Vaginal Anatomy

The vagina is a distensible fibromuscular tube extending from the cervix to the vaginal orifice, the opening at the inferior end of the vagina.  Its major functions include copulation and parturition. During coitus, the vagina receives the penis and ejaculate, which facilitate the ascent of spermatozoa into and through the cervix, up into the uterus and fallopian tubes. The vagina is the distal birth canal and serves as an efflux pathway for menstrual blood (menses). ^[2]

The vagina is posterior to the urinary bladder and urethra, anterior to the rectum, and medial to the levator ani (puborectalis) muscles. The vaginal fornix is a recess around the cervix and has anterior, posterior, and lateral parts. The posterior vaginal fornix is associated with the rectouterine pouch (of Douglas). The pubovaginalis, external urethral sphincter, urethrovaginal sphincter, and bulbospongiosus are the four muscles that compress the vagina and act as sphincters.

Embryology

Table 1 summarizes the developmental changes occurring approximately between the 12th and 22nd postmenstrual weeks. ^[2]

Table 1. Embryology: Vagina (Open Table in a new window)

Gross Anatomy

Location

The vagina is located within the pelvis and its proximal upper end surrounds the vaginal projection of the cervix of the uterus. It opens externally via a midline orifice positioned inferior to the external urethral orifice. ^[2]  In the standing position, the vagina ascends posteriorly and superiorly, forming an angle of 60-70° with the horizontal plane. It lies at a 90° angle in relation to the uterus in most cases and this angle varies with the contents of the urinary bladder and rectum as well as the position of the uterus and its supporting structures. ^[2]

Structure and Relations

The vagina is an oblique canal as its anterior wall (7.5 cm) is shorter in length than its posterior wall (9 cm). The inner surfaces of the anterior and posterior vaginal walls are in contact with each other, forming a transverse slit. Its width increases as it ascends. It is held in place by endopelvic fascia and ligaments. It is a potential space that is easily distended. It has the following structural features: ^[2]

1. Vaginal fornix: It is a recess formed between the cervix and the vagina. It includes ^[2]

          a) Anterior fornix: Between the anterior lip of the cervix and the anterior vaginal wall

          b) Posterior fornix: Between the posterior lip of the cervix and the vaginal wall; it is an access point to the rectouterine pouch (pouch of Douglas) to obtain oocytes during IVF and to needle biopsy anything in the pouch. It is also a location where tampons can embed and be difficult to remove.

          c) Lateral fornices: Spaces on either side between the cervix and the lateral vaginal walls 

2. Vaginal wall, which includes:

          a) Anterior wall: It is fibromuscular in nature and supports the fundus of the urinary bladder in the middle and superior portions and the urethra (which is superior to the distal vagina).

          b) Posterior wall: It is fibromuscular in nature and supports the rectum.

The upper quarter of the posterior vagina is separated from the rectum by the peritoneum of the rectouterine pouch (pouch of Douglas). The middle half is separated by moderately dense fibromuscular tissue while the lower quarter is separated from the anal canal by the fibromuscular perineal body. ^[2]

3. Supportive structures:

         a) Proximal vagina: Supported laterally by levator ani, cardinal ligaments, and uterosacral ligaments

         b) Mid-vagina: Pubovaginalis provides a U-shaped muscular sling around this part.

         c) Distal vagina: Surrounded by bulbospongiosus

         d) The sphincter urethrae and the transverse perineus muscles, perineal membrane, and pelvic diaphragm support the vagina. The term urogenital diaphragm is no longer used; formerly, it included the sphincter urethrae and the deep transverse perineus muscle, together with their inferior fascia, the perineal membrane. These muscles are innervated by perineal branches of the pudendal nerve. The pelvic diaphragm primarily refers to the levator ani and coccygeus muscles and is innervated by branches of S2-S4 from the sacral plexus. 

4. Vaginal orifice: The vagina opens externally via a sagittal orifice positioned inferior to the external urethral orifice. It varies in size and can stretch significantly during childbirth and sexual intercourse. Just within and surrounding the vaginal orifice lies a membrane known as hymen, which has no established function. The hymen, in most cases, is open from internal to external vagina, with variations ranging from cribriform to stellate to completely closed (imperforate hymen). An imperforate hymen can be a surgical emergency. It varies in shape and can rupture during the first sexual intercourse. Its remnants, called carunculae hymenales, remain after rupture. ^[2]

The ureters pass anteromedially as they course through the pelvis to reach the fundus of the urinary bladder, close to the lateral parts of the fornix. As they enter the urinary bladder anterior to the vagina, each ureter is crossed superiorly by a uterine artery. ^[2]   This relationship can be remembered by the mnemonic: water (ureter/urine) under the bridge (uterine artery). ^[2]

Vasculature, Nerve Supply, and Lymphatic Drainage

Arteries

The vasculature of the vagina is supplied primarily by the uterine artery (superior/proximal part), and vaginal and internal pudendal arteries (middle and inferior portions). The vaginal artery anastomoses with the uterine artery, forming a rich arterial supply to the vagina. These vessels supply the bulb of the vestibule, fundus of the urinary bladder, and adjacent part of the rectum. Internal pudendal and middle anorectal arteries also contribute to the rich anastomotic blood supply to the vagina. ^[2]

Veins

The vaginal veins, one on each side, originate from lateral venous plexuses, which communicate with the uterine, vesical, and anorectal venous plexuses and drain into the internal iliac veins. The uterine and vaginal venous plexuses can serve as collateral venous drainage pathways for the lower limb. ^[2]

Nerve supply

The pelvic splanchnic nerves enter the inferior hypogastric plexus from ventral rami of the S2-4 spinal nerves. Pelvic splanchnic nerves (parasympathetic) innervate the proximal (inner) 4/5^th of the vagina and the distal 1/5^th is supplied by the somatic pudendal nerve. The pudendal nerve carries sensitive fine touch and temperature information from the distal 1/5^th of the vagina, while the pelvic splanchnic nerves are controlling glandular secretions and carrying visceral afferent feedback. 

The uterovaginal plexus in the female crosses the pelvic floor in the base of the broad ligament and is distributed with branches of the uterine and vaginal arteries.  The vaginal plexus turns downward on the lateral vaginal wall and then in the groove between the vagina and urethra, supplying both organs. Pain from the uterine body is conveyed by sympathetic fibers (T11-L2), while that from the cervix and upper vagina passes back through the parasympathetic pelvic splanchnic nerves (S2-4). ^[2]

Lymphatic drainage

Vaginal lymphatic vessels link with those of the cervix, rectum, and vulva and form three groups that are summarized in Table 2. ^[2]

Table 2. Lymphatic Drainage From the Vagina (Open Table in a new window)

Disorders of Pelvic Support

The American Urogynecologic Society has published various scholarly works based on cadaver dissections that describe the normal and abnormal anatomic relationships and quantification of defects that involve different structures of human female pelvic support and continence mechanisms. The pelvic organ prolapse interactive assessment tool (POPQ) helps to grade pelvic support and can assist patients and clinicians as they decide on treatment methodology.

The structure of the vagina is a network of connective, membranous, and erectile tissues. The internal lining of the vaginais rugattede, throughout its length. These allow for distention, especially during childbearing and coitus. Two median longitudinal ridges are present on the epithelial surface: the anterior and posterior. These rugatted sites increase under the influence of estrogen during puberty and pregnancy, are well developed before parturition, and decrease after menopause. Numerous transverse bilateral vaginal rugae arising from these ridges give the appearance of conical papillae, which are most numerous on the posterior wall and near the orifice. ^[2]

Histologically, the vagina has three distinct layers. The first layer is the mucosa. The epithelium of the mucosal layer is composed of non-keratinized stratified squamous cells, similar to and continuous with the ectocervical mucosa.

After puberty, the epithelium thickens, and its superficial cells accumulate glycogen, giving them a clear appearance in histological preparations. The vaginal epithelium's glycogen content increases after ovulation and diminishes towards the end of the cycle. Natural vaginal bacteria, particularly Lactobacillus acidophilus, break down glycogen in the desquamated cellular debris to produce lactic acid, resulting in a highly acidic environment (pH 3) that inhibits the growth of most other microorganisms. There is less glycogen before puberty and after menopause, leading to a higher incidence of vaginal infections during these periods. The vaginal epithelium lacks mucous glands, but a fluid transudate from the lamina propria, supplemented by mucus production from the cervical glands, maintains its moisture. ^[2]

The lamina propria is composed of loose connective tissue that has a vast amount of elastic fibers, giving the vagina its capability to distend. The second layer is muscular, mainly smooth muscle, and consists of a thick outer longitudinal and an inner circular layer interconnected by oblique interlacing fibers. The longitudinal fibers are continuous with the superficial muscle fibers of the uterus. ^[2] The final layer is the adventitia, which is also rich in elastic fibers. A large plexus of blood vessels is also present within the adventitia. ^[1]

Development of the vagina necessitates the fusion of the urogenital sinus and Müllerian structures, forming the Müller's tubercle. The upper four fifths of the vagina are Müllerian in origin, while the lower one fifth arises from the urogenital sinus. Anomalies of paramesonephric (Müllerian) duct fusion can produce related vaginal anomalies. ^[2] As ovaries and uterine tubes develop independently of the uterovaginal canal, they are not associated with Müllerian anomalies. However, shared mesodermal origins link paramesonephric and renal anomalies. ^{[3, 6]}

Initial studies on the female genital tract embryogenesis proposed that uterine development occurs through the fusion of the two Müllerian ducts followed by unidirectional septal reabsorption from a caudal to a cephalic direction. However, it failed to account for rare complex Müllerian malformation characterized by a complete uterine septum, double cervix, and vaginal septum). Thus, McBean et al. in 1994 proposed bidirectional reabsorption theory in which septal reabsorption begins at the isthmus and proceeds simultaneously in both cranial and caudal directions that could explain certain uterovaginal anomalies. ^[4]

Vaginal Agenesis

Congenital vaginal and renal anomalies are often linked with conditions like obstructed hemivagina and ipsilateral renal anomaly syndrome and Müllerian duct anomalies, being associated with renal abnormalities like renal agenesis, ectopic ureters, and dysplastic kidneys.

Vaginal agenesis, a congenital defect, is the complete absence of the vagina. Vaginal and renal agenesis, in the presence of other paramesonephric duct (Müllerian duct) anomalies, is termed the Mayer-Rokitansky-Küster-Hauser syndrome, ^[2] characterized by an absence of the vagina and uterus (46,XX karyotype). This syndrome is thought to be a developmental accident rather than an inherited condition.

Vaginal Septum

The vaginal lumen is formed when the paramesonephric (Müllerian) ducts join the sinovaginal bulb at the paramesonephric (Müllerian) tubercle. There are two types of vaginal septum:

1. Transverse vaginal septum: It is formed due to defective fusion or recanalization of vaginal and Müllerian organs. It is broadly classified into perforated or imperforated septum depending on the presence of communication. ^[5] This septum may be partial or complete; different variations are possible; and the most common site of occurrence is at the junction of the upper third and lower two thirds of the vagina. This is sometimes referred to as a double vagina (see the image below), although the presence of two separate vaginas is also possible. If the septum is complete, the diagnosis is made when the female experiences primary amenorrhea with cyclic cramping and hematocolpos. Treatment of a vaginal septum is surgical, by resection of the septum.
2. Longitudinal vaginal septum: It is caused by partial or total failure of fusion of the terminal portion of the paramesonephric (Müllerian) ducts. ^[2] It is usually associated with uterine anomalies such as septate uterus and didelphys uterus. ^[6] It can be obstructive, communicative, or non-obstructive. Incomplete longitudinal vaginal septum is formed due to incomplete fusion of the Müllerian ducts and is often associated with duplication of the Müllerian ducts. Obstruction and communication can cause symptoms such as dysmenorrhea, lower abdominal pain, intermenstrual bleeding, dystocia, and dyspareunia, whereas a non-obstructive septum typically remains asymptomatic. ^[6]

Double vagina.

Vaginal Dysplasia

Vaginal dysplasia very rarely can result in cancer if left untreated.  This is more frequently seen in immunocompromised individuals and is HPV related. Diagnosis typically results from detection of atypical vaginal cells followed by colposcopy and vaginal biopsy.

Vaginal intraepithelial neoplasia (VIN) can range from simple to high grade dysplasia. Typically, if abnormal cells are ablated, the recurrence risk is low. The modalities used to ablate this tissue include laser and cautery. For the removal of the affected tissue, or in the case of cancer, a partial, complete, or radical vaginectomy may be performed.

Vaginal Infections

The three most common vaginal infections are candidiasis, bacterial vaginosis, and trichomoniasis.

Vaginal candidiasis

Vaginal candidiasis (also known as yeast infection) is a fungal infection and is caused by an imbalance of the normal vaginal flora with an overgrowth of yeast. The predominant organism is Candida albicans, followed by C. glabrata and C. krusei. Recognized risk factors for candidal overgrowth include: uncontrolled diabetes mellitus, systemic antibiotic treatment for other infections or exacerbation by immunosuppression (i.e., chemotherapy or antimetabolite medications, human immunodeficiency virus (HIV) infection, or transplant patients), and broad-spectrum antibiotic use. ^[7]

While Candida albicans is the causative agent of over 90% of vulvovaginal candidiasis cases, non-albicans Candida (NAC) species also account for a significant number of cases. These NAC species include C. glabrata, C. krusei, C. parapsilosis, and C. tropicalis that constitute the majority of remaining cases. ^[7]

Typical symptoms of vaginal candidiasis include internal and external vaginal itching as well as increased thick white discharge. External vulvar irritation may also be involved. Diagnosis is made by microscopic identification of pseudohyphae on potassium hydroxide slide preparation. Treatment is with either oral or vaginal antifungal medication, available both over the counter and by prescription.

Bacterial vaginosis

Bacterial vaginosis is characterized by a decline in Lactobacillus abundance and an overgrowth of pathogenic bacteria such as Gardnerella vaginalis, Atopobium vaginae, Megasphaera spp., Prevotella spp., and Sneathia spp . Women with bacterial vaginosis are at an increased risk of preterm birth, sexually transmitted infections (STIs) including HIV, pelvic inflammatory disease (PID), and post-operative complications, such as vaginal cuff cellulitis. ^[8]  Bacterial vaginosis is characterized by increased vaginal discharge (thin, yellow/gray), strong malodor (fishy smell), and mild itchiness.

Diagnosis at the point of care involves noting at least three of the four Amsel criteria: thin white discharge, clue cells on microscopy, vaginal pH > 4.5, and a fishy odor with potassium hydroxide. The Food and Drug Administration-approved laboratory-based molecular tests can identify DNA from bacterial vaginosis-associated species. ^[8]

Treatment is with oral or vaginal metronidazole and intravaginal clindamycin, available by prescription only. A major drawback to antibiotic-based treatment is its high recurrence rate, with 50-80% of women experiencing recurrence within 6-12 months due to factors such as reinfection from sexual partners, antimicrobial resistance, biofilm presence, and the failure to reestablish a healthy vaginal microbiota. ^[8] Many studies are exploring the role of probiotics, vaginal microbiome transplantation, pH modulation, and biofilm disruption as preventive measures for bacterial vaginosis. ^[8]

Trichomoniasis

Trichomoniasis is a sexually transmitted vaginal infection caused by the parasitic organism Trichomonas vaginalis. It is linked to several adverse reproductive health outcomes in women, including preterm birth and pre-labor rupture of membranes, low birth-weight, higher risk of acquiring HIV and other STIs, PID, infertility, and cervical cancer. ^[9] T. vaginalis uses its surface glycolipids and glycoproteins to attach with the surface proteins on host genital squamous epithelial cells. This attachment, combined with the release of proteases helps in cytoadherence, mucus membrane degradation, and cytotoxicity thereby, eliciting a host immune response characterized by increased levels of various cytokines, including interleukin (IL)-1b, IL-6, IL-8, IL-17, IL-22, IL-23, regulated and normal T cell expressed and secreted protein, C-C motif chemokine ligand 2, interferon beta, macrophage inflammatory protein-3 alpha, and tumor necrosis factor. ^[9]

Symptoms include increased vaginal discharge (thin, watery, yellow/green), vulvovaginal irritation, and malodor. Other symptoms include genital pruritis, dysuria, and dyspareunia. ^[9] Diagnosis is made by microscopic identification of the motile organisms, trichomonads, on a saline slide preparation. Treatment is with oral metronidazole, available by prescription only.

Gonorrhea

Gonorrhea is a STI caused by the bacterium Neisseria gonorrhoeae and it affects about 0.8% of women. Infected females may experience burning with urination, vaginal bleeding between periods, pelvic pain, or vaginal discharge. It can lead to pelvic inflammatory disease thereby causing scarring of the fallopian tubes, ectopic pregnancies and problems with fertility. Treatment is usually a single injection of ceftriaxone. It is imperative the partner also be treated, and a test of cure be obtained 4 weeks after treatment. ^[10]

Chlamydia

Chlamydia is an STI caused by the bacterium Chlamydia trachomatis, and it affects about 4.2% of women. It is known as the “silent epidemic” as nearly 70% of genital C. trachomatis infections are asymptomatic at the time of diagnosis. Some have symptoms of vaginal discharge or burning with urination, but most go undiagnosed. Half of asymptomatic infections still progress to pelvic inflammatory disease which can lead to scarring of the fallopian tubes, ectopic pregnancies, and problems with fertility. Treatment is usually doxycycline for 7 days unless the patient is pregnant then azithromycin by mouth is the preferred option. It is imperative the partner also be treated, and a test of cure be obtained four weeks after treatment. Secondary to the silent nature of how chlamydia presents the American College of Ob/Gyn recommends screening anyone 25 or younger for this STI after they are sexually active with a new partner. Finally, chlamydia used to be the #1 cause of blindness worldwide, but effective treatments have lessened this malady.