Benign vulvar lesions

Dr Sally Sayed El-Tawab

Lecturer of Gyne-oncology
Alexandria University
 Lichen sclerosus
is commonly characterized by whitish lesions of the vulva.
It is asymptomatic, but intractable pruritus can sometimes
be present. Burning and pain are less likely manifestations.
Clinically, the lesions are characterized by a wrinkled
("cigarette-paper") or parchment like (shiny, delicate, pale)
appearance of the skin that commonly extends around the
anal area in a figure-8 or keyhole configuration.
 The etiology of this condition is unknown. A higher prevalence of the disease in postmenopausal women
suggests hormonal factors, but this has not been confirmed.

A 2008 study demonstrated that oral contraceptives with antiandrogenic properties might trigger the early
onset of lichen sclerosus in susceptible young women.

Lichen sclerosus has been weakly linked to autoimmune diseases and genetic factors. Approximately 21% of
patients have an autoimmune disease, most commonly a thyroid disorder.

Familial occurrence is also well recognized. Forty-four percent of patients have one or more autoantibodies,
and 22% percent have a positive family history.

The role of local factors (eg, trauma, friction, chronic infection, and irritation) is well recognized, and
ocurrence near vulvectomy scars has been observed.
In late stages of the disease, normal architecture may be
lost. Additionally, atrophy and fusion of the labia minora,
constriction of the vaginal orifice (kraurosis), synechiae,
ecchymoses, fissures, and telangiectases may be noted.
Squamous cell carcinoma develops in 3-6% of women
affected by vulvar lichen sclerosus, which is therefore now
regarded as a preneoplastic condition.
The presence and the duration of symptoms and the loss of
vulvar architecture are not useful indicators of potential
cancer risk.
Histologic findings include hyperkeratosis, epithelial thinning
with flattening of the rete pegs, cytoplasmic vacuolation of
basal keratinocytes, follicular plugging, homogenization of
the subepithelial layer, and inflammatory cell infiltration
consisting of lymphocytes with few plasma cells.
A skin biopsy is necessary to confirm the diagnosis and to
exclude the presence of malignant degeneration.
Treatment
Patients with lichen sclerosis typically present with thin,
parchment like skin, which is a poor barrier to the loss of
moisture. Patients should avoid excessive drying of this
skin after bathing. Bland emollients should be used to
improve moisture retention. For instance, a thin layer of
petrolatum (eg, Vaseline) may be helpful. Aqueous creams
or emulsifying ointments are safe and cheap. Many
proprietary preparations of moisturizing lotions, creams, or
ointments are available.
Careful hygiene, avoidance of irritants and allergens, use of
cotton underwear, and avoidance of constricting and heat-
inducing clothing are sensible adjuncts of local care. The
condition is independent of whether the patient is taking
hormone replacement therapy.
Currently, potent topical corticosteroids provide the best
outcomes. Clobetasol propionate 0.05% ointment, applied
twice daily for 1-3 months (with the dose gradually tapered)
provides short-term relief and long-term control in most
patients.

 Maintenance therapy with 1-2 applications per week may

be useful. In using a potent corticosteroid, the amount used
should be monitored, with 30 g over 3 months providing a
dosage level below which few local or systemic adverse
effects are likely to occur.
Long-term sequelae of potent topical corticosteroids (eg,
atrophy and thinning of skin and subcutaneous tissues) have
not been clinically significant in persons with this disorder.
A protective effect from malignant evolution has been
suggested but not proved.
 Long-term maintenance therapy of vulvar lichen sclerosus
with a moisturizing cream (both safe and inexpensive) can
maintain the symptom relief induced by topical
corticosteroids.
Estrogen and testosterone creams have little or no role in
the treatment of lichen. Topical progesterone has been used
for adults who did not respond to steroids or testosterone
and for children.
As with testosterone, pruritus must first be controlled with
steroid cream before use of the progesterone cream.
 Alternative treatments include intralesional steroid
injections and/or cryosurgery, focal ultrasonography,
photodynamic therapy, and surgery.

Surgery may occasionally be necessary to excise

hyperplastic or fissured areas of lichen sclerosus
unresponsive to medical therapy, but patients must realize
that recurrence rates after excision are high. This applies
even after skin grafting, when lichen sclerosus may recur in
the grafted skin. Surgery is reserved for patients in whom
biopsy has identified associated vulvar intraepithelial
neoplasia or invasive SCC.
Squamous cell hyperplasia
atypical epithelial hyperplasia (dysplasia), vulvar dystrophy,
vulvar atypia, atrophic dystrophy, mixed dystrophy, and
vulvar intraepithelial neoplasia
inhibit effective communication between clinicians and
pathologists. These terms have different meanings to
dermatologists, pathologists, and gynecologists, further
complicating the problem.
 Squamous cell hyperplasia appears as ill-defined, single or
scattered, asymmetrical, whitish, thickened, and sometimes
verrucous plaques that may be accompanied by excoriations
or fissurations that cause pain and soreness.
Itching is a common symptom. If hyperkeratosis is not
prominent, lesions may appear as reddish plaques. The
clitoris, labia minora, and inner aspects of the labia majora
are more commonly affected.
Extensive lesions may result in stenosis of the vaginal
introitus.
 Histologic examination reveals thickening of the keratin layer
(hyperkeratosis) greater than that seen with lichen sclerosus, and
epithelial hyperplasia with elongation, widening, and distortion
(acanthosis) of the rete pegs. Retention of nuclei in the keratin layer
(parakeratosis) is a common finding.
An inflammatory response in the dermis usually occurs, consisting
of lymphocytic and plasma cell infiltration. Varying degrees of
cellular atypia with increased mitotic activity and loss of polarity
may be observed in the epidermis.
This vulval squamous epithelial hyperplasia with atypia corresponds
to the entity formerly indicated as leukoplakia, which has a
malignant potential. It appears to be related to conditions that
approximate vulvar intraepithelial neoplasms (VINs) and has been
found to progress to invasive carcinoma in 10% of cases.
The diagnosis is one of exclusion after psoriasis, lichen
sclerosus, lichen planus, and chronic eczematous dermatitis
have been ruled out.
In doubtful cases, a biopsy is suggested. This also helps
identify cases of squamous cell hyperplasia with atypia that
may have a propensity to develop carcinoma
 Treatment of squamous cell hyperplasia is the same as that
for lichen sclerosus and is aimed at halting the itch-scratch-
itch cycle. General attention to proper hygiene is suggested.
If the skin is moist or macerated, aluminum acetate 5%
(Burow) solution applied 3-4 times daily for 30-60 minutes
is beneficial.
Systemic antihistamines or tricyclic antidepressants,
especially when taken at bedtime, may help.
 Benign tumors, hamartomas, and cysts
Mucous cysts
Mucous cysts usually cause no symptoms and appear as a
lump or mass that may be found at the introitus and labia
minora.
Cysts of the canal of Nuck can give rise to a hydrocele
located high in the labia majora and are associated with a
concurrent inguinal hernia in 30% of cases.
 Bartholin cyst and Skene duct cyst
Bartholin cysts are the most common vulvar cystic growths.
They usually occur in the lower and lateral portion of the
labia majora, although lesions expanding anteriorly have
also been described, and, if large, they may cause variable
discomfort, hampering sexual intercourse and micturition.
Skene duct cysts arise adjacent to the urethral meatus and,
if large enough, may cause urinary obstruction.
In both conditions, acute infection with abscess formation
may occur, thus causing considerable pain.
 Epidermal inclusion cyst
Epidermal inclusion cysts are most commonly observed in
the vagina, but they can also be found on the vulva. Such
cysts are subcutaneous and generally asymptomatic unless
they become infected. Spontaneous rupture often occurs.
Fibroma, fibromyoma
Fibromas, fibromyomas, and dermatofibromas usually
appear as solitary, slightly raised, gray-brown, mobile
indurated lesions (3-8 mm in diameter) developing along
the insertion of the round ligament into the labia majora.
Fibromas may be pedunculated and may rarely reach a
considerable size.
 Lipoma
On the labia majora, lipomas may appear as soft sessile or
pedunculated masses varying in diameter from 1 cm to
several centimeters.
Large lesions may gradually ulcerate.
Hidradenoma
Hidradenomas usually occur in postpuberty as single
mobile nodules (~1-1.5 cm in diameter) arising in the
interlabial sulcus.
Ulceration may occur, and in these cases, the lesions may
show an exophytic proliferation clinically resembling a
malignant neoplasm.
 Hemangioma
Most genital hemangiomas involve the labia majora, but the
labia minora, the perineal area, and the perianal area may
also be involved to varying degrees. They appear as red
macules that rapidly progress to well-circumscribed, raised,
red, and soft lesions of variable size.
Endometriosis
Often painful, vulvar endometriosis manifests as an ill-
defined, dark red, brown, or blue-black cystic papule or
nodule, usually located on the posterior fourchette. A case
of endometriosis infiltrating the Bartholin gland has been
observed.
It sometimes shows a cyclical variation in size and
symptoms according to menses. More widespread
involvement is a significant cause of pain and distress.
 Vulval Pain Syndromes
Include :
Vulval vestibulitis and dysaesthetic vulvodynia
Before a diagnosis : infections and vulval dermatoses should
be excluded.
 Vulval vestibulitis
Def: a cause of superficial dyspareunia and is characterized
by vestibular tenderness on light touch.

Can be generalized or focal (openings of Bartholin glands

or posterior fourchette)
 Clinical picture:
Age 20-40 years
History of provoked pain e.g. superficial dyspareunia,
tampon intolerance and pain during gyne examination.
Chronic with a high level of psychological morbidity.
Q-tip applicator can identify vestibular tenderness.
A defining feature: labial skin is not tender.
 Aetilogy is unknown, multifactorial.
Recurrent attacks of vaginal candidiasis are frequently
cited, but this may be due to initial misdiagnosis.
Prognosis:
30% resolution without treatment, 50% of these resolutions
can occur within 12 months.
management
General measures: Reassurance and explanation
Strict vulval hygiene to reduce the chance of contact
sensitivity.
Local anaesthetic gel/ointment, vaginal dilators to densitize
the pelvic floor.
Pain management and psychosexual counselling
Surgery modified vestibulectomy: excision of a horse-shaped
area of the vestibule and inner labial fold followed by
dissection of the posterior vaginal wall. The vaginal wall is
advanced to cover the skin defect. Improvement rate 60%.
 vulvodynia
A cutaneous dysaesthesia causing non-localized vulval pain.
Constant (non-provoked) neuropathic-type pain in the vulva
and occasionally the peri-anal area.
C/P
Perimenopausal or post-menopausal
Superficial dyspareunia is not constantly reported (less sexually active)
Many experience rectal, perineal and urethral discomfort.
Etiology, prognosis : unknown
Management:
Reassurance and explanation
Strict valval hygiene
Tricyclic antidepressants (amitriptyline) : address the central
ad peripheral componants of pain seen in vulvodynia.
10mg/day increased every week till pain is controlled
Average dose (60mg/day) up to 150mg can be used.
3-6months.
Neuroleptic gabapentin (2nd line treatment)
Surgery: contraindicated
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