Despite vaginal birth being  identified as the leading risk factor for pelvic floor muscle injury mechanisms of damage remains unclear. The purpose of this original exploratory study was to determine if the cause of the injury is due to the common practice of external thigh rotation during pushing in the 2nd stage.

A systematic review was conducted of the literature on finite-element models to elucidate the common mechanical changes of the pelvic floor muscles during the active second stage of labor to determine the potential influence of external leg rotation.

Finite element simulations show that pelvic floor muscles are subjected to large deformations in the levator ani during the second stage, with estimated stretch ratios of between 2.2 to 4.3. When correlating the stretch ratios shape analysis results, it was found that increases in muscle thickness, reduction in circumference and elongated axial span of the muscles, increased the maximum stretch.

The maximum principal stresses occurred at consistent positions in the pelvic floor: around the tendinous arch region, which connects with the inner obturator muscle, the insertion points of the rectal area of the levator ani in the coccyx, and also the symphysis pubis (right and left insertion points.

All of these findings may be explained by a common practice in the 2nd stage of placing the mother's thighs in external rotation (ER) during pushing. Movement of the thigh anteriorly toward the trunk (hip flexion) and laterally to the side away from the midline (abduction) is usual during pushing. However, this position will invariably be combined with external rotation of the thigh laterally around its longitudinal axis away from the midline, while its anterior surface rolls outward. An MRI study shows that  ER externally rotates the iliac bone such that the ischial spine orients towards the interior of the pelvis reducing the bony outlet where the levator ani muscle (LAM) is attached. 
This shape change of the outlet during is only a few mm but it makes the cross-sectional area of the LAM attached to it smaller. This smaller area is also theoretically stiffer, for if the origin and insertion of a muscle moves closer together, its dynamic elasticity decreases. However, more significantly, this stiffness may also come about because the  LAM originates from the linear thickening (arcus tendineus levator ani - ATLA) of the fascia covering the obturator internus (OI) muscle. a major external rotator of the leg.   We hypothesize that contraction of the OI  during ER  creates reciprocal tensioning in the fascia by way of attachment and line of pull, influencing the length-tension of the LAM, shortening and stiffening it. 
This intriguing hypothesis, of stiffness around the ATLA with ER, is supported by the evidence from finite element studies which show the maximum stress distribution localized around the tendinous arch. Such that increasing stiffness of the lateral attachments of the pelvic sidewall caused an increased stretch of the attached LAM. However, when the stiffness of the lateral attachments of LAM to ATLA was decreased  5-fold it resulted in a 14% decrease in the maximal stretch ratio. Also unwittingly the stiffness was created by various studies taking the approach of fixing the muscles spatially at their attachment points to pubis, arcus tendineus, and coccyx providing lateral constraints for the deformation of the LAM.

We believe the higher stretch rates seen are created by ER causing the baby to be shifted onto a smaller stiffer outlet less able to stretch. Such that as it progresses through the canal the baby needs to extend its head and neck backward in relation to its body and use greater force and more time to overcome the tighter inelastic area, causing enormous pressure on vulnerable anterior structures.  This is in keeping with the findings of a longer 2nd stage in those with injuries, and finite element studies which show the greatest increase in stress in the LAM occurs during fetal head extension.  There is also the fact that most injuries to the pelvic floor and perineum occur within the anterior triangle and anterior portion of the posterior triangle where the anal sphincters lie. 

The use of greater force would theoretically also be limited by resistance exerted by the LAM which will reflexly contract in response to the force being exerted on it, producing inward squeezing around the pelvic openings which counternutates the sacrum and closes the outlet further. This may compound the risk of injury as it means the LAM is unable to relax and thus recover part of its initial properties which is seen as an important feature needed for viscoelastic tissues to sustain less stiffness and withstand larger deformations without trauma. Then pushing forces of the uterus may be insufficient to overcome the resistance of the LAM, so the mother must also voluntarily push which will increase intra abdominal pressure which will also automatically contract the pelvic floor. Whilst fascial ligaments such as the uterosacrals, holding the anterior vaginal wall and apex in place and designed to limit the excursion of the pelvic organs during periods of increased force, will also be placed on tension and possibly disrupted. Biomechanical models suggest that such disruption can lead the urogenital hiatus being forced to open when exposed to any increase in the intra-abdominal pressure, and apical descent leading to prolapse.

This tense stiff floor has the potential to create a spiral of  2nd stage complications and injuries. For instance, not allowing flexion and internal rotation of the head which simulation shows will create a larger circumference with a corresponding increase in LAM stretch and thus trauma. Increased stiffness laterally with ER also offers an explanation for how striated muscle atrophy, owing to pudendal denervation is caused. Because the tunnel in the fascia of the obturator internus called Alcock’s canal where the pudendal nerve, artery, and vein pass through can theoretically get compressed by stiffness caused by ER. 

ER may also contribute to postpartum pelvic floor issues.  For instance, a stiffer pelvic floor may become a habit that continues after birth explaining the overactive pelvic floor commonly found postpartum,  which over time is known to contribute to pain, bladder symptoms, constipation, and pudendal nerve compromise.

This analytic evidence represents a major advance in understanding the injury mechanics of the pelvic floor during birth. Avoiding ER in the 2nd stage is a simple low-cost change to practice that can radically transform both clinical research and patient care. Further studies are needed to explore the effects of external hip rotation on the pelvic floor.