Stergios K Doumouchtsis (ed.)Childbirth Trauma10.1007/978-1-4471-6711-2_3

3. Epidemiology of Childbirth Trauma and Associated Pelvic Floor Disorders

Lieschen H. Quiroz¹ and S. Abbas Shobeiri²

(1)

Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences, 910 Stanton L. Young Blvd, WP 2430, Oklahoma City, OK 73034, USA

(2)

Gynecologic subspecialties, Inova Fairfax Hospital, 3300 Gallows Rd. Fairfax, VA 22042, USA

Lieschen H. Quiroz

Email: Lieschen-Quiroz@ouhsc.edu

S. Abbas ShobeiriProfessor and Vice Chairman (Corresponding author)

Email: Abbas.Shobeiri@inova.org

Abstract

Pelvic floor disorders such as urinary incontinence, pelvic organ prolapse and anal incontinence affect women of all ages and are strongly associated with a significant economic burden and detriment to a woman’s quality of life. Clinical and epidemiologic findings indicate that women who undergo vaginal childbirth are at an increased risk of developing pelvic floor disorders. Trauma to the pelvic floor in the process of vaginal childbirth is common, yet symptomatic development of pelvic floor disorders is difficult to predict. Imaging modalities have provided further information as to the mechanism of pelvic floor trauma, yet the effects of mode of delivery and other modifiable risk factors to implement secondary prevention methods need further investigation.

Keywords

Pelvic organ prolapseLevator ani traumaUrinary incontinenceVaginal deliveryAnal incontinenceChildbirth traumaPelvic floor disorders

Introduction

Pelvic floor disorders include urinary incontinence, pelvic organ prolapse and fecal incontinence. Pelvic floor disorders affect 24 % of US females [1]. In addition to having a strong association with aging, pelvic floor disorders are more prevalent in women who have delivered at least one child, and it is known that pelvic floor trauma commonly occurs at the time of the first vaginal delivery [2–5]. The continuing rising trend towards elective cesarean section [6] is due in part to a growing awareness of the potential deleterious effects of vaginal childbirth and future repercussions on the pelvic floor. Both patients and their doctors increasingly opt for cesarean delivery without maternal or neonatal indications, in part to avoid future morbidity such as urinary incontinence, pelvic organ prolapse or fecal incontinence, all of which have been associated with vaginal childbirth in epidemiologic studies [7, 8]. In addition, women may be at increased disposition to pelvic floor trauma due to inherent weakness in the collagen within the pelvic floor structures [9, 10].

Traditionally, this trauma was thought to involve the anal sphincter complex and the perineal body. Recently, there have been advances in imaging in the form of magnetic resonance imaging (MRI) and three-dimensional (3D) ultrasound, and the role of the levator ani muscle (LAM) as an important component of pelvic floor trauma has become evident. We currently have a better understanding that about 50 % of all women after vaginal delivery have a significant alteration of the pelvic floor anatomy affecting the levator ani muscle [2].

The Pelvic Floor in Childbirth: Risk Factors and Mechanisms

The levator ani muscle plays a major role in childbirth as it is the most substantial soft tissue structure defining the dimensions and biomechanical properties of the birth canal [11]. At the time of vaginal delivery, the birth canal undergoes substantial distension, varying between individuals by at least a factor of 5 [12, 13]. According to research on muscle physiology, skeletal muscle will not stretch to more than twice its length without some structural or macroscopic trauma [14]. Skeletal muscle studies have shown that in passive muscles, a stretch of 50 % is necessary to cause significant injury, whereas in maximally activated muscles a stretch of 30 % results in injury [14]. This finding may explain the suggested protective effects of epidural anesthesia from developing a LAM injury [2].

The association between vaginal parity and POP has been known to have a non-linear effect, with the first vaginal delivery having its greatest impact as a risk factor for POP [15–19]. Several obstetrical factors have been associated with levator muscle injury after vaginal birth [2, 3, 20, 21]. Results from a small study by Miller et al. reported MRI findings of LA injury in 19 high risk postpartum women, showing 47 % to have LAM injury. However, current experience comes from small studies, or case control data with limitations in clinical application. Based on recent literature, women at highest risk for LAM injury have exposure to risk factors such as perineal injuries, prolonged second stage of labor, instrumented delivery, and fetal head circumference >35.5 cm. Although these individual risk factors may be associated with LAM injury, little is known about the combination of factors, which increase the risk of LAM injury. While 10–30 % of women will undergo macroscopic LAM trauma, there is an even greater number that will undergo microtrauma, or irreversible distension of the levator hiatus [2–5]. Obstetric predictors of microtrauma may differ from those of levator “avulsion,” which is the traumatic dislodgement of the LAM from its bony insertion.

The pelvic floor is a complex three-dimensional structure, with a variety of functional and anatomical areas. It consists of a musculotendinous sheet that spans the pelvic outlet and consists of paired levator ani muscle (LAM). It is broadly accepted that the LAM consists of subdivisions that have been characterized according the origin and insertion points, consisting of the pubococcygeal, puborectal and iliococcygeus portions [22]. The levator ani is further divided into the puboperinealis, pubovaginalis and puboanalis, according to its relationship to the surrounding viscera [22]. Lateral to the LAM is the puborectal division, which forms a sling around and behind the rectum, just cephalad to the external anal sphincter. Lastly, the iliococcygeus division forms a flat, horizontal shelf, spanning both pelvic side walls [23]. Recently, the use of 3D EVUS has been validated to visualize LAM subdivisions previously characterized by MRI studies [24]. These subdivisions were localized in cadaveric dissections, then correlated with images seen in nulliparous women, based on origin and insertion points and were shown to have excellent inter-observer reliability.

The pelvic floor muscles have the unique role of supporting the urogenital organs and the anorectum. Unlike most other skeletal muscles, the LAM maintains constant tone, except during voiding, defecation and a valsalva maneuver [25]. At rest, the LAM keeps the urogenital hiatus closed, by compressing the vagina, urethra and rectum against the pubic bone, and maintains the pelvic floor and pelvic organs in a cephalad direction [23]. Pelvic floor muscles are integral to pelvic organ support, and while functioning properly, provide support to the pelvic organs, keeping the ligament and fascial attachments tension-free.

Consequences of Levator Ani Trauma: The Implications of Childbirth

During parturition, the LAM stretches beyond its limits [12, 26] in order to allow passage of a term infant. Studies have shown that LAM injuries occur in 13–36 % of women who deliver vaginally [3, 27, 28]. There are various definitions of levator ani injury, according to mode of assessment and imaging modality. Assessment of the levator muscles is essential for a complete understanding of pelvic floor anatomy abnormalities, as well as of pelvic floor dysfunction.

Given that skeletal muscle will not stretch to more than twice its length without tearing [14], it is surprising that more women do not sustain LAM injuries. The degree of distension as well as the point of maximum strain of the tissue varies based on MRI-based models [12, 29].

There are numerous definitions of LAM injury depending on the mode of assessment, namely clinical palpation, ultrasonography, or MRI. It is widely believed that nulliparous women do not suffer from LAM injuries [30].

Childbirth and Prolapse

Pelvic organ prolapse is defined as descent of the uterus and vaginal walls into the vaginal canal. Most women have at least some degree of prolapse. Objective prolapse severity is weakly correlated with symptom burden [31–33]. The general trend in clinical studies is that prolapse becomes symptomatic when it descends beyond the hymen, and therefore the hymen represents a clinically significant threshold [33–35]. Women with symptomatic prolapse may experience a high degree of bother and substantial negative impact on physical function and quality of life [36]. Additionally, the public health impact of prolapse is substantial with respect to the incidence of surgery: the lifetime incidence of surgically managed pelvic organ prolapse is as high as 19 %, which is higher than previously estimated [37].

The research on the epidemiology of prolapse has been limited. The gold standard for “evidence-based medicine” is the randomized trial, but the ability to perform a randomized trial in this area is hampered by the long follow-up needed, since there is an inherent latency between obstetric exposures and clinically significant symptom development. As such, most studies have used surrogate markers for prolapse symptoms [38, 39] or surgical management [40, 41]. These surrogate measures may not be reliable and can lead to bias in the estimation of prevalence [19].

More recently, studies using a quantitative or graded approach to measuring prolapse suggest that prolapse is more common among parous compared to nulliparous women [42]. In addition, vaginal childbirth, particularly operative vaginal delivery, has been shown to increase the risk of pelvic organ descent to or beyond the hymen [19, 43]. As early as 6 months postpartum, stage 2 pelvic organ prolapse was noted in 18 % of primiparous spanish women delivered vaginally compared to 7 % of women who delivered by cesarean [44]. Similar findings were shown in a multicenter study from the United States [45]. Current evidence supports that the mode of delivery is a more critical component, rather than the process of labor itself. As such, no difference was seen in prevalence of prolapse in women who delivered by unlabored cesarean, compared to women who delivered by cesarean after active labor and complete cervical dilation [19].

Recently, the role of episiotomy and the development of pelvic organ prolapse have come into question. Episiotomy was first recommended in the 1930s as a means of preventing obstetric lacerations, and many argued that by protecting the mother’s perineum this would result in better, pelvic organ support [46]. In 2005, a systematic review observed that the evidence does not support routine episiotomy as means of providing maternal benefit, and the role of episiotomy as it impacts the development of pelvic organ prolapse remains unknown [47].

The potential for an association between spontaneous lacerations and prolapse is suggested by recent literature involving vaginally parous women 5–10 years after delivery. This study found that women who had more than one spontaneous laceration were more likely to have prolapse to or beyond the hymen [43]. In addition, no increase in pelvic organ prolapse was observed in association with episiotomy. Interestingly, there are recent data suggesting an association between mediolateral episiotomy as a protective factor against developing central support defects of the anterior vaginal wall, which is the most common site of prolapse [48]. The question of episiotomy vs spontaneous lacerations remains, with respect to the risk of prolapse; there is a clear need for future research in this area.

Childbirth and Urinary Incontinence

It is general assumption that urinary incontinence is a sign of a weak pelvic floor, but this assumption is not evidence-based.

Viktrup et al. interviewed 305 primiparous women and found that 39 % had stress incontinence before, during or after pregnancy, and 7 % developed de novo stress incontinence after delivery [10]. In a follow up of this cohort, up to 30 % reported stress incontinence 5 years later. Those without symptoms of urinary incontinence after their first delivery had an incidence of 19 % as compared with 92 % in those who had symptoms at 3 months postpartum [49]. In another prospective study of 949 women, urinary incontinence was experienced by 22 % of women before pregnancy, 65 % during the third trimester and 31 % after delivery [50]. New onset of urinary incontinence was found to be more common in parous as compared with nulliparous women. Even among those having cesarean section, postpartum urinary incontinence was independently associated with incontinence prior to and during pregnancy. Current evidence highlights the high proportion of women who suffer from urinary incontinence and confirm previous observations that prepregnancy and antenatal urinary incontinence increases the risk of future urinary incontinence [51].

There is conflict in the evidence regarding the relative contribution of different obstetric factors in the development of urinary incontinence. It is not clear whether it is pregnancy or the delivery itself, the major contributor to new onset urinary incontinence. Obstetric factors that have been investigated include the duration of the second stage of labor and birthweight [52]. Other investigators have not found a significant correlation between stress incontinence and fetal head circumference [53, 54], second stage of labor [50, 54], or birth weight [53, 55, 56]. In the largest community-based epidemiologic study of incontinence, involving 15,307 participants, (EPICONT study) women who were younger than 65 years, had not delivered or had cesareans or vaginal deliveries only reported that the prevalence of any urinary incontinence was 10 % in the nulliparous group [57]. There was a prevalence of 16 % in the cesarean group, and a prevalence of 21 % in the vaginal delivery group. This implies that pregnancy itself, rather than the process of delivery may also be an important causal factor in the development of urinary incontinence.

Urinary urgency or overactive bladder is reported by 27–45 % of women above the age of 40 [58]. In comparison to other pelvic floor disorders, the association between overactive bladder and vaginal childbirth has not been well established. For instance, it is not completely clear whether overactive bladder is associated with greater parity since urgency incontinence is reported by similar proportion of both, women who delivered vaginally and nulliparous women [57]. It is also unclear whether overactive bladder is associated more with vaginal versus cesarean birth. For example, the odds of overactive bladder in women 5–10 years after childbirth do not appear to significantly differ in women after a vaginal versus cesarean birth [19]. Interestingly, operative vaginal birth, particularly forceps, may be associated with overactive bladder [19, 43].

Childbirth and Fecal Incontinence

Trauma and laceration of the anal sphincter complicates 2–16 % of vaginal deliveries [59, 60]. Injury to the anal sphincter complex, even those without recognition or repair, contributes to the development of anal incontinence. Several studies have demonstrated significant short-term risk of anal incontinence after exposure to anal sphincter laceration after vaginal childbirth [61, 62]. The prevalence of postnatal fecal incontinence symptoms was reported by a postal questionnaire by 906 women 10 months after delivery to be 4 %. Flatal incontinence was more commonly reported in about 29 % of women at 9 months after delivery in a study of 349 primiparous women [63]. Fecal incontinence is especially common after anal sphincter disruption, with a reported prevalence of 16–47 % [64–67].

Injury to the anal sphincter complex during childbirth is likely due to both, mechanical trauma and denervation injury. The latter injury may occur from traction and straining during the expulsive efforts associated with vaginal childbirth, similar to the mechanisms of nerve damage reported in patients with chronic constipation, which may result in anal incontinence [68]. The presence of neuropathy has been observed to be associated to the length of the second stage of labor, size of baby and instrumental delivery [69]. In studies involving 5 years of follow-up Snooks et al. observed that pudendal nerve terminal motor latencies (PNTML) as measures at the external sphincter were increased after childbirth [69, 70], indicating pudendal nerve damage. As compared to controls, PNTML was increased from 1.9 ms in control subjects to 2.2 ms in normal vaginal delivery and 2.4 ms in forceps delivery. Cesarean delivery appeared protective from such changes.

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