Radioguided Surgery and Vulvar Carcinoma

Edward C. Grendys, Jr., James V. Fiorica

Introduction l42

Epidemiolo gy l43

Anatomy and Lymphatic Drainage l44

Surgical Management and Stagingof Vulvar Carcinoma l44

Intraoperative Lymphatic Mapping for Vulvar Carcinoma l47

Technique of Vulvar Lymphoscint igraphy l47

Vulvar Melanoma l48

Conclusion and the Future l48


Overall, carcinoma of the vulva is a relatively rare malignancy representing approximately 5% of all female genital tract cancers1 and 1% of all malignancies in women. The incidence has risen slightly over the past 50 years, perhaps because of an overall rise in the average age of women in the U.S.,2 or an increase in the prevalence of human papillomavirus (HPV) genital tract infection. The reported increase in vulvar carcinoma in situ, a precursor lesion, has nearly doubled from 1.1-2.1 per 100,000 woman-years between 1973 and 1987,3,4 mostly in younger women.

Fortunately, the majority of lesions are diagnosed at a relatively early stage and are thus amenable to local surgical extirpation with high overall cure rates. Generally, these tumors are readily visible on the external vulvar surface and produce the typical symptom of pruritus in over 90% of patients.5 Other signs and symptoms associated with vulvar carcinoma include a visible, palpable vulvar mass, pain, bleeding, ulceration, dysuria and/or an abnormal vaginal, perineal discharge. Unfortunately, even given the high prevalence of early symptoms, patient reporting and subsequent diagnostic evaluation is often delayed, most commonly due to patient denial or embarrassment. A histologic diagnosis should always be considered before initiating any topical therapy for women with these complaints.

Vulvar malignancies with the rare exception of vulvar sarcomas appear most commonly in women between the ages of 65 and 75 while the median age of the precursor in situ lesion is approximately 45-50. However, 15% of vulvar carcinomas occur in women less than 40 years of age6 with multifocal disease being more prevalent._

The vulva is covered by keratinized squamous epithelium and the majority of these neoplasms are of squamous cell (epidermoid) histology (see Table 13.1). Though relatively uncommon, vulvar melanoma represents about 5-10% of malignant vulvar neoplasms and overall about 17% of melanomas diagnosed in females will originate on the vulva. The aggressive biopsy of hyperpigmented vulvar lesions using standard criteria should be considered (See Table 13.2).


Several infectious agents have been proposed as possible etiologic factors in the development of vulvar carcinoma, including various granulomatous infections, herpes simplex virus and human papillomaviruses (HPV). The molecular role of the human papillomavirus in cervical dysplasia and carcinoma as well as the association between viral induced vulvar condylomata and subsequent development of vulvar carcinoma has been well established.7 Many investigators have identified HPV DNA in both invasive and precursor carcinoma in situ vulvar lesions.8 With the increasing incidence of HPV related dysplasias in the younger female population and the reported trend toward a younger age of diagnosis9 there is certainly cause for concern that an increase in related vulvar cancer may be forthcoming. In a study by Mitchell et al10 169 women with invasive vulvar carcinomas were noted to have a secondary genital squamous neoplasm in 13% of

Table 13.1.Histologic distribution of malignant vulvar neoplasms Tumor type Percent

Epidermoid 86.2

Melanoma 4.8

Sarcoma 2.2

Basal cell 1.4

Bartholin gland 1.2

Squamous 0.4

Adenocarcinoma 0.6

Undifferentiated 3.9

Plentl, AA, Friedman, EA, Lymphatic system of the Female Genitalia Philadelphia, 1971, WB Saunders

Table 13.2. Indications for excisional biopsy of vulvar nevi

Change in surface area of nevus Change in lesion contour or surface Change in lesion color Change in sensation cases. Brinton et al11 concluded that women with a history of genital warts, previous abnormal Papanicolaou smears as well as a history of smoking are at increased risk for vulvar cancer. Chronic immunosuppression has also been linked to an increased incidence of both vulvar and cervical disease.9 Other observational associations have been made between hypertension, diabetes mellitus, and obesity.12


The vulva, including the mons pubis, labia majora and minora, clitoris, vaginal vestibule, perineal body and the supporting subcutaneous structures, develops embryologically from the genital tubercle of the cloacal membrane, as does the distal vagina. Because of their embryologic derivation the vulva and distal vagina share common routes of lymphatic drainage. The vulvar lymphatics run anteriorly through the labia majora, turn laterally at the mons pubis and drain primarily into the superficial inguinal lymph nodes. Previous lymphatic dye mapping studies by Parry-Jones13 demonstrated that the vulvar lymphatic channels do not cross to the contralateral lymph nodes unless the dye is injected in the midline structures (clitoris or perineal body). There may be some minimal, direct drainage to the pelvic lymph nodes though the clinical relevance of these communications appears negligible. Most studies indicate an orderly progression of lymphatic drainage from the vulva to the superficial inguinal lymph nodes then directly to the deep inguinal nodes prior to proceeding to the pelvic nodal structures (See Fig.13.1).


Vulvar cancers have three modes of spread: 1) direct extension into adjacent organs; 2) embolization into locoregional lymph nodes; and 3) hematogenous spread. Fortunately well documented clinical investigations have revealed that early spread is almost always confined to the local inguinal lymphatic basins. Although lymphatic drainage usually proceeds from the superficial to the deep inguinal (femoral) lymph nodes, care must be taken before adopting too cavalier an approach in that deep nodal involvement has been reported without evidence of superficial inguinal lymph node disease.15-17

Few radical procedures in gynecologic oncology have been as successful and yet continue to change as much as the surgical approach to vulvar carcinoma. Original radical procedures as described by Taussig18 and Way19 defined the procedure that dramatically reduced the mortality from vulvar carcinoma. These traditional "Longhorn" resections included the entire vulva, mons and laterally extending over and including the inguinal lymph nodes and inferiorly to the urogenital diaphragm. Until recently, this procedure was the treatment of choice for all resectable vulvar lesions regardless of clinical size or location. The conventional radical vulvectomy and bilateral inguinofemoral lymphadenectomy had been

Fig. 13.1. Lymphatic drainage from the external genitalia to the inguinal lymph nodes. Reprinted with permission from DiSai and Creasman, Clinical Gynecologic Oncology, Copyright 1997; 206-207. © 1997 Mosby-Year Book Inc.

extremely successful from a curative standpoint as has been well documented in the literature.12,20,21 The overall uncorrected 5-year survival following this procedure is approximately 65% and operability rates in this generally older population about 95%.22 Unfortunately postoperative morbidity remained extremely substantial. Reported operative and perioperative mortality rates in modern series range from 1-5%.20-22 The incidence of acute wound breakdown approaches 85%22 and often disabling chronic lower extremity edema in 30-70%.23 Genital prolapse, urinary incontinence, and vaginal stricture occurs in 15-20% of women postoperatively with Hacker et al reporting a reoperation rate of 15% for correction of postsurgical complications.20

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