Levator ani muscle complex integrity is very important to pelvic floor support. Comprising puborectalis, pubococcygeus and ileococcygeus, this muscle provides support to urethra, distal vagina and rectum. During labor, stretching and damage of these muscles can occur, particularly to the pubococcygeus, since it is the shortest and most medial muscle of the complex [7–9].

Levator trauma can lead to widening of the genital hiatus and thus be a risk factor for pelvic organ prolapse. It can also be associated with urinary incontinence.

Imaging studies may help in elucidating the types of injuries of levator ani muscle, especially transvaginal or transperinaeal ultrasonography and magnetic resonance imaging of the pelvis with or without three-dimensional reconstruction [7–9].

In three-dimensional reconstruction, it is possible to observe the distinct anatomical difference of the levator ani when comparing nulliparous, asymptomatic multiparous, symptomatic multiparous and elderly, as shown in Fig. 7.2 [10].

Injury to pudendal nerve can also be associated with pelvic floor disorders, especially urinary and fecal incontinence. The pudendal nerve innervates the external urethral and anal sphincters. During labor, nerve compression and stretching can occur, leading to incontinence. This process is reversible in most cases, with complete return to continence in the postpartum period. Severe cases of injury can lead to persistent incontinence [11, 12].

During pregnancy, collagen and elastin, components of connective tissue, experience some modifications in order to increase vaginal distensiblity [13].

During labor, extensive stretching promotes collagen degradation. The endopelvic fascia and other connective tissue elements are at risk of stretch and detachment from their bony attachments during childbirth [13]. Pubic bone edema and subcortical fracture are common, and magnetic resonance shows that they persist until 7 weeks after delivery without clinical findings [14]. In rare cases, pubic symphysis rupture can occur [15].

After delivery, there is a substantial remodeling of the connective tissue components. However, this new tissue is not as strong as the original [13].

Injuries at level I of DeLancey are responsible for the appearance of prolapse of the uterus. The increase in intra-abdominal pressure generated by the pregnancy itself can cause rupture or stretching of these structures, especially if it is a twin pregnancy, macrosomic fetus or increased amniotic fluid as in gestational diabetes.

At level I, proximal transverse defect may occur with a detachment of the rectovaginal fascia from the pericervical ring, leading to the descent of the small bowel, omentum or sigmoid through the vaginal canal, called enterocele or protrusion of the rectum, called high rectocele [3, 16].

Structures of level II of DeLancey in labor are molded to hold the fetus. However, especially in cases of large fetuses or prolonged labor or even accelerated labor, rectovaginal fascia can break or stretch or it can detach from arcus tendineus. These injuries may result in the appearance of rectoceles in varied degrees and types, associated with central or transverse rupture of fascia or side rupture of fascia [17].

At level II, if there is a lesion of pubocervical fascia, the anterior vaginal wall may protrude into the vagina. When this prolapse involves the protrusion of the bladder it is called cystocele. Rarely, enterocele may occur via anterior vaginal wall, but is anatomically classified as apical prolapse; it originates from the detachment of the pubocervical fascia from the pericervical ring [7, 17]. Moreover, vaginal childbirth is associated with loss of tenting of the vaginal fornices, independent of levator trauma, and also with impaired anterior vaginal wall support. The existence of paravaginal defects may imply a role for such defects in the causation of anterior vaginal wall prolapse [18].

The expulsion phase of labor can cause injuries to level III of DeLancey as pubocervical fascia and the urethra can prolapse into the vaginal lumen, called urethrocele. In some cases it can cause hypermobility of the bladder neck and stress urinary incontinence (usually during medium or large efforts). Still, if there is injury to the urethral sphincter during the expulsion phase, it will decrease the intra-urethral pressure and, therefore, also cause stress urinary incontinence (usually during minimal efforts) [7, 17].

The second stage of labor can also be associated with level III lesions in the posterior compartment. Lesions in the rectovaginal fascia at this level cause rectoceles. Lesions in the perineal body and perineal muscles can cause perineal rupture. In these cases the patient complains of “a large or gaping vagina.” If the anal sphincter is affected, the patient may develop fecal incontinence [19].

Table 7.1 summarizes the time of pregnancy or childbirth, the types of injuries that can occur according to DeLancey levels and their clinical consequences.

It is important to note that in some cases urinary urgency and urgency incontinence/overactive bladder can be caused by anterior vaginal prolapse. Vesical receptors present in the base of the bladder in contact with the vaginal epithelium are activated during bladder filling. However, in most cases, the etiology of overactive bladder is unknown [20].