses including dysthetic vulvodynia and

pudendal neuralgia secondary to sensory nerve damage and vaginismus, or

spasm of the muscles at the vaginal introitus. Because VV presents a

challenging differential diagnosis, complete a thorough history and physical

examination.

Physical Examination and Diagnosis:

Patient history, clinical presentation, and diagnostic testing form

the basis of diagnosis for VV. VV is a diagnosis of exclusion because it can

be definitively diagnosed only after tests rule out other pathology. Base a

diagnosis on the symptoms described by Friedrich.

The initial work-up includes a thorough vulvar assessment. First,

inspect the vulva for HPV lesions, ulcerations, or other abnormalities that

would lead to a diagnosis other than VV. The patient with VV will present

with erythema and edema in the affected areas, usually near the minor

vestibular glands. Tenderness on palpation of these areas will also be

present. The erythema, which can vary from slight to marked, is usually

located at 5 and 7 o’clock on the vulva, the location of the minor

vestibular glands. Document the location and degree of erythema and pain for

tracking and follow-up.

The most classic finding of VV is point tenderness during the

cotton-tipped swab test. Applying pressure to the affected areas of the

vulva with a cotton-tipped swab will provoke a significant pain response. 2

, 4

In addition to the vulvar assessment, perform a speculum examination

to rule out other diagnoses. First, conduct a gross examination of the

vagina to look for discharge or other signs of infection or pathology. Next,

obtain a wet smear to assess for yeast spores, clue cells, and Trichomonas.

Take saline and potassium chloride preparations to adequately assess for

yeast presence. Consider performing cultures for Candida , gonorrhea,

Chlamydia , and herpes to rule out these infections. Using litmus paper to

determine the vaginal pH will help in the differential diagnosis of any

vaginal infection. During the bimanual examination, assess pelvic muscle

instability and vaginismus, both common findings in VV.

If diagnosis remains uncertain, consider performing a detailed

examination of the vulvar mucosa. With a large cotton-tipped swab, place

acetic acid on the vulvar area to assess for acetowhitening of the tissue.

Acetowhitening can result from HPV, dysplasia, inflammation, trauma,

allergic or contact dermatitis, or lichen sclerosus.

After examining the whitened area with a colposcope, or high-powered

microscope, perform a biopsy on tissues suspicious for other pathology. In a

patient with VV, colposcopy will reveal capillary ectasia in the affected

areas of the vestibule. The biopsy findings in VV show nonspecific

inflammation in the subepithelial tissue surrounding the minor vestibular

glands.

Treatment:

Unfortunately, an agreed-upon protocol for VV treatment doesn’t exist.

Optimal treatments, however, should be comprehensive and include

nonpharmacologic, pharmacologic, psychosocial and, if needed, surgical

measures. 15 Most interventions are palliative and don’t provide a cure for

the disorder.

Nonpharmacologic Treatment

Because many nonpharmacologic measures are conservative and easy to

implement, the patient can instigate and manage them. This places the

patient in control of her disease management, and she can use trial and

error to conclude which measures decrease individual discomfort (see Patient

Education, “Reduce Your Symptoms of Vulvar Vestibulitis”).

Along with other treatment regimens, consider physical therapy and

biofeedback. Gynecologic physical therapists comprehensively evaluate the

pelvic floor’s musculoskeletal structure and function to identify muscle

spasm and other dysfunctions that exacerbate vulvar pain. After an

evaluation, most therapists teach stretching, strengthening, and relaxation

techniques and may also use modalities such as ultrasound and electrical

stimulation.

Gynecologic physical therapists also instruct patients on biofeedback

and dilatation exercises. Dilatation of the vaginal introitus and Kegel

exercises help decrease pelvic floor and vulvar tension and help patients

overcome anxiety and fear of vulvar pain. 16 Many women who performed

biofeedback-assisted, pelvic floor muscle exercises at home for 16 weeks

found that their pain substantially decreased and their sexual activity

increased. 5 , 17

Pharmacologic Treatment

Numerous pharmacologic regimens for treating VV exist. Before treating

VV, resolve any vaginal infections such as Candida or HPV. When beginning

treatment for VV, start with the least invasive and costly interventions and

proceed to more extensive treatment as needed.

A conservative, frequently used, first-line approach involves applying

2% to 5% topical lidocaine gel to the vulva as needed 10 to 15 minutes

before intercourse. This may allow for intercourse with minimal or absent

pain. While intervention will decrease the pain at the introitus where it’s

applied, it won’t alter intravaginal or clitoral sensation. Instruct the

patient to avoid overapplication of the lidocaine gel to minimize or prevent

alterations in penile sensation.

Another strategy involves limiting dietary oxalates. A metabolic

by-product excreted in the urine, urinary oxalates are sharp crystals that

irritate the vulvar mucosa in women with VV. 10 Oxalates can also induce a

histamine release, particularly in those suffering from connective tissue

disorders. A low-oxalate diet requires limiting the intake of certain fruits

and vegetables, as well as chocolate, alcohol, wheat, and other foods.

Calcium citrate inhibits the formation of oxalate crystals, decreasing

crystalluria and histamine release, reducing the inflammation and pain of

VV. Taking 400 mg of calcium citrate three times daily over a 3-month period

may decrease vulvar pain. A conservative, inexpensive option, consuming a

low-oxalate diet and taking calcium citrate presents a logical first-line

approach. 18

Some clinicians prescribe low-potency topical corticosteroids applied

twice daily to the vulva. Although this can provide short-term relief, it

isn’t recommended because long-term application of topical corticosteroids

can lead to epidermal atrophy and other skin changes that exacerbate VV. In

addition, taper the patient off topical corticosteroids when discontinuing

use to prevent rebound inflammation.

Topical hormones, including progesterone, estrogen, and testosterone

creams, have met with some success. Many clinicians have seen the most

clinical success with topical 0.01% estradiol cream applied to the vulva

twice daily. 19

Oral Medications

Some women with VV experience point tenderness of the vulva with

applied pressure as well as constant vulvar burning and irritation. The

description of burning is similar to the discomfort of neuralgias, such as

those resulting from herpes zoster. Thus, VV may involve a problem with

cutaneous perception.

Because of its success in decreasing neuropathic pain, consider

prescribing amitriptyline (Elavil) for women with this symptom pattern.

Begin with a dose of 10 mg per day increased every 2 to 4 weeks up to 100 mg

as needed.

For many patients, a dose of 60 mg a day for 6 to 7 months resolves

symptoms. Some patients can taper completely off the drug after this period

of time, while others require a lower maintenance dose to control symptoms.

Other medications to treat neuropathic pain are also used to treat VV.

The literature reports the use of carbamazepine, phenytoin, acyclovir, and

neurontin. 20 Consider the costs and benefits of these therapies carefully

and discuss them with the patient because of their potential adverse

effects.

Surgical Treatment

For women with severe VV who don’t respond to more conservative

treatments, vestibular surgery is an option. Surgeons perform different

surgical procedures, some more radical than others. A need for comparative

studies exists to explain success and complication rates for the various

procedures. 13

Surgical procedures can have complications. Infection, scarring, and

stenosis, as well as recurrent pain can sometimes result; therefore, surgery

isn’t appropriate for all patients with VV. Women with dyspareunia since

their first experience with intercourse and those experiencing constant

vulvar pain have a low success rate with surgery. 21

Psychosocial Treatment

Comprehensive treatment of VV requires addressing the psychosocial

issues surrounding the disorder. Women with dyspareunia have more physical

pathology, psychological symptoms, and negative attitudes about sexuality.

They also have lower levels of relationship adjustment and sexual function

than women without dyspareunia. 6 , 22

Women with VV often suffer from depression, low self-esteem, and many

other psychological symptoms. Because of the disorder’s intimate nature and

the fear of an underlying disease, many women find discussing their pain

with significant others difficult and withdraw from intimate interpersonal

relationships. Fear and shame may also discourage them from involvement in

new relationships.

Women may feel guilty because they can’t tolerate sexual intercourse

with their partner; relational stress can occur. Because a clear etiology

doesn’t exist, women suffering from VV may feel frustrated and become

demoralized as they try different treatments without success. Clinicians can

assist women with VV to regain their psychological well-being and help

prevent further stress in interpersonal relationships.

First, reassure the patient that her pain is real and caused by a

physical entity, not a psychological dysfunction. Provide education related

to the etiology, course of illness, and treatment options. Encourage

patients to express their questions and concerns to you and encourage open

communication with their partners.

Provide educational materials and encourage the patient to find other

ways of expressing sexuality if she can’t tolerate intercourse, despite

treatment. A partner’s support can make a significant difference in a woman’

s ability to cope with VV and manage its symptoms. Also consider referral to

a mental health clinician, if indicated.

VV in Practice:

Early recognition of VV, coupled with a comprehensive,

multidisciplinary approach, is vital to treating this condition. Research

should continue to investigate the etiology of VV, including the role of

genetics and VV’s association with connective tissue disorders. Finally,

researchers must evaluate treatments to determine an effective protocol for

managing VV. More research of nonsurgical treatment options is vital.

ACKNOWLEDGMENTS:

The author gratefully acknowledges Joyceen S. Boyle, RN, PhD, FAAN, of

the Medical College of Georgia, ElDonna Hilde, RNC, OGNP, MSN, of Georgia

Southern University, and the Vulvar Pain Foundation’s Scientific Research

Committee for their editorial assistance.

REFERENCES