Childbirth Trauma 1st ed., 2017

12. Childbirth Trauma and Lower Gastrointestinal Tract Complications

Filippo La Torre Giuseppe Giuliani2 and Francesco Guerra2

(1)

Colorectal and Pelvic Surgery Unit, Emergency Department and Surgical Sciences Department, Policlinico Umberto 1°, “Sapienza” Rome University Hospital, Rome, Italy

(2)

Department of Surgery, Policlinico Umberto I, “Sapienza” University of Rome, Rome, Italy

Filippo La Torre

Email: filippo.latorre@uniroma1.it

Abstract

Pelvic floor and lower gastrointestinal tract complications as a consequence of vaginal childbirth are issues that have a great impact on women’s well-being. They are also of great social and economic importance, even if the role of childbirth on pelvic and anorectal disorders is still an area of debate. Levator ani and anal sphincter injuries are associated with several complications, and women seem to be only partially protected by caesarean section. Pelvic organ prolapse (POP) and fecal incontinence (FI) are clinical consequences of childbirth trauma. In postpartum women, the first-line approach with medical and behavioral treatments often proves ineffective in treating FI. Rehabilitative therapy and less invasive procedures are preferred before performing standard intervention, while invasive procedures are to be discouraged.

Keywords

Childbirth traumaFecal incontinenceLevator ani muscle injuryPelvic organ prolapseRehabilitative therapy

Introduction

Despite an increased use of caesarean section, often chosen as elective option with the intent of decreasing morbidity associated with vaginal delivery [12], the incidence of pelvic floor and lower gastrointestinal tract lesions as a result of vaginal childbirth remains an issue of great impact on women’s well-being as well as an issue of social and economic importance. The higher prevalence of morbid obesity in the female population and the higher age of primiparous females, especially in western countries, have led to an increase in complications associated with vaginal delivery.

In fact, the role of the main protagonist in the pathogenesis of anorectal and perineal lesions is attributed by some authors to pregnancy per se, rather than to the trauma sustained at the time of delivery. To date there is no consensus about the real risk of serious injury from trauma associated with vaginal delivery [35].

What are the traumatic effects to the pelvic floor, and particularly anorectum, during vaginal childbirth? Anorectal tract disorders will be discussed, focusing on anatomical defects, specifically muscular structures, describing pathophysiology and symptoms associated with them, addressing clinical and diagnostic evaluation and general principles of medical and surgical treatment.

Injuries affecting lower gastrointestinal function will be treated separately, primarily muscle injuries associated with pelvic floor and those associated with anal sphincteric apparatus.

Pelvic Floor Injuries

Pelvic floor muscles, which can be identified as the complex of the levator ani muscle (LAM), is shaped like a slingshot that starts from the lateral pelvic wall, envelops the distal gastrointestinal tract – the anorectal junction – and runs on the opposite side to fit on the contralateral pelvic wall. The levator hiatus, which includes the urethra anteriorly, the vagina in its central part, and the anorectum posteriorly, has a surface of about 5–40 cm when stimulated with straining. The risk of injury that can result from the passage of the fetus is particularly related to the passage of the head, which has an approximate area of 70–100 cm2 [6].

Numerous imaging studies have been conducted in this regard, often using MRI methods. The advent and spread of radiologic methods based on the use of 3D ultrasound allowed a much more detailed and dynamic study of the changes present in multiparous compared to nulliparous women [6]. In this regard, the size of the levator hiatus varies consistently if measured in nulliparous women, but prospective studies have demonstrated that the lesion of levator ani muscles is present in 13–36 % of women following vaginal delivery. It seems that the degree of muscle stretch varies widely in general population. Brooks and colleagues demonstrated that in passive muscles, individual strains of 50 % are necessary to produce significant lesions, while muscles in maximum activity exposed to a stretching of 30 % can be damaged, even if the degree of distension which can be considered maximal varies widely among individuals, according to MRI-based models. Lien and collaborators have shown that the largest tissue strain occurs in the medial component of the pubococcygeus muscle due to its small original length and for its location at the midline. Overall, there are differences in ability to be strained due mainly to changes in muscle length at maximum Valsalva maneuver and the intrinsic properties of muscle. Indeed, it has been assumed that the hormonal effects of pregnancy may affect the properties of levator ani muscles. In this regard, Balmforth and coworkers have explored the importance of connective tissue’s biochemical configuration, as an important factor in the development of pelvic organ prolapse (POP), stress incontinence, and normal progress of labor [712].

Even today, there are different definitions of LAM injury, based on clinical or imaging evaluations, by means of ultrasound or MRI assessment.

The definition of LAM injury according to Novellas and colleagues includes one of the following abnormalities: hypersignal muscle thickening or thinning, ruptured muscle’s insertion, and abnormality in the iliococcygeus muscle, which can unilaterally or bilaterally appear flat or concave. Regardless of the definition used, the prevalence of trauma affecting the LAM in parous women varies depending on the technique used from 13 to 36 % [81314]. Comparisons between different studies are often difficult, due to heterogenous patient selection or difference in obstetric practice. Certainly the lack of a universal definition of LAM injury remains the key issue on which a further clarification is strongly needed.

One of the main risk factors is forceps delivery: damage was demonstrated by means of ultrasound evaluation in 35–64 % of women after childbirth, with an odds ratio of 3.4–14.7. Anyway, it is not clear if the real injury is caused by the rapid passage of the head or by the type of forceps used [81517].

There is also evidence that a prolonged second stage of labor is associated with LAM injury, while ventouse delivery does not seem to increase the risk of LAM injury. Indeed, as stated by Kearney and coworkers, a second stage of labor longer than 78 min is associated with LAM injury. Furthermore Valsky revealed an OR of 2.3 when a second stage of labor was greater than 110 min [71819].

The age at first birth also appears to be a risk factor (RF). The greater the age at first delivery, the greater the probability of LAM injury, although this correlation was not found significant by all study groups. The role of body mass index (BMI) does not seem to be clear: Shek and Dietz found that women with low BMI had a higher risk of LAM injury, although the clinical significance is quite questionable. On the other hand, epidural anesthesia proved to have a protective effect against LAM injuries [8].

Concerning lower gastrointestinal tract, the major problems associated with damage to the pelvic floor can be traced to fecal incontinence and pelvic organ prolapse.

Bowel Disorders

As described by Sultan et al. [20], up to 13 % of primiparous will develop fecal incontinence mainly to flatus.

There seems to be a clear relationship between LAM injury and fecal incontinence (FI) in older women, highlighting the importance of the LAM in preserving anal continence. This was demonstrated in a study conducted by Weinstein, in which an US-detected abnormality of LAM was correlated with an increased risk of developing FI compared to controls. On the other hand, major LAM injuries are significantly more common in women with sphincter tears than in those who delivered vaginally without sphincter tears or by caesarean. One in five women with a sphincter tear had a major LAM injury on MRI in a study by Heilbrun and colleagues, who found no major LAM injuries in women who delivered by caesarean without labor [2122].

Although the probability to develop postpartum fecal incontinence is highest in women after a vaginal delivery, an elective caesarean is not completely protective against the development of fecal incontinence [23]. Postpartum fecal incontinence is more likely if birth follows a late stage of labor with an emergency caesarean section.

Other risk factors to the development of fecal incontinence seem to be epidural anesthesia prolonging the second stage of labor resulting in pudendal nerve injury by stretching and compression lesions; the use of episiotomy and of forceps in women with epidural anesthesia are other risk factors to the development of fecal incontinence [24].

If a clear relationship between childbirth and fecal incontinence is really consistent, the link of constipation to childbirth is not so clear. Parity in general has been considered a predisposing factor for the outlet-type constipation due to pelvic floor prolapse and particularly rectocele. Although these conditions are present among patients who suffer from constipation, a correlation between the severity of prolapse and the prevalence of constipation and other bowel dysfunctions has not been confirmed [25].

Pelvic Organ Prolapse (POP)

Parity increases the risk for both POP and surgery for POP. In a study of Samuelsson et al., 31 % of 487 Swedish women had some degree of POP on examination: parity and age increased the risk of POP, after adjusting for other variables.

In a study designed to determine risk factors for surgical interventions for POP in women less than 45 years of age, Rinne and coworkers demonstrated that women with POP had more deliveries and babies with higher birthweight than age-matched controls operated for benign ovarian tumors.

LAM injury increases the risk of POP. Avulsion of levator ani appears to double the risk of anterior and central compartment prolapse, with minor effect on prolapse of the posterior compartment, although a link between rectal intussusception and avulsion has been suggested. A direct correlation between the size of the defect and symptoms and/or signs of prolapse has been suggested, and women with a bilateral lesion are more likely to suffer from uterine prolapse.

However, it is unclear if all women with LAM injuries develop a prolapse: is it only a question of time? In a case control study including a group of 151 women with POP and 135 controls, DeLancey and colleagues found a significant OR of 7.3 for major LAM injuries but an equal number of minor defects. It was also demonstrated that, in women with major LAM defects, outcomes following surgical correction of POP appear to deteriorate in the short term and the risk of recurrence is increased [4152627].

Acute LAM injury can be clinically diagnosed at inspection and digital examination, when the levator ani avulsion is associated with a large vaginal laceration; also a chronic detachment from the lower aspect of the pubis can be clinically detected, with the finger positioned laterally and parallel to the urethra and pushed up to the bladder neck: in this way the insertion of the puborectalis muscle on the pubic bone can be palpated immediately lateral to the finger.

According to Laycock [28], a strong pubococcygeus muscle of a young woman can be palpated like an elastic band of about 1–2 cm. An avulsion defect is diagnosed if the lower aspect of the pubis feels free from the muscle when moving the finger sideways. Palpation should be performed at rest and during contraction, to identify the presence of small portions of muscle. Overall, clinical evaluation by different clinicians was proved to moderately correlate with LAM defects. On the contrary, it has been shown that US evaluation leads to highly reproducible findings among different operators. Avulsion is diagnosed if a discontinuation between hyperechogenic fibers of puborectalis muscle and pelvic wall is present, with the insertion being replaced by a hypoechoic area representing the vaginal wall [212935].

Injuries to Anal Sphincteric Apparatus

The damage caused to the anal sphincters is common but underdiagnosed at the time of delivery. Between one-third and two-thirds [36] of women who have a significant laceration recognized during childbirth will suffer from fecal incontinence. In those women who present with symptoms of anal incontinence which continue to exist postpartum or those in whom FI develops subsequently, the incidence of anal sphincter injury (both external and internal anal sphincter, or EAS and IAS) is high, although severity of symptoms does not strongly correlate with damage entity. Bidimensional endoanal ultrasound (EAUS)-based studies suggest that injury involving one or both anal sphincter muscles occurs in up to one-third of primiparous women [20], although the true incidence of injuries is probably closer to 11 % [37] (Fig. 12.1).

A308966_1_En_12_Fig1_HTML.gif

Fig. 12.1

EAUS of postpartum EAS lesion

On the other hand, many patients with significant defect at ultrasound may be clinically asymptomatic.

Afro-Caribbean women have a lower incidence of severe trauma at delivery than white European or Hispanic. Conversely, Asian women have an increased risk, which might be related to their relatively shorter stature [38]. Again, both obesity and high birthweight seem to increase the risk of perineal trauma [3940]. Furthermore, in women with a history of intermittent episodes of fecal incontinence after first delivery, there is an increased risk of overt fecal incontinence after subsequent delivery. In fact, in women with sphincter injury, the risk of further severe lesions is seven times greater compared to women with healthy muscles [36].

A persistent occipito-posterior position of fetal head is associated with higher risk of third- to fourth-degree anal sphincter injury. Instrument-assisted delivery, episiotomy, and conversion to caesarean section are often required in such cases. With occipito-posterior position, sphincter laceration occurs in 42 % of patients undergoing assisted deliveries with suction cup and in 52 % of those with forceps [36].

Likewise, the prolongation of the second stage of labor is associated with an increased risk operative vaginal delivery and anal sphincter injuries, with one-third of women who have a second stage of labor more than 4 h sustaining a third- or fourth-degree injury. Women encouraged to push immediately after full cervical dilatation have an increased risk of perineal trauma compared to those where pushing is delayed. Traditionally, it is taught that applying pressure against the perineum and the descent of the baby’s head during delivery reduce the incidence of perineal injury. According to other studies, using the “hand-poised” method of childbirth whereby the accoucheur avoids touching the perineum and verbally guides the parturient, with occasional gentle support of the head, severe anal sphincter injuries and the need of episiotomy seem to be reduced, although these findings failed to reach significance [4142].

The risk of fecal incontinence following a non-extended midline episiotomy is three times higher when compared with spontaneous laceration. Injuries are more significant in cases of midline than those of mediolateral episiotomies.

Forceps-assisted delivery is associated with symptoms of fecal incontinence in more than 59 % of women with an incidence varying from 13 to 83 % in different studies. The risk seems to increase with occipito-posterior presentation.

Vacuum extraction compared with forceps delivery is associated with a lower incidence of clinically significant anal and perineal trauma. Delivery by caesarean section appears to play a protective role against anal sphincter injury when carried out as elective procedure or in the early stage of labor. Conversely, pelvic floor does not seem to be fully protected by caesarean section, and abdominal delivery should be considered in women at risk of further trauma after precedent vaginal delivery resulting in anatomical defects, as well as in women with symptoms of fecal incontinence after previous vaginal birth [364347].

Diagnostic Aspects

Clinical Examination

The presence of pelvic floor or even perineal skin trauma should raise suspicion for injury to sphincters, immediately after childbirth.

For example, the presence of a large vaginal laceration after childbirth may be associated with acute LAM injuries [48]. A chronic detachment of LAM from the inferior ramus of the pubic bone can be diagnosed by vaginal examination. With the patient in lithotomy position, a finger is inserted 4 cm laterally and parallel to the urethra, with the fingertip at the level of the bladder neck. The puborectal muscle insertion to the pubic bone can be palpated lateral to the index finger about 2 cm proximal to the introitus and the pubococcygeus of a young women, and according to Laycock [17], it is felt like a 1- to 2-cm firm band. Hence a chronic detachment of LAM from the inferior ramus of the pubic bone is diagnosed when moving the finger laterally, whereby the inferior ramus appears free of muscle [4].

A rectal examination is necessary before any type of instrument assessment: low anal sphincter resting tone associated with a low pressure during the contraction raises the suspicion of anal sphincter injuries. It must be considered that significant injury of one or both sphincters may be evident in the absence of LAM injuries.

Imaging

Transanal bidimensional ultrasound is still the fastest method to study anal canal anatomy, although evaluating childbirth-related trauma provides discordant results according to the timing of investigation. An EAS or IAS is simple to recognize with endoanal ultrasound, a hyperechoic (EAS) or hypoechoic (IAS) ring.

As demonstrated by Santoro et al. with endovaginal ultrasound, it is possible to achieve good visualization of the LAM described as a hyperechoic sling lying posterior to the anorectum and attaching to the pubic bone, which resembles a “gothic arch” [4]; moreover with endovaginal ultrasound, LAM injuries can be diagnosed, with good to very good interobserver and interdisciplinary reliability [4950].

MRI is a second-line investigation that can be performed after an ultrasound assessment, if an ultrasound examination is inconclusive.

Functional Investigations

Functional tests remain useful after imaging evaluation to obtain clinically relevant information. The first, simple, and fast examination that must be performed is anorectal manometry that can measure resting and squeeze pressures and also anal canal length. Resting pressure is impaired if an IAS defect is present; a reduction of squeeze pressure is typical finding of EAS injury.

The use of an intrarectal balloon can also evaluate the rectal compliance, sensitivity, and the rectoanal inhibitory reflex.

Altered rectal sensitivity or anal incontinence is usually transient after childbirth, with anorectal manometry showing a reduction in both resting and squeezing pressure immediately after delivery; but clinical evidence is generally poor and when significant tends to spontaneously heal. It seems that this condition is due to traction pudendal neuropathy postpartum; but clinical symptoms usually recover in about 2 months in 60 % of women. Anal incontinence may persist when weakness of pelvic floor coexists, but not all studies confirm this [5155].

Another functional test is the pudendal nerve terminal motor latency testing (PNTML) that assesses the pudendal nerve function: although normal latencies do not exclude nerve damage, this examination is important before sphincter repair surgery because a prolonged value is a prognostic indicator of poor long-term functional success after surgery [56].

Finally there is no correlation between altered PNTML examination and presence of a sphincter defect [57].

Treatment

Pharmacological treatments are employed substantially in order to solidify the stool and prolong the intestinal transit. Constipating agents are indicated in most cases of postpartum women suffering from passive incontinence (leakage) or urgency with the intent of reducing the fecal mass and the frequency of bowel emptying. Reductions in episodes of fecal incontinence, fecal urgency, and loose stools have actually been demonstrated. Associated to clinical improvement, in patients treated with constipating agents, a reduction in weight and fecal content has been achieved. Loperamide is the most commonly used agent due to its minimal side effects and because of its greater efficacy compared to codeine and difenoxin associated with atropine. Agents promoting evacuation such as osmotic laxatives or glycerine suppositories can be adopted in cases of post-defecatory leakage or when overflow incontinence is present, often due to the presence of fecal impaction in chronically constipated individuals.

Rehabilitative therapy in the form of pelvic floor muscle training (PFMT) involves training on the right use of the pelvic floor muscles during contracting and straining, breathing, and changes in abdominal pressure, based on the use of electrostimulation and/or biofeedback. Biofeedback consists of exercises to strengthen anal sphincter and pelvic floor muscles, by improving rectal sensation and voluntary contraction of the EAS. Pelvic floor physiotherapy associated with changes in lifestyle is effective in treating patients suffering from fecal incontinence of different causes. In a study conducted by Norton and Kamm on 100 patients, it was demonstrated that a lesion of EAS alone does not seem to affect the efficacy of treatment with biofeedback, while a lesion of the IAS appears to decrease the effectiveness of the treatment. In a subsequent randomized controlled trial on 171 women conducted by Norton, in both patients with intact sphincter muscles and those with sphincter disruption, including women with childbirth trauma, effectiveness rate was comparable. However, there seems to be a direct relationship between the extent of the defect in the EAS and the effectiveness of the treatment [6869].

Normally only patients suffering from severe anal incontinence, in whom conservative treatment failed, require surgery. Anal sphincter injury repair can be performed at the time of childbirth or later. Delayed surgery is performed by colorectal surgeons. EAS repair may have a short-term effectiveness in up to 54 % of patients, but symptoms can worsen over time. Indeed at 3-month follow-up, a residual muscle defect at ultrasound is still detectable in more of 90 % of patients and between 30 and 61 % of patients present with fecal incontinence. Although at the short term sphincter repair seems to improve symptoms, with increased resting and squeezing manometric pressures, symptoms seem to deteriorate progressively. In fact, 10 years after surgery, only 20 % of patients remain continent to liquids and solids [36].

Other surgical procedures, such as graciloplasty, the implantation of an artificial anal sphincter (AAS), or prosthetic trans-obturator sling (TOT) (Fig. 12.2), are far more invasive and generally not recommended due to frequency and number of complications and low success rates [5859].

A308966_1_En_12_Fig2_HTML.gif

Fig. 12.2

(a) Anal sling: elastic structure that surrounds anorectal canal bilaterally fastened to obturator foramen. (b) Anal sling: the device patented in Italy, not on the market, includes the device and the hammockinstruments to implant the prosthesis formed by a central body in biological material and four ends in nonabsorbable material to “suspend” the rectum and reposition it in the anatomical position

Sacral nerve stimulation (SNS) and tibial nerve stimulation (TNS) improved stool continence in several studies. SNS consists of a direct electrical stimulation to sacral plexus by means of an inplanted electrode. TNS (Fig. 12.3) provides electrical stimulation with a needle electrode (percutaneous tibial nerve stimulation) or from two pad electrodes (transcutaneous tibial nerve stimulation) both inserted into the lower, inner aspect of the leg, slightly cephalad to the medial malleolus aiming to transmit stimulation through the tibial nerve to the sacral plexus. Both SNS and PTNS showed low rate of complications and morbidity. PTNS treatment has shown an efficacy in the short term of up to 83 % [60] and in the long term, 53 %, reported by La Portilla after 2 years without treatment [61]. While for TTNS there are no studies with long-term outcomes, in the short term the efficacy is up to 60 %; in patients treated with bilateral TTNS, the efficacy is 85 % [6263].

A308966_1_En_12_Fig3_HTML.gif

Fig. 12.3

PTNS device (Uroplasty®)

In a meta-analysis that examined 34 studies published between 2000 and 2008 and included 790 patients, of whom 665 received a SNS permanent implant, SNS is an effective treatment for patients with FI compared to conservative treatment. In a multicenter, prospective nonrandomized trial that evaluated SNS in patients with FI, 83 % of 106 patients had a 50 % improvement and 40 % became fully continent, maintaining the improvement for 3 years [6465].

According to Wexner et al, the presence of an IAS defect, compared with its absence, is statistically associated with a lower likelihood of SNS treatment success [65].

According to Tan et al, the most common complications related with permanent SNS implantation are pain o local disconfort (6%), infection (3%) or seroma (3%),lead displacement or breakag (4%) [64].

Use of perianally injected bulking agents (BA) is a minimally invasive method for treating fecal incontinence, especially useful in those patients with higher risk of comorbidity in whom an open surgical procedure should be avoided, such as postpartum females. The procedure involves injecting prosthetic or autologous fillers into the submucosal tissues of the anorectum increase their volume and coaptation, thus preventing from incontinence episodes. Numerous studies have reported favorable short-term results with injectable perianal bulking agents, but according to Guerra et al. in the long-term follow-up, bulking agents seem to lose effectiveness and the ultrasound assessment of bulking agents suggests they are absorbed almost completely with time and the implants are no longer effective in treating incontinence [6667].

References

1.

Fisk NM. Caesarean section for all patients? In: Ben-Rafael Z, Lobo R, Shoham Z, editors. Controversies in obstetrics, gynaecology and infertility. Bologna: Monduzzi Editore; 2002.

2.

Minkoff H, Chervenak FA. Elective primary cesarean delivery. [comment]. N Engl J Med. 2003;348:946–50.CrossRefPubMed

3.

Quigley MM. Impact of pregnancy and parturition on the anal sphincters and pelvic floor. Best Pract Res Clin Gastroenterol. 2007;21(5):879–91.CrossRefPubMed

4.

Schwertner-Tiepelmann N, Thakar R, Sultan H, Tunn R. Obstetric levator ani muscle injuries: current status. Ultrasound Obstet Gynecol. 2012;39:372–83.CrossRefPubMed

5.

Gregory WT, Nygaard I. Childbirth and pelvic floor disorders. Clin Obstet Gynecol. 2004;47(2):394–403.CrossRefPubMed

6.

Dietz HP, Schierlitz L. Pelvic floor trauma in childbirth – myth or reality? Aust N Z J Obstet Gynaecol. 2005;45:3–11.CrossRefPubMed

7.

Valsky DV, Lipschuetz M, Bord A, Eldar I, Messing B, Hochner-Celnikier D, et al. Fetal head circumference and length of second stage of labor are risk factors for levator ani muscle injury, diagnosed by 3-dimensional transperineal ultrasound in primiparous women. Am J Obstet Gynecol. 2009;201:91e1–7.CrossRef

8.

Shek KL, Dietz HP. Intrapartum risk factors for levator trauma. BJOG. 2010;117:1485–92.CrossRefPubMed

9.

Hoyte L, Damaser MS, Warfield SK, Chukkapalli G, Majumdar A, Choi DJ, et al. Quantity and distribution of levator ani stretch during simulated vaginal childbirth. Am J Obstet Gynecol. 2008;199(198):1–5.

10.

Brooks SV, Zerba E, Faulkner JA. Injury to muscle fibres after single stretches of passive and maximally stimulated muscles in mice. J Physiol. 1995;488:459–69.CrossRefPubMedPubMedCentral

11.

Lien KC, Mooney B, Delancey JO, Ashton-Miller JA. Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol. 2004;103:31–40.CrossRefPubMedPubMedCentral

12.

Balmforth J, Toozs-Hobson P, Cardozo L. Ask not what childbirth can do to your pelvic floor but what your pelvic floor can do in childbirth. Neurourol Urodyn. 2003;22:540–2.

13.

Blasi I, Fuchs I, D’Amico R, Vinci V, La Sala GB, Mazza V, Henrich W. Intrapartum translabial three-dimensional ultra- sound visualization of levator trauma. Ultrasound Obstet Gynecol. 2011;37:88–92.CrossRefPubMed

14.

Dietz HP, Steensma AB. The role of childbirth in the aetiology of rectocele. Br J Obstet Gynaecol. 2006;113:264–7.CrossRef

15.

Delancey J, Morgan DM, Fenner D, Kearney R, Guire K, Miller JM, et al. Comparison of levator ani muscle defects and function in women with and without pelvic organ prolapse. Obstet Gynecol. 2007;109:295–302.CrossRefPubMed

16.

Dietz HP, Kirby A. Modelling the likelihood of levator avulsion in a urogynaecological population. Aust N Z J Obstet Gynaecol. 2010;50:268–72.CrossRefPubMed

17.

Krofta L, Otcenasek M, Kasikova E, Feyereisl J. Pubococcygeus–puborectalis trauma after forceps delivery: evaluation of the levator ani muscle with 3D/4D ultrasound. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20:1175–81.CrossRefPubMed

18.

Novellas S, Chassang M, Verger S, Bafghi A, Bongain A, Chevallier P. Features of the levator ani muscle in the immediate postpartum following cesarean delivery. Int Urogynecol J. 2010;21:563–8.CrossRefPubMed

19.

Kearney R, Miller JM, Ashton-Miller JA, Delancey JO. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol. 2006;107:144–9.CrossRefPubMedPubMedCentral

20.

Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med. 1993;329:1905–11.CrossRefPubMed

21.

Heilbrun ME, Nygaard IE, Lockhart ME, Richter HE, Brown MB, Kenton KS, et al. Correlation between levator ani muscle injuries on magnetic resonance imaging and fecal incontinence, pelvic organ prolapse, and urinary incontinence in primiparous women. Am J Obstet Gynecol. 2010;202:488.e1–6.CrossRef

22.

Weinstein MM, Pretorius DH, Jung SA, Nager CW, Mittal RK. Transperineal three-dimensional ultrasound imaging for detection of anatomic defects in the anal sphincter complex muscles. Clin Gastroenterol Hepatol. 2009;7:205–11.CrossRefPubMed

23.

Borello-France D, Burgio KL, Richter HE, Zyczynski H, Fitzgerald MP, Whitehead W, et al. Fecal and urinary incontinence in primiparous women. Obstet Gynecol. 2006;108:863–72.CrossRefPubMed

24.

Fitzgerald MP, Weber AM, Howden N, Cundiff GW, Brown MB, Pelvic Floor Disorders Network. Risk factors for anal sphincter tear during vaginal delivery. Obstet Gynecol. 2007;109:29–34.CrossRefPubMed

25.

Weber AM, Walters MD, Ballard LA, Booher DL, Piedmonte MR. Posterior vaginal prolapse and bowel function. Am J Obstet Gynecol. 1998;179:1446–50.CrossRefPubMed

26.

Samuelsson EC, Victor FTA, Tibblin G, Svärdsudd KF. Signs of genital prolapse in a Swedish population of women 20–59 years of age and possible related factors. Am J Obstet Gynecol. 1999;180:299–305.CrossRefPubMed

27.

Rinne KM, Kirkinen PP. What predisposes young women to genital prolapse? Eur J Obstet Gynecol Reprod Biol. 1999;84:23–5.CrossRefPubMed

28.

Laycock J. Clinical evaluation of the pelvic floor. London: Springer; 1994.

29.

Model AN, Shek KL, Dietz HP. Levator defects are associated with prolapse after pelvic floor surgery. Eur J Obstet Gynecol Reprod Biol. 2010;153:220–3.CrossRefPubMed

30.

Dietz HP, Shek KL. Levator defects can be detected by 2d translabial ultrasound. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20:807–11.CrossRefPubMed

31.

Dietz HP, Abbu A, Shek KL. The levator–urethra gap measurement: a more objective means of determining levator avulsion? Ultrasound Obstet Gynecol. 2008;32:941–5.CrossRefPubMed

32.

Dietz HP. Repeatability of digital palpation for the detection of levator trauma. Int Urogynecol J Pelvic Floor Dysfunct. 2007;18:156.

33.

Dietz HP. Quantification of major morphological abnormalities of the levator ani. Ultrasound Obstet Gynecol. 2007;29:329–34.CrossRefPubMed

34.

Kearney R, Miller JM, Delancey JO. Interrater reliability and physical examination of the pubovisceral portion of the levator ani muscle, validity comparisons using mr imaging. Neurourol Urodyn. 2006;25:50–4.CrossRefPubMedPubMedCentral

35.

Fernandi M, Shek KL, Dietz HP. Diagnosis of levator avulsion injury: a comparison of three methods. Neurourol Urodyn. 2010;29:1019–20.

36.

Dudding TC, Vaizey CJ, Kamm MA. Obstetric anal sphincter. Injury Ann Surg. 2008;247:224–37.CrossRefPubMed

37.

Williams AB, Bartram CI, Halligan S, Spencer JA, Nicholls RJ, Kmiot WA. Anal sphincter damage after vaginal delivery using three-dimensional endosonography. Obstet Gynecol. 2001;97(5, Pt 1):770–5.PubMed

38.

Howard D, Davies PS, DeLancey JO, Small Y. Differences in perineal lacerations in black and white primiparas. Obstet Gynecol. 2000;96:622–4.PubMedPubMedCentral

39.

Kabiru W, Raynor BD. Obstetric outcomes associated with increase in BMI category during pregnancy. Am J Obstet Gynecol. 2004;191:928–32.CrossRefPubMed

40.

Castro LC, Avina RL. Maternal obesity and pregnancy outcomes. Curr Opin Obstet Gynecol. 2002;14:601–6.CrossRefPubMed

41.

Mayerhofer K, Bodner-Adler B, Bodner K, Rabl M, Kaider A, Wagenbichler P, et al. Traditional care of the perineum during birth. A prospective, randomized, multicenter study of 1,076 women. J Reprod Med. 2002;47:477–82.PubMed

42.

McCandlish R, Bowler U, van Asten H, Berridge G, Winter C, Sames L, et al. A randomised controlled trial of care of the perineum during second stage of normal labor. Br J Obstet Gynaecol. 1998;105:1262–72.CrossRefPubMed

43.

Nicholls CM, Nam M, Ramakrishnan V, Lamb EH, Currie N. Anal sphincter defects and bowel symptoms in women with and without recognized anal sphincter trauma. Am J Obstet Gynecol. 2006;194:1450–4.CrossRef

44.

Pinta TM, Kylanpaa ML, Salmi TK, Teramo KA, Luukkonen PS. Primary sphincter repair: are the results of the operation good enough? Dis Colon Rectum. 2004;47:18–23.CrossRefPubMed

45.

de Leeuw JW, de Wit C, Kuijken JP, Bruinse HW. Mediolateral episiotomy reduces the risk for anal sphincter injury during operative vaginal delivery. BJOG. 2008;115(1):104–8.CrossRefPubMed

46.

Coats PM, Chan KK, Wilkins M, Beard RJ. A comparison between midline and mediolateral episiotomies. BJOG. 1980;87:408–12.CrossRef

47.

Fitzpatrick M, Behan M, O’Connell PR, O’Herlihy C. A randomized clinical trial comparing primary overlap with approximation repair of third degree obstetric tears. Am J Obstet Gynecol. 2000;183:1220–4.CrossRefPubMed

48.

Dietz HP, Gillespie AV, Phadke P. Avulsion of the pubovisceral muscle associated with large vaginal tear after normal vaginal delivery at term. Aust N Z J Obstet Gynaecol. 2007;47:341–4.CrossRefPubMed

49.

Santoro GA, Wieczorek AP, Stankiewicz A, Wozniak MM, Bogusiewicz M, Rechberger T. High-resolution three-dimensional endovaginal ultrasonography in the assessment of pelvic floor anatomy: a preliminary study. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20:1213–22.CrossRefPubMed

50.

Santoro GA, Wieczorek AP, Shobeiri SA, Mueller ER, Pilat J, Stankiewicz A, Battistella G. Interobserver and interdisciplinary reproducibility of 3D endovaginal ultrasound assessment of pelvic floor anatomy. Int Urogynecol J. 2011;22:53–9.CrossRefPubMed

51.

Snooks SJ, Henry MM, Swash M. Fecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology. Br J Obstet Gynaecol. 1985;92:824–8.CrossRefPubMed

52.

Delancey JO, Kearney R, Chou Q, Speights S, Binno S. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol. 2003;101:46–53.PubMedPubMedCentral

53.

Zhuang RR, Song YF, Chen ZQ, Ma M, Huang HJ, Chen JH, et al. Levator avulsion using a tomographic ultrasound and magnetic resonance-based model. Am J Obstet Gynecol. 2011;205:232.e1–8.CrossRef

54.

Handa VL, Lockhart ME, Fielding JR, Bradley CS, Brubakery L, Cundiffy GW, et al. Racial differences in pelvic anatomy by magnetic resonance imaging. Obstet Gynecol. 2008;111:914–20.CrossRefPubMedPubMedCentral

55.

Dietz HP, Shek KL. Validity and reproducibility of the digital detection of levator trauma. Int Urogynecol J Pelvic Floor Dysfunct. 2008;19:1097–101.CrossRefPubMed

56.

Tetzschner T, Sorensen M, Rasmussen OO, Lose G, Christiansen J. Pudendal nerve damage increases the risk of fecal incontinence in women with anal sphincter rupture after childbirth. Acta Obstet Gynecol Scand. 1995;74:434–40.CrossRefPubMed

57.

Oberwalder M, Dinnewitzer A, Baig MK, Thaler K, Cotman K, Nogueras JJ, et al. The association between late-onset fecal incontinence and obstetric anal sphincter defects. Arch Surg. 2004;139:429–32.CrossRefPubMed

58.

O’Brien PE, Dixon JB, Skinner S, Laurie C, Khera A, Fonda D. A prospective, randomized, controlled clinical of placement of the artificial bowel sphincter (acticon neosphincter) for the control of fecal incontinence. Dis Colon Rectum. 2004;47:1852–60.CrossRefPubMed

59.

Altomare DF, Binda GA, Dodi G, La Torre F, Romano G, Rinaldi M, Melega E. Disappointing long-term results of the artificial anal sphincter for fecal incontinence. Br J Surg. 2004;91:1352–3.CrossRefPubMed

60.

Findlay JM, Yeung JMC, Robinson R, Greaves H, Maxwell-Armstrong C. Peripheral neuromodulation via posterior tibial nerve stimulation—a potential treatment for fecal incontinence? Ann R Coll Surg. 2010;92:385–90.CrossRef

61.

de la Portilla F, Laporte M, Maestre MV, Dıaz-Pavon JM, Gollonet JL, Palacios C. Percutaneous neuromodulation of the posterior tibial nerve for the treatment of fecal incontinence – mid-term results: is retreatment required? Colorectal Dis. 2013;16:304–10.CrossRef

62.

Queralto M, Portier G, Cabarrot PH, Bonnaud G, Chotard JP, Nadrigny M, et al. Preliminary results of peripheral transcutaneous neuromodulation in the treatment of idiopathic fecal incontinence. Int J Colorectal Dis. 2006;21:670–2.CrossRefPubMed

63.

Thomas GP, Dudding TC, Nicholls RJ, Vaizey CJ. Bilateral transcutaneous posterior tibial nerve stimulation for the treatment of fecal incontinence. Dis Colon Rectum. 2013;56:1075–9.CrossRefPubMed

64.

Tan E, Ngo NT, Darzi A, Shenouda M, Tekkis PP. Meta-analysis: sacral nerve stimulation versus conservative therapy in the treatment of fecal incontinence. Int J Colorectal Dis. 2011;26:275–94.CrossRefPubMed

65.

Wexner SD, Coller JA, Devroede G, Hull T, McCallum R, Chan M, et al. Sacral nerve stimulation for fecal incontinence: results of a 120-patient prospective multicenter study. Ann Surg. 2010;251:441–9.CrossRefPubMed

66.

Maeda Y, Vaizey CJ, Kamm MA. Long-term results of perianal silicone injection for fecal incontinence. Colorectal Dis. 2006;9:357–36.CrossRef

67.

Guerra F, La Torre M, Giuliani G, Coletta D, Amore Bonapasta S, Velluti F, La Torre F. Long-term evaluation of bulking agents for the treatment of fecal incontinence: clinical outcomes and ultrasound evidence. Tech Coloproctol. 2015;19(1):23–7. Epub 2014 Nov 9.CrossRefPubMed

68.

Norton C, Kamm MA. Outcome of biofeedback for fecal incontinence. Br J Surg. 1999;86:1159–63.CrossRefPubMed

69.

Norton C, Chelvanayagam S, Wilson-Barnett J, Redfern S, Kamm MA. Randomized controlled trial of biofeedback for fecal incontinence. Gastroenterology. 2003;125(5):1320–9.CrossRefPubMed



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