eMedicine Specialties > Obstetrics and Gynecology > Gynecologic Surgery

Surgical Treatment of Vulvar Cancer

Author: Robert V Higgins, MD, Clinical Associate Professor, Department of Obstetrics/Gynecology, University of North Carolina School of Medicine; Vice-Chairman of Academic Affairs, Associate Director of Gynecologic Oncology, Residency Director, Department of Obstetrics and Gynecology, Carolinas Medical Center
Coauthor(s): R Wendel Naumann, MD, Clinical Assistant Professor of Obstetrics and Gynecology, University of North Carolina at Chapel Hill; Associate Director, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Carolinas Medical Center; James Hall, MD, Director, Division of Gynecologic Oncology, Clinical Associate Professor, Department of Obstetrics and Gynecology, Carolinas Medical Center, University of North Carolina
Contributor Information and Disclosures

Updated: Nov 20, 2008

Introduction

History of the Procedure

In the early part of the 20th century, patients with vulvar cancer usually died of disease. The overall survival rate for vulvar cancer after simple surgical excision was less than 25%. Attempts to improve outcomes for patients with vulvar cancer by performing more radical surgery were first described by Basset in 1912.1  Way described an improved survival rate using an en bloc dissection radical vulvectomy with an inguinal and pelvic lymphadenectomy.2  The Bassett-Way operation resulted in a 5-year survival rate of 74% as reported by Morley.3 This success rate convinced most surgeons to use this operation for all patients with vulvar cancer regardless of tumor size. Major morbidity from this procedure included poor wound healing and long-term lymphedema.

Fred Taussig collected a large series of vulvar cancer cases from 1911-1940.4  He initially started his series with a radical excision of the primary tumor with an en bloc dissection of the inguinal lymph nodes. Later, he modified his technique for patients with small lesions in an attempt to decrease operative morbidity. He used separate incisions for the groin dissection and the vulvar excision. This less radical operation for small lesions was not routinely used until Hacker reported his experience with 100 patients in 1981.5 He reported using 3 separate incisions, as described by Taussig, for patients with clinical stage I disease. The 5-year survival rate was 97%.

Problem

Vulvar carcinoma encompasses any malignancy that arises in the skin; glands; or underlying stroma of the perineum, including the mons, labia minora, labia majora, Bartholin glands, or clitoris. Tumors can also arise in ectopic breast tissue that can be located in the vulva along the milk line. Metastatic tumors have also been described but occur relatively infrequently.

For related information, see eMedicine's article on Malignant Vulvar Lesions.

Frequency

Cancer of the vulva is the fourth most common malignancy of the female genital tract. The American Cancer Society estimates 3,460 women will be diagnosed with vulvar cancer in 2008.6 Currently, approximately 75% of patients with vulvar carcinomas will be cured, making vulvar carcinoma responsible for approximately 900 deaths annually in the United States.

Unfortunately, the incidence of preinvasive disease of the vulva has almost doubled over the past decade, and this may translate into a marked increase in the incidence of invasive vulvar carcinoma in the future. Since vulvar cancer is rare and is not monitored by the World Health Organization, the global incidence of this disease is not precisely known.

Etiology

The incidence of vulvar carcinoma has a bimodal peak. Currently, development of vulvar carcinoma in situ in young women is suggested to correlate to human papillomavirus (HPV) infection. In older women, the etiology of the carcinoma is attributed to chronic irritation or other poorly understood cofactors. Estimates indicate that women who smoke cigarettes have a 4- to 5-fold increase in the incidence of carcinoma in situ of the vulva and a 20% increase in vulvar carcinoma. The incidence of vulvar carcinoma in situ and vulvar carcinoma is higher in women with multiple sexual partners and in women with a history of HPV infection. For women who report a history of genital warts or HPV-related disease, the relative risk for carcinoma in situ is 18.5 and for invasive cancer is 14.5.

Pathophysiology

The development of vulvar dysplasia and cancer in most patients is related to HPV infection. Certain strains of HPV are known to be more oncogenic than others. HPV types 16, 18, 31, 33, 35, 45, and 54 are more likely to be associated with cervical neoplasia and cancer and are suspected to also be responsible for vulvar cancers. The DNA from HPV 16 and 18 has been detected in up to 60% of patients with vulvar cancer.

The mechanism of HPV transformation into dysplasia and cancer is not well understood. Two gene products from HPV are known to immortalize cells in culture and are probably responsible for malignant transformation. The HPV E6 protein does have the ability to bind the host p53 protein. The HPV E7 protein binds the Rb gene product. The oncogenic viral types are thought to have a greater affinity for these cellular proteins, which would explain the increased risk of malignant transformation. Some infections may lead to integration of the viral DNA into the host, with disruption of the normal regulation of the E6 and E7 oncoproteins. This increased production of the E6 and E7 gene products could then result in oncogenic transformation.

Presentation

Diagnosis of vulvar carcinoma is often delayed. Women neglect to seek treatment for an average of 6 months from the onset of symptoms. In addition, a delay in diagnosis often occurs after the patient presents to her physician. In many cases, a biopsy of the lesion is not performed until the problem fails to respond to numerous topical therapies. A biopsy should be performed when any discrete lesion of the vulva is discovered.

The most common presentation is a pruritic lesion of the vulva or a mass detected by the patient herself. However, early vulvar cancer may be asymptomatic and recognized only with careful inspection of the vulva. A biopsy should be performed on all visible lesions on the vulva. More advanced vulvar carcinomas present with bleeding, pain, or discharge.

Indications

Choosing the proper surgical procedure for vulvar cancer is important. Patients with vulvar dysplasia can have a wide local excision. The advantage of this procedure is that the removed tissue is sent for pathologic examination. Pathologic examination allows for assessment of surgical margins and assures the absence of invasive disease. Ablative procedures can be used for dysplastic lesions if vulvar cancer can be excluded with reasonable certainty. 

Patient with biopsy-proven squamous cell carcinoma of the vulva are usually candidates for surgical excision. Patients with a lesion involving the upper urethra or anus or is fixed to the pelvic bone can be treated with neoadjuvant radiation and chemotherapy prior to surgical intervention.7 This type of therapy can allow future resection with preservation of the urethral or rectal sphincter in most cases. Radiation can also be used in an attempt to spare the clitoris.

Relevant Anatomy

The vulva includes all external genital structures, including the mons pubis, labia majora, labia minora, clitoris, vaginal vestibule, perineum, and supporting structures exterior to the urogenital diaphragm.

The femoral triangle is bounded by the inguinal ligament superiorly, the adductor longus medially, and the sartorius laterally. The superficial groin nodes lie above the cribriform fascia in the femoral triangle. Careful dissection generally reveals 5 vessels in the femoral triangle above the cribriform fascia, the largest of which is the saphenous vein. Often, a lateral accessory saphenous vein can be identified. The other vessels include the superficial circumflex, the superficial epigastric, and the external pudendal. Below the cribriform fascia are the deep inguinal nodes. Three to 4 nodes can be found medial to the femoral vein. The most superior of these is the sentinel node to the pelvic lymphatics and is known as the node of Cloquet.

The lymphatics of the vulva and distal third of the vagina drain into the superficial inguinal node group and travel through the deep femoral lymphatics and the node of Cloquet to the pelvic nodal groups (see Media file 1).8  Direct spread to the deep nodal groups without metastasis to the superficial group has been documented using lymphatic mapping. This type of direct spread is uncommon and represents fewer than 5% of cases.

Lymphatic mapping studies have also demonstrated that radioactive colloid injected into the vulva can accumulate more readily in the lateral external iliac nodes than in the medial group, which suggests that not all lymphatics flow to the medial pelvic nodes through the node of Cloquet. Studies suggest that 10-20% of lymphatic flow from the superficial node group travels directly to the pelvis without passage through the deep inguinal nodes. A direct pathway from the clitoris or vulva to the pelvic nodes has not been identified.

Contraindications

Because few alternatives to surgery are available for vulvar carcinoma, resection of the primary lesion should be attempted in most cases. Regional or general anesthesia can be used for this type of surgery. A combination of radiation and chemotherapy is an alternative to surgery. However, this regimen can have significant morbidity. For this reason, women who are not candidates for surgery are generally poor candidates for chemoradiation. The use of radiation alone can be used for palliation but should not be considered a curative treatment.

More on Surgical Treatment of Vulvar Cancer

Overview: Surgical Treatment of Vulvar Cancer
Workup: Surgical Treatment of Vulvar Cancer
Treatment: Surgical Treatment of Vulvar Cancer
Follow-up: Surgical Treatment of Vulvar Cancer
Multimedia: Surgical Treatment of Vulvar Cancer
References
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Further Reading

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Keywords

vulvar cancer, vulvar carcinoma, vulva cancer, vulva carcinoma, vulva cancer treatment, carcinoma in situ of the vulva, vulvar CIS, Bowen disease, Bowen's disease, squamous cell carcinoma of the vulva, vulvar carcinoma, vulvectomy, vulvar malignancy, gynecologic cancer, gynecologic carcinoma, female genital cancer, human papilloma virus infection, HPV infection, sarcoma, leiomyosarcoma, malignant fibrous histiocytoma, epithelioid sarcoma, basal cell carcinoma, verrucous carcinoma, Buschke-Lowenstein giant condyloma, adenocarcinoma

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Contributor Information and Disclosures

Author

Robert V Higgins, MD, Clinical Associate Professor, Department of Obstetrics/Gynecology, University of North Carolina School of Medicine; Vice-Chairman of Academic Affairs, Associate Director of Gynecologic Oncology, Residency Director, Department of Obstetrics and Gynecology, Carolinas Medical Center
Robert V Higgins, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Surgeons, North Carolina Medical Society, and Society of Gynecologist Oncologists
Disclosure: Merck Speaker's Bureau Honoraria Speaking and teaching

Coauthor(s)

R Wendel Naumann, MD, Clinical Assistant Professor of Obstetrics and Gynecology, University of North Carolina at Chapel Hill; Associate Director, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Carolinas Medical Center
R Wendel Naumann, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and American College of Surgeons
Disclosure: Nothing to disclose.

James Hall, MD, Director, Division of Gynecologic Oncology, Clinical Associate Professor, Department of Obstetrics and Gynecology, Carolinas Medical Center, University of North Carolina
James Hall, MD is a member of the following medical societies: American Cancer Society, American College of Obstetricians and Gynecologists, American Medical Association, and Association of Professors of Gynecology and Obstetrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

 
 
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