Diagnosis and Treatment of Vulvar

Diagnosis and treatment of vulvar precancerous lesions and cancer

 uncommon, representing about 4% malignancies of female genital tract.  squamous cell ca account for about 90% of the cases (much less common:

melanomas, adenoca, basal cell ca, sarcomas) "  in situ vulvar ca - doubled between mid-1970s and mid-1980s (rate of invasive squamous cell ca remained sable)

VIN - Vulvar Intraepithelial Neoplasia - in 1986 this term was recommended (erythroplasia Queyrat, Bowen's disease, Ca in situ simplex, Paget's disease) ,

VIN is graded as: 1 (mild) 2 (moderate) 3 (severe dysplasia = ca in situ)

VIN 1 - immature cells, cellular disorganisation, mitotic activity in the lower one- third of the epithelium, VIN 2 - immature cells with scanty cytoplasm and severe chromatinic alterations occupy most of the epithelium (changes of HPV info : perinuclear halos with displacement of the muclei by the intracytoplasmic viral protein, thickened cell borders, binucleation, multinucleation) VIN 3 - unifocal or multifocal: small hyperpigmented lesions on the labia major, (clinically: multiple small, pigmented papules less than 5 mm - 40% cases (bowenoid papulosis = dysplasia)

Paget's disease of the vulva (adenoca in situ) - most cases intraepithelial, must be distinguished from superficial spreading melanoma, Clinical: affects postmenopausal Caucasian woll)~n, symptoms - pruritus and ,- vulvar soreness. Eczematoid lesion, begins on the hair-bearing portion of the vulva.

VIN treatment:  varied from wide excision to superficial vulvectomy  therapeutic alternatives: 1- simple excision, 2- laser ablation (used for multifocal lesion, can be painful, costly, no specimen) 3- superficial vulvectomy with or without split- thickness skin grafting (extensive or recurrent VIN.

Invasive Vulvar Cancer

Epidemiology:  history of vulvar condylomata or granulomatous venera disease,  v. ca ocassionally arise from areas of ca-in-situ,  occur more frequently in women who have been treated for invasive squamous carcinomas of the cervix or vagina,  more than half of the patients are between 60 and 79, fewer than 15% are under age of 40. obese, hypertensive, diabetic or nulliparous patients - more common

Etiology: HPV DNA has been reported in 20-60% of patients with invasive vulvar cancer (HPV- positive group: younger mean age, more tabacco use, presence of VIN associated with the invasive cpmponent).

Approximately 90-92% of all invasive vulvar cancers are of the squamous celr type.

Physical examination: the lesion is usually raised and may be fleshy, ulcerated, leukoplakic or warty (20%). Most squamous ca occur on the labia majora (labia minora, clitoris, perineum also may be primary sites). About 5% cases - multifocal, 10% too extensive to determine a site of origin.

Diagnosis: requires a wedge biopsy specimen, usually taken under local anesthesia. About 1 cm lesion - excisional biopsy is preferable.

Symptoms: a history of chronic vulvar irritation or soreness, a visible lesion on the labia, often sore.

Patterns of spread: 1- Local expansion (involves the contiguous structures of the urethra, vagina, perineum, anus, rectum, pubic bone. 2- Lymphatic spread: superficial inguinal nodes, deep femoral groups, pelvic nodes, 3- Hematogenous spred (advanced or recurrent cases).

Treatment:

Microinvasive ca (less than 1 cm, focal invasion no greater than 5 mm in depth, no Iymphovascular space involvement): wide (3 cm) local excision and sampling of the ipsilateral superficial inguinal nodes.

Invasive squamous ca: Stage I and II - radical vulvectomy, pelvic ratiotherapy is recommended for p. with involved nodes Stage III and IV - radical or exenterative surgery alone or in combination with radiotherapy. Five Year Survival rates: Stage 1- 71,4% Stage 2- 47,2% Stage 3- 32,0% Stage 4 - 10,5%.