Clinical Anatomy 15:321334 (2002)

REVIEW

Anatomy and Physiology of the Female Perineal Body With Relevance to Obstetrical Injury and Repair
PATRICK J. WOODMAN1*
1 2

AND

DANIEL O. GRANEY2

Department of Obstetrics and Gynecology, Madigan Army Medical Center, Tacoma, Washington Department of Biological Structure, University of Washington School of Medicine, Seattle, Washington

The female perineal body is a mass of interlocking muscular, fascial, and brous components lying between the vagina and anorectum. The perineal body is also an integral attachment point for components of the urinary and fecal continence mechanisms, which are commonly damaged during vaginal childbirth. Repair of injuries to the perineal body caused by spontaneous tears or episiotomy are topics too often neglected in medical education. This review presents the anatomy and physiology of the female perineal body, as well as clinical considerations for pelvic reconstructive surgery. Clin. Anat. 15:321334, 2002.

2002 Wiley-Liss, Inc.

Key words: perineal body; central tendon; perineum; episiotomy; incontinence; episiorrhaphy

INTRODUCTION
I learned how to repair a fourth-degree (episiotomy) long before I learned how to protect the perineum -Quote from a second-year Ob-Gyn resident Ironically, the perineal body is commonly damaged, but poorly repaired, due in large part to suboptimal knowledge of its anatomy (Sultan et al., 1995). Other factors contributing to poor repair include time pressures of a busy clinical schedule, fatigue, inadequate analgesia, or inexperience (Sultan et al., 1995). A poor episiorrhaphy can cause pain, dyspareunia (painful intercourse), aerovagina (air trapping within the vagina), pelvic organ prolapse from a gaping introitus, and fecal or urinary urgency or incontinence. The perineal body is a complex bromuscular mass into which many structures insert. It is bordered cephalad by the rectovaginal septum (Denonvilliers fascia), caudad by the perineal skin, anteriorly by the posterior wall of the vagina, posteriorly by the anterior wall of the anorectum, and laterally by the ischial rami. What follows is a description of the form and function of the female perineal body. Terminologia Anatomica has been used to standardize anatomical nomenclature (Federative Committee on Anatomical Terminology, 1998).

CLASSIC ANATOMY
MacAlister rst named the perineal body in 1889 (Oh and Kark, 1973). It marks the embryologic site of fusion between the anal tubercles and the pelvic bar, which separate the cloacal sphincter into anal and urogenital portions. The urorectal septum grows caudally until it reaches the cloacal membrane, dividing the cloaca into two parts: an anterior urogenital sinus and a posterior anorectum (DeLancey, 1989). The urorectal septum becomes the perineal body in the adult. The perineal body is the central point between the urogenital and anal triangles of the perineum. Its three-dimensional form has been likened to that of the cone of the red pine (Pinus resinosa, Fig. 1) with each petal representing an interlocking structure,
The opinions and assertions contained herein are the private views of the authors and are not to be construed as ofcial or reecting the views of the Department of the Army or the Department of Defense. *Correspondence to: MAJ Patrick J. Woodman, MC, USA, 115 Colorado Ct., Southern Pines, NC 28387. E-mail: Patrick.Woodman@na.amedd.army.mil Received 28 July 2000; Revised 2 August 2000, 7 January 2002 Published online in Wiley InterScience (www.interscience.wiley. com). DOI 10.1002/ca.10034

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Fig. 1. The owering pattern of Pinus resinosa.

such as an insertion site of fascia or a muscle of the perineum. Pelvic musculo-tendinous and brous fascial attachments to the perineal body show a similar pattern (Fig. 2). The perineal body is devoid of subcuticular fatty tissue. Upon removal of the fatty tissue in the adjacent urogenital and anal triangles, however, the supercial perineal space can be explored. The bulbospongiosus muscles, located lateral and deep to the introitus and labia majora, respectively, insert into the inferior limit of the perineal body with the supercial transverse perineal muscles and the subcutaneous portion of the external anal sphincter. The deep part of the perineal body occupies the upper half of the space anterior to the anal canal. Oh and Kark (1972) suggested that the external anal sphincter forms a single muscle bundle in the female, unlike the male that appears to form distinct portions. Shak (1975, 1976a,b) described the anat-

omy of the external anal sphincter as a triple-loop system of muscle bundles for both males and females. The deep part of the external anal sphincter and a reection of the levator ani (puborectalis) form the top loop, and the subcutaneous part of the external anal sphincter forms the bottom loop, both of which attach anteriorly to the perineal body; the supercial part of the external anal sphincter, which forms the middle loop, is tethered posteriorly to the coccyx. Shaks work modernized the understanding of the anal continence mechanism. Anteriorly, the perineal body is rmly adhered to the vaginal muscularis submucosa (DeLancey, 1992). It is suspended anteriorly to the pubic bone by the puborectalis and pubovaginalis. The perineal body is also connected anteriorly to the posterior border of the perineal membrane (Wilson, 1967). Laterally, the perineal body is rmly attached to the ischiopubic rami by the supercial transverse perineal muscles. Along its upper lateral borders, the perineal body is attached to the pubococcygeus, pubovaginalis, and puborectalis portions of the levator ani muscle group. Posterior and superiorly, the perineal body communicates with the longitudinal brous sheath of the internal anal sphincter, which starts to curve anteriorly toward the posterior wall of the vagina at the level of the anorectal junction (Oh and Kark, 1973). The pudendal nerve supplies most of the innervation to the perineal body. It is formed from the ventral rami of S2 4 spinal nerves inferomedial to the sciatic nerve, descends between the coccygeus and piriformis

Fig. 2. Female perineal body (shaded area). Note the cut-aways of the pubococcygeus, bulbospongiosus, and supercial transverse perinei muscles. Illustration by Mr. Tom Pierce.

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muscles, and leaves the pelvis through the greater sciatic foramen. It then crosses the posterior surface of the ischial spine and enters the perineum through the lesser sciatic foramen to travel along the lateral wall of the ischioanal fossa within the pudendal (Alcocks) canal (Benson, 1989). The inferior rectal nerve usually branches off as the pudendal nerve wraps around the ischial spine and subsequently supplies the external anal sphincter, which is involved in maintaining fecal continence, and provides sensory innervation to the anal canal below the pectinate line. At the level of the joined superior fascia of the pelvic diaphragm and the endopelvic fascia, the pudendal nerve divides again into the dorsal nerve of the clitoris and the perineal nerve. The perineal nerve supplies the perineal body and the labia. Other branches of the perineal nerve supply the external urethral sphincter muscle, which is involved in maintaining urinary continence. The anal canal above the pectinate line is innervated by the uterovaginal portion of the inferior hypogastric plexus and the pelvic splanchnic nerves. Because of its proximity to the anal canal and its close association with the internal anal sphincter, small autonomic nerve branches to the perineal body are possible (Moore, 1992). Perineal branches of the posterior femoral cutaneous nerve may also provide innervation. Arterial supply to the perineal body comes primarily from the internal pudendal artery, one of the branches of the anterior trunk of the internal iliac artery. The internal pudendal artery accompanies the pudendal nerve through the pudendal canal and divides into the inferior rectal and perineal arteries and the dorsal artery of the clitoris (Platzer and Monsen, 1989). The bulk of the perineum is supplied by the transverse branch of the perineal artery and the inferior rectal artery. Another branch of the internal iliac artery, the middle rectal artery, supplies the middle third of the rectum and may also send minor branches to the superior portion of the perineal body (Wilson, 1988). The perineal body may also receive minor branches from the superior rectal artery, a branch of the inferior mesenteric artery (Netter, 1989). Venous drainage of the perineal body is primarily accomplished via the internal pudendal veins and the venae comitantes of the branches of the internal pudendal artery (Moore, 1992). Drainage is assisted by the vaginal venous plexus, as well as veins that communicate with the uterine, vesical, and rectal venous plexuses and with the bulb of the vestibule. Posteriorly, the perineal body is drained by the internal rectal venous plexus and inferior rectal veins (Platzer and Monsen, 1989). Superiorly, the middle rectal and superior rectal veins also provide venous drainage. Most lymph vessels pass to the supercial and deep ingui-

nal lymph nodes, and internal iliac lymph nodes, in order of importance (Netter, 1989).

MODERN ANATOMY
The classic description of the urogenital diaphragm includes the deep transverse perineal muscles, encapsulated within layers of the superior and inferior fasciae of the urogenital diaphragm (Netter, 1989). Oelrich (1983) contended that he could not identify the urogenital diaphragm of Henle as a distinct anatomical entity. He conducted an extensive review of the literature, performed gross and histological sections on 43 fetal pelves and 43 adult pelves at various stages of development (66 mm crown-rump length fetuses to 30-year-old adults) and concluded that teachings about the existence of the urogenital diaphragm were unfounded, notwithstanding their promulgation throughout the anatomical and medical literature for most of the 20th century. All of the following contribute to the confusion: difculty of dissection in the area, few and small skeletal muscle bers, the replacement of skeletal muscle bers by collagen bundles with age, the large amount of surrounding smooth muscle, and an extensive connective tissue investment. Oelrichs (1983) major contribution was to describe the external urethral sphincter as encircling the middle third of the length of the urethra (Fig. 3). More caudally the compressor urethrae and the urethrovaginal sphincter pass anterior to the urethra. The compressor urethrae originates from the ischiopubic ramus and compresses the urethra, as well as pulls it inferiorly, thus assisting in elongating the urethra. The urethrovaginal sphincter complements the compressor urethrae as they pass together ventral to the urethra, and they may be reciprocal in size. In early development, the urethrovaginal sphincter is distinct as it passes dorsally along the lateral wall of the urethra and vagina immediately deep to the cephalic edge of the vestibular bulb. It is separated from the vestibular bulb by a thin layer of perineal membrane and interdigitates with the corresponding muscle of the opposite side and the perineal body. With age, there is an increased density of connective tissue in the perineal body and it becomes difcult to identify the skeletal muscle bers of the urethrovaginal sphincter behind the vagina. Because of Oelrichs studies (1983), the transversus vaginae muscles have replaced the deep transverse perineal muscle. The transverse vaginae parallel the compressor urethrae and radiate from it and the ischiopubic rami to attach to the anterior portion of the lateral vaginal wall. These bers form a very thin, fan-shaped muscle that attaches to the perineal membrane and to the anterior midpoint of the anorectal

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Fig. 3. Components of the former urogenital diaphragm. B, bladder; CU, compressor urethrae; IR, ischial ramus; SM, smooth muscle; TV, transverse vaginae; V, vaginal cavity; U, urethra; US, urethral sphincter; UVS, urethrovaginal sphincter; VW, vaginal wall. From Anatomical Record by T.M. Oelrich, 1983, Wiley-Liss. Reprinted with permission of WileyLiss, Inc., a subsidiary of John Wiley & Sons, Inc.

junction. The superior and inferior fasciae of the urogenital diaphragm are produced by a combination of the superior fascia of the pelvic diaphragm and the endopelvic fascia as it passes around the margins of the urogenital hiatus. Oelrichs ndings (1983) started to be reported in the scientic literature, in part due to his participation on the 1989 International Anatomical Nomenclature Committee. The term deep transverse perineal muscle, however, still appears in Nomina Anatomica, 6th ed. (International Anatomical Nomenclature Committee, 1989) and Terminologia Anatomica (Federative Committee on Anatomic Terminology, 1998). At the writing of this article, 29 scientic journal articles have quoted his original work over the past 16 years. Oelrich has several proponents in the gynecological and urological elds and his ndings have been conrmed utilizing other technologies (Myers et al., 1998), and have been incorporated into anatomical texts (Woodburne and Burkel, 1988; Platzer and Monsen, 1989; Moore, 1992; Slaby et al., 1994; Williams et al., 1995). In other texts, his ndings have been overlooked (Wilson, 1988; Netter, 1989; Frick et al., 1990; Spence, 1990; Snell, 1992; Hall-Craggs, 1995; Rohen et al., 1998). Some gynecology texts have incorporated his concepts, but Oelrichs ndings (1983) may as yet be considered minutiae.

and descriptions of the perineal body, few authors have chosen to examine the perineal body directly; however, there is a wealth of information from physiologic studies. What follows is a discussion of the clinically important functions of the perineal body, which are multiple and diverse (Table 1).
Anchors the Anorectum

Wilson (1967) examined the pelves of four embryos, 27 fetuses, six full-term infants, and 129 adults, both histologically and grossly, and described how the sphincter vaginae (pubovaginalis) muscle passes through the perineal body and blends with the deep part of the external anal sphincter, anchoring the perineal body to the anal canal. In addition, the upper surface of the perineal body joins with the rectovaginal septum (Denonvilliers fascia) and into its very posterior and superior aspects pass bers from the longitudinal muscle layer of the muscularis externa of the anterior wall of the rectum. The perineal body is also attached to the muscles in the supercial and deep perineal spaces. Thus, through the perineal body, the various components of the external anal
TABLE 1. Clinical Importance of the Perineal Body Anchors the Anorectum Anchors the Vagina Prevents Expansion of the Urogenital Hiatus Provides a Physical Barrier Between the Vagina and Rectum Episiotomy Maintains the Orgasmic Platform Maintains Urinary Continence Pudendal Nerve Injury Maintains Fecal Continence

CLINICAL IMPORTANCE OF THE PERINEAL BODY

Because of the difculties that Oelrich (1983) and Oh and Kark (1973) experienced in their dissections

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sphincter, supercial transverse perineal muscles, levator ani (pubococcygeus, pubovaginalis and puborectalis) and the median part of the posterior border of the perineal membrane anchor the anterior anorectal region to the pelvic ring.
Anchors the Vagina

DeLancey (1992) described the support of the vagina at three distinct levels. The immobile inferior one-third of the vagina, Level III, fuses with the perineal membrane, levator ani muscles, and perineal body. DeLancey reported that an important function of Level III supporting structures includes keeping the vagina closed. Defects in Level III support commonly predispose to total uterine procidentia or vaginal eversion. An intact perineal body can delay or prevent these conditions by maintaining the prolapsing tissues above the levator plate (the central tendon of the levator ani muscles) and the urogenital hiatus. In 1999, DeLancey histologically and macroscopically examined 42 fresh and 22 xed female pelves in serial section. He described how the perineal body served as the central connection between the two halves of the perineal membrane. As force is directed upon the vagina from above, the bers of the perineal membrane, which are laterally and posteriorly attached to the ischiopubic rami and perineal body, respectively, become taut and resist downward displacement. At Level II (middle one-third of the vagina), the lateral attachments of the vaginal canal, including the levator ani muscles and the tendinous arches of the pelvic fascia (arcus tendineus fasciae pelvis) also become taut. This anatomical arrangement underlies the structural interdependence between the support offered by the perineal body at Level III through its attachment to the perineal membrane and the suspension of the vagina by the perineal body at Level II through its multiple connections with the tendinous arches of the pelvic fasciae (and the levator ani musculature).
Prevents Expansion of the Urogenital Hiatus

selection of the A-P diameter measurement in the American Urogynecologic Society/International Continence Society sanctioned Pelvic Organ Prolapse Quantication Exam (Bump et al., 1996). Kelly (1928) observed that it was actually the levator ani and not the perineal body that closes the urogenital hiatus. DeLancey and Hurds (1998) data were consistent with this nding. The urogenital hiatus is sealed by the vaginal walls, endopelvic fascia, and urethra. As the urogenital hiatus increases in size, however, an open space develops in the pelvic oor and gravity tends to ll this space with a cystocele, rectocele, or the uterine cervix. Once the urogenital hiatus has opened up, the vaginal wall and cervix lie unsupported, and the endopelvic fascia is called upon to hold the pelvic organs in place. In predisposed individuals the constant load from abdominal pressure on this fascia can cause its failure with the development of signicant prolapse. Ultimately, it is the perineal body that acts as the nal mechanism for preventing prolapse beyond the urogenital hiatus. As the perineal membrane and tendinous arches of the pelvic fasciae tighten, the entire perineal body redirects abdominal pressure and dissipates gravity to prevent expansion of the urogenital hiatus.
Provides a Physical Barrier Between the Vagina and Rectum

DeLancey and Hurd (1998) examined the relationship between pelvic organ prolapse and the size of the urogenital hiatus. They found that the average size of the urogenital hiatus in the levator ani muscles was 5 cm2 (calculated using the anteroposterior measurement from the external urethral meatus to the frenulum of the labia minora [fourchette] and the greatest transverse diameter). An increase in the size of the urogenital hiatus was directly related to progressively larger pelvic organ prolapses that were correlated more to the anterior-posterior (A-P) diameter than to the transverse diameter. This fact was key in the

Hakelius (1979) proposed that the perineal body was integral in maintaining the structural integrity of the fecal continence mechanism by acting as a physical barrier or spacer between the rectum and vagina, thus protecting the rectum during childbirth. The shortening of the puborectalis sling pulls the anorectal junction anteriorly and superiorly, making the anorectal angle more acute, and thereby maintaining fecal continence. Damage to the perineal body or the attached puborectal sling may lead to anal incontinence. Hakelius (1979) used perineorrhaphy (repair of the perineal body) as the primary procedure for anal incontinence in 15 patients and achieved an 80% resolution of incontinence. Henry et al. (1982) measured the distance between the perineal body and an imaginary line drawn between the ischial tuberosities and reported an average distance of 2.5 cm. They also describe a descending perineum syndrome, where the perineal body lies at a lower level than normal and descends an average of 2 cm with the Valsalva maneuver. In this condition, the acute anorectal angle, so important in fecal continence, is disrupted; it may be caused by a loss of perineal body volume, detachment of the rectovaginal septum, or a widening of the urogenital hiatus after childbirth.

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TABLE 2. Layers Traversed During Uncomplicated Second-degree Episiotomy* Midline type Epithelium Supercial transverse perinei Bulbospongiosus Perineal membrane Urethrovaginal sphincter and transversus vaginae Rectovaginal septum (possible) *Adapted from Sultan et al. (1995). Mediolateral type Epithelium Bulb of vestibule Greater vestibular (Bartholins) gland (possible) Bulbospongiosis Supercial transverse perinei Perineal membrane Urethrovaginal sphincter and transversus vaginae

Zetterstroem et al. (1998) used endoanal ultrasound measurements of the perineal body to assess anterior anal sphincter defects. A perineal body thickness of less than 10 mm was found in 93% of patients with sphincteric defects. This ultrasonographic measurement may be an important reection of the relationship between the status of the perineal body and the anal sphincter musculature.
Episiotomy

In addition to spontaneous damage to the perineal body, damage also occurs iatrogenically through the performance of an episiotomy. Episiotomy is one of the most common procedures performed in obstetrics; unfortunately, it is often the least-experienced intern or resident who is relegated to repair an episiotomy. Experience and knowledge of the applicable anatomy contribute signicantly to good repair. Sultan et al. (1995) surveyed the training in episiotomy and its repair and found it to be wholly insufcient. Less than 20% of physicians felt their training in perineal anatomy to be of high standard, and more than 50% of physicians and midwives misidentied the muscles cut during an uncomplicated episiotomy (Table 2). A great deal has been written about episiotomies in the last 130 years. Thacker and Banta (1983) performed an extensive review of the English-language scientic literature (1860 1980) on the risks and benets of episiotomy. Notwithstanding a lack of clear evidence of its efcacy, episiotomy was performed in 60% of all deliveries in the US and in 50 90% of primigravid patients. Subsequently, Wooley (1995a,b) published two review articles that dealt with episiotomy from 1980 94. He reported that episiotomy was shown to reduce anterior vaginal lacerations, but, more signicantly, episiotomy did not provide the maternal and fetal benets normally reported by its proponents. These benets included prevention of perineal damage and its sequelae, prevention of pelvic oor relaxation and its sequelae, and protection of the newborn from intracranial hemorrhage or intrapartum asphyxia. In fact, episiotomy has been shown to subject the patient to increased risk caused by greater

maternal blood loss, increased perineal body injury and anal sphincter damage, improper wound healing, and postpartum pain. Episiotomy techniques differ according to geographic location. Midline episiotomy (where a linear surgical incision is made in the midline of the vagina and perineum to increase vaginal capacity) is predominant in the United States and at some centers in Canada. Beynon (1974) advocated the use of midline episiotomy over mediolateral episiotomy (where the incision is toward the ipsilateral ischial tuberosity), the general preference of obstetrical providers in Great Britain. Midline episiotomy was deemed to be easier to repair and to heal better than mediolateral episiotomy. Median episiotomy, however, has been associated with severe perineal lacerations in primiparous women. Labrecque et al. (1997) reported an overall 15.4% incidence of anal sphincter disruption; 20.6% occurred in women with midline episiotomy and 4.5% in women who did not have an episiotomy. This difference persisted even after adjustment for delivery type, birth weight, experience of physician, babys head circumference, shoulder dystocia, and epidural anesthesia. The relationship between midline episiotomy and anal sphincter disruption has been extensively documented by other investigators as well (Klein et al., 1994; Handa et al., 1996; Klein et al., 1997; Sultan, 1997; Wood et al., 1998; Albers et al., 1999; Zetterstroem et al., 1999). Although mediolateral episiotomies are technically more difcult to repair, their use appears to be protective, at least in nulliparous women (Poen et al., 1997). Wood et al. (1998) reported a 1.2% incidence of third degree anal sphincter tears in a retrospective study of 9,631 women who received a mediolateral episiotomy. Studies of occult sphincter damage with endoanal ultrasonography, however, have shown that neither midline nor mediolateral episiotomy prevents anal sphincter disruption (Sultan, 1997). See Table 3 for a comparison between midline and mediolateral episiotomy.

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TABLE 3. Comparison of Midline Versus Mediolateral Episiotomy* Episiotomy type Characteristic Surgical repair Faulty healing Postoperative pain Anatomical results Blood loss Dyspareunia Extensions Midline Easy Rare Rare Excellent Less Rare Common Mediolateral More difcult More common Common Occasionally faulty More Occasional Uncommon

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Maintains the Orgasmic Platform

*Adapted from Ramin and Gilstrap (1994).

Because of the concern about the relationship between episiotomy and severe perineal damage, physicians have begun to speak out against the routine or liberal use of episiotomy (Helewa, 1997; Meyers-Helfgott and Helfgott, 1999). When a conscious change in the liberal use of episiotomy was attempted, the incidence of tears in the external anal sphincter remained unchanged; however, women had an increased incidence of delivering with an intact perineum (Henriksen et al., 1994). McCandlish et al. (1998) described a hands-on method of supporting the perineum and assisting the delivery of the shoulders, resulting in a lower episiotomy rate. Besides an unsupported perineum, other factors favoring severe perineal damage include: forceps delivery, increased fetal size (4,000 g), prolonged second stage (pushing) of labor, primiparous delivery, and occiput posterior position. Other factors that protect against severe perineal damage include vacuum-assisted delivery and cesarean section before labor (Sultan et al., 1994; Handa et al., 1996). When evaluating the use of episiotomy in the management of labor, an obvious concern is pain. Albers et al. (1999) investigated genital tract trauma in secondstage labor with a restrictive episiotomy policy and found that painful trauma occurred in 85% of births (59% required suturing); even with a rst- or seconddegree tear, pain and dyspareunia were signicant. Gordon et al. (1998) compared women who had received episiotomy repair by the performance of a two-layered closure leaving the skin unsutured, vs. by the traditional three-stage closure with skin closure. They found that by leaving the skin unsutured women had less pain and dyspareunia at three-month follow-up. Ramin and Gilstrap (1994) reported that 1 in 20 women with a fourth-degree tear develop early infection, wound dehiscence, or both, which can also result in pain and dyspareunia. Mackrodt et al. (1998) found that post-episiorrhaphy pain, analgesic use, and wound breakdowns can be limited with the use of polyglactin 910 suture, as compared to catgut.

Masters and Johnsons (1966) book, Human Sexual Response, suggested that the perineal body was an integral part of the orgasmic platform, an area of localized vasocongestion during the plateau level of the sexual response. This platform, which encompasses the entire inferior one-third of the vagina, together with the labia minora, reects the vaginas anatomico-physiologic expression of orgasm. When the perineal body is damaged, this platform is damaged. Klein et al. (1994) investigated primiparous and multiparous women and found that sexual functioning was best in women with spontaneous or no tears and that during the rst three months of the postpartum period, perineal pain was least for women who gave birth over an intact perineum. Perineal suturing itself may be associated with an increased incidence of perineal pain (Gordon et al., 1998). Benyon (1974) advocates midline episiotomy over the mediolateral technique because it is associated with less pain and dyspareunia. Sleep and Grant (1987), however, reported on a three-year follow-up study that compared liberal use of episiotomy to a restrictive policy and found no benet in the prevention of long-term dyspareunia. If perineal damage and its attendant pain are signicant, so can be the corresponding sexual consequences. Haadem et al. (1988) surveyed women who received episiotomy and found that 48% had pelvic oor symptoms, such as perineal pain and dyspareunia, particularly when childbirth perineal damage included extension into the anal sphincter. Great importance is often placed on a womans body image and sexual functioning. In Brazil, body image and sexual functioning are perceived as threatened by vaginal delivery, leading to a comparatively high cesarean-section rate (Souza, 1994). Episiotomy has even been viewed as a form of genital mutilation (Wagner, 1999). Compared to a natural tear, episiotomy results in more bleeding and pain, more permanent vaginal deformity, and more temporary and longterm sexual dysfunction (Ramin and Gilstrap, 1994).
Maintains Urinary Continence

The urinary continence mechanism is complex and depends, in large part, upon the coordination of the involuntary detrusor and intrinsic urethral sphincteric muscles. The levator ani muscle and external urethral sphincter muscle function as back-up mechanisms, both of which are under voluntary control. The levator plate also provides a dynamic backdrop for the normal continence mechanism, resisting posterior rotational

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descent of the vagina and overlying urethrovesical junction during levator contraction. Childbirth can damage the pelvic musculature; consequently, posterior rotational descent of the bladder neck necessary for normal voiding can also occur at times of increased intra-abdominal pressure. Benson (1996) summarized the neurogenic hypothesis of urinary incontinence. Weakening of the pelvic oor musculature after childbirth occurs secondary to direct damage and partial denervation. Ninety-ve percent of women with stress urinary incontinence have prolonged perineal nerve conduction times, compared to only 4% of women without stress urinary incontinence. This suggests a double neuromuscular pathology: direct compression, stretch, and devascularization of the pudendal nerve resulting in levator ani atrophy and loss of urethral and bladder support. Ryhammer et al. (1995) reported on the relationship between urinary incontinence symptomatology and the number of repeated vaginal deliveries. The risk for urinary incontinence was additive: 3.3%, 1.0%, and 6.8% after one, two, and three deliveries, respectively. The difference was signicant after three vaginal deliveries, as compared to the rst two. In a survey of Danish women, Foldspang et al. (1999) investigated factors associated with urinary incontinence. Episiotomy and perineal suturing correlated to incontinence; however, using a multivariate analysis, only perineal suturing continued to be associated with urinary incontinence. Sleep and Grant (1987) found no benet from episiotomy in the prevention of urinary incontinence. It appears that both spontaneous or deliberate trauma to the perineal body is associated with urinary incontinence. The urethrovaginal sphincter attaches into the perineal body and contributes to the external urethral sphincter (Oelrich, 1983). Because neurologic and direct damage to the pelvic oor can occur during delivery, subsequent loss of urethrovaginal sphincter function may be just enough to make a woman incontinent.
Pudendal Nerve Injury

The terminal ends of some of the perineal and inferior rectal branches of the pudendal nerve are tethered in the perineal body. Thus, Kiff and Swash (1984) suggested that because the pudendal nerve is bound tightly by connective tissue as it wraps around the ischial spine, it is predisposed to damage distal to this site when it is stretched by the perineal descent that occurs during the second stage of labor or with excessive straining at defecation (Henry, 1982; Benson, 1989). Henry et al. (1982) estimated that a perineal descent of 2 cm, which may occur during labor,

stretches the pudendal nerve by 20% of its length. Disruption of Denonvilliers fascia during vaginal delivery can separate the perineal body from this immobile fascia and allow perineal descent with a simple Valsalva maneuver of up to 1.1 cm (Snooks and Swash, 1984; Snooks et al., 1986). Descent of as little as this distance (and stretching of the pudendal nerve by 12% of its length) can cause permanent pudendal neuropathy, and repeated events are additive. Similar to carpal tunnel syndrome, the terminal branches of the pudendal nerve undergo demyelination. Ho and Goh (1995) suggested a linear relationship between perineal descent and pudendal nerve damage, based on an increase in pudendal nerve terminal motor latency. Benson (1996) summarized other common neurogenic mechanisms of injury. Pressure as low as 80 mm Hg on the perineurium can lead to cessation of blood ow to the axons, and pressure during a vaginal delivery can easily surpass this limit (up to 240 82 mm Hg). Cessation of blood ow for more than 8 hr may lead to thrombosis without recovery of neural function. Thus, vascular compression during delivery may lead to neuropathic and myopathic dysfunction. Dissection neuropathy may occur as a result of vaginal pelvic reconstructive surgery. Because pudendal neuropathy has been shown to be an etiologic factor in both urinary and fecal incontinence (Snooks and Swash, 1984; Snooks et al., 1986), electrophysiologic studies may allow the identication of the most effective pelvic reconstructive surgery. Pudendal neuropathy may affect the efcacy of traditional procedures and may indicate that a more targeted procedure should be recommended. Direct branches of the ventral rami of the S3S4 spinal nerves (and perhaps branches of the pudendal nerve) supply the puborectalis portion of the levator ani muscle (Hollabaugh et al., 1997), and these nerves may also be involved in traction injury. Allen et al. (1990) used concentric needle EMG, pudendal nerve conduction, and perineometer measurements to determine the extent of levator ani damage during childbirth. In 80% of women, there was EMG evidence of denervation at 2 months postpartum and impairment of pelvic oor contraction. Women who delivered by elective cesarean section before labor commenced were spared electrophysiologic damage to the pelvic oor musculature. Cesarean section was not protective if the patient labored, however, suggesting that labor itself is an important cause of denervation. Deindl et al. (1994) reported that birth trauma was associated with asymmetric denervation of the pelvic oor and suggested that coordination of levator ani contraction is also important in urinary continence.

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Multiparity, forceps delivery, increased duration of the second stage of labor, a third-degree perineal tear, and a linear relationship with increasing birth weight were associated with pudendal nerve damage.
Maintains Fecal Continence

The most important functional role of the perineal body, because of its very intimate relationship to the anal canal and anal sphincter muscles, is its contribution to fecal continence. Shak (1975, 1976a,b) described the external and internal anal sphincters as inserting into, passing through, and being invested by the perineal body. It follows that when damage to the perineal body occurs, direct (or indirect) extension into the anal sphincters and a loss of fecal continence is possible. Fecal incontinence is a disturbing and life-altering disorder. Sphincteric control is fundamental in human socialization and its impairment may result in severe emotional and social disruption. Schoetz (1985) said loss of voluntary control of bowel movements results in progressive isolation of the affected individual and alienation from family members, with devastating psychosocial impact. Because of the sensitive nature of the problem, embarrassment, and perceived social stigmata of the condition, fewer than 50% of women will report it to their doctors. Estimates of fecal incontinence incidence range from 0.4 17% of adult ambulatory women, and may be as high as 50% in institutionalized patients (Kamm, 1994; Jackson and Hull, 1998). Approximately 13% of women have fecal urgency and 30% have structural changes on ultrasound (Kamm, 1994). Sultan et al. (1993) reported that 13% of primiparous and 23% of multiparous women have fecal urgency or incontinence at 6 weeks postpartum. Zetterstroem et al. (1999) described the vagina as slightly J-shaped with the bottom of the J being closely associated with by the rectum, anal canal, and the perineum. Therefore, most of the uterine pressure during the second stage of labor is directed toward the perineal body and anorectum. Anal rupture during labor carries a high risk (20 50%) of anal incontinence (Haadem et al., 1988; Bek and Laurberg, 1992; Sultan, 1997). The internal anal sphincter is responsible for up to 80% of anal resting pressure and for liquid stool continence. The external anal sphincter is primarily responsible for atal continence and produces about 80% of the maximum squeeze pressure on manometric testing (Mitrani et al., 1998). Sultan et al. (1994) demonstrated that those patients with anal incontinence or fecal urgency had both internal and external anal sphincter defects on ultrasound, and signicantly lower manometric anal pressures.

DeLancey et al. (1997) examined the anatomy of the internal and external anal sphincter in relation to acute fourth-degree midline perineal body lacerations. These investigators reported that the internal anal sphincter lies over the submucosa of the anal canal as a distal condensation of the longitudinal layer of the muscularis externa of the rectum. Of clinical importance was the observation that the internal anal sphincter in these patients retracted laterally into the surrounding tissue because of its constant muscular activity. If a physician is not vigilant in repairing a severe perineal body laceration, the internal anal sphincter can retract, not be repaired, and result in the loss of internal anal sphincter function with subsequent anal urgency or liquid stool incontinence. As women age, the strength of both the external and internal anal sphincter musculature decreases, evidenced by a decrease in resting and squeeze manometric pressure (Poos et al., 1986). As anal sphincter muscle strength deteriorates, a patient may no longer be able to compensate for long-term anal sphincter disruption. Nygaard et al. (1997) questioned women with anal sphincter disruption 30 years after delivery. Those women with anal sphincter disruption had signicantly more bowel sequelae than women with a simple episiotomy or cesarean section; however, as the women aged, the three groups became very similar suggesting that age acts as an equalizer, rather than exacerbating previously existing symptoms. A normal perineum on clinical examination does not preclude underlying sphincter damage. Nielsen et al. (1992) reported that digital anal examination detects only 85% of cases of persistent anal sphincter damage. Frudinger et al. (1997) reported a 43% occult sphincter disruption rate with a normal digital exam and no visible perineal evidence of trauma. The advent of endoanal ultrasonography has allowed physicians to determine unrecognized anal sphincter muscle damage postpartum. Burnett et al. (1991) demonstrated ultrasonographic sphincter defects in patients suffering from anal incontinence: 90% had external anal sphincter defects, 65% had internal anal sphincter defects, and 44% had disruption of the perineal body suggested by signicant attenuation during imaging. In a groundbreaking study, Sultan et al. (1993) reported that 35% of primiparous women and 44% of multiparous women had occult sphincter disruption on ultrasound 6 weeks after delivery and concluded that most damage occurred during the rst vaginal delivery. They identied no sphincteric disruption in women undergoing cesarean section or vacuum deliveries.

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Several authors have suggested that anal sphincter disruption is the most important contributing factor to fecal incontinence (Bek and Laurberg, 1992; Kamm, 1994; Sultan, 1997) and that the most common predisposing factor for sphincter disruption is the use of forceps (Haadem et al., 1988; Sultan et al., 1993; Kamm, 1994; Poen et al., 1997; Wood et al., 1998). Johanson et al. (1993) compared forceps to vacuum extraction and found an incidence of 17 and 11%, respectively, of anal sphincter damage. Other risk factors for anal sphincter rupture include primiparity (Haadem et al., 1988; Poen et al., 1997; Wood et al., 1998), abnormal presentations other than occiput anterior (Haadem et al., 1988), large babies 3,800 4,000 g birth weight (Haadem et al., 1988; Poen et al., 1997; Wood et al., 1998), oxytocin administration (Haadem et al., 1988; Poen et al., 1997), episiotomy (Wood et al., 1998), second stage of labor 1 hr (Poen et al., 1997; Wood et al., 1998), and epidural anesthesia (Poen et al., 1997). The traditional end-to-end anal sphincter repair has been associated with up to a 50% failure rate and, therefore, has come into question. Stricker et al. (1988) compared four different anal sphincteroplasty procedures and found that deep external anal sphincter plication with perineal body reconstruction and anoplastic skin closure was superior. This procedure involves dissecting up the rectovaginal septum and serial plication of the medial part of the levator ani and the supercial and deep external anal sphincters. Unfortunately, success rates were not cited. Sultan (1997) suggested that the techniques found most effective in secondary episiorrhaphy may also be effective in primary closure under the appropriate conditions. There are several ongoing investigations of overlapping sphincteroplasty (in which the internal anal sphincter is plicated in the midline and the external anal sphincters are divided in the midline, overlapped, and sutured) for the repair of sphincter rupture at the time of delivery. For example, LondonoSchimmer et al. (1994) reported a 75% fair to excellent result after 5 years in women who underwent overlapping sphincteroplasty for fecal incontinence. The outcomes were not related to the cause of injury, but an anterior overlap was signicantly better than a posterior one. Pudendal neuropathy, infection, and impaction were often associated with procedure failure. Sultan (1997) reported that poor outcomes after primary repair are often related to persistent sphincteric disruption rather than to pudendal neuropathy. The persistence of sphincteric disruption occurs in 50 58% of women (Nielsen et al., 1992; Sultan et al., 1994). Although some patients with persistent disruption improve, 29% continue to have bowel sequelae

(Nielsen et al., 1992). Eighty-ve percent of anally incontinent women have persistent structural defects after a third-degree repair and 50% of women remain symptomatic despite repair immediately after delivery (Kamm, 1994). Transient postpartum anal incontinence is a reliable predictor of future anal incontinence (Bek and Laurberg, 1992). We have already discussed pudendal neuropathy in relation to urinary incontinence; the neurogenic basis of fecal incontinence is even better established (Snooks et al., 1984, 1985; Sultan et al., 1994; Ryhammer et al., 1995; Kafka et al., 1997; Jackson, 1998). Pudendal nerve injury and traumatic anal sphincter disruption subsequent to vaginal delivery are the two primary causes of fecal incontinence (Jackson, 1998). Snooks et al. (1985) investigated patients with anterior external anal sphincter damage and fecal incontinence through physical examination, anal ultrasonography, and pudendal nerve terminal motor latency studies. They found a 60% incidence of pudendal neuropathy, suggesting that muscle and nerve damage often coexist, producing a double pathology. Some authors suggest that pudendal neuropathy is the predominant factor differentiating patients with minor leakage versus gross anal incontinence. For instance, Kafka et al. (1997) prospectively measured pudendal nerve terminal motor latencies (PNTML) in women presenting with abnormalities of defecation. Less than 35% of patients with leakage alone had abnormal PNTMLs, whereas 77.4% of PNTMLs were abnormal for women with gross incontinence. Each group showed signicant decreases in the following manometric parameters: resting and squeeze manometric pressures, volume pressures, and functional sphincter length. Snooks et al. (1984) suggested that the pudendal nerve damage caused by vaginal delivery might be cumulative in multiparous women. Ryhammer et al. (1995) distributed a questionnaire examining anal incontinence symptomatology with repeated vaginal deliveries without obstetrical tears of the anal sphincter. They found a risk of permanent atal incontinence of 1.2, 1.5, and 8.3% after one, two, and three vaginal deliveries, respectively.

RECOMMENDATIONS
Protection of the perineal body is integral to vaginal delivery and its ancillary procedures, which are themselves common causes of perineal body damage. Shipman et al. (1997) suggested that perineal massage during the second-stage of labor may reduce the episiotomy rate, the incidence of instrumental deliveries, and anal sphincter damage. Controlling the speed of

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vaginal delivery with a hands-on approach is important to minimize shearing neuropathy and uncontrolled delivery of the shoulders, which may extend a perineal laceration or episiotomy. Episiotomy has not proven effective in preventing maternal or fetal morbidity and, consequently, should be restricted to certain indications, such as cases of fetal distress, malpresentation, persistent occiput-posterior position, and shoulder dystocia (Sultan and Kamm, 1997). Prophylactic episiotomy in women who have had previous anal sphincter disruption does not seem to be effective in preventing recurrence of such damage (Sultan, 1997). Henriksen et al. (1994) recommend keeping episiotomy rates below 30% and, if instrumental assistance is necessary, vacuum extraction has proven safer than forceps (Poen et al., 1997). Vacuum extraction is currently the procedure of choice recommended by the Royal College of Obstetricians and Gynaecologists for instrumental deliveries (Sultan and Kamm, 1997). The work of Allen et al. (1990) suggests that women who are delivered by elective cesarean section before the onset of labor are spared electrophysiologic damage to the pelvic oor musculature. Despite the benets of the modern surgical methods, however, cesarean section is not without risk. Few physicians have been bold enough to recommend elective cesarean section to their patients; nonetheless, Sultan and Stanton (1996) warn that the request rate for elective cesarean section may rise as more women worry about their quality of life after the trauma of a vaginal delivery. Souza (1994) reported on the status of Brazils Cesarean Section On Demand policy. He warned that patients rights could become confused with the transference of physicians attitudes through patient counseling. Selected women may benet from cesarean delivery, but it should be restricted to women who have undergone repair for incontinence or pelvic organ prolapse. If damage occurs during vaginal delivery, steps can be taken to minimize morbidity and reestablish anatomy. When used for primary repair, Mackrodt et al. (1998) found polyglactin sutures superior to catgut in decreasing postoperative pain, analgesic use, and wound breakdowns. Gordon et al. (1998) demonstrated that women had less pain and dyspareunia at three months postpartum when a layered perineal repair was performed in women who had rst- and second-degree perineal lacerations, leaving the skin unsutured. For women with complicated deliveries, such as forceps usage (a predictor of occult sphincter damage; Sultan, 1997), endoanal ultrasonographic evaluation may be useful in identifying occult sphincteric injuries. If a patient appears to suffer a second-degree

laceration, but is found on ultrasonography to have an asymptomatic occult third-degree defect, it would be difcult to justify not repairing the whole defect. The best type of perineal repair is yet to be determined. However, physicians repairing rst- and second-degree lacerations or incomplete anal disruptions might be well-advised to perform a layered anatomical technique in the fashion described by Stricker et al. (1988) and Wheeless (1998). Patients with complete anal sphincter disruption may benet from a primary overlapping anal sphincteroplasty procedure. Nonetheless, perineorrhaphy and reattachment of the perineal body to Denonvilliers fascia and the anal sphincters must be the goal. Sultan et al. (1995) demonstrated that the training of midwives and trainee doctors in perineal anatomy and repair has been shown to be poor and demanded that education in this area be enhanced. Unfortunately, because delivery rates have consistently fallen over the last 30 years in the United States, trainee exposure to episiotomy and repair is limited. It is not uncommon for a trainee or a physician with a limited obstetrical practice to repair only one or two fourthdegree lacerations per year. Without adequate instruction, practice models, and supervision by trained surgeons, the number of women with urinary or fecal incontinence and pelvic organ prolapse may grow. Wheeless (1998) proposed the development of an early-morning episiorrhaphy service. All patients with severe perineal trauma from the previous evenings deliveries would be kept at bed rest, hydrated, and given antibiotics and pain medication until the morning. A senior gynecologic surgeon would then attend the repair of all third- and fourth-degree tears in a controlled setting, with adequate instrumentation, lighting, and assistance. This would provide an optimal environment for formal episiorrhaphy teaching and improvement of outcomes. Secondary repair of sphincter defects may be less straightforward, especially if patients present with incontinence. Electrophysiologic studies that indicate neuropathy can be used to enhance the selection of the ideal pelvic reconstructive surgical candidate: if a neurologic decit is present, the physician could withhold traditional reconstructive procedures in lieu of more complicated procedures (Benson, 1996). More targeted procedures may be indicated if intrinsic urethral sphincteric deciency or an end-stage external anal sphincter are encountered.

SUMMARY
The perineal body is a complex structural entity between the terminal ends of the urogenital and gas-

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Woodman and Graney damage following childbirth revealed by anal endosonography. Br J Radiol 64:225227. Deindl FM, Vodusek DB, Hesse U, Schuessler B. 1994. Pelvic oor activity patterns: comparison of nulliparous continent and parous urinary stress incontinent women. A kinesiological EMG study. Br J Urol 73:413 417. DeLancey JOL. 1989. Anatomy and embryology of the lower urinary tract. Obstet Gynecol Clin 16:717731. DeLancey JOL. 1992. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166:17171728. DeLancey JOL, Toglia MR, Perucchini D. 1997. Internal and external anal sphincter anatomy as it relates to midline obstetric lacerations. Obstet Gynecol 90:924 927. DeLancey JOL, Hurd WW. 1998. Size of the urogenital hiatus in the levator ani muscles in normal women and women with pelvic organ prolapse. Obstet Gynecol 91:364 368. DeLancey JOL. 1999. Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 180:815 823. Federative Committee on Anatomical Terminology. 1998. Terminologia anatomica. Stuttgart: Thieme. Foldspang A, Mommsen S, Djurhuus JC. 1999. Prevalent urinary incontinence as a correlate of pregnancy, vaginal childbirth, and obstetric techniques. Am J Public Health 89:209 212. Frick H, Kummer B, Platz R. 1990. Wolf-Heideggers atlas of human anatomy. 4th Ed. Basel: Karger. Frudinger A, Bartram CI, Spencer JAD, Kamm MA. 1997. Perineal examination as a predictor of underlying external anal sphincter damage. Br J Obstet Gynaecol 104:1009 1013. Gordon B, Mackrodt C, Fern E, Truesdale A, Ayers S, Grant A. 1998. The Ipswich Childbirth Study. I. A randomized evaluation of the two stage postpartum perineal repair and leaving the skin unsutured. Br J Obstet Gynaecol 105:435 440. Haadem K, Ohrlander S, Lingman G. 1988. Long-term ailments due to anal sphincter rupture caused by deliverya hidden problem. Eur J Obstet Gynecol Reprod Biol 27:27 32. Hakelius L. 1979. Reconstruction of the perineal body as treatment for anal incontinence. Br J Plastic Surg 32:245252. Hall-Craggs ECB. 1995. Anatomy as a basis for clinical medicine. 3rd Ed. London: Williams & Wilkins Waverly Europe. Handa VL, Harris TA, Ostergard DR. 1996. Protecting the pelvic oor: obstetrical management to prevent incontinence and pelvic organ prolapse. Obstet Gynecol 88:470 478. Helewa ME. 1997. Episiotomy and severe perineal trauma: of science and ction. Can Med Assoc J 156:811 813. Henriksen TB, Bek KM, Hedegaard M, Secher NJ. 1994. Methods and consequences of changes in use of episiotomy. BMJ 309:12551258. Henry MM, Parks AG, Swash M. 1982. The pelvic oor musculature in the descending perineum syndrome. Br J Surg 69:470 472. Ho Y-H, Goh HS. 1995. The neurophysiological signicance of perineal descent. Int J Colorect Dis 10:107111. Hollabaugh RS, Dmochowski RR, Steiner MS. 1997. Neuroanatomy of the male rhabdosphincter. Urology 49:426 434.

trointestinal systems. The interlocking muscular, fascial, and brous components make dissection and description of the anatomy difcult. Despite the paucity of literature on the perineal body, it is an extremely important structure. It is commonly injured during labor, and an unrepaired or improperly repaired laceration can compromise the functional capacity of the urogenital and gastrointestinal systems, as well as associated peripheral nerves and the muscles they innervate. Components of the urinary and fecal continence mechanism insert into the perineal body, which serves as the central anchor for the vagina and anorectum, and a terminal insertion site for part of the external urethral sphincter (urethrovaginal sphincter). The perineal body is stimulated during intercourse and inasmuch as it attaches to the various levator ani muscles, narrows the urogenital hiatus. Unfortunately, repair of a perineal laceration or episiotomy is often relegated to an inexperienced resident or physician. Because of the functional importance of perineal anatomy, proper education is extremely important. Only through the teaching of anatomy and knowledge of the indications for and against episiotomy can quality obstetrical and gynecologic medical care be ensured. Perineal massage and controlled speed of fetal descent will minimize the extent of perineal damage. Optimal primary repair of the perineal body can help prevent the development of pain, dyspareunia, aerovagina and, potentially, pelvic organ prolapse (caused by a gaping introitus) and fecal or urinary urgency or incontinence.

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