Vulvar atypias: Intraepithelial neoplasia

Lichen sclerosus ( Fig. 30.2 ) is a change in the vulvar skin that often appears whitish; microscopically the epithelium becomes markedly thinned, with a loss or blunting of the rete ridges. In some cases there is also a thickening or hyperkeratosis of the surface layers ( Fig. 30.3 ), and inflammation is usually present. In a study of 3038 women in the Netherlands, Bleeker and associates found that the cumulative incidence of squamous cell carcinoma of the vulva for women with a prior diagnosis of lichen sclerosis was 6.7% ( ). The latency period between diagnosis of lichen sclerosis and subsequent vulvar cancer in those who developed the malignancy was 3.3 years. Concurrent VIN and age 70 or older at the time of the diagnosis of lichen sclerosis were independent risk factor for subsequent development of vulvar cancer. For women with lichen sclerosis, the standard incidence ratio (SIR) for developing vulvar cancer is 33.6 and 3.69 for developing vaginal cancer ( ). For women who are compliant with topical corticosteroid therapy, the risk of developing vulvar dysplasia or carcinoma approaches 0% compared with noncompliant women, whose risk is 4.7% ( ). Squamous hyperplasia (formerly called hyperplastic dystrophy) involves the elongation and widening of the rete ridges, which may be confluent ( Fig. 30.4 ). There may also be hyperkeratotic surface layers, and the tissue grossly is often whitish or reddish.

Lichen sclerosus et atrophicus. Homogeneous collagen in the papillary dermis is accompanied by a scattered lymphocytic infiltrate and atrophy of the epithelium (hematoxylin and eosin stain, ×80).

(Courtesy Dr. Anthony Montag, Department of Pathology, University of Chicago, Chicago.)

Lichen sclerosus. Hyperkeratosis is occasionally present.

(From Friedrich EG, Wilkinson EJ. The vulva. In: Blaustein A, ed. Pathology of the Female Genital Tract. New York: Springer-Verlag; 1982.)

Squamous hyperplasia (formerly hyperplastic dystrophy), benign. Hyperkeratosis, acanthosis, and mild inflammation are present.

(From Friedrich EG, Wilkinson EJ. The vulva. In: Blaustein A, ed. Pathology of the Female Genital Tract. New York: Springer-Verlag; 1982.)

Atypical changes may appear in the vulvar epithelium. These are often marked by a loss of the maturation process usually seen in squamous epithelium, as well as an increase in mitotic activity and nuclear/cytoplasmic ratio ( Fig. 30.5 ). Mild dysplasia (atypia) is diagnosed if these changes involve the lower third of the epithelium, moderate dysplasia (atypia) if half to two-thirds of the epithelium is involved, and severe dysplasia (atypia) if more than two-thirds of the epithelium is affected. Carcinoma in situ involves the full thickness of the epithelium. The term VIN I is used for mild atypia, VIN II for moderate atypia, and VIN III for severe atypia and carcinoma in situ. It is sometimes difficult to distinguish between squamous hyperplasia and intraepithelial neoplasia. Crum has suggested that VIN usually contains nuclei that are fourfold or greater different in size, whereas differences in the size of nuclei in condyloma or nonneoplastic epithelia are threefold or less ( ). Furthermore, abnormal mitoses are usually observed in VIN.

A, Vulvar intraepithelial neoplasia from which human papillomavirus type 16 was isolated. Characteristic features displayed here include abnormal mitoses (a two-group metaphase is denoted by the arrowhead ), a full-thickness population of abnormal cells, and abnormal differentiation. Superficial cells contain perinuclear halos, which in contrast to condylomata are small and concentric. B, The higher-power photomicrograph of vulvar intraepithelial neoplasia illustrates the marked variability in nuclear size and staining, with both enlarged nuclei and multinucleated cells. Coarsely clumped mitoses (small arrowheads) and a three-group metaphase (large arrowhead) are present.

(From Crum CP. Pathology of the Vulva and Vagina. New York: Churchill Livingstone; 1987.)

Carcinoma in situ (vin III)

Carcinoma in situ is diagnosed if the full thickness of the epithelium is abnormal ( Fig. 30.6 ). Occasionally the process may histologically resemble carcinoma in situ of the cervix, and in many lesions there are multinucleated cells, abnormal mitoses, an increased density in cells, and an increase in the nuclear-to-cytoplasmic ratio.

A, Carcinoma in situ, histology. The full thickness of the epithelium is replaced by hyperchromatic cells with poorly defined cellular borders (×80). B, Carcinoma in situ, cytology. Cells derived from carcinoma in situ of the vulva may exhibit varying sizes and shapes, as depicted in this photomicrograph. Note variation in nuclear pattern from one nucleus to another. Degenerated polymorphonuclear leukocytes are present in the background (×800). C, Invasive squamous carcinoma, histology. Tumor nests and cords infiltrate stroma. The squamous nature of the tumor is more apparent on surface (left), where cells have abundant dense cytoplasm. Keratin is also seen (×80).

Paget disease

Paget disease is a rare intraepithelial disorder that occurs in the vulvar skin and histologically resembles Paget disease in the breast. Paget cells are large pale cells ( Fig. 30.7 ). The cells often occur in nests and infiltrate upward through the epithelium. Histologic abnormalities of the apocrine glands of the skin often may be noted in these lesions. There has been an increased association of Paget disease of the vulva with underlying invasive adenocarcinoma of the vulva, vagina, and anus, as well as distant sites, including the bladder, cervix, colon, stomach, and breast. Paget disease of the vulva tends to spread, often in an occult fashion, and recurrences are common after treatment.

Vulvar epidermis with Paget disease. Malignant cells (arrows) are seen infiltrating the epidermis and spreading along the dermal-epidermal junction (hematoxylin and eosin stain, ×160).

(Courtesy Anthony Montag, MD, Department of Pathology, The University of Chicago.)

Clinical presentation

Atypias of the vulva present with a variety of symptoms and signs. Irritation or itching is common, although some patients do not report these symptoms. The vulva often has a whitish change because of a thickened keratin layer. In the past, the term leukoplakia was used. This term has been discarded, in part because abnormal lesions of the vulva require biopsy to establish a correct diagnosis. When lichen sclerosus is present, there is usually a diffuse whitish change to the vulvar skin ( Fig. 30.8 ). The vulvar skin often appears thin and there may be scarring and contracture. In addition, fissuring of the skin is often present, accompanied by excoriation secondary to itching. Areas of squamous hyperplasias (formerly called hyperplastic dystrophy without atypia ) also appear as whitish lesions in general, but the tissues of the vulva usually appear thickened and the process tends to be more focal or multifocal than diffuse ( Fig. 30.9 ).

Vulva, lichen sclerosus. The tissue of the labia minora and perineum have a white, brittle, cigarette paper appearance.

(From Kaufman RH, Gardner HL, Merrill JA. Diseases of the vulva and vagina. In: Romney SL, Gray MJ, Little AB, et al, eds. Gynecology and Obstetrics. New York: McGraw-Hill; 1980.)

Vulva, hyperplastic dystrophy. A sharply demarcated, raised, white area is noted at lower tip of white pointer.

(From Kaufman RH, Gardner HL, Merrill JA. Diseases of the vulva and vagina. In: Romney SL, Gray MJ, Little AB, et al, eds. Gynecology and Obstetrics. New York: McGraw-Hill; 1980.)

Abnormal areas of vulvar atypia or VIN may also appear as white, red, or pigmented areas on the vulva, although the clinical appearance of VIN is variable. Friedrich and colleagues estimated that approximately one-third of patients with carcinoma in situ present with pigmented lesions, emphasizing the importance of a biopsy to establish the diagnosis ( ). The lesions tend to be discrete and multifocal and occur more commonly in those who have had squamous cell neoplasia of the cervix. In addition, reddish nodules may be foci of Paget disease as well as of carcinoma in situ, and Paget disease often has a reddish eczematoid appearance. However, it should be reemphasized that these conditions cannot be accurately diagnosed from their clinical appearance, and biopsies are needed.

Diagnostic methods

In general, cytologic evaluation (Papanicolaou [Pap] smear) of the vulva has not proved helpful, in part because the vulvar skin is thick and keratinized and does not shed cells as readily as the epithelium of the vagina and cervix; however, in some cases, particularly if there is ulceration of the vulva, a cytologic smear can be helpful diagnostically (see Fig. 32.6 , B ). A tongue depressor moistened with normal saline or tap water is scraped over the surface portion of the vulva to be sampled, and the specimen is placed on a glass slide and then fixed.

The toluidine blue test (1% toluidine blue applied for 1 minute, followed by 1% acetic acid) with biopsy of the retained blue-staining areas has generally been discarded because it appears to be very nonspecific.

Colposcopy of the vulva is difficult because the characteristic changes in vascular appearance and tissue patterns that are seen in the cervix are not present (see Chapter 28 ). Nevertheless, the magnification of the colposcope may be used to help follow patients with VIN and to identify the discrete whitish or pigmented areas that warrant biopsy. The colposcope is not used for routine vulvar examination but is primarily used for those who are being evaluated or followed for vulvar atypia or VIN. The addition of 3% acetic acid highlights whitish areas for biopsy.

Biopsy of the vulva can be conveniently accomplished with a Keyes dermal punch biopsy ( Fig. 30.10 ). Usually, a 3- to 5-mm diameter punch is used. Each area in which a biopsy sample is to be obtained is usually infiltrated with local anesthesia using a fine 25-gauge needle. The punch is then rotated and downward pressure applied so that a disk of tissue is circumscribed. When the entire thickness of the skin has been incised, the specimen is elevated with forceps and removed with a sharp scissors. Occasionally, a larger biopsy is needed, in which case a larger field is anesthetized and a small scalpel or cervical punch biopsy (see Fig. 30.14 later in the chapter) is used to obtain the specimen. Little bleeding typically is encountered, and generally can be controlled by applying silver nitrate or ferrous subsulfate (Monsel solution). Depending on the size of the atypical area and the variety of atypical-appearing areas, one or multiple biopsy specimens may be needed.

Diagnostic Keyes punch biopsy.

(From Friedrich EG. Vulvar Disease. 2nd ed. Philadelphia: WB Saunders; 1983.)

Carcinoma of the vulva, patients treated from 1990 to 1992; survival by International Federation of Gynecology and Obstetrics stage (epidermoid invasive cancer only; N = 611). ^a Hazards ratio and 95% confidence intervals obtained from a Cox model adjusted for country.

(From Pecorelli S, Creasman WT, Pettersson F, et al. FIGO Annual Report on the Results of Treatment in Gynaecological Cancer. Vol. 23. Milan, Italy: International Federation of Gynecology and Obstetrics; 1998.)

Vulvar atypias

Most vulvar atypias have pruritus as the major symptom, so the relief of itching is often the woman’s main concern. Once the correct diagnosis has been established by biopsy, appropriate therapy can be undertaken. Most whitish lesions will be benign because lichen sclerosus is the most common condition encountered.

Topical steroids can be used for atrophic conditions of the vulva, particularly lichen sclerosus. The most commonly used option for the treatment of lichen sclerosus is 0.05% clobetasol propionate ointment. This can be used anywhere from nightly to twice weekly for up to 12 weeks and then used to retreat as necessary. Although lichen sclerosus can be associated with the development of squamous cell carcinoma as described previously, use of a potent steroid cream may offer protection from malignant evolution.

A newer class of drug, topical calcineurin inhibitors (TCIs), has been evaluated as a nonsteroidal treatment of lichen sclerosis. Both the TCIs, pimecrolimus and tacrolimus, have been compared with clobetasol. In one study, twice daily usage of pimecrolimus 1% cream was compared with once daily application of clobetasol 0.05% cream in 38 women with biopsy-proven vulvar lichen sclerosis ( ). Although clobetasol was superior in improving inflammation, patients who used pimecrolimus did have some reduction in inflammation and showed equivalent improvement in pruritus and burning/pain. Another study compared nightly tacrolimus 0.1% ointment with nightly clobetasol 0.05% cream in 55 women with lichen sclerosis ( ). Both groups had significant improvement in disease-related symptoms, although the clobetasol group had a larger improvement. Most would agree that clobetasol should still be used as first-line therapy in the treatment of lichen sclerosis, with consideration of TCIs in women who fail clobetasol or have other contraindications to topical steroid therapy.

When clobetasol and TCIs are ineffective, some advocate the use of hormonal creams, although results from small clinical trials using testosterone and progesterone creams have been mixed. A preparation of 2% testosterone propionate in petrolatum can be used twice daily, with once-daily maintenance after the first week. Often, reducing the dosage of testosterone cream to twice weekly is a sufficient maintenance dose. Side effects, such as clitoral hypertrophy and increased hair growth, can occur. If there are undesirable side effects with testosterone, local progesterone cream is sometimes tried, with variable success. Those who have a beneficial response to testosterone should be continued on the medication indefinitely.

The control of local irritation of the vulva is discussed in Chapter 18 (Benign Gynecologic Lesions). In addition to local measures to diminish irritation (e.g., cotton underclothes, avoidance of strong soaps and detergents, avoidance of synthetic undergarments), topical fluorinated corticosteroids are helpful to control itching. Commonly used preparations are 0.025% or 0.1% triamcinolone acetonide (Aristocort, Kenalog), fluocinolone acetonide (Synalar), and 0.01% or 0.1% betamethasone valerate. These are usually applied twice daily to control the itching, which is often relieved in 1 to 2 weeks. Unfortunately, the prolonged use of fluorinated topical steroids can lead to vulvar atrophy and contraction, and thus once the symptoms of itching are controlled, the dose of topical corticosteroids is tapered off or, if long-term therapy is needed, a nonfluorinated compound such as 1.0% hydrocortisone is used to avoid vulvar contraction. Occasionally, 1% hydrocortisone is sufficient for initial therapy. In some cases the corticosteroids are not successful, and numerous types of topical therapy must be tried to control symptoms. Gentle soaps are helpful. Burow’s solution (5% solution of aluminum acetate) is often used as a wet dressing to help control irritation and itching. Doak tar, 3%, in petrolatum (USP) or in 1% hydrocortisone ointment is useful for severe cases.

In some patients with lichen sclerosus, severe contracture of the vulva, particularly in the area of the posterior fourchette, occurs with concomitant scarring and tenderness. Intercourse may then become painful for these patients. Woodruff and coworkers described a useful surgical technique to treat these vaginal outlet disorders by repair of the perineum ( ). The contractured and fissured area in the posterior fourchette is excised, which results in an elliptic defect. This is then closed by undermining the distal 3 to 4 cm of the posterior vaginal mucosa and suturing the freed mucosa to the perineal skin ( Fig. 30.11 ).

Surgical correction of perineal scars.

(From Woodruff JD, Julian C. Surgery of the vulva. In: Ridley JH, ed. Gynecologic Surgery: Errors, Safeguards, Salvage. Baltimore: Williams & Wilkins; 1974.)

Vulvar intraepithelial neoplasia

Once the diagnosis of VIN has been established by biopsy, therapy is performed to eradicate the area containing the neoplasia. The clinician must be aware that the progress of vulvar atypia (mild dysplasia [VIN I]) to moderate dysplasia (VIN II) to severe dysplasia and carcinoma in situ (VIN III) and then to invasive carcinoma is not as well documented for vulvar neoplasia as it is for squamous cell neoplasia of the cervix. Moreover, vulvar neoplasia is often multifocal, requiring treatment of several areas. An additional complication is that some cases originally diagnosed as intraepithelial neoplasia have been reported to regress spontaneously.

In 1972, Friedrich reported bowenoid atypia (histologically similar to carcinoma in situ) in a pregnant woman that regressed spontaneously postpartum ( ). Others also reported spontaneous regression of this lesion. These spontaneously regressing lesions tend to be discrete elevations in young women. Some may be explained by studies of the nuclear DNA content of vulvar atypias that suggest that not all lesions with this designation are premalignant. Fu and colleagues noted that only four of eight cases of vulvar atypia had an aneuploid (neoplastic) distribution. A polyploid distribution was noted in four of the cases, which is consistent with a benign process, whereas aneuploidy is consistent with intraepithelial neoplasia ( ).

Although VIN has been diagnosed more commonly in younger women, the risk of progression to invasive cancer is higher for those who are older and for those who are immunosuppressed, such as women with acquired immunodeficiency syndrome (AIDS) or transplant recipients. Chafe and associates studied 69 patients with a diagnosis of VIN treated by surgical excision ( ). Unsuspected invasion was found in 13 patients. The median age was 36 years for those without invasive carcinoma, whereas the median age was 58 years ( P = .003) for those with invasion found in the excision specimen, emphasizing the increased risk of invasion in the older patients. Furthermore, the risk of invasion was higher in those who had raised lesions with irregular surface patterns. Thus patients who were older and those with irregular raised lesions had the greatest risk of unrecognized invasive carcinoma. A study by Modesitt and colleagues of 73 women, with a mean age of 45 years, found an invasive carcinoma in 22% of VIN III excision specimens ( ). Not surprisingly, the risk of recurrence was almost 50% if the margins were positive and only 17% if they were negative. The risk of progression from intraepithelial disease to invasive carcinoma appears to be less for vulvar cases than for cervical disease (see Chapter 28 ).

Women with HIV and AIDS are also more likely to develop vulvar carcinoma in situ and invasive cancer than the general population. In a large population-based study, Chaturvedi and colleagues found a relative risk (RR) of 1.59 for developing VIN III in the 28 to 60 months after the onset of AIDS and an RR of 4.91 for developing invasive carcinoma in this group ( ).

Studies have suggested that the potential of VIN to develop into invasive cancer is low. Buscema and coworkers followed 102 patients with vulvar carcinoma in situ for 1 to 15 years without treatment; 4 patients developed invasive disease, 2 of whom were immunosuppressed ( ). Unfortunately, current techniques do not allow precise prediction of which lesions of VIN are at the greatest risk of progression to invasive disease. A population-based study from Norway has confirmed an increasing frequency of VIN III that nearly tripled from the mid-1970s to 1988 to 1991 but, during the same period, the age-adjusted frequency of invasive vulvar carcinomas remained almost constant ( ). Iversen and Tretli further noted an estimated conversion rate of VIN III to invasive carcinoma of approximately 3.4% for these in situ lesions ( ). For women with a known diagnosis of VIN, risk factors for progression to invasive disease include immunosuppression (odds ratio [OR], 4.0), multifocal lesions (OR, 3.1), and smoking (OR, 3.0) ( ).

HPV types 6 and 11 have generally been recognized as being found most often in benign vulvar warts, whereas primarily HPV types 16, 18, 31, 33, and 35 are more often associated with intraepithelial neoplasia or invasive carcinoma (see Chapter 28 ). The Centers for Disease Control and Prevention (CDC) has estimated that 80% of women aged 50 will have acquired a genital HPV infection at some point in their lives. Beutner and associates predicted that as many as 1 million new cases of perineal warts will occur annually in the United States ( ). An additional complication is that HPV type 16 infection is not always accompanied by histologic evidence of VIN. Moreover, HPV types 6, 11, and 16 can be recovered from a single site, including those that show only condyloma as well as those that show carcinoma. Thus a unique role for HPV types in VIN has not been elucidated. With current data, therapy should be based on histologic findings and not on the presence or absence of HPV infection or specific HPV types. Studies by Buscema and associates have suggested that HPV type 16 is often found in vulvar neoplasia and, as noted, HPV 16 has been commonly associated with some vulvar carcinomas ( ).

Paget disease of the vulva

Paget disease generally occurs in postmenopausal women with an average age of approximately 65 years and is more common in white women. The disease typically appears grossly as a diffuse erythematous eczematoid lesion that has usually been present for a prolonged time. Itching is a common problem. The major importance of Paget disease of the vulva is the common association with other invasive carcinomas. Squamous cell carcinoma of the vulva or cervix, adenocarcinoma of the sweat glands of the vulva, or Bartholin gland carcinoma may be present. Cases of adenocarcinoma of the gastrointestinal (GI) tract and breast accompanying Paget disease have also been reported. Once a diagnosis of Paget disease of the vulva is made, it is important for the gynecologist to rule out the presence of breast and GI malignancies. In a review by Fanning and associates, 20% of patients with vulvar Paget had nonvulvar malignancies, including cancers of the breast, uterus, pancreas, lung, stomach, thyroid, and skin. In addition, 12% had invasive Paget disease of the vulva and 4% had invasive adenocarcinoma of the vulva ( ).

If no local or distant primary malignancy is uncovered, a wide excision of the affected area can be performed. It is important to remove the full thickness of the skin to the subcutaneous fat to ensure that all the skin adnexal structures are excised because they may have a subclinical malignancy. Bergen and coworkers evaluated 14 patients with Paget disease of the vulva treated by surgery, usually vulvectomy, skinning vulvectomy with graft, or hemivulvectomy ( ). With a median follow-up of 50 months, all patients were free of disease, although 2 with positive margins and 1 with negative margins required treatment for recurrence. Fishman and colleagues studied 14 patients with Paget disease treated by various surgical procedures ( ). Frozen-section or gross visual inspection was used to judge the operative margins. In this series, visual estimation was as useful as frozen section insofar as the error rate for judging margins by the final pathology report was approximately 35%. In addition, 2 of 5 patients with positive margins had a recurrence after the initial operation compared with 3 of 9 with negative margins. This small series therefore suggests that gross visual inspection may be as useful as frozen section when judging the extent of surgical operation. Other small series evaluating Mohs micrographic surgery for treating vulvar extramammary disease have failed to reduce recurrence significantly. A conservative approach involving removal of gross Paget disease with approximately a 1-cm margin appears to be the most appropriate, with the understanding that reexcision may be required for recurrence in the future. The full thickness of the vulvar skin to the adipose layer should be removed.

Even if resection margins are free of Paget disease at the time of surgical excision, local recurrence remains a risk. Women who have been treated for Paget disease of the vulva should have as part of their routine follow-up an annual examination of the breast, cytologic evaluation of the cervix and vulva, and screening for GI disease, at least by testing for occult blood in the stool. Progression of Paget disease of the vulva to invasive adenocarcinoma has been rarely reported.

Investigators have also explored using topical imiquimod cream as a nonsurgical therapy for extramammary Paget disease of the vulva. In one retrospective study, 21 women with Paget disease were treated with imiquimod cream and 11 (52%) had a complete response to therapy, whereas an additional 6 (29%) had a partial response with no cases of progressive disease ( ). In another small study, 6 of 8 patients with vulvar Paget disease (75%) treated with imiquimod cream had a complete pathologic response at 12 weeks; however, 4 of the 6 patients who had a complete response (67%) eventually did have recurrent disease ( ). Because treatment of Paget disease not associated with underlying malignancies is largely for symptom control, a trial of imiquimod may be a reasonable approach for patients who do not desire surgery or are not surgical candidates. In addition, because achieving negative margins with surgical resection is rare, some may consider using a course of imiquimod adjuvantly after surgical resection in an effort to reduce recurrence.

Morphology and staging

Grossly, vulvar carcinomas usually appear as raised, flat, ulcerated, plaquelike, or polypoid masses on the vulva ( Fig. 30.12 ). A biopsy sample of the lesion reveals the characteristic histologic appearance of squamous cell carcinoma (see Fig. 30.6 , C ).

A, Radical vulvectomy specimen. B, Vulvectomy with operative incision lines shown. Note groin incisions.

Four clinical stages are defined for carcinoma of the vulva according to the International Federation of Gynecology and Obstetrics (FIGO), similar to the system used for other gynecologic malignancies. In addition, many centers use the TNM system (tumor, nodes, metastases) for classification; T denotes the size and extent of the tumor, N the clinical status of the nodes, and M the presence or absence of metastatic disease.

In the clinical staging system, lymph node status was assessed clinically and incorporated into the stage. Enlarged or clinically suspicious lymph nodes were assigned a higher stage, regardless of disease status documented at surgery. Clinically negative nodes were assigned an earlier stage, which was upheld even if they were found to harbor metastasis after surgical removal and pathologic examination. Therefore in 1988 the FIGO staging was modified to a surgical staging system for vulvar cancer to reflect lymph node status more accurately. In addition, a location on the perineum is no longer assigned to stage III. This system, with the modifications introduced in 2009 by FIGO and in 2017 by the American Joint Committee on Cancer (AJCC) for new definitions of stages I to IV, is shown in Box 30.3 .

Natural history, spread, and prognostic factors

The vulvar area is rich in lymphatics, with numerous cross connections. The main lymphatic pathways are illustrated in Fig. 30.13 . Tumors located in the middle of either labium tend to drain initially to the ipsilateral inguinofemoral nodes, whereas perineal tumors can spread to the left or right side. Tumors in the clitoral or urethral areas can also spread to either side. From the inguinofemoral nodes, the lymphatic spread of tumor is cephalad to the deep pelvic iliac and obturator nodes. Although there has been concern in the past that tumors in the clitoral-urethral area would spread directly to the deep pelvic nodes, this rarely, if ever, occurs. The characteristics of lymph drainage of the vulva have been evaluated by Iversen and Aas, who injected technetium-99m colloid subcutaneously into the anterior and posterior labia majora, anterior and posterior labia minora, clitoral area, and perineum ( ). They then measured the radioactivity in the pelvic lymph nodes, which were surgically removed 5 hours later. More than 98% of the radioactivity was found in the ipsilateral node and less than 2% on the contralateral side. The anterior labial injections resulted in a 92% concentration of radioactivity in the ipsilateral side, with 8% on the contralateral side. The clitoral and perineal injections developed a bilateral nodal distribution of radioactivity in all the patients. It is of interest that two-thirds of the patients with labial injections had a small amount of detectable radioactivity in the contralateral nodes. Thus anastomoses of the lymphatics do exist, but a direct connection from the clitoris to the deep nodes was not demonstrated.

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