Annotation N: The vaginal architecture

Click here for Key Points to Annotation

The vagina (Latin, sheath) connects the lower portion of the uterine cervix to the vulvar vestibule. Depending on rectal and bladder contents, the vagina forms a 90 degree angle with respect to the uterine axis, ascending postero-superiorly. The fibromuscular tube has anterior, posterior, right, and left lateral walls. The anterior and posterior walls are slack and remain in contact with each other; the lateral walls are more rigid and remain separated.

Thus, viewed in cross section, the vagina has an H-shaped appearance.1 The urethral and clitoral bodies are embedded in the anterior wall. The cervix projects into the upper end of the vagina, and, as the vaginal mucosa merges with cervical mucosa circumferentially, divides the upper vagina into the anterior fornix (Latin, arch or vault), posterior and lateral fornices.

The vagina measures 8 to 8.5 cm from the hymenal ring to the top of the anterior fornix, 7 to 7.5 cm to the top of the lateral fornix; and 9.to 9.5 cm to the top of the posterior fornix. The proper way to measure total vaginal length when the cervix is present is to document the distance from the hymenal ring to the posterior vaginal fornix.2 The anterior wall length does not change, even with hysterectomy.

Although the length and width of the vagina show considerable individual variation, anatomic narrowness or lack of length in a properly sexually aroused woman is not responsible for dyspareunia because of the elastic nature of the surrounding muscles.

The vagina develops in the embryo from the urogenital sinus, advancing from inferior to superior to meet with the Müllerian ducts, approaching from superior to inferior. The plate their union forms canalizes to a tube with upper, middle, and lower thirds of approximately the same length with different blood supply, innervation and relationship to other organs. In the upper third, the anterior wall of the vagina is closely applied to the bladder, separated only by loose areolar tissue (fibrous connective tisse with the fibers arranged in a mesh or net). Inferior to the bladder, the urethra and the clitoral bodies are embedded into the anterior vaginal wall. The upper third of the posterior vaginal wall is covered with cul-de sac peritoneum with direct access into the peritoneal cavity at this point. Under the mid portion of the posterior vaginal wall lie fibrofatty tissue, the rectovaginal septum, and the rectum. The lower third of the posterior vaginal wall is separated from the anal canal and sphincter by the rectovaginal septum and the muscles of the perineal body. The lateral walls are the pelvic fascia and the levator ani muscles.3

The vaginal architecture is formed by four layers: (1) The innermost lining of multilayered, nonkeratinized, squamous epithelium; (2) A lamina propria containing a labyrinthine network of blood vessels contributing to the diffusion of vaginal fluid across elastic fibers, lymphatic vessels and nerves to the epithelium; (3) A strong external longitudinal and internal circular layer of smooth muscle connected by oblique criss-crossing muscle bundles. The muscularis layer is autonomically innervated and contains a variety of transmitters; the function of most of these is still unclear; (4) An external adventitial layer laced with collagen and elastic fibers, giving structural support to the vaginal wall and allowing expansion during intercourse and labor. The entire vaginal wall thickness in a reproductive age woman measures 2-3 mm.

Transverse epithelial folds dip into the third layer of muscle, collagen, and elastic tissue. These rugae account for the elasticity of the vaginal walls during intercourse and delivery. They are not as well developed in parous women.

The vagina contains no glands but is moisturized by transudation and mucus secreted from the cervix, paraurethral, vestibular, and Bartholin glands, all in close proximity.4

Human female sexual physiology is still being unraveled. Challenges arise in evaluation of vaginal physiology because of individual differences (explaining many discrepancies in scientific literature), locoregional differences between anterior and posterior vagina, and the fact that the vagina is hormone-dependent and therefore cyclic in function.5

Nerves that utilize neuropeptide Y, vasoactive intertinal peptide or calcitonin gene-related peptide as a neurotransmitter may play a role in controlling blood flow and capillary permeability in the vagina. Vasoactive intestinal peptide administration, both intravenously and by subepithelial injection in the vaginal wall, increases blood flow and induces lubrication.6

The nitric oxide-cyclic guanosine monophasphate (cGMP) –phosphodiesterase type 5 pathway is an important, if not the primary, regulator of vaginal hemodynamics.7 Nitric oxide is the key pathway mediating clitoral and vaginal smooth muscle relaxation.

The upper and middle thirds of the vagina are supplied by branches of the superior and inferior vesical arteries that connect with branches of the uterine artery. The lower third is supplied by a branch of the perineal division of the pudendal artery. The dorsal clitoral arteries also supply the distal vagina where it is adherent to the urethra and the bulbs of the clitoris.

Until recently, the vagina was considered devoid of nerves and sensation. In the last two decades, immunohistochemical markers have allowed progress in identification of vaginal innervation, a mixture of both sensory and autonomic nerve fibers. The nerve supply of the introitus, hymen and vagina comes from the autonomic nervous system’s vaginal plexus. The sensory nerve fibers come from the pudendal nerve. The anterior vaginal wall has more nerve fibers than the posterior. There are few free nerve endings in the upper two thirds of the vagina. In some areas, an extreme number of richly innervated and non-innervated blood vessels immediately beneath the epithelium are noted.8 These are postulated to mediate pleasure from an area devoid of typical tactile receptors. Their presence is used as support of the existence of the G-spot.9


Introduction

Architectural abnormalities of the vagina are diverse; time of presentation varies from birth to postmenopause. Many are asymptomatic and are detected by careful speculum examination; others present with dyspareunia or vaginal bleeding.

Congenital abnormalities

Vaginal agenesis

Prevalence

Vaginal agenesis is estimated to occur in one in 4000 to one in 7,000 female births.

Etiology

More than 90% of patients with vaginal agenesis have Rokitansky-Mayer-Küter-Hauser syndrome (RMKH). Women who have this are genetically female with 46XX chromosomes. The ovaries and external genitalia are normal but there is maldevelopment or absence of the vagina, fallopian tubes, cervix, and/or uterus. There may also be problems with the kidneys, the skeleton and hearing. Etiology of RMKH is unknown.

7-8% of others with vaginal agenesis have androgen insensitivity syndrome (AIS), have 46XY chromosomes and do not have a vagina, cervix, uterus, fallopian tubes or ovaries. External genitalia may look like those of a normal female or may have male attributes.10

Other genetic or developmental abnormalities account for the remainder of patients with this condition.

Symptoms and clinical features

Physical findings vary from complete agenesis, with only a dimple demarcating the potential vaginal opening, to a short vaginal pouch. As a leading cause of primary amenorrhea, agenesis is usually detected during adolescence.

Treatment

Referral for surgical reconstruction at a major medical center is indicated.

Longitudinal vaginal septum

Prevalence

Rare

Etiology

A longitudinal vaginal septum develops during embryogenesis when there is an incomplete fusion of the lower parts of the two Müllerian ducts.11 As a result, there is a double vagina. There may be associated duplications of the more cranial parts of the Müllerian derivatives, a double cervix, and either a uterine septum, or a uterus didelphys (double uterus). Studies are essential to rule out possible associated anomalies of the genital and urinary tract.

Symptoms and clinical features

A woman with a longitudinal vaginal septum may be completely asymptomatic. Various clinical symptoms, such as severe dysmenorrhea, lower abdominal pain, paravaginal mass, excessive, foul, mucopurulent discharge, and intermenstrual bleeding, which are dependent on the existence of uterine or vaginal communications, have also been described.12

Treatment

Referral to a gynecologist for evaluation for resection is recommended. The traditional surgical method requires transvaginal resection of the obstructed septum, and continues to be the most widely used approach. However, this conventional excision requires hymenal disruption and wide exposure of the vagina, and can be technically difficult.13

Hysteroscopic resection of an obstructed septum is simple and fast, and does not require any specialized surgical technique. Hysteroscopy preserves hymenal integrity, and facilitates intervention as it considerably enlarges the surgical view. In addition, transabdominal ultrasound guidance improves interventional accuracy.14

Transverse vaginal septum

Prevalence

Rare

Etiology

A transverse septum, as well as an imperforate hymen, can form during embryogenesis when the Müllerian ducts fuse improperly to the urogenital sinus. Incomplete canalization of the vagina occurs.

Symptoms and clinical features

A complete transverse septum will block menstrual flow and is a cause of primary amenorrhea. The accumulation of menstrual debris behind the septum is termed cryptomenorrhea. Some transverse septa are incomplete and may lead to dyspareunia or obstruction in labor.15

These disorders usually present at puberty with primary amenorrhea and the cyclic pain of hematocolpos. Imperforate hymen is almost always an isolated finding whereas transverse septum may be associated with urinary tract anomalies. Both abnormalities can be corrected surgically by a gynecologist.16

Treatment

Referral to a gynecologist for excision.

Vaginal cysts

Introduction

A vaginal cyst is a closed sac containing fluid or semisolid material located on or under the vaginal epithelium. A vaginal cyst can be an embryological derivative, ectopic tissue, or a urologic abnormality. Benign vaginal cystic lesions can range in size from the size of a pea, to the size of an orange, large enough for urological obstruction and include inclusion cysts, Gartner’s duct cysts, urethral diverticulae, endometriosis, and adenosis.

Vaginal inclusion cyst

Prevalence

Common

Etiology

These arise from inclusion, beneath the epithelial surface, of tags of mucosa resulting from perineal lacerations or from imperfect approximation during surgical repair of the perineum, usually after delivery.

Symptoms and clinical features

Vaginal inclusion cysts are common near the introitus. Occasionally, such cysts are found at the apex of the vagina after hysterectomy in the region of the scar. They are lined by a stratified squamous epithelium, and the content is usually cheesy or clear.

Treatment

Vaginal inclusion cysts do not require excision unless they produce discomfort.

Gartner’s duct cyst

Prevalence

A Gartner duct represents the vestigial remnant of a duct from the excretory organ of the fetus (mesonephros) that develops and degenerates as the mature fetal kidney forms. The duct may be detected in up to one fourth of adult women, although Gartner’s cysts arise only in approximately 1%–2% of the population.

Etiology

Cysts develop in the space formerly occupied by the Gartner’s (Wolffian mesonephric duct remnants) duct, usually between the layers of the broad ligament of the uterus and in the sidewalls of the vagina. This duct is active during fetal development of urinary and reproductive organs but ordinarily disappears after birth. In some cases, however, remnants of the duct persist and may collect fluid, developing into a vaginal wall cysts later in life.

Symptoms and clinical features

Gartner’s cysts can be multiple, tiny, cystic protrusions palpable on the surface of the vaginal fornices, and are rarely symptomatic. Other such cysts are small (< 3 cm), and they are usually paravaginal and in the anterolateral position; however, they can be large and cause urethral or even ureteric obstruction.17

When the cysts enlarge, they may be mistaken for other structures, such as anterior vaginal wall prolapse (cystocele) or urethral diverticulum. The largest Gartner duct cyst reported measured 16 cm x 15 cm x 8 cm.18 Large cysts can cause dyspareunia or interfere with normal vaginal delivery.19

Vaginal cysts may present in adolescence as an obstruction to tampon insertion or as dyspareunia. Most often, they are an incidental finding on pelvic exam.

Treatment

Most need no treatment, but they can be excised, although it may be safer to simply marsupialize deep cysts to avoid significant bleeding. In rare cases, a Gartner’s duct cyst may communicate with an ectopic ureter. For this reason, imaging of the urinary tract is indicated prior to excision of a vaginal wall mass in a patient with congenital urinary tract anomalies or unexplained leakage of urine.20

Urethral diverticula

Prevalence

The reported prevalence of urethral diverticula ranges from 1 to 5 percent of adult females.21 The true prevalence may be higher, since accurate diagnosis of diverticula is difficult.

Etiology

The etiology of urethral diverticula is not clearly understood. A widely accepted theory suggests repeated infection with E. coli, gonococcus, and chlamydia in the periurethral glands leading to obstruction and formation of a suburethral abscess. With the eventual abscess rupture into the urethral lumen, a communication between the abscess cavity and the urethra develops. Fibrosis and adhesion to adjacent structures follow.22

Other possible causes include trauma from childbirth, or vaginal or urethral surgery, including repetitive transurethral surgical procedures. Urethral diverticula have now been reported after the tension-free vaginal tape sling procedure and transurethral collagen injection.2324

Symptoms and clinical features

While anterior wall masses may be vaginal wall cysts, urethral diverticula are more common in the distal two thirds of the urethra at this location, and can sometimes be palpated. Urethral diverticulua have been historically described as a classic triad of three D’s: Dysuria, Dyspareunia, and Dribbling, but these symptoms are present in about one third of cases.25 Diverticulae can be asymptomatic, may be incidentally detected, or may present with painful vaginal mass, chronic pelvic pain, or recurrent urethritis or cystitis.26 In a significant percentage, there are nonspecific symptoms and no palpable masses. While diagnostic techniques are improving, the most important tool in the evaluation of a urethral diverticulum is still a high index of suspicion.27

Diagnosis

A urogynecologist can help with the diagnosis and treatment.

Ultrasonography is used to evaluate the urethra since it has the ability to visualize the entire length of the urethra and surrounding tissues for evaluation of periurethral lesions, and the capacity to differentiate between solid and cystic masses. Ultrasound is, however, operator dependent.28 MRI is the most sensitive study for diagnosing diverticula.29 Voiding cystourethrography (VCUG) has long been used to identify a urethral diverticulum, but is no longer recommended because of its low sensitivity.

Differential diagnosis

The differential diagnosis of urethral diverticulum includes vaginal wall inclusion cyst, Skene’s gland abscess, Gartner’s duct cyst, ectopic ureterocele, periurethral fibrosis, urethrocele, vaginal leiomyoma, and urethral or vaginal neoplasm.30

Treatment

Surgical management remains the treatment of choice, although expectant observation may be appropriate in some cases.

Vaginal endometriosis

Prevalence

Endometriosis in the vagina is rare.

Etiology

Endometriosis is the ectopic implantation of endometrial glands and stroma in the vagina; it is thought to occur by implantation after surgery or procedures such as endometrial curettage. Extra-pelvic lesions are reported in women with no history of endometriosis and in the absence of prior surgery, with pathogenesis presumed to be vascular or lymphatic migration, cellular metaplasia, and iatrogenic metastasis.31

Symptoms and clinical features

Many patients with pelvic endometriosis have nodules palpable through the posterior vaginal fornix. Rarely, the disease may extend into the vaginal vault, especially after hysterectomy, causing red-blue to yellow-brown nodules visible on speculum examination and palpable in the posterior fornix. Presentation with a tender mass, cyclic pain with menses, or continuous bleeding may also occur.

Diagnosis

Biopsy must show two of the three: endometrial glands, stroma, hemosiderin-laden macrophages. Foreign body giant cells may be found.32

Differential diagnosis

Melanoma, vaginal intraepithelial neoplasia, squamous cell carcinoma

Treatment

Excisional biopsy is the usual treatment.33

Diethylstilbestrol (DES) exposure

Besides uterine and cervical abnormalities, (Annotation M: Evaluation of the cervix, vagina and STIs), DES exposure (during the years 1938-1971) is associated with vaginal ridges, transverse vaginal septa, and vaginal adenosis. (Annotation O: The vaginal epithelium.) These benign cellular changes often regress over time, and treatment is unnecessary in asymptomatic women.34 Vaginal adenosis is discussed in Annotation O.

Benign solid vaginal tumors

Vaginal fibroepithelial stromal polyp (FSP)

Prevalence

Rare; only a handful of cases exist.

Etiology

Vaginal fibroepithelial stromal polyps were first described in the female genital tract in 1960. The pathology is not well understood. FSP may be a reactive lesion, or possibly a modified counterpart of a normal constituent cell of the distal genital tract. Hormonal influences may play a role in their formation.35 Suggestive evidence includes: (1) the propensity of these lesions to occur during pregnancy and spontaneously regress following delivery; (2) the association with hormone replacement therapy in the postmenopausal patient; and (3) the stromal cells of FSP can be estrogen and progesterone receptor positive. Furthermore, FSP are extremely uncommon before the menarche.36 A recent study of 34 cases, however, could not establish a direct association with a particular hormone or hormone modulator.37

Symptoms and clinical features

Fibroepithelial stromal polyps (FSP) of the vulvovaginal region are remarkable for their ability to exhibit a wide range of morphological appearances. FSP usually occur in young to middle aged women in their reproductive years, presenting more commonly in the vagina, but also occurring in the vulva and rarely the cervix.38 They can occur as a single lesion, polypoid or fronded, or can be multiple, an occurrence particularly associated with pregnancy.39 FSP that occur during pregnancy tend to exhibit a greater degree of cellularity and nuclear pleomorphism, which in the past contributed to the use of the term ‘pseudosarcoma botryoides’ by some authors.40 These lesions are benign but have the potential for local nondestructive recurrence, particularly if incompletely excised.41

Diagnosis

Biopsy

Differential Diagnosis

These can be hypercellular with marked pleomorphism and frequent mitoses leading to inaccurate diagnosis of sarcoma.

Treatment

A vaginal polyp that is not enlarging or causing symptoms does not require treatment, but since it can be difficult to determine the identity of the lesion, excisional biopsy is often performed. FSP occurring during pregnancy can spontaneously regress afterwards.42

Vaginal leiomyoma

Prevalence

Rare. approximately 300 cases have been reported since the tumor was first documented in 1733. 43

Etiology

Unknown, thought to be hormonally related

Symptoms and clinical features

A vaginal leiomyoma may vary in size from small (1.5 to 4.5 cm in diameter)  to obstructive of the vaginal canal. It can arise anywhere within the vagina, most often on the anterior wall. Unlike a uterine myoma, the vaginal myoma is single. Dyspareunia or vaginal bleeding are possible, especially if the myoma ulcerates the overlying mucosa. Prolapse of a large myoma through the vaginal introitus can occur.44

Diagnosis

Imaging by ultrasound; biopsy

Differential diagnosis

Anterior wall myoma may be confused with prolapse (cystocele), urethral diverticulum, developmental cyst, or uterine myoma. Posterior vaginal wall tumors must be distinguished from prolapse (rectocele), enterocele, inclusion cyst.45

Treatment

Small tumors can be observed if stable. Excision is recommended in pregnancy.

Fibroma

Prevalence

Rare

Etiology

Fibroma is a rare solid tumor that may arise de novo from the connective tissue and smooth muscle elements of the vaginal wall. Some are intraligamentary uterine fibromas which have separated from the uterus and dissected into the paravaginal area.

Symptoms and clinical features

The lesions are seldom symptomatic. Soft fibroma or fibroepithelial tags (achrochordon) are also rare.

Diagnosis
Biopsy or excision

Differential diagnosis
Leiomyoma, fibroepithelial stromal polyp

Treatment

Excision is performed if the lesion is enlarging or symptomatic.

Vaginal condylomata

Prevalence

Common

Etiology

Caused by the human papilloma virus, vaginal condyloma are often associated with vulvar or anal condyloma and with abnormalities of the Pap smear, necessitating a referral for full evaluation of these areas. Vaginal condylomata may become exuberant with pregnancy, filling the vagina with vascular, edematous tissue that may interfere with vaginal delivery.

Diagnosis

Lesions vary from pinhead-sized soft papules to large verrucous, cauliflower-like masses. If not classically recognizable in clinical appearance, biopsy.

Differential diagnosis

Adenosis or VaIN

Treatment

Treatment of vaginal condylomata is more challenging than treatment of vulvar lesions. Small isolated lesions could be treated with trichloracetic acid, but more extensive lesions require laser ablation. Podofillox and Imiquimod are not recommended for vaginal use. 5-FU is poorly tolerated because of burning, pain, inflammation, edema, and ulceration. Cryotherapy is also not recommended for the vagina since there is risk of vaginal perforation and fistula formation from the depth of freeze from nitrous oxide.46

Malignant and pre-malignant tumors of the vagina

Vaginal intraepithelial neoplasia

Vaginal intraepithelial neoplasia (VaIN) is defined by the presence of squamous cell atypia without invasion. VaIN lesions are classified as VaIN (vaginal intraepithelial neoplasia) I, II, or III, corresponding to mild, moderate, or severe dysplasia, respectively. The relative rarity of VaIN, which is far less common than cervical or vulvar intraepithelial neoplasia (VIN), has prevented complete understanding of the disease and its natural history. As a result, much information is an extrapolation of the knowledge of the pathophysiology of cervical and vulvar intraepithelial neoplasia. The propensity of VaIN lesions to progress to a higher grade is less well established than for CIN, but nevertheless evokes the same concern.

Prevalence

Rare.

Etiology

Although rare, vaginal neoplasia is more common in patients who have previously been treated for cervical or vulvar neoplasia. 50 to 90 percent of patients with VaIN had or currently have either intraepithelial neoplasia or carcinoma of the cervix or vulva.47 While it is estimated that 9 of every 10 truly premalignant lesions of the vagina occur in women over 40 years of age, the incidence of such lesions may be rising in younger women. The increasing incidence may correspond to a similar rise in vulvar intraepithelial neoplasia, possibly reflecting the increased incidence of infection with human papilloma virus (HPV) generally noted in the younger population.48

Symptoms and clinical features

Vaginal intraepithelial neoplasia is usually asymptomatic, although patients can present with post-coital spotting or vaginal discharge. VaIN should be excluded in all women with an abnormal Pap smear who are post-hysterectomy or who do not have identifiable cervical lesions that could account for their Pap smear abnormality.

Diagnosis

Aceto-white vaginal lesions may appear in tissue contiguous to areas previously involved with condyloma, i.e., at the vaginal apex, in the fornices, or about the vestibule and lower vagina. The premalignant vaginal lesions appear to be more homogenous than their vulvar counterparts, which may present in a variety of colors and textures.

The examination should include digital palpation to assess for thickening or irregularity of the vaginal wall and a thorough colposcopic assessment of the entire vagina. In the postmenopausal patient, a few weeks of topical estrogen treatment will often accentuate visualization and improve detection of VaIN. After the insertion of a speculum and the application of acetic acid, lesions will appear as raised or flat, white, granular, epithelium with sharply demarcated borders and may contain areas of vascular punctation. The majority of lesions are located in the upper one-third of the vagina. A biopsy should be taken from any suspicious areas.

Differential diagnosis

Parabasal cells present from vaginal atrophy have large nuclei, and are a common cause of false-positive vaginal Pap tests in postmenopausal women. Whitened plaques from condyloma, reticulations or leukoplakia from lichen planus, adenosis, vaginal endometriosis are also part of the differential.

Treatment

A broad range of treatment options is available for therapy of VaIN: surgical excision, or laser ablation are common modalities. Topical chemotherapy and radiation of lesions are also possibilities. Previous treatment failures, the presence of multifocal disease, the patient’s general health, her medical risks from surgery, her desire to preserve sexual function, and the certainty with which invasive disease has been excluded are factors considered in selecting a therapeutic course.49

Vaginal cancer

Prevalence

Primary invasive cancer is rare, representing 0.3 percent of all malignant neoplasms of the female genital tract.50 About 75% of patients with squamous cell cancer of the vagina are over 50. Adenocarcinomas of the vagina more commonly affect younger women. The average age at which adenocarcinoma of the vagina is diagnosed is 19.

Etiology

The majority (80-90%) of vaginal malignancies are metastatic, often arising from the endometrium and cervix, but also from the vulva, ovary, breast, rectum, and kidney. Vaginal metastases may occur by direct extension (e.g. cervix, vulva, endometrium) or by lymphatic or hematogenous spread (e.g, breast, ovary, kidney).51 Women whose mothers took diethylstilbestrol (DES) during the first 3 months of pregnancy are at increased risk for developing adenocarcinoma.

Symptoms and clinical features

The majority of patients with vaginal carcinoma present with vaginal bleeding, whether postmenopausal or post-coital. Other symptoms include a watery, blood-tinged, or malodorous vaginal discharge, vaginal mass, urinary symptoms (e.g. frequency, dysuria, or hematuria), or gastrointestinal complaints (e.g. tenesmus, constipation, or melena). Pelvic pain from extension of disease beyond the vagina is present in 5 percent of patients. 20 percent of women are asymptomatic at time of diagnosis. The majority, however, have a clinically evident lesion. The posterior wall of the upper one-third of the vagina is the most common site of primary vaginal carcinoma.

Diagnosis

The diagnosis of vaginal carcinoma can be difficult. The lesion may be missed on initial examination if it is small and situated in the lower two-thirds of the vagina. During visual examination of the vagina, the anterior and posterior blades of the speculum obscure this area, so the tumor may be missed unless the vagina is inspected as the speculum is rotated and removed, or the lesion is palpated on bimanual examination. Papanicolaou (Pap) smear may detect malignant cells; 20 percent of vaginal tumors are detected incidentally as a result of cytologic screening for cervical cancer. Definitive diagnosis is accomplished by biopsy of the suspected lesion, which may appear as a nodule or mass, a plaque, or an ulcer.52

Types of vaginal cancer include:

  • Invasive squamous cell carcinoma is the most common vaginal cancer affecting 89-90% of cases. It tends to start in the upper vagina near the cervix. The mean age at diagnosis of squamous cell carcinomas is approximately 60 years, although the disease is seen occasionally in women in their 20s and 30s. Squamous carcinoma is more common as the age of the patient increases.53
  • Adenocarcinomas (approximately 6% of all vaginal cancers) represent nearly all of the primary vaginal cancers in women less than 20 years old.54 Adenocarcinomas may arise in areas of vaginal adenosis, Wolffian rest elements, periurethral glands, and foci of endometriosis. Clear-cell variants are the best-known type of adenocarcinoma, primarily because of their occurrence in young women who have been exposed in utero to diethylstilbestrol (DES).55 DES exposure can result in both cervical and vaginal clear cell adenocarcinomas. Grossly, clear cell carcinomas of the vagina usually present as polypoid masses, most often on the anterior wall of the vagina. FDA advised against DES use in 1971; therefore, the incidence has dropped dramatically
  • Sarcoma: Leiomyosarcomas, endometrial stromal sarcomas, malignant mixed müllerian tumors, and rhabdomyosarcomas are the major types of primary vaginal sarcomas, representing about 3% of vaginal cancers. The most common of these is the embryonal rhabdomyosarcoma (sarcoma botryoides), a highly malignant tumor that occurs in the vagina during infancy and early childhood.
  • Melanoma: Melanomas arising on the vaginal mucosa are rare but account for 3-5% of vaginal cancer. Melanomas are thought to originate from mucosal melanocytes in areas of melanosis or from atypical melanocytic hyperplasia.56 Almost all of the reported melanomas have been in Caucasian women. These malignancies occur at a mean age of 58 (range 22 to 83 years). They appear as a blue-black or black-brown masses, plaques, or ulcerations, most frequently on the distal one-third of the anterior vaginal wall. However, they are often non-pigmented.

Differential diagnosis

VaIN, adenosis, condyloma

Treatment

Women with vaginal cancer need referral to a gynecologic oncologist. Clinical staging is performed for all vaginal cancers, and an individualized treatment plan is based on location, size and stage of the tumor. Surgery, radiation and/or chemotherapy are common treatment modalities.

Vaginal wall defects (prolapse)

Pelvic organ prolapse (POP) includes descent of the cervix and uterus (not considered a vulvovaginal problem and not discussed here), and defects of the anterior, apical, and posterior vaginal wall that allow herniation of the urethra, bladder, rectum or bowel into the vagina. Prolapse is mainly a urogynecological problem but is discussed here in view of its vaginal involvement.

Anterior compartment prolapse is defined as herniation or descent of the anterior vagina so that the urethrovesical junction or any other point on the anterior vaginal wall is less than 3 cm from the hymenal ring. Anterior compartment defect replaces the previously used terms of cystocele and urethrocele; the current definition utilizes the actual site of vaginal wall prolapse (anterior vaginal wall), rather than the structures underlying it (bladder or urethra). Vaginal topography does not reliably predict the location of associated viscera.57

Apical compartment prolapse includes descent of the apex of the vagina into the lower segment of the vagina, to or beyond the hymen. The apex can be either the uterus and cervix, cervix alone, or vaginal vault if the woman has had a hysterectomy. Enterocele often accompanies apical prolapse.58

Posterior compartment prolapse is defined as hernia of the posterior vaginal wall usually associated with descent of the rectum. Posterior compartment defect or prolapse replaces the term rectocele since the location of the rectum cannot reliably be predicted based on vaginal topography.

Enterocele represents protrusion or herniation of the intestines to or through the vaginal wall.

Defects of pelvic support often do not occur in isolation. In a series of 384 women undergoing surgical repair of POP there were: anterior defects only (40 percent), posterior defects only (7 percent), apex only (6 percent), anterior and posterior defects (16 percent), anterior defect and apex defect (9 percent), posterior defect and apex defect (5 percent), and all three defects (18 percent).59

Prevalence

Prevalence is probably common, but difficult to assess since various classification systems have been used. In addition, prolapse is best defined by whether it is symptomatic or not, since treatment is indicated only for women with symptoms. It is unknown how many women exist with asymptomatic POP, and high quality evidence regarding symptomatic POP is limited. While 200,000 inpatient surgical procedures for prolapse are performed yearly in the USA,60 there are still many symptomatic women with POP who do not elect surgery. Estimates of prevalence of POP range from 3-11 percent of women.61

Etiology

In the past, vaginal wall defects were believed to be due to stretching or thinning of the anterior vaginal wall and its supports, thereby allowing herniation of neighboring organs into the vagina. Based on this assumption, surgical plication or tightening of the weak and redundant vaginal wall (i.e. anterior colporrhaphy) became the treatment. We now know that vaginal wall prolapse is not as simple as a stretch defect in this area, but is the result of a specific defect in the support structures of the vagina. Lack of attention to the specific defect in these support structures is a major reason that anterior vaginal wall prolapse recurs in as many as 40 percent of patients after anterior colporrhaphy alone.62

The last decade has seen significant progress in our understanding of the pathophysiology and anatomy of pelvic prolapse. We now know that the pelvic organs are supported through a complex interplay between the uterosacral/cardinal ligament complex, the levator ani muscles, the endopelvic fascia, and the nervous system. These structures attach the pelvic organs to the bony pelvis and form a continuous and interdependent organ complex. Pelvic prolapse occurs, in part, due to site-specific fascial defects that result in anterior, apical, or posterior vaginal segment weakness. Damage to any of the muscles and fibrous structures results in descent of the vaginal walls and pelvic organs through the urogenital hiatus. Understanding this process has led to improvement in the surgical approach to a challenging clinical problem.63

Symptoms and clinical features

Vaginal wall defects may or may not be symptomatic. Symptoms tend to become bothersome when the prolapse extends beyond the hymenal ring,64 but severity of the symptoms does not correlate well with the degree of prolapse.65

Symptomatic women who have prolapse do not describe common vulvovaginal complaints of itching, burning, or rawness. Prolapse is not an etiology of pain and dyspareunia. Therefore, women with irritative complaints and pain need evaluation for other causes besides prolapse.

Sexual dysfunction is, however, common as women avoid sexual activity because of fear of discomfort or embarrassment regarding bulges, or urinary or bowel incontinence during sexual activity.66 Women with POP may also have sexual dysfunction because of mechanical issues from prolapsed tissue, or difficulty with penetration because of the obstacle from protrusion of the fecal-filled rectum into the vagina.

Pelvic pain and low back pain are classically associated with POP, but well designed studies do not validate the association.67 68

Women do speak of vaginal or pelvic fullness, heaviness, pressure, or discomfort that often worsens over the course of the day. These symptoms are most noticeable after prolonged standing or straining. Patients with POP frequently describe feeling as if they are sitting on an egg.

The report that something is protruding or falling out of the vagina is common, and some women may actually be able to see the prolapsed tissue. Exteriorization may result in vaginal discharge; vaginal bleeding from friction and ulceration may occur.

Women with anterior vaginal wall defects may have stress urinary incontinence, incontinence with intercourse, urgency, frequency, nocturia, or enuresis.69 70 Advanced anterior vaginal compartment prolapse can cause urethral obstruction or “kinking”, resulting in slow stream, incomplete emptying, or urinary retention.71 Women may need to reduce or splint the prolapse of the anterior wall and urethra manually in order to empty their bladders.

Constipation is the most common bowel symptom associated with all types of prolapse,72 but with posterior compartment defects there may also be tenesmus, and either fecal incontinence or obstructive symptoms such as incomplete emptying and straining.73 Women with posterior compartment defects report that they may need to apply digital pressure (splinting) to the posterior bulge in the vagina, or to the perineum, in order to move their bowels. Incontinence of stool may occur during sexual intercourse.74

Diagnosis

Pelvic organ prolapse quantification (POPQ)

In the past, prolapse has been graded in severity by several imprecise classification systems with poor reproducibility as well as poor potential for standardized communication between clinicians. These deficiencies have been replaced with POPQ, an objective, site specific system for describing and staging POP.75 A “map” of the vagina is created from quantitative measurements of points representing anterior, apical, and posterior vaginal prolapse. These anatomical reference marks are then used to determine the stage of the prolapse.  The POPQ test  With a brief office examination, the clinician can identify prolapse to make an appropriate referral.

Anterior compartment defects are best demonstrated with the woman in the lithotomy position. A retractor or the posterior blade of a Graves speculum is used to depress the posterior wall of the vagina. The patient is then asked to bear down, and, if present, the anterior wall bulge may be seen.

Posterior compartment defects may be identified by retracting the anterior vaginal wall upward with the blade of a Graves or Pederson speculum and again having the patient strain. If prolapse is present the rectum will bulge into the vagina. Placement of one finger in the rectum and one in the vagina allows palpation of the herniation.

Enterocele is challenging to diagnose. It represents a hernia of the peritoneal cavity along a weakened pouch of Douglas between the uterosacral ligaments and into the rectovaginal septum. It occurs frequently after abdominal or vaginal hysterectomy. If large enough, it may prolapse through the vagina. It may be palpated as a separate bulge above the posterior wall prolapse. Frequently, the diagnosis is established only at them time of surgery.76

Differential diagnosis

Anterior compartment: myoma, inflamed and enlarged Skene’s glands, urethral diverticula, bladder tumors, bladder diverticula. Differentiation of posterior compartment: herniation from enterocele as above, and myoma.

Treatment

Vaginal wall defects should be evaluated and treated by a urogynecologist or gynecologist experienced with POP. Conservative medical management includes pessaries and pelvic floor muscle exercises. Numerous surgical procedures for POP include vaginal and abdominal approaches with and without use of graft materials.

Vaginal changes after surgery

Techniques for hysterectomy and procedures for correction of prolapse and incontinence emphasize the preservation of a functional vagina with caliber and length adequate for sexual intercourse, but few data are available regarding what dimensions are necessary to avoid dyspareunia. Shortcomings in methodology have been problematic. Differences in types of hysterectomy cause varying changes in the post-operative vagina.

The type of closure of the vaginal cuff at the time of vaginal hysterectomy results in significant vaginal length differences: horizontal closure results in a 16% shorter vagina compared with vertical closure when length of the vagina is properly measured. There is no evidence on the effect of the shorter vagina on post-hysterectomy dyspareunia.77

There is a recent Cochrane Database meta-analysis showing morbidity-related advantages of the vaginal versus the abdominal approach. However, there was no significant difference in sexual dysfunction among vaginal, laparoscopic, or abdominal approaches.78

One study of 104 women concluded that vaginal anatomy, measured by introital caliber, length, and vulvovaginal atrophy, does not correlate well with sexual function, particularly symptoms of dyspareunia.79


Erosive lichen planus

Vaginal lichen planus may be seen with or without vulvar involvement, and can lead to telescoping, stricturing, or complete obliteration of the vagina. (Annotation O: The vaginal epithelium and Atlas of Vulvar Disorders.)

Fixed Drug Eruption(Annotation O: The vaginal epithelium and Atlas of Vulvar Disorders)

Bullous erythema multiforme (Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN)) (Annotation O: The vaginal epithelium and Atlas of Vulvar Disorders)

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