Pelvic floor
Anatomy and composition
The pelvic floor is a highly complex, heterogeneous structure that supports the pelvic organs. In certain cases, such as childbirth, substantial stretch and accommodation of the pelvic floor must occur. Although the precise physiology by which the pelvic floor provides support to the vagina is not understood, it is known to comprise a combination of striated muscles, connective tissues, and bones. Together, this support mechanism serves to maintain the location and orientation of the uterus, vagina, bladder, urethra, and anorectum in the pelvis while allowing appropriate motion for physiological functions, such as defecation ( ).
Pelvic floor muscles are largely composed of striated muscle. The predominant muscle group is the levator ani, but the pelvic floor includes superficial muscles (bulbocavernosus, ischiocavernosus, and deep and superficial transverse perinei) that lie inferiorly and the coccygeus that lies posteriorly and superiorly to the levator ani ( Fig. 4.1 ). The pelvic floor extends anteriorly to the pubis, laterally to the arcus tendineus levator ani (ATLA), and posteriorly to the sacrum and coccyx via the anococcygeal raphe (or levator plate).
The levator ani have historically been defined as being composed of three muscles; the iliococcygeus, pubococcygeus, and puborectalis ( ) (see Chapter 1 ). Using these terms, the iliococcygeus is the most superior, posterior, and lateral of the levator ani, while the puborectalis is the most inferior and medial, although the literature contains a large variety of terms for the same pelvic floor muscles, some of which may imply incorrect origin-insertion pairs ( ). This led to use the term “pubovisceral muscle” as a replacement for the terms puborectalis and pubococcygeus, as the latter imply that muscle fibers connect the pubis and coccyx directly, whereas the former is thought to be more representative of actual origin-insertion pairs ( ). The pubovisceral muscle includes any muscle that originates at the pubis and inserts into or acts as a sling to support pelvic viscera ( ). However, using the term “pubovisceral” has resulted in its own confusion, as studies have equated it the pubococcygeus [as suggested by ], the puborectalis, or both. Additionally, there is variation in which muscles define the levator ani. Although used the terms iliococcygeus, pubococcygeus, and puborectalis, referred to the pubovisceral (including the puborectalis), iliococcygeus, and coccygeus muscles. substituted “puborectalis” for “puboanal sphincteric sling” to emphasize that some muscle fibers insert into the external anal sphincter. suggested using “puborectalis” instead, although they agreed on the puboanalis’ origin-insertion pairs.
To remain consistent with previous literature, and based on our own studies, we suggest defining the levator ani as the pubovisceral and iliococcygeus muscles, where the pubovisceralis is composed of the puborectalis, puboanalis, puboperinealis, and pubovaginalis. However, it is worth noting that the term “pubovisceral muscle” is not officially recognized by Terminologia Anatomica (see Chapter 1 ).
The pubovisceral muscle attaches bilaterally to the pubic bone just lateral to midline. This bilateral attachment creates the levator hiatus—an opening where the urethra, vagina, and rectum pass through the pelvic floor. The puborectalis attaches at the pubic bone, and the left and right portions meet behind the rectum, forming a sling observed anatomically as the anorectal angle. The puboanalis, puboperinealis, and pubovaginalis insert into the intersphincteric groove, perineal body, and vagina, respectively. The iliococcygeus originates from a connective tissue condensation (the ATLA) of the lateral pelvis and attaches to the coccyx. The left and right sections of the levator ani coalesce along a midsagittal, posterior line between the sacrum and coccyx, forming the levator plate upon which the upper two-thirds of the vagina, uterus, and rectum rest nearly horizontally. The levator plate is also called the anococcygeal raphe, but should not be confused with the more superficial anococcygeal ligament that runs directly between the external anal sphincter and coccyx. As the levator ani muscles contract, they squeeze the structures within the levator hiatus by pulling them toward the pubic rami, which generates pressure in those organs by reducing available space.
In humans, the nervous system is divided in two (see Chapter 3 ). The central nervous system (CNS) includes the brain and spinal cord, whereas the peripheral nervous system (PNS) comprises the somatic and autonomic nervous systems. Somatic nerves primarily innervate striated muscle and allow execution of voluntary actions. Conversely, the autonomic nervous system underlies baseline, homeostatic functions that occur without conscious thought. This includes innervation of the smooth muscle of visceral organs and glandular functions. Somatic innervation to the levator ani is provided by efferent (motor) nerves arising primarily from the nerve to the levator ani (originating from spinal cord levels S2–S4), which innervates the superior portion of the levator ani, and to a lesser extent from the pudendal nerve (also from S2–S4), innervating the inferior portion. The levator ani maintain a baseline contractile tone that preserves the orientation of the pelvic organs ( ; ). This constant tone relies on proprioceptive afferent input processed by the dorsal root ganglia in the spine and afferent sensory nerves. Humans can voluntarily increase pelvic muscle contractions, but the muscles rapidly fatigue, and tone returns to baseline after roughly 1 minute ( ).
Smooth muscle fibers are primarily contained within viscera, allowing for stretch during filling and evacuation of visceral contents in combination with autonomic reflexes. Connective tissue contains varying amounts of smooth muscle cells. Many components of the pelvic floor are altered by menopause or prolapse, including smooth muscle cells. determined via computational analyses that the predicted ratio of smooth muscle cells in the round ligament is decreased in women with prolapse.
In orthopedic terminology, ligaments are dense connective tissues bridging bone to bone, whereas tendons are connections between muscle and bone. Within the abdomen and pelvis, the term “ligament” is used more variably. It may refer to a fold of peritoneum formed during embryonic development, like the hepatoduodenal ligament, which contains the portal triad (the hepatic artery, portal vein, and common bile duct). In the pelvis, ligaments usually refer to connective tissue suspensions tethering the viscera to the pelvic sidewall and bony pelvis. Connective tissue condensations that provide support to the vagina and uterus include the cardinal-uterosacral ligament complex and the paravaginal attachments to the arcus tendineus fasciae pelvis (ATFP). This is collectively known as the endopelvic fascia.
The endopelvic fascia is a continuation of the web of connective tissue originating at the level of the uterine artery’s insertion at the uterus and extending bilaterally to the pelvic sidewalls and caudally to suspend the cervix and vagina, periodically solidifying into ligaments. Close to the uterus and cervix, it is termed the parametrium, and at the level of the external cervical os it becomes the paracolpium ( ). These connective tissue attachments have been organized into a conceptual framework of levels corresponding to different anatomic sites on the vagina ( ; ) (see Fig. 1.15 ). Level I refers to the support of the vagina at its apex provided by the cardinal and uterosacral ligaments. Level II is the lateral support of the midportion of the vagina where the endopelvic fascia coalesces with the ATFP on either side. More distally, the vagina attaches to the arcus tendineus fascia rectovaginalis. Level III support for the distal vagina is provided by the perineal body, the perineal membrane, and the superficial muscles. The transverse perinei and bulbocavernosus intersect at the perineal body, which is composed of multiple layers with varying fiber orientations ( ; ). Injury at different levels of vaginal support will cause distinct anatomic defects.
Connective tissue is composed of collagen, elastin, proteoglycans, and the extracellular matrix (ECM) acting as a scaffold for the other components. Collagen provides tensile strength, which is the stress a material can undergo before breaking while being pulled. Elastin provides resilience, or elasticity, which is a tissue’s ability to snap back into place after being deformed. Proteoglycans are extracellular proteins that are vital for cell-to-cell connections or connections between cells and the ECM. Small proteoglycans (decorin, fibromodulin, biglycan, luminican, and chondroadherin) bind with glycosaminoglycans to form complexes in the ECM and resist compression by restricting the motion of water molecules ( ). Other proteoglycans, including fibronectin, vitronectin, and laminin, serve to create cell-to-cell bindings ( ). Connective tissue composition is dynamic, with production and degradation of collagens occurring as the tissue endlessly remodels in response to stresses, aging, and injury. Tissue breakdown occurs through the enzymatic activity of acid cathepsins and matrix metalloproteinases (MMPs), which break down collagen fiber cross-links and lead to cleavage of the collagen fibers themselves, respectively ( ).
Of the 19 known types of collagens, types I and III are found most commonly in epithelial tissues ( ). Type I is the most common throughout the body. It forms large fibers and is a main contributor to tensile strength, although types II and III also form strong fibers that resist tension. Type III fibers are smaller than type I fibers and are found more frequently in tissues that require flexibility, such as blood vessel walls ( ). Type IV collagen assembles into a network configuration instead of distinct fibers and helps form the basement membrane beneath fibers ( ). Type V collagen forms small fibrils, is frequently found in wound healing, and likely directs fibrillogenesis. Heterogeneous fibrils are formed when type I collagen copolymerizes with type III or V collagen. As the proportion of type III and IV collagens increases relative to type I collagens, tissues become weaker. Hormones may influence the balance of collagen types within the tissues. After menopause, if hormone therapy is not initiated, the amount of type I collagen decreases by 75% (compared with premenopausal women), and the ratio of type I to type III/V collagen decreases in the ATFP ( ). Thus, after menopause, there is an increased amount of type III and V collagens in human connective tissue. Changes in collagen composition are also likely to be associated with pelvic organ prolapse. found that total collagen content and collagen solubility were decreased in premenopausal women with prolapse compared with controls. They also found that MMP and cathepsin activity increased in prolapse patients, leading to more rapid turnover of collagen ( ). Overall, the changes in collagen found in women with prolapse likely decrease the tensile strength of the tissue, a risk factor for prolapse.
Function and biomechanical properties
In nonhuman mammalian species, especially quadrupeds, the levator ani primarily control tail movement, and the connective tissues alone act as the primary support ( ). For example, the rat has connective tissue attaching the upper vagina to the spine, similar to the human uterosacral ligaments; paravaginal attachments from the lateral vagina to the dense connective tissue, similar to the ATFP; and attachments connecting the distal vagina to the anterior surface of the ischiopubic rami, emulating level III support ( ). Although the connective tissues are similar, the pelvic floor muscles differ considerably. In humans, portions of the pubovisceral muscle attach directly to the vagina and rectum, whereas in rodents these attachments are provided by loose connective tissues. Anatomical differences should be considered when choosing appropriate animal models for research studies.
In humans, because of the adoption of an upright posture, the levator ani and connective tissues work together to support the pelvic organs. When pelvic floor muscles contract at baseline, the tension experienced by supportive ligaments is reduced. If the muscles are damaged, as may occur with vaginal birth, or if those muscles are compromised because of nerve damage, then the shelf supporting the pelvic organs may sag. This may cause organs to change orientation or descend through the urogenital hiatus (the opening in the levator ani anterior to the perineal body where the urethra and vagina pass through the pelvic floor), and can cause excessive straining of connective tissues attached to those organs. Vaginal birth likely serves as an instigating event for damage, but progressive muscle deterioration may also occur as women age. Some suspect that pudendal nerve trauma (i.e., stretch during childbirth) may play a role, although this is a point of contention, as some studies suggest that most nerve injury that occurs with vaginal birth resolves ( ), whereas others show worsening neuropathy and organ function over time ( ). Other risks include chronic increased intraabdominal pressure or repetitive high-pressure straining, as occurs in patients with obesity, chronic cough conditions, chronic obstructive pulmonary disease, habitual heavy lifting, or chronic constipation.
Recent work has sought to elucidate the biomechanical properties of the pelvic floor, which supports the pelvic organs against the effects of gravity and increased intraabdominal pressure. The biomechanical parameter of deformation, a general term for the change in size or configuration of a material due external forces or changes in temperature, is applicable to this discussion. Deformation can be referred to more specifically as strain or stretch, where a state of no deformation is indicated by a strain of 0 and a stretch of 1, and stretch can be converted to strain by subtracting 1. Forces may be tensile, applied by pulling; compressive, applied by pushing; shear, applied by sliding; or torsion, applied by twisting. Ligaments typically exhibit viscoelastic behavior—the ability to initially resist strain, then stretch, and then regain their previous configuration once forces are removed—because they contain water, collagen, and elastin. Water aids with resisting compression, collagen with resisting tension, and elastin with the recovery of the tissue after deformation. When a tissue undergoes excessive strain, meaning the yield strength (the stress value at the yield point) and the elastic, or linear, region of the stress-strain curve are surpassed, it experiences microdamage that may cause loss of this recoil ability and permanent deformation ( Fig. 4.2 ). If the tissue is stretched even further, it will suffer structural failure and rupture. Collagen remodels in damaged ligaments as they heal. After healing, the ligament composition does not perfectly resemble that of the ligament before injury; the ligament is frequently stiffer and may be permanently elongated, both of which contribute to the loss of its recoil ability and increased susceptibility to future injury ( ).
Biomechanical properties may be structural or mechanical, as described by ). Both describe how tissues respond to an applied load; but structural properties are dependent on the size of the tissue sample tested. Thus, a larger sample generally performs better. One common mechanical test is a uniaxial, tensile load to failure test ( Fig. 4.3 ; ). In this test, one edge of a tissue is rigidly fixed to the base of the mechanical testing system, while the other end is connected to a movable arm containing a load cell. The arm displaces that end of the tissue until it fails, while the system generates a load-elongation curve. The linear stiffness of the tissue is the slope of the linear portion of this curve. In contrast, mechanical properties describe tissue behavior independent of size. These properties can also be obtained from a load to failure test by converting the forces and elongations to stresses and strains, respectively, resulting in a stress-strain curve ( Fig. 4.4 ; ). Stress is calculated by dividing the applied force by the tissue’s cross-sectional area, whereas strain is the change in length of the sample divided by its original length. The tangent modulus (called the elastic modulus or Young’s modulus when describing the linear region) is the slope of this stress-strain curve. The tensile strength of the tissue is the maximal stress it can support before rupture and corresponds with the ultimate strain—the maximal strain it can support. As these properties are calculated per unit area, they offer a more direct measurement of the composition of the tissue and the results are more generalizable.
Biomechanical properties of a tissue can differ depending on the axis in which the sample is stretched, termed anisotropy. This is common in biological tissues, as there are preferred collagen alignments. For example, tendons and ligaments are considered transversely isotropic, a type of anisotropy, as collagen is predominantly aligned along one axis. These tissues will behave differently if pulled perpendicularly versus in parallel to that collagen alignment. Using the uniaxial tensile test example, when pulling parallel to collagen fibers, collagen is the dominant contribution to the measured mechanical properties. If pulling perpendicularly, the ground substance (for connective tissues) or the tissue between collagen fibers is the main contribution.
Stretch must occur during childbirth. After the fetal head descends through the cervix and into the vagina, it must pass through the urogenital hiatus. The bones of the fetal skull differentially deform based on whether the fetus is preterm or at term, the shape of the mother’s pelvis, and expulsive labor forces, but the head still must narrow and elongate as molding occurs during the second stage of labor ( ). The average suboccipitobregmatic diameter, the smallest aspect of the presenting fetal head, is roughly 9.2 cm ( ) after molding. The average frontooccipital diameter, the longest distance between the occipital and frontal bones, is 10.3 cm at the initiation of the second stage of labor, 10.8 cm once expulsion begins, and 11.2 cm at crowning ( ). The urogenital hiatus is approximately 2.5 cm transversely between medial borders in an average nonpregnant woman without prolapse ( ). It must rapidly dilate during delivery, similar to the dilation of the cervix but over a much shorter time frame. determined that the maximum stretch ratio, another term for stretch, before muscle undergoes structural failure with subsequent rupture of muscle fibers, is 1.5. Several finite element simulations of vaginal delivery have been created to predict the stretch in maternal soft tissues, specifically at the pubovisceral muscle enthesis and perineal body, two common sites of injury during vaginal delivery that have been linked with the later development of pelvic floor disorders, such as pelvic organ prolapse. These models predicted maximum stretch ratios of maternal soft tissues that surpass this 1.5× threshold, with values ranging from 1.6 to 4.1 ( ; ; ). Thus, it is likely that most vaginal deliveries lead to some degree of stretch injury. Although, owing to tissue remodeling during pregnancy, it is also likely that this 1.5× stretch injury threshold may be higher in women at term. Further investigation is required, but found, using a rat model, that remodeling of the pelvic floor resulted in increased muscle stiffness in pregnancy, a plausible mechanism for protecting pelvic floor tissues from injury during delivery.
Compared with other medical fields, such as orthopedic surgery, female pelvic medicine and reconstructive surgery research is still in its infancy. We are only beginning to understand the effect of childbirth injuries, chronic pressure, chronic constipation or cough, or other trauma to the pelvic floor. We poorly understand pelvic floor tissue healing and repair and how variations in healing may predispose women to pelvic floor disorders later in life. In the future, it will be critical to improve our knowledge of these components if we are to elucidate the mechanisms of pelvic organ prolapse and to improve the longevity and specificity of our surgical corrections.
Vagina
Anatomy and composition
The vagina is made of muscle and connective tissues and is richly vascular. It is a fibromuscular tube extending from the cervix to the perineum. Vaginal layers include an epithelial surface, the lamina propria, muscularis, and adventitia, whereas its surface is lined with nonkeratinizing stratified squamous epithelial cells. Histologically, there are four main epithelial layers: (1) most superficially, nonkeratinized cells with small, pyknotic nuclei; (2) an intermediate glycogen-containing cellular layer; (3) proliferating parabasal cells; and (4) the basal epithelial layer ( ). Adjacent to the epithelium is the lamina propria, or subepithelium, a layer of dense connective tissue composed of collagen and elastin. Next is the muscularis, composed of smooth muscle cells with blood vessels intercalated between smooth muscle bundles. The smooth muscle has a circular configuration in its inner layer and a longitudinal orientation in its outer layer ( ). Lastly, the adventitia is made of loose connective tissue, containing collagen, elastin, and additional smooth muscle and vasculature. The connective tissue composition here includes 84% collagen and 13% elastin ( ; ). The vagina and the endopelvic fascia have very similar collagen configurations ( ), so clinically obtained vaginal biopsies may allow extrapolation to the collagen composition of the endopelvic fascia.
Embryology and innervation (see also Chapter 2 )
The innervation between the proximal and distal vagina differs, beginning early in embryogenesis. The distal two-thirds of the vagina arise from an outgrowth of the endoderm of the urogenital sinus, the paired sinovaginal bulbs. The proximal third of the vagina, the cervix, and the uterus arise from the uterovaginal primordium, which results from fusion of the paramesonephric ducts in the midline. The solid sinovaginal bulbs fuse together, grow cephalad, and then fuse with the uterovaginal primordium. This structure then canalizes to form the vagina. Reflecting differential embryologic origins, innervation to the upper vagina is via the inferior hypogastric nerve plexus, whereas innervation to the lower vagina and skin is from the pudendal nerve. The spinal origin of these nerves is the sacral levels S2 to S4 ( ).
Important to note is the convergence of sensory input from the pelvis at the level of the spinal cord and brain. Although afferent sensations are tracked independently from various end organs, there is dynamic processing of the inputs centrally, so pathophysiology from one organ may affect others. This explains the expression of several pelvic pain syndromes within one individual, such as endometriosis, interstitial cystitis, irritable bowel syndrome, and fibromyalgia. There may also be overlap of sensory nerve fibers within the pelvic nerve plexus.
Orientation and structural support
The epithelium contributes little to the structural integrity of the vagina, which is instead supplied by deeper layers of connective tissue and smooth muscle, whereas the levator ani and connective tissues provide external support ( ; ). In the midsagittal plane, the vagina contains a convex angle; the uppermost portion is nearly horizontal as it rests on top of the levator ani, and the distal portion descends more vertically. The angle occurs as the vagina descends through the levator hiatus and is caused, in part, by contraction of the levator ani at baseline. found this angle to be 130 degrees on average in the supine position on x-ray vaginogram, and others noted that it can be influenced by pregnancy and hysterectomy ( ; ). If this angle is lost owing to lack of puborectalis muscle tone or compromised connective tissues, the urogenital hiatus will widen, and the risk of prolapse and herniation through that hiatus will increase ( ). A 20% larger urogenital hiatus before development of prolapse symptoms and a four times larger increase in hiatus size over a 5-year period was noted in women who developed pelvic organ prolapse compared with controls ( ). This has practical effects when considering the approach for a prolapse repair. Any repair that changes the vaginal angle may circumvent this normal anatomic support. Postoperative angles were measured after abdominal sacrocolpopexy with Burch colposuspension (137–149 degrees) and sacrospinous ligament fixation (215–220 degrees) ( ; ). In these cases, it is worth noting that the normal anatomy has already been disrupted, leading to the prolapse. However, based on imaging studies, it seems that sacrocolpopexy restores the normal vaginal angle better than sacrospinous ligament fixation.
Because of its attachments to the ATFP and arcus tendineus rectovaginalis, the midvagina in axial cross-section for a woman with normal support often has an “H” or a “W” configuration. This has been confirmed on magnetic resonance imaging, although more robust characterization of vaginal configuration and variation is required ( ; ).
Function
Normal vaginal functions include response to hormonal stimulation, lubrication and stretching during sexual activity, immunologic protection against infectious diseases, mechanical support of pelvic organs, and remodeling and stretching to allow for vaginal childbirth.
One consequence of sexual excitation is genital congestion in the lower third of the vagina, which is a reflexive autonomic response regulated by the CNS and PNS. The major neurotransmitters involved are nitric oxide and cyclic guanosine monophosphate (cGMP), which act on the clitoris, and vasoactive intestinal polypeptide (VIP), which affects the vagina ( ). With this reflexive response, the genitals become engorged, and lubrication increases. This is partly mediated by increased vascular flow and capillary permeability and is dependent on estrogen. Both cGMP and cyclic adenosine monophosphate (cAMP) aid in the regulation of vaginal smooth muscle tone, the loss of which allows for engorgement during sexual arousal ( ). Inhibition of phosphodiesterase type 5, which degrades cGMP, enhances the relaxation of the clitoris and vagina, which can also be relaxed by VIP with a concomitant increase in cAMP ( ). After menopause, paravaginal vasodilation is compromised because of a decrease in the number of estrogen receptors on the vascular endothelium, which may lead to deficits in the genital congestion response ( ). Hormone therapy decreases autonomic and sensory vaginal innervation density in postmenopausal women, corresponding with reduced VIP immunoreactivity, which may explain how hormone therapy reduces vaginal pain and discomfort ( ).
Before menarche, the vaginal epithelium is thin, and the vaginal pH is high (>4.7) ( Fig. 4.5 ). As the ovaries initiate endogenous estrogen production, the epithelium thickens. The vagina maintains an acidic pH (<4.5) once menstruation begins ( ). This pH level is thought to be established as the naturally predominant Lactobacillus bacteria ferment glycogen in the epithelium, converting it into antimicrobial lactic acid that protects against infection and adverse pregnancy outcomes ( ; ; ). collected vaginal biopsies from women throughout the menstrual cycle and found that the epithelium thickens, and the superficial epithelial cells mature when circulating estrogen levels are high. With high progesterone levels, superficial cell layers are shed, and the basal portion of the epithelium is more quiescent. At the time of ovulation, the epithelium is maximally thickened and mature. After menopause, serum estrogen levels decrease, and estrogen receptors are downregulated. The ratio of epithelial intermediate and parabasal cells increases, with few superficial basal cells observed. There is less vaginal blood flow, reduced elasticity, and a decrease in normal vaginal secretions. The microbiome is altered in this new milieu, with the disappearance of lactobacilli and emergence of rectal bacteria. The latter increase susceptibility to urinary tract infections, which occur more frequently after menopause, likely by altering endogenous bladder flora. Estrogen receptors are restored, and vaginal lactobacilli return, if hormone therapy, particularly estrogen, is administered ( ; ). The frequency of urinary tract infections may also be reduced through the restoration of vaginal flora with lactobacilli using probiotics—an alternative for postmenopausal women unable to use estrogen ( ).
