Squamous Intraepithelial Lesion (SIL, Cervical
Invasive Carcinoma of the Cervix
Hydatidiform Mole: Complete and Partial
Preeclampsia/Eclampsia (Toxemia of
The vulva is the external female genitalia and includes the hair-bearing skin (labia majora) and mucosa (labia minora). Disorders of the vulva most frequently are inflammatory, rendering them more uncomfortable than serious. Malignant tumors of the vulva, although life-threatening, are rare.
One of the most common causes of vulvitis is reactive inflammation in response to an exogenous stimulus, which may be an irritant (contact irritant dermatitis) or an allergen (contact allergic dermatitis). Scratching-induced trauma secondary to associated intense “itching” (pruritus) often exacerbates the primary condition.
Contact irritant eczematous dermatitis manifests as well-defined erythematous weeping and crusting papules and plaques and may be a reaction to urine, soaps, detergents, antiseptics, deodorants, or alcohol. Allergic dermatitis has a similar clinical appearance and may result from allergy to perfumes; additives in creams, lotions, and soaps; chemical treatments on clothing; and other antigens.
Vulvitis also may be caused by infections, which often are sexually transmitted. The most important infectious agents in North America are human papillomavirus (HPV), the causative agent of condyloma acuminatum, vulvar intraepithelial neoplasia (VIN), and one type of vulvar squamous carcinoma (discussed later); herpes simplex virus (HSV-1 or HSV-2), the agent of genital herpes; N. gonorrhoeae, a cause of suppurative infection of the vulvovaginal glands; and Treponema pallidum, which causes primary chancre at vulvar sites of inoculation. Candida also is a cause of vulvitis, but is not sexually transmitted.
An important complication of vulvitis is obstruction of the excretory ducts of Bartholin glands. This blockage may result in painful dilation of the glands (Bartholin cyst) and abscess formation.
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Lichen sclerosus is characterized by thinning of the epidermis, disappearance of rete pegs, a zone of acellular, homogenized, dermal fibrosis, and a bandlike mononuclear inflammatory cell infiltrate (
Fig. 19.1 ). It appears as smooth, white plaques (termed leukoplakia) or papules that in time may extend and coalesce. When the entire vulva is affected, the labia become atrophic and stiffened, and the vaginal orifice is constricted. Lichen sclerosus occurs in all age groups but most commonly affects postmenopausal women and prepubertal girls. The pathogenesis is uncertain, but the presence of activated T cells in the subepithelial inflammatory infiltrate and the increased frequency of autoimmune disorders in affected women suggest an autoimmune etiology. Lichen sclerosus is benign; however, 1% to 5% of women with symptomatic lichen sclerosus develop HPV negative squamous cell carcinoma of the vulva.
Lichen simplex chronicus is marked by epithelial thickening (particularly of the stratum granulosum) and hyperkeratosis. Increased mitotic activity is seen in the basal and suprabasal layers; however, there is no epithelial atypia (