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Benign Disorders of the Vulva:

Pruritus (itchy) Vulva


Vulval Skin and Pain Disorders

Dr Michelle M Fynes MB BAO BCH (Hons) MD (Research) MRCOG DU DipUS


Locum Consultant Reproductive Medicine
Subspecialist Uro-Gynaecologist
Department of Obstetrics and Gynecology
Cambridge University Hospitals NHS Foundation Trust 2017-2018
Objectives of this presentation:

• Introduce and overview the topic


• Review anatomy of the vulva
• Outline the relevant neurological innervation
• Describe assessment of the vulva
• Detail causes of vulval pain and pruritus
• Focus on specific disorders; Lichen simplex (dermatitis), Vulval atrophy,
Lichen Sclerosus, Lichen Planus
• Focus on pain disorders; vulvodynia, vestibulitis, non-infective vulvitis
• Discuss the causes of chronic vulval pruritus (itching)
• Review best practice management of vulval pain and pruritus (itching)
• Provide references for further reading
Introduction:

• The vulva refers to the female external genitalia that lie within the anterior
perineal triangle, spanning from the anterior mons pubis to the posterior perineal
body and laterally from the inguinal crease to the hymenal ring, encompassing the
labia majora, minora, clitoral hood, external urethral meatus, vaginal introitus, and
greater (Bartholin’s)/lesser (Skene’s) vestibular glands.
• Vulval skin disorders are not common and may be asymptomatic or present with
pruritus (itching), skin changes, discomfort or pain including dyspareunia.
• A wide variety of benign skin disorders may affect the Vulva including; Lichen
Sclerosus, Lichen Planus, Lichen Simplex, Atrophy, Contact dermatitis, as well as
common infective skin changes seen with candidiasis.
• Vulval Intra-epithelial Neoplasia (VIN) may exist independently or co-exist with
any of these other benign skin disorders and Vulval Cancer accounts for <2% 0f all
genital tract tumours.
Introduction:

• Vulval pain can be divided into two categories: Pain secondary to a specific,
identifiable, underlying disorder and idiopathic pain with no recognisable cause.
• Pain: This may include a variety of unpleasant symptoms including burning,
soreness, and throbbing, and some insist that they do not have pain but describe
the sensation in words which can be misleading for clinicians
• Prevalence: The prevalence of benign vulval skin disorders and pain is unclear.
A population based survey from the USA found 16% of women had at some time
experienced chronic burning, knife-like pain, or pain on contact with the vulva.
• QoL: Vulval disorders not infrequently have a debilitating effect on QoL, sexual
function, and may be associated with increasing anxiety and depression.
Vulval Anatomy:
Vulval Anatomy
Vulval Anatomy
Vulval Anatomy (sagittal and internal anterior)
Vulval Anatomy: Innervation
Vulval Anatomy: Innervation
Vulval Anatomy: Innervation
Vulval physiology

• Vulval epithelium: There are two types separated by Hart’s line (medial to the labia minora).
The labia are covered by keratinized epithelium. Medially the mucosal vulvar vestibule is lined
by non-keratinized transitional epithelium. Unlike the external genitalia, the vestibule is derived
from embryonic endoderm (urogenital sinus) and morphologically resembles vaginal mucosa.

• Vulval skin: Exposed to many physiologic contact irritants (i.e. sweat, vaginal secretions, urine,
occlusion by underwear, sanitary pads, skin-skin contact, and mechanical trauma from sexual
activity). Because the vulva is almost always covered in some way, the degree of occlusion is a
unique factor to consider, and the effects can be significant.

• Hydration: Vulval skin has increased skin hydration and elevated Trans-Epidermal Water Loss
(TEWL). Increased friction coefficient predisposes to mechanical skin damage. TEWL also
measures hydration/barrier function. Vulvar skin is not as effective a barrier to water loss as
other skin. TEWL also relates to permeability being x7 higher in the vulva compared to forearm
skin. Contributing factors include a >numbers sweat glands, hair follicles, blood flow, hydration.
Vulval physiology

• Hormones: Vulvar epithelium is hormone responsiveness (e.g. oestrogen). The stratum


corneum of labia majora thickens with age until menopause. As circulating E2 levels fall tissue
atrophy and elasticity occurs breaching the vulval skin’s barrier to external exposures.

• Menopause: Elastic degeneration post-menopause in the vulvar dermis is similar to that seen
with years of sun exposure and actinic damage in the aged population. E2 fall increases the
acidic pH of the area with <produced lipids (2 factors contributing to skin’s protective function

• Low oestrogen: This increases the vulva/vaginal risk of injury in a post-menopausal population.
Low oestrogen states are also observed postpartum, with breastfeeding, on certain medications
(e.g. OCP and tamoxifen), and removal of the ovaries. Women to whom these apply are thus
also at increased risk for developing vulvar contact dermatitis.
Vulval Assessment:
Vulval assessment:
Detailed history;
- Itching or pruritus
- Pain/ soreness (character, severity, radiation, relieving/exacerbating factors)
- Erythema (redness), Localised lesions, Any discharge
- Onset and progression of any pain tenderness or itching
- Do these symptoms wake the patient up or impair sleep
- Sexual history including any previous STIs, sexual pain
- Hygiene/cleansing routine (check specific products ?allergy)
- Menopausal status (? Is the patient on local or systemic HRT)
- Contraception including use of condoms or lubricants (impact on pain or itching)
- Cervical screening history and vaccination
- Medical, psychological (anxiety/depression), surgical and social history (e.g. cigarettes)
- Psychosexual symptoms (e.g. vaginismus, loss of libido)
- Impact on QoL of pain and itching (VAS 0-100)
- Any treatment to date and effect of therapy and side effects
- Any lesions elsewhere on the body or history dermatoses (e.g. dermatitis, psoriasis)
- Any history atopy, chest infection, sore throat etc
- Current or recent medications
Vulval examination:
Detailed vulvovaginal and general examination;
1. Inspect external/internal vagina then exam including bi-manual
2. Qualify the rash lesion(s); (erythema, petechiae, ulcer, type lesion, colour)
3. Tender non tender
4. Assess the quality of the surrounding skin
5. Hygiene
6. Identify any vaginal discharge
7. Cusco speculum exam; visualise cervix and vaginal walls (document tenderness)
8. Consider microscopy, wet mount (LM assess) and/or HVS and/or PID screen
9. Document findings (consider photo)
10. Palpation vulva using swab; any pain tenderness, character, radiation
11. Check the anus and peri-anal skin (consider PR)
12. Consider vulvoscopy
13. Consider the Q-tip test

14. General medical exam of the body skin remembering to look at the scalp and behind
the ears. Oral exam using tongue depressor identify and oral mucosal /gingival lesions
and tongue. Check elbows and behind the knees.
Vulval Biopsy:
Vulval biopsy procedure:
1. Keyes Biopsy
2. Different sizes
3. LA cover
4. Only every biopsy
the edge of a lesion
5. Always take a clinical
photo were possible
6. Review histology and
adjust treatment as
required
7. Refer to specialist
dermatologist if unclear
8. Discuss histology at
MDT if fails to
respond to therapy
Vulval Skin: Normal histology
Review of Benign Vulval Skin Disorders
Benign vulval Skin Disorders
• Lichen Sclerosus
• Lichen Planus
• Vulval Dermatitis (Lichen Simplex)
• Vulval Atrophy
• Vulval Candidiasis
• Vulval Intra-epithelial Neoplasia (VIN)
• Contact Allergic Dermatitis
• Psoriasis

Normal vulval skin


Lichen Sclerosus
Lichen Sclerosus Aetiology: All 1 in 300 females of all ages and 1 in 30
elderly women. Ratio F:M is 5:1
Presentation: White patch (leukoplakia) which
coalesce leading to a paper-thin-like skin, stiff labia
with a constricted vaginal orifice and loss of
architecture. Figure of ‘8’ appearance.
Symptoms: None (rare), itching (worse at night),
sore, pain, dyspareunia (introitus tight), concerns re-
appearance, constipation peri-anal involvement.
Other sites: Less common but may have patches of
LS elsewhere (picture below left). > risk other
autoimmune disorders.
Differential skin lesions: Can co-exist with LP and
must exclude neoplastic lesions or VIN. Biopsy: If
fails to respond to therapy or suspicious lesions.
Pathogenesis: Unknown (autoimmune?). Some
research autoantibodies to ECM protein.
Histology: Benign thin, flat squamous epidermal cells
w/ fibrosis, degeneration of basal epidermal cells
(picture above left).
Hallmark at histology: Band of Fibrosis.
Lichen Sclerosus (et atrophicus)

21.5% have 1 or more and 21% a family history of


Auto-Immune (AI) disorders. 42% have AI
antibodies. The most common AI disorders linked
to LS are AI thyroiditis, alopecia areata, vitiligo, and
pernicious anaemia. Genetics also have a
pathogenetic role and 12% of LI patients have a
positive family history of LS.
Histology: Lichen Sclerosus et atrophicus
Signs
. Pale atrophic areas affecting the vulva
. Purpura (ecchymosis) is common
. Fissuring
. Erosions, but blistering is very rare
. Hyperkeratosis can occur
. Changes may be localised or in a ‘figure of
eight’ distribution of the perianal area
. Loss of architecture may be manifest as loss of
the labia minora and/or midline fusion with
introital stenosis. Clitoral hood may beburied or
may have clitoral psudocyst formation.
. Dysaesthesia

Corresponding Histology:
• Epidermal atrophy, hyperkeratosis
• Sub-epidermal hyalinization of collagen
• Lichenified infiltrate
• Early disease may be difficult diagnosis
Lichen Sclerosus: Histological features
Lichen Planus
Lichen Planus
Aetiology: All ages, mostly post-menopausal ♀
Presentation: White patch (leukoplakia) which
coalesce leading to a paper-thin-like skin, stiff
labia with a constricted vaginal orifice and loss
of architecture.
Symptoms: None, itching (worse at night),
soreness, pain, dyspareunia, concerns
regrading appearance.
Other sites: Less common but may have
patches of LS elsewhere (picture below left).
Differential skin lesions: Can co-exist with LP
and must exclude neoplastic lesions or VIN.
Biopsy: If fails to respond to therapy or
suspicious lesions.
Pathogenesis: Unknown (autoimmune?)
Histology: Benign thin, flat squamous
epidermal cells w/ fibrosis, degeneration of
basal epidermal cells (picture above left).
Hallmark at histology: Band of Fibrosis.
Lichen Planus: Other sites and symptoms
Lichen Planus: Other sites and symptoms
Lichen Simplex Chronicus
Lichen Simplex Chronicus (squamous hyperplasia)
Presentation: White patches (leukoplakia)
with thick leathery vulval skin.
Symptoms: None, itching, soreness, concerns
regarding appearance.
Differential skin lesions: Can co-exist must
exclude neoplastic lesions or VIN.
Biopsy: If fails to respond to therapy or
suspicious lesions.
Pathogenesis: Benign hyperplasia of the
vulvar epithelium secondary to rubbing and
scratching due to pruritus.
Histology: Hyperkeratosis, no nuclear atypia.
No increased risk squamous cell cancer.
Hallmark at histology: Hyperkeratosis.
Lichen Simplex Chronicus (squamous hyperplasia)
Lichen Simplex Chronicus of the vulva is the end
stage of the itch-scratch-itch-scratch cycle.
The initial stimulus itch may be due to;
- Underlying seborrrhoeic dermatitis
- Intertrigo
- Tinea
- Psoriasis
In most cases the underlying cause is not evident
and may have been transient vulvitis or vaginal
discharge
Any itching disease of the vulva may become
secondarily lichenified

Psychological factors may play a role in the


development or exacerbation of Lichen Simplex
and some specialists may use the term
neurodermatitis.
Lichenification: Examples elsewhere on the body
Vulval Atrophy
Vulval Atrophy

• Vulvar and vaginal atrophy is a condition


associated with menopause and reduced
oestrogenization.
• Its symptoms include dryness, discomfort,
and pain in the vaginal and vulvar areas.
• Some women have itching, burning
sensations, and vaginal discharges as well.
• Symptoms include dryness, irritation,
soreness, and dyspareunia with urinary
frequency, urgency, and urge
incontinence.
• Experienced by up to 40% women
• Progressive condition normally presents
>65 years.
• May be associated with secondary
opportunistic candidal infection or
lichenification rom chronic itching.
Vaginal-vulval Atrophy: Pre and during therapy
Vulval Contact Dermatitis
Contact Irritant Dermatitis
• Irritant Contact Dermatitis (ICD) is a common problem and vulvar
irritation is a frequent complaint among women.
• It occurs after exposure/contact with exogenous irritants as
opposed to Allergic Contact Dermatitis (ACD), and can present in
acute, subacute, or chronic forms.
• While vulvar pruritus and pain can be seen in a number of
different conditions, ACD is one of the most common causes
encountered and its effects on QoL can be dramatic.
• With a thorough history and a complete physical exam, this
prevalent condition can be diagnosed and addressed.
• Treatment aims to identify/eliminate underlying cause, restoring
the damaged epithelial barrier, and calming the inflammation.
• Although numerous options are available for addressing the itch
and pain, the only true ”cure” for contact dermatitis is to avoid
the responsible exposures.
Irritant Contact Dermatitis (ICD):

• Unlike ACD, irritant (ICD) reactions are not typically vesicular or bullous, although erosions can
occur and give the appearance of compromised vesicles.
• Involved areas are often symmetric, with sharp demarcations if there is a well-defined area of
exposure. As with diaper rash, there is often sparing of the inguinal creases where the
offending agent is not as capable of contacting the skin.
• A variety of substances can cause irritant contact dermatitis of the vulva (see table on next
slide), including body fluids such as urine or stool, hygiene products like douches or soaps, or
various topical medications.
• Sodium lauryl sulfate (SLS) is an anionic detergent and surfactant used as a foaming agent in
many soaps and shampoos, and it has been implicated in the induction of dermatitis of the
vulva. Sodium lauryl sulfate has been postulated to contribute to hyperalgesia by inducing
pro-inflammatory cytokines.
Vulval skin contact irritants predisposing to an allergic reaction and ICD

Body Fluids: urine (ammonia), faeces (enzymes), vaginal discharge, sweat, semen

Feminine Hygiene Products: douches, feminine wipes, sanitary pads/napkins, panty liners,
tampons, deodorants, lotions, powders, perfumes, shampoos, soaps

Sexual Support: lubricants, condoms, diaphragms, spermicides, arousal stimulants

Laundry: detergent, bleach, fabric softener


Topical Medicaments: antifungals, anti-itch creams, antibiotics, Vagisil R, A+DR ointment, tea tree
oil, alcohol based creams or gels, cantharidin, 5-fluororacil, Imiquimod R, phenol, podophyllin,
bichloroacetic acid, trichloroacetic acid

Physical Irritants: tight fitting clothes, nylon, latex, wash cloths, sponges, hot water, excessive
washing, vigorous drying with towel, hair dryer (on hot).
Allergic Contact Dermatitis (ACD):

• ACD a type IV delayed hypersensitivity reaction involves antigen-presenting Langerhans cells


within the epidermis. These dendritic cells sample/process antigens at the tissue surface and
then transport them to lymph nodes presenting to T lymphocytes. This induces T cell
proliferation and production of inflammatory cytokines. Because this immune process takes
time, physical manifestations can take 48 to 72 hours to appear following exposure.

• With such delay before symptoms develop the allergen is often difficult to identify. Itching is a
prominent feature of ACD, which can be somewhat helpful in distinguishing from ICD, in which
pain is often a primary, although both symptoms can be seen with ICD/ACD.

• The characteristic appearance of ACD includes erythema, oedema, and possible vesicles or
bullae with weeping. Because the vulvar skin is thinner oedema may be more prominent and
vesicles may form geometric patterns consistent with application or contact with the allergen.
Vulval skin contact irritants predisposing to an allergic reaction and ACD
Antibiotics: neomycin, bacitracin, sulfonamides, polyline
Antifungals: imidazoles (itraconazole, miconazole, clotrimazole, etc.), nystatin
Antiseptics: chlorhexidine, gentian violet, povidone iodine
Anesthetics: esters (benzocaine, tetracaine, procaine), amides (lidocaine, bupivacaine)
Emollients: lanolin, jojoba oil, glycerin, propylene glycol
Corticosteroids: all
Fragrance: Balsam of Peru, cinnamic alcohol, cinnamic aldehyde, hydroxy citronellal
Nail polish: toluene, sulfonamide, formaldehyde resin
Preservatives: stearyl alcohol formaldehyde, formaldehyde releasers (quaternium), urea
Sanitary wipes: acetyl acetone, fragrance, methacrylates, formaldehyde
Douches: fragrance, oil of eucalyptus, thymol, oxyquinoline, methyl salicylate benzethonium Cl
Metal (jewelry, buttons, etc.): nickel, palladium, gold
Spermicides: quinine hydrochloride, oxyquinoline sulfate nonoxynol, phenylmercuric butyrate
Rubber (diaphragms, condoms, gloves, etc.): latex, thiurams, mercaptobenzothiazole
Plants (poison ivy/sumac/oak): urushiol
Body fluids: semen, saliva
Patch testing
Chronic Allergic Contact Dermatitis:

• Chronic ACD may present more as scaling plaques with varying degrees of erythema,
hyperpigmentation, and lichenification, possibly complicated by comorbid lichen simplex
chronicus (discussed below). Vesicular responses are less common in African Americans and
others of dark complexion, and hyperpigmentation may be so prominent as to overpower any
erythema, so lack of these elements should not distract from the diagnosis. Besides
appearance, timing is also important to consider, as intermittent or recurrent itching is a
common presentation suggesting episodic exposure to an allergen.

• Because topical corticosteroids are commonly used to treat a variety of vulvar dermatoses, it’s
important to keep in mind their potential for inducing comorbid ACD. Positive patch test rates
as high as 10.7% have been reported, with many reacting to multiple different steroids.
Corticosteroids have been classified into four groups (A-D) based on chemical structure and
patch test results (see next slide), that may guide management in suspected steroid allergy.

• High cross-reactivity exists within each group as well as between Group D2 and Groups A and B.
Groups C-D1 demonstrate low cross-reactivity with others and are less likely to induce ACD.17
Coopman classification of cross-reactivity in
topical corticosteroid allergy:

Corticosteroid Group Examples:

A - hydrocortisone (acetate, succinate, phosphate), cortisone, cortisone acetate,


fludrocortisone, methylprednisolone (acetate, succinate, phosphate), prednisone,
prednisolone acetate, tixocortol pivalate
B - amcinonide, budesonide, desonide, flunisolide, fluocinolone acetanide,
fluocinomide, halcinonide, triamcinolone, triamcinolone acetonide
C - betamethasone, desoxymethasone, dexamethasone, paramethasone, fluocortolone
D1 - beclamethasone dipropionate, betamethasone (valerate, dipropionate),
clobethasone 17 butyrate, clobetasol 17 propyonate
D2 - fluticasone, mometasone, prednicarbate, hydrocortisone (17 butyrate, 17
propionate), methylprednisolone aceponate
Vulval Psoriasis
Psoriasis
A detailed general examination is imperative to delineate
other body sites affected. Skin cells normally turn over every 3-
4 weeks. In psoriatic lesions this happens every 3-4 days
resulting in the psoriasis plaques. Believed to be immune
related it can run in families (implies a genetic component)

The typical sites are the; elbows, knees, scalp, skin flexures and
behind the ears. The hand and toe nails may also be affected.
The most common type is plaque like and less often pustular
psoriasis type.

Generally starts <35years and affects men as well as women


equally. It is a chronic disease where the lesions and symptoms
may vary in expression/severity over time. Psoriasis symptoms
start or become worse because of a certain "trigger" including
skin skin, infections, medication.

Treatments fall into 3 categories:


topical – creams and ointments applied to your skin
phototherapy
systemic – oral and injected medications or combined therapy.
Vulval Psoriasis

• Psoriasis is a chronic, inflammatory epidermal skin disease with a population prevalence of 2% .


• It is the 3rd most common dermatoses of genital skin where it may affect the pubic area, vulva,
skin folds and buttocks. Isolated genital psoriasis presents in only 2–5% cases whereas patients
with generalized psoriasis have involvement of the genitalia in 40% cases.
• Genital Psoriasis is often associated with considerable morbidity, discomfort , embarrassment
and psychosexual sequelae. Genital psoriatic lesions often present as well-demarcated, brightly
erythematous, thin plaques and usually lack, due to maceration, the typical scaling that is
apparent on other parts of the body. However, scales may be seen on the more keratinised
regions of the genital skin. When scaling is present, it is often minimal and can easily be scraped
off, leaving pinpoint bleedings.
• The appearance of vulvar psoriasis is often symmetrical and can vary from silvery, scaling
patches adjacent to the outer parts of the labia majora to moist greyish plaques or glossy red
plaques without scaling in the skin folds.
• Most genital psoriatic lesions represent plaque-type but the genital area may also be affected
by pustular psoriasis (generalised and localised).
• The diagnosis of psoriasis is based on appearance. Histologically there is no difference between
genital and non genital psoriasis.
Vulval Psoriasis Therapy
Genital psoriasis can be difficult and frustrating to treat. Generally responds to treatment. Due to
the sensitivity of genital skin Rx needs special consideration. Response times vary among individuals.
Symptoms of psoriasis vary but a few common signs include:
- red patches of skin covered with silvery scales
- small, scaly spots that are common in children
- dry, cracked skin prone to bleeding, itching, burning, soreness
thickened, pitted, or ridged nails
- swollen and stiff joints
Treatment: Topical preparations and UV light are most often used.
- Moisturize
- Emollients can cover and protect the skin
- Low strength topical steroids
- Topical Vitamin D preparations
- Coal tar preparations
- UV light (risk burns with excess)
Over-use of steroids may cause thin skin and striae
Refractory psoriasis may require systemic medications: Calcineurin inhibitors: Tacrolimus and
Pimecrolimus can treat genital psoriasis without thinning skin. May cause a burning sensation,
reactivate STI’s (Herpes/ warts). Topical cyclosporin may also be considered 3rd line.
Vulval Candidiasis
Vulvo-Vaginal Candidiasis (VVC)

1. VVC is symptomatic inflammation of the vagina / vulva caused by a superficial fungal infection most commonly Candida albicans in
90% of cases and 1 in 20 Candida glabrata . Other fungal infections are caused by Saccharomyces cerevisiae (brewer’s yeast) and rarely,
Trichosporon spp . Unlike Candida spp , these are not present in normal vaginal flora. Thrush is not an STI but can be passed on to a
sexual partner.

2. Predisposing factors include: DM, Immunosuppression, disturbance of vaginal flora (with broad-spectrum antibiotics), pregnancy,
OCP, HRT, scented cleansing products, Tampons and wearing nylon tights, some women are more prone to developing thrush than
others even without any obvious predisposing conditions.

3. Symptoms: All women have a natural vaginal discharge. With VVC the discharge is thick and white often described as “cottage
cheese-like” and does not usually smell. The discharge may be heavy and cause vulval itching. The vulva may be inflamed and swollen.
Sex may be uncomfortable and dysuria may occur.

4. Signs of vaginal candidiasis include: erythema, fissuring, discharge – may be thin or curdy, oedema, satellite lesions, excoriation.
Note: 10-20% women of reproductive age may be colonised with candida without any symptoms or signs. These women do not need
any treatment.

5. Differential diagnoses includes: BV, dermatitis, allergic reactions, HS infection and lichen sclerosis. A proportion of women with VVC
also have other infections, for example chlamydia or gonorrhoea.

6. Investigations: Not usually needed empirical treatment can be considered based on the history. Vaginal vulval swabs should be taken
if symptoms are persistent or recurrent. The pH is normal in candida infections.
Vulvo-Vaginal Candidiasis (VVC):
Candidiasis therapy:
Recurrent candidiasis therapy:
• Recurrent VVC (RVVC) is defined as >4 episodes in a year,
with at least partial resolution of symptoms between episodes.
RVVC is very common and affects 1 in 20 women.
• Consideration should be given for any predisposing factors for RVVC and relevant
investigations undertaken (e.g. fasting glucose, HIV test).
• The British Association for Sexual Health/HIV guidelines state +ve microscopy or a
moderate or heavy growth of C. albicans should be documented on at least 2 occasions
to diagnose RVVC.
• Treatment of RVVC aims to control rather than cure infection and following measures
may be useful:
 Avoid using bubble baths and spermicides, as these may alter the normal vaginal flora
 Emollients should be used instead of soaps
 Avoid nylon underwear or tight-fitting jeans
 Women prone to thrush after taking antibiotics may find it useful to have antifungal treatment prescribed
 Friction during intercourse may cause minor damage to the vaginal wall, which may make candida more likely
to thrive. Some women may be advised to use a lubricant.
• If sexual intercourse takes place when one or both partners has thrush then they should
be advised to use a condom to prevent reinfection. If the woman’s partner is
symptomatic, then they should be treated with a topical imidazole cream at the same
time.
• Any reversible predisposing factors for RVVC need to be eliminated. However, in most
women with RVVC, no underlying or predisposing factor is identified.
RVVC therapy:

• Oral fluconazole (150mg) for3 days/3doses followed by one dose every week for
six months. Initially intravaginal topical imidazole for 10-14 days followed by
clotrimazole vaginally (500mg pessary) once every week for six months.
• Initially intravaginal topical imidazole for 10-14 days twice a week followed by itraconazole
orally (50-100mg/day) for six months (These are unlicensed uses).
• The first regimen results in around 90% remission at six months and around 40% at one year.
These regimens can be repeated if recurrent infection occurs; there is currently no good
evidence regarding the optimum duration of suppressive treatment.
• Treatment with cetirizine (10mg od) for six months may cause remission in women who fail to
get resolution of symptoms with suppressive fluconazole.

• Some women take antifungal treatment whenever they take antibiotics to prevent thrush from
occurring. There is little scientific evidence to show that natural remedies are effective.
• Neither suppositories nor yogurt containing Lactobacillus spp are likely to prevent recurrences
of VVC so their use is not recommended.
• Non-albicans species; C. glabrata does not form pseudohyphae or hyphae and is not easily
recognised on microscopy. C. glabrata and other non-albicans candida species are seen in
around 10-20 per cent of patients with RVVC and are usually still sensitive to standard
treatment
Vulval Intra-epithelial Neoplasia
Vulval Intra-epithelial Neoplasia (VIN)
Presentation: Older postmenopausal women. Leukoplakia
and may have obvious tumour mass.
Symptoms: None, itching, soreness, specific lesion.
Differential skin lesions: Can co-exist with other skin
lesions (LP/LS) and also differing stages of VIN with areas
invasive tumour. Needs expert input.
Aetiology: HPV (30%)- Sex active, Non-HPV(70%).
Biopsy: Biopsy edge of lesion to confirm or direct referral
to Dermatology and Gynaeoncology.
Pathogenesis: Pre-malignant proliferation of vulva
squamous epithelium. 1. HPV- High risk types 16, 18 & 31.
Arises from VIN a dysplastic precursor lesion characterized
by KOILOCYTIC change, disordered cellular maturation,
nuclear atypia & ↑ mitotic activity. 2. NON HPV- Chronic
irritation, Lichen Sclerosis, squamous hyperplasia
Histology: Architectural disorder & enlarged, dark nuclei.
KERATIN and INTRACELLULAR BRIDGES (desmosomes)
STAGE; <2cm (good) or >2cm + lymph nodes (bad) 3
grades- ◙ VIN I= mild dysplasia (66% of thickness)-
reversible ◙ VIN II= moderate dysplasia (33% of thickness)-
reversible ◙ VIN III= severe dysplasia (slightly less than
entire thickness)- reversible, but usually progresses ◙
Carcinoma in situ (not yet invaded)- Non-reversible
Complications: Invasive squamous cell cancer.
Vulval Intra-epithelial Neoplasia (VIN)
VIN
1. Pre and post
treatment at 5
months, 5-6 years.
2. Treated with LASER
Vulval Cancer

Vulval Cancer accounts for 5% of


all female genital tract tumours.
Mostly postmenopausal women.

Risks increased by;


1. Persistent VIN
2. Lichen Sclerosus which
causes persistent pruritus and
scarring of the vulva
3. HPV infection
4. Cancer vagina or cervix
5. Heavy cigarette smoking
6. Chronic granulomatous
disease. Hereditary disorder
impairing immune system.
Vulval cancer:
Vulval Skin Disorders:
Differentials to exclude
Condyloma Acuminatum (genital warts)
Presentation: Numerous often large white
warty neoplasms of vulvar skin. .
Symptoms: None, itching, concerns regarding
appearance.
Differential skin lesions: Can co-exist must
exclude neoplastic lesions or VIN.
Biopsy: If fails to respond to therapy or
suspicious lesions.
Pathogenesis: Usually benign genital warts
caused by HPV (subtypes 6,11).
Histology: Koilocytosis (clear halo around
raisin like nuclei, a viral effect) in
papillomatosis formations . Usually benign
but rarely progress to squamous cell cancer.
Hallmark at histology: Halo raisin like nuclei.
Extra-mammary Pagets (risk of adenocarcinoma)
Presentation: Erythematous , puritic,
ulcerated crusted vulval skin (often extends
grossly beyond visible lesion).
Symptoms: None, itching, soreness, concerns
regarding appearance.
Differential skin lesions: Can co-exist must
exclude neoplastic lesions or VIN.
Biopsy: Biopsy from edge of lesion and/or
direct referral to Dermatology and
Gynaeoncology specialists.
Pathogenesis: Arises from sweat glands and
10% patients have underlying sweat gland
adenocarcinoma.
Histology: Glandular tissue visible with
normal squamous cells, no invasion, PAS+
(mucin secreting cells), Keratin +
(intermediate fillaments), S100-.
Complications: Invasion.
Bechet’s Disease
Behçet's disease is a diffuse inflammatory
disorder. The most common symptoms
include painfu mouth, genital sores,
inflammation of parts of the eye, and arthritis.
The sores last a few days. Less commonly
there may be inflammation of the brain or
spinal cord, VTE, aneurysms or blindness.
Symptoms come and go and the cause is
unknown but believed to be partly genetic.
There is no cure.
Treatments may include immunosuppressants
such as steroids, lidocaine mouthwash may
help pain. Colchicine may decrease attack
frequency. The condition often improves with
the passage of time.

While rare in the USA it is more common in


the Middle East (2 per 1,000). The usual onset
is 20-40 years of age. Makes> females.
Vagina Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)

Presentation: Female child <5yoa. Lesion looks like red


bunches of grape at vulva but protruding from the vagina.
Symptoms: None, itching, soreness, spotting, bleeding.
Differential skin lesions: None or warts.
Aetiology: Congenital.
Biopsy: No biopsy. Direct referral to Paediatrics.
Pathogenesis: Malignant mesenchymal proliferation of
immature skeletal muscle Prognosis moderate if localized .
Histology: Small blue cell tumor w/ RHABDOMYOBLASTS
(Big pink cells) w/ cytoplasmic CROSS STRIATIONS (Dx
hallmark); Desmin+ (intermediate filament in muscle cells),
Myogenin+ (Nuclear transcription factor in immature
skeletal muscle
Complications: Invasive aggressive lesion
Vulval Infections to exclude
Bartholin’s Gland and Cyst
Swollen inflamed Vulva: Underlying Bartholin’s
abscess with inflammation of the Vulva

• Painful swollen gland

• Fluctuant tender

• May have expressible purulent


discharge

• Located at the 4 and 7 o’clock


position of the vestibule.

• 2% have adenocarcinoma
Treatment Bartholin’s Cyst or Abscess
Management:
1. Consider antibiotics if extensive
inflammation vulval tissues.
2. If small may settle alternately for
persistent cysts and or larger
cysts/absecess 2 options.
3. First consider insertion of Word
Catheter in OPD and prescribe
antibiotics. Allow free drainage
remove catheter when settled
4. Send swab for C&S
5. Marsupialization of Bartholin’s
abscess or cyst alternative option
6. Recurrent abscess or cyst consider
excision Bartholin’s cyst/gland
7. Older females tissue for histology
sent as 2% risk adenocarcinoma
8. Antibiotics: Chlamydia cover with
Doxycycline 200mg BD for 10 days
and broad spectrum cover with a
Cephalopsporin 500mg TDS for 5-7
days or Metronidazole 400mg TDS
for 5-7 days
Infective Vulvitis
Streptococcal B vulvitis; check history sore throat or chest infection.
Fungal groin infections (Tinea)
Herpes Simplex: HSV 1 and 2
Management of Benign Vulval Disorders
and
The role of the Vulval Clinic:
Setting for managing
Benign Vulval Disorders:

• Most straight forward benign disorders of the vulva may be managed first-line in
a primary care (GP) or outpatient Gynaecology Clinic.
• Persistent or recurrent disorders, suspected VIN or cancer, and any unusual
lesions or conditions should be managed within a designated Vulval Clinic.
• The Vulval Clinic services should incorporate a multidisciplinary team (MDT) of
named health professionals interested in vulval disorders across different
specialities. It should include core members from; Gynaecology, Dermatology and
Genitourinary medicine (GUM). They should be senior clinicians and have
experience in the assessment and management of vulval disease.
• The extended-core members of a vulval service should include representation
from; Nursing, Psychosexual therapy, Pain management, Clinical psychology,
Specialist physiotherapy, Reconstructive surgery, Continence advisory service,
Oral physicians and Colorectal surgeons.
Setting for managing
Benign Vulval Disorders:

• Extended service role; This extended team structure is important in ensuring


access to a toolkit of clinical skills (ie sexual therapy for those patients with sexual
dysfunction, pain management for those with intractable vulvodynia, colposcopy
for those with multifocal intraepithelial neoplasia, and specialist physiotherapy
for those with pelvic floor dysfunction). Patch testing should also be available to
patients with suspected contact dermatitis and the service should work closely
with a histopathologist with a special interest in vulval skin disease.
• Care pathways; Clear access and referral paths to gynaecological oncology
services are crucial.
• Role of MDT; The ideal vulval service should comprise a virtual MDT – a
multidisciplinary network of channels of communications between the different
core and extended-core members.
Setting for managing
Benign Vulval Disorders:

• Leadership: 1-2 named leads should take a formal lead role within the MDT service.
Their responsibilities should include: Overall clinical governance, ensuring service
sustainability, co-ordinate clinical meetings. They’re usually a consultant/associate specialist
• Teamwork and communication: Regular MDT meetings to discuss difficult cases every 1-2
months. These meetings should also look at service delivery, audit and clinical governance.
• Models of care (care pathways): Models of care for patients with vulval conditions should
be developed to ensure they’re seen by the right person, in the right place, at the right time
and can move readily between the levels of care as necessary.
• Local pathways should be developed between the vulval service and primary and secondary
health care to ensure that the most appropriate patients are sent to the service. Within the
vulval service itself, there should be clear referral pathways to different members of the
team when they are not operating as part of a multidisciplinary clinic.
• Care Pathways; Should be complaint with national RCOG and ACOG guidance
Guidance on appropriate practitioners and
levels of care for vulval conditions:

Practitioner Roles and responsibilities


Level 2 Care;
General practitioner (GP) or specialist secondary care (dermatology, gynaecology, genitourinary medicine)
Patient assessment (history taking, clinical examination, microbiological swabs)
Uncomplicated vulvovaginal infections (eg candidiasis) Follow-up of vulval conditions (eg uncomplicated lichen sclerosus)

Level 3 care;
Patient assessment (history taking, clinical examination, microbiological swabs, biopsy)
Treatment for common and uncommon conditions (eg lichen sclerosus, psoriasis) and follow-up
Referral of certain patients to supra-specialist care (vulval service)
Skin disease (eg lichen sclerosus), Vulvodynia , Unifocal VIN, Complicated infections (ie resistant to basic treatment)

Level 4 care;
Supra-specialist care; Assessment and management of uncommon and rare skin disease, uncommon conditions
Vulval dermatoses; e.g. LS, LP (erosive/ hypertrophic), multifocal VIN, refractory symptoms, rare conditions (e.g. bullous disorders)

Level 4 care
Gynae-oncology team; Patient assessment and treatment of premalignant and malignant vulval disease
Liaison with the extended cancer team
Examples appropriate referred disorders- Vulval cancer, VIN (all types including Pagets )
Diagnosis and management of specific
Benign Vulval Skin Disorders:
Management Lichen Sclerosus:

A. Diagnosis: Symptoms and signs


B. Inivestigations;
1. Biopsy: mandatory if diagnosis uncertain, atypical features , coexistent VIN or SCC is suspected.
.
2. Investigation autoimmune disease: If clinically indicated (e.g. T4 TSH) is often asymptomatic .
3. Skin swab: only to exclude co-existing infection if there are symptoms or signs suggestive .
4. Patch testing: rarely required and only if secondary medicament allergy was suspected.
5. Consider referral to dermatologist or Vulval Clinic if chronic, complicated or diagnosis unclear.

C. Treatment General advice;


1. Patients information ether written or web-based and should be made aware of the small risk of
neoplastic change.
3. Advise to contact doctor if notice a change in appearance or texture (e.g. lump/ hardening skin)
or major change in symptoms.
Treatment Lichen Sclerosus:
1. Recommended regimen: Ultra-potent topical steroids (e.g. Clobetasol proprionate (level
evidence I A). Various regimens are used. The most common is daily use for 1-month,
alternate days 1-month, x2 weekly for 1-month , review at three months. Then use as
required. No evidence on optimal regimen. 30 g ultra-potent steroid should last at least three
months. .Ointment bases better for anogenital skin because reduced need for ointment
preservatives and <risk irritation or secondary contact allergy.

2. Alternative regimens: Ultra-potent topical steroid with antibacterial /antifungal


(e.g. Dermovate/generic equivalent, Clobetasol with neomycin/nystatin), alternative
preparation that combats secondary infection (e.g. Fucibet cream) . Use for short period or#
to clear infection and void development contact allergy (Level evidence IV, C).
Refractory LS:
New and novel therapies
• Topical calcineurin inhibitors (e.g topical
tacrolimus 0.1%)
• Avocado and soya beans extracts
• Methyl aminolevulinate photodynamic
therapy (MAL-PDT)
• Cyclopsporin
• Methotrexate (dosing e.g.
Methylprednisolone 1g for 3 days then
15mg once weekly for 6 months)
• Retinoids (e.g. elretinate)
• Surgical excision
• Demasilk pants
Ano-genital and refractory Vulval LS therapy:

1. CP 0.05% ointment on a regimen for 3 months (OD for a month, alternative days for a
month, twice weekly for a month), combined with a soap substitute and a barrier
preparation.
2. Discuss the amount of topical treatment to be used, the site of application and the
safe use of an ultrapotent topical steroid with the patient.
3. Continued use of CP 0.05% for ongoing active LS disease.
4. Consider an individualized treatment regimen of topical steroid to maintain disease
control and prevent scarring in females with ongoing active LS disease despite good
compliance. Treatment should be titrated to maintain symptoms and resolution of
skin thickening and ecchymosis although pallor may not completely resolve.
5. Consider referral to a specialist vulval clinic in all females (including children & young
people) with LS not responding to a topical steroid, or if any surgical procedure is
being considered.
6. Consider intralesional triamcinolone (10-20 mg) in females with LS with topical
steroid-resistant, hyperkeratotic areas after intra-epithelial neoplasia or malignancy
has been excluded by biopsy .
Management Lichen Planus:
A. Diagnosis: Symptoms and signs
B. Inivestigations;
1. Biopsy: mandatory if diagnosis uncertain, atypical features , coexistent VIN or SCC is suspected. .
2. Investigation autoimmune disease: If clinically indicated (e.g. T4 TSH) is often asymptomatic .
3. Skin swab: only to exclude co-existing infection if there are symptoms or signs suggestive .
4. Patch testing: rarely required and only if secondary medicament allergy was suspected.
5. Consider referral to dermatologist or Vulval Clinic if chronic, complicated or diagnosis unclear.

C. Treatment General advice;


1. Patients information ether written or web-based.
2. Recommended regimen: Ultra-potent topical steroids (e.g. Clobetasol proprionate (level evidence I A).
Various regimens are used. The most common is daily use for 1-month, alternate days 1-month, x2 weekly for 1-
month , review at three months. Then use as required. No evidence on optimal regimen. 30 g ultra-potent
steroid should last at least three months. .Ointment bases better for anogenital skin because reduced need for
ointment preservatives and <risk irritation or secondary contact allergy.
3. Alternative regimens: Ultra-potent topical steroid with antibacterial /antifungal (e.g. Dermovate/generic
equivalent, Clobetasol with neomycin/nystatin), alternative preparation that combats secondary infection (e.g.
Fucibet cream) . Use for short period or to clear infection and void development contact allergy (Level evidence
IV, C).
4. New and novel therapies: Topical calcineurin inhibitors are not licensed for LS. Long-term safety and efficacy
is not clear.. Tacrolimus 0.1% effective used for 16-24 weeks (IIb, B) with use for genital and extra genital LS
studies show 77% of patients responding had a 43% resolution LS (absence of symptoms and skin findings
excepting induration and atrophy) at 24 weeks.at 18 months follow-up.
Vulval Pain Disorders:
VulVoDynia (VVD)
Classification Vulval Pain
and Vulvodynia:

A. Vulval pain related to a specific disorder:


1 Infectious (e.g. candidiasis, herpes, etc.)
2 Inflammatory (e.g. lichen planus, lichen sclerosus, immunobullous, disorders, etc)
3 Neoplastic (e.g. Paget’s disease, squamous cell carcinoma, etc.)
4 Neurological (e.g. herpes neuralgia, spinal nerve compression, etc.)

B. Vulvodynia
1 Generalized
1 Provoked (sexual, nonsexual, or both)
2 Unprovoked
3 Mixed (provoked and unprovoked)
2 Localized (vestibulodynia: previously known vulval vestibulitis, clitorodynia, hemivulvodynia, etc.)
1 Provoked (sexual, nonsexual, or both)
2 Unprovoked
3 Mixed (provoked and unprovoked)
International Society for the Study of Vulvovaginal Diseases (ISSVD)
Vulvodynia
Vulvodynia
• Vulvodynia is a chronic pain syndrome that
affects the vulvar area and occurs without an
identifiable cause affecting up to 16% women.
• Symptoms typically include a feeling of burning
or irritation. For diagnosis symptoms must last at
least 3 months.
• The exact cause is unknown but is believed to
involve a number of factors, including genetics,
immunology, and possibly diet.
• Diagnosis is by ruling out other possible causes
that may include biopsy of the area.
• Treatment may involve a number of different
measures. None is universally effective, and
evidence to support effectiveness is often poor.
• These include; improved vulvar care, dietary
changes, medications, counselling, and, if
conservative treatment not effective, surgery.
Vulvo-vestibulitis

The term Vestibulitis should be avoided as there is no inflammation associated


with This pain disorder. There are also no skin changes as with Lichen Sclerosus or
Lichen Planus. Occasionally, there may be some transient erythema with acute
VVD. The term provoked and unprovoked vulvodynia or vulvovestibulodynia are
the correct terms to use
Vulvodynia
Aetiology
Management of Vulval Pain Disorders - Pain

• Detailed assessment as described earlier


• Pain history taken to assess symptoms, severity and impact on QoL and activities
• Categorize subgroup of vulvodynia on ISSVD definitions (e.g. provoked ⁄unprovoked)
• Management will be different for each subset. Removal of terms as ‘vestibulitis’ from the
ISSVD terminology in preference for ‘provoked vulvodynia’ avoids confusion as the suffix ‘itis’
implies inflammation, which is not proven to be present in this condition.
• Visual Analogue Scales (VAS) for pain and pain diaries are helpful
• Quantitative assessment of pain levels may involve standardized pain assessment tools such as
the McGill Pain Questionnaire.
• Pudendal neuralgia, an entrapment nerve syndrome, can present with symptoms similar to
vulval pain but the management may be different. Patients with pudendal neuralgia usually
experience pain on sitting and the pain is relieved by standing or lying.

Grade of recommendation C evidence level IV


Management of Vulval Pain Disorders- Sex

• Sexual History: If there are problems patients an adequate sexual history taken asking
specifically about the presence of vaginismus, adequate lubrication during intercourse,
anorgasmia and partner problems.
• Identification of psychosexual morbidity: Is important as psychosexual counselling may be
necessary to complement the medical treatments being offered. Sexual dysfunction is common
and frequently reported with VVD.
• Dyspareunia: Unfortunately most studies focus on provoked pain where superficial
dyspareunia is the presenting feature. However, reduced sexual arousal, more negative sexual
feelings and less spontaneous interest in sex (not elicited by a partner) are all described.
• Psychological morbidity: Is significantly higher in women with vulvodynia compared with
asymptomatic women with studies demonstrating high degrees of anxiety, depressive
symptoms, somatization disorders and hypochondriacal symptoms with no evidence for
primary psychological cause for pain.

Grade of recommendation C evidence level IV


Management of Vulval Pain Disorders

• Team aproach: The diagnosis of vulvodynia is clinical and a team approach may be necessary
to address the different components of vulvodynia.
• A lead clinician should triage patients and consider referral to other health professionals who
have a role in vulvodynia management, e.g. psychosexual medicine, physiotherapy, pain
management teams. Combining treatments should be encouraged
• Involving the patient: Patients should be given an adequate explanation of their diagnosis,
relevant written information and suggested contact information.
• Clear instructions and treatment plans: When prescribing treatments clear instruction should
be given on how to take medication
• Support information: Details and contacts for IVVD support groups, appropriate web sites for
reference, printed information and leaflets.
Management of Vulval Pain Disorders- Therapy

• Steroids: Topical agents should be used with caution to avoid the problem of irritancy.
• Local anaesthetic : Topical agents may be considered in all vulvodynia subsets
• Oral analgesics: Paracetamol, NSAIDs. Referral to the Pain Clinc should be considered as they
can often offer a more structured MDT approach to chronic pain management including
education, psychotherapy, dietician and specialist physiotherapy. They can also offer more
specific therapies for refractory VVD including nerve blocks, spinal cord stimulation.
• TCAD’s: Tricyclic antidepressant drugs (TCAs), e.g. amitriptyline or nortriptyline, are an
appropriate initial treatment for unprovoked vulvodynia. And may also have an antidepressant
mood elevating effect as well as promoting sleep.
• Neuromodulators of pain: Other drugs may be considered including gabapentin and
pregabalin which can be given in addition to a TCADs.
• Surgery: Surgical excision of the vestibule may be considered in patients with local provoked
vulvodynia (vestibulodynia) after other measures have been tried. Only a minority of patients
may be suitable for surgery. If surgery is offered, adequate counselling and support should be
given to the patient both pre- and postoperatively
Vulvodynia: Topical steroid therapy and potencies
Management VVD- Drug Therapy

• TCADs: Effective particularly for unprovoked VVD.


• Dosage: Amitriptyline best studied and dose increased according to the patient’s pain level.
Start 10 mg OD increasing weekly until pain controlled . Average dose 60 mg divided daily up
to 100 mg.
• Side-effects: Will influence the compliance with treatment and these should be discussed
with the patient.
• Response rate: 47% complete response TCAs for generalized pain
• Other drugs: Refractory VVD or side effects with TCADs trial of Gabapentin and Pre-gabalin
at increasing dosages. Start 300 mg Gabapentin orally. Increased by 300 mg every 3 days to
max dose of 3600 mg daily. The optimal drug treatment for VVD remains unclear due to a
lack of well-conducted trials.
Management VVD- Combining Therapies
Combining treatments: Should be encouraged (Grade of recommendation C; evidence level IV). This
may tackle different facets of chronic vulval and sexual pain. Research shows combining medication
with psychotherapy, physiotherapy and dietary advice significantly improves pain free outcome rates.
Surgical removal of the vestibule also has a better outcome when patients have psychosexual input.
General measures: Minimizing exposure to contact irritants from everyday products will help, and use
of inappropriate topical agents, e.g. antifungal creams, should be discouraged. Topical agents should be
used with caution to avoid the problem of irritancy.

Topical agents:
Local Anaesthetic (LA): A trial of LA may be considered in all VVD subsets (Grade C; evidence level IV).
Topical lidocaine gels or ointments can be for provoked VVD making penetrative sex possible. This is
applied 15–20 mins prior to sex.
Side effects/risks: There is a risk of irritancy and potential effects to the partner of penile numbness.
They may want to wear condoms and avoid oral contact. Regular uses of LA on the areas of tenderness
with VVD reduces the allodynia response on the vulva.
Outcome: In a study by Zolnoun et al., 5% lidocaine ointment was applied liberally to the affected VVD
area for provoked VVD at night. A cotton wool ball soaked in 5% lidocaine was also inserted into the
vestibule and left overnight. At follow-up improvement observed with 36-76% able to have sex.20 This
management option would be best suited to those with
provoked vulvodynia.
Other agents: Many other topical agents have been suggested including capsaicin cream, ketoconazole
cream, oestrogen creams, steroid creams, interferon and nifedipine with mixed results.
Management of VVD- Surgery

• Surgical excision of the vestibule: May consider with refractory local provoked VVD
(vestibulodynia). Only minority suitable. If offered, adequate counselling and support given.
(Grade recommendation B evidence level IIb ). The procedure that yields best results is a
modified vestibulectomy. Horseshoe-shaped excision of vestibule and inner labial fold wit
advancement posterior wall.
• Case selection: Those who respond to lidocaine gel prior to sex have a more successful
outcome and a failure to do so should be considered as a relative contraindication to surgery.
• Success: Provoked VVD 59% complete response, 30% partial response and 11% no response
at1 year. Long-term success unclear may be as high as 83%.
• Adjunctive therapy: Success improved with postoperative sex therapy including vaginal
dilators.
• Alternate therapies: LASER used to destroy hyperaesthetic skin poor response.
• RCT surgery vs behavioural therapies: RCT compared sex education, partner therapy and PFM
exercises with surgery. Both arms same results but behavioural therapy preferred by patients.
Management of VVD -Physical Therapy
• Pelvic floor muscle dysfunction: Should be addressed in for vulvodynia with have sex-related
pain. Techniques to desensitize the Pelvic Floor Muscles (PFM) are beneficial (Grade of
recommendation B; evidence level IIb).

• Vaginismus: VVD is often associate with vaginismus a specific PFM dysfunction. This vaginismus
‘response’ can be addressed with physical therapy. Patients can be taught a variety of self-help
techniques; PFM exercises, external and internal soft tissue self-massage, trigger point pressure,
biofeedback and use of vaginal trainers. One study reported success with a vaginal
transcutaneous ES. No studies report on the optimal technique and success will depend on a
number of factors including the therapist, degree of patient support, and time and number of
sessions. These therapies aim to desensitize the pelvic floor area.

• Success of physical therapy: 51% resolution and 20% moderate improvement for provoked VVD
less with unprovoked VVD. Whilst EMG studies of the PFM in unprovoked VVD (pain) show
differences compared with asymptomatic patients no studies have been carried out to address
the value of physical treatment.
Management of VVD-Adjunctive Therapy

• Acupuncture: May be considered in the treatment of unprovoked VVD (Grade of


recommendation C evidence level IIb); In one study of refractory unprovoked VVD 25%
responded/resolved and 25% significantly improved with acupuncture treatment. A large part of
its beneficial effect, as recognized by the authors, may come from the regular specialist contact.
The role of acupuncture in provoked VVD pain is not clear.

• Intra-lesional injections : May be of value for provoked VVD (Grade of recommendation B;


evidence level III). Various drugs have been suggested.
- LA and steroid; subcutaneous injections 40 mg methylprednisolone acetate/lidocaine in 10 mL
of saline into the vestibule (vestibulodynia) with a 1/3 remission rate. Similar results with
betamethasone /lidocaine. Hylase may augment effect.
-Botulinum Toxin A: Botox injections to treat allodynia has unclear benefits. Effects likely to be
temporary meaning repeat treatment may be necessary.
Conclusions: Benign Vulval Skin Disorders

• Benign vulval skin disorders and pain disorders; These are not uncommon and may be debilitating
to the affected female significantly and adversely impacting on QoL and sexual function.
• Quality of care; Women with benign vulval and pain disorders are entitled to expect equitable
access to high-quality care provided at a level appropriate to their condition in an environment that
meets their clinical needs and respects dignity.
• The multidisciplinary team and models of care; The complex and cross-disciplinary nature of many
vulval conditions means that any effective vulval service must be based on the MDT approach,
creating a virtual network of care between core and non-core team members and a set of clear
care pathways, both into the service from generalist care and within and across the service at
specialist and supra-specialist levels.
• Appropriately trained staff; A historical and ongoing lack of training in vulval conditions (across
almost all disciplines) makes it particularly important that clinical leads are both experienced and
competent and that every effort is made to promote and share knowledge and training across the
extended network.
• Clinical governance; This is essential across a vulval service and depends on good, regular
communication and on analysis of and responsiveness to the data generated by continual
assessment of outcomes and patient experience.
• Patient and public involvement in service development; When setting up or further developing a
vulval service it is important to seek input from patients (via PREMs and PROMs and through
contacting patient groups) and members of the public whose care could be affected.
Conclusions: Vulval Pain Disorders

• This talk and slides act as a starting point to aid doctors and other
healthcare professionals in the diagnosis and management VVD and to
increase awareness and education on the condition.
• The clinician should play a role in the assessment and diagnosis of
vulvodynia and liaise with colleagues in difficult cases.
• Team work should be nurtured and developed.
• A structured approach to assessment and therapy with follow-up involving
objective/subjective outcome measures is integral to further
understanding VVD.
• Support groups and PILs are an essential part of the therapeutic package.
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Thank You
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