Impact of pregnancy and parturition on the anal sphincters and pelvic floor

Best Practice & Research Clinical Gastroenterology Vol. 21, No. 5, pp. 879–891, 2007 doi:10.1016/j.bpg.2007.06.001 available online at http://www.sciencedirect.com

8 Impact of pregnancy and parturition on the anal sphincters and pelvic floor Eamonn M.M. Quigley *

MD, FRCP, FACP, FACG, FRCPI

Professor Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland

Incontinence and defecatory difficulties are commonly reported among women and are often ascribed to traumas sustained during childbirth. Specifically, injuries to the anal sphincters (tears) and conformational changes in the various structures that comprise the pelvic floor (prolapse and perineal descent) have been considered as important contributors to the development of anal incontinence, or difficult defaecation (straining, incomplete evacuation), in later life. An understanding of both the effects of pregnancy and parturition on these structures and the natural history of any traumas sustained are, therefore, of key importance. Unfortunately, the literature on these issues, though vast, is far from complete. While it is evident that pregnancy, per se, imposes changes, primarily through hormonal influences, on colonic, ano-rectal and pelvic floor physiology, the long-term impact of such effects is far from clear. Risk factors for the occurrence of significant, though often occult, anal sphincter injuries during birth have been identified and the role of these tears in the etiology of post-partum incontinence has been well delineated. In contrast, the contribution of such intra-partum events to the later onset of incontinence is far from clear and may well have been over-estimated. Key words: pelvic floor; anal sphincters; constipation; parturition; pregnancy; faecal incontinence; anal incontinence; defaecatory difficulty.

BASIC PHYSIOLOGY OF THE ANAL SPHINCTERS AND PELVIC FLOOR: IMPACT OF PREGNANCY The pelvic floor refers to all of the structures supporting the abdominal wall and pelvic cavity and, in the female, includes those organs and tissues that are contained between the perineum and the vulvar skin: * Corresponding author: Department of Medicine, Clinical Sciences Building, Cork University Hospital, Cork, Ireland. E-mail address: [email protected] 1521-6918/$ - see front matter ª 2007 Elsevier Ltd. All rights reserved.

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the peritoneum; the pelvic viscera and endopelvic fascia; the perineal membrane; the levator ani muscles [comprising the pubovisceral (which, in turn, is composed of puborectalis and pubococcygeus portions) and the iliococcygeus muscles], and;  the external genital muscles. Support for the pelvic floor comes from its connections to the bony pelvis and its attached muscles. In the female, the pelvic floor is conveniently divided into anterior and posterior components by the genital tract, injury to the anterior pelvic floor resulting primarily in urinary incontinence and to the posterior floor in problems with anal continence and the act of defaecation.1 In their primary functions of facilitating and controlling defaecation and maintaining continence, the pelvic floor, the intrinsic neuromuscular apparatus of the colon and rectum and the anal sphincters act in a highly coordinated and integrated manner. This integration is illustrated by even a cursory examination of the anatomy of the region: 1. the internal anal sphincter and its innervation represent an extension of the circular muscle layer and the enteric nervous system of the rectum; 2. the external anal sphincter muscle is intimately associated with the muscles of the pelvic floor, such as the pubo-rectalis; 3. fibres of important pelvic floor muscles, such as the puborectalis, interdigitate with the longitudinal muscle layer of the rectum and anal canal. These interrelationships, which extend to the neural control of these muscle groups, are critical to the coordination of a process as complex as defaecation, which includes the following steps: 1. transfer of stool to the rectum, through the propulsive forces generated by giant migrating contractions in the colon;2 2. sensing of the arrival of stool in the rectum with activation of the recto-anal inhibitory and sampling reflexes which allow stool to enter the anal canal and to be distinguished from flatus; 3. a voluntary decision to proceed, and, finally; 4. the act of defaecation itself which involves the integrated, and appropriately timed, actions of the:  pelvic floor musculature, and the puborectalis, in particular, which relaxes to straighten out the anal canal and facilitate defaecation (Figures 1 and 2);  external sphincter, which relaxes;  internal sphincter, which relaxes;  diaphragm and abdominal wall muscles, which contract, increase intra-abdominal pressure and generate the pressure gradient between the rectum and anal canal that propels stool out of the body. The maintenance of continence is a similarly complex and coordinated process involving: 1. the anal canal high pressure zone which is, in turn, generated by the internal and external anal sphincters, the latter being intimately related to the musculature of the pelvic floor;

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Contracted Puborectalis Increases Ano-Rectal Angle

Relaxed Puborectalis Decreases Ano-Rectal Angle Figure 1. The role of the pelvic floor in the maintenance of continence and the facilitation of defaecation. Diagrammatic representation of the manner in which the puborectalis muscle influences continence (when contracted) and defaecation (when relaxed), through its effects on the ano-rectal angle.

2. the pelvic floor; contraction of the puborectalis, for example, increases the ano-rectal angle and promotes the retention of stool in the rectum (Figure 2), and; 3. ano-rectal sensation and reflexes. One can appreciate how susceptible many of these parameters may be to alteration and injury during pregnancy and parturition and also the difficulties that may be

Figure 2. Frames from a normal defaecography study. At rest, the ano-rectal angle is maintained and facilitates continence. Voluntary contraction of the pelvic floor (and puborectalis muscle, in particular) accentuates the ano-rectal angle and promotes stool retention. On straining, the ano-rectal angle straightens out and defaecation is facilitated.

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encountered in determining the precise pathophysiology of incontinence or constipation in a particular instance. BOWEL FUNCTION DURING PREGNANCY Constipation Constipation is common during pregnancy and has several potential causes, as listed in Table 1.3 Hormonal effects, such as those related to the effects of progesterone and other hormones on gastrointestinal smooth muscle as well as on the musculature and supportive tissues of the pelvic floor, have traditionally been invoked to explain the occurrence of constipation (presumably of slow-transit type) during the first and second trimesters, while ‘mechanical’ effects of the gravid uterus on the pelvic floor, diaphragm and abdominal muscles have been reported to lead to difficult defaecation in the last trimester. It is worth noting that while the effects of various sex hormones on intestinal muscle have been well characterised in vitro, there is scant consensus on the impact of these same hormones on gut motor function in vivo, under physiological conditions. It must be cautioned that there have been few investigations of the mechanisms of constipation in pregnancy and the above-described classification of etiology by trimester is, indeed, scarcely supported by data. In one prospective study, for example, while constipation was more common at 12 than at 36 weeks (8.9 vs 4.5%), symptoms suggestive of difficult defaecation (painful defaecation, sensation of anal blockage, feeling of incomplete evacuation) were, contrary to expectations, equally common at 12 and 36 weeks.4 All bowel symptoms, with the exception of a feeling of incomplete evacuation, were less prevalent 12 months postpartum than at any stage during pregnancy.4 These findings were recently, and, for the most part, confirmed by Derbyshire and colleagues who found that the prevalence of both straining (21–39%) and incomplete evacuation (12.5–22%) was high in all trimesters, with the prevalence of incomplete evacuation and the time to complete the act of defaecation falling dramatically when evaluated six weeks post-partum.5 In the latter study, indeed, the prevalence of incomplete evacuation was, if anything, highest in the first trimester. Taken together, these studies speak against the ‘mechanical’ hypothesis and suggest that changes in bowel function during pregnancy are more likely explained by a hormonal effect which is sustained throughout pregnancy, or by the impact of pre-existing bowel dysfunction.6 While progesterone would be

Table 1. Causes of constipation in pregnancy. 1. Hormonal 2. Mechanical 3. Iatrogenic: a. Medications 4. Multiparity 5. Pre-existing disease: a. Chronic slow-transit constipation b. Irritable bowel syndrome c. Congenital or acquired megacolon d. Chronic idiopathic intestinal pseudo-obstruction

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regarded as a leading candidate hormone in this regard,6 studies of the effects of progesterone (in doses which simulated levels that would occur during the luteal phase of the menstrual cycle) on gastrointestinal transit demonstrated quite clearly, if surprisingly, that this hormone accelerated, rather than delayed, colonic emptying.7 A lack of responsiveness to progesterone has, indeed, been suggested as playing a role in the pathogenesis of slow transit constipation.8 Use of oral iron supplements has, traditionally, been blamed for the occurrence of constipation in pregnancy; the failure of Milman and colleagues to demonstrate any effect of increasing doses of oral iron on gastrointestinal symptoms (including constipation) questions this assumption.9 There have been few controlled trials of any intervention to alleviate constipation during pregnancy. Jewell and Young, in their 2001 Cochrane review, could identify only two trials which they considered of sufficient merit and concluded that management should commence with a high fibre diet or fibre supplements and proceed to osmotic laxatives if the former approach fails.10 The use of fibre supplements11 and poly-ethylene glycol-based laxatives12 have been further supported by other clinical trials. In choosing further interventions, the clinician needs to be mindful of the classification of the drug in relation to use in pregnancy and any risk of precipitating premature labour. Impact of pregnancy on irritable bowel syndrome (IBS) and motility disorders Irritable bowel syndrome (IBS) is one of the most common of all medical disorders, whether surveyed in the community, in a primary care practice or at a specialist gastroenterology referral centre.13 Its prevalence has long been appreciated in the West; evidence now accumulates to indicate that IBS is also highly prevalent in the East and even in developing nations. Though the vast majority of IBS sufferers in the community do not seek medical attention and either attempt to ignore their symptoms or self-medicate, the minority who do seek medical attention may suffer significant impairments in quality of life and consume considerable health care resources and costs. For these individuals, treatment is often challenging. IBS is predominantly a disorder of females and young-to-middle aged females, in particular; it should come as no surprise, therefore, that many IBS sufferers become pregnant. Clinically, IBS is defined on the basis of a combination of abdominal pain or discomfort and altered or disturbed bowel function but may also feature bloating, distension, tiredness and a host of related nongastrointestinal symptoms.14 While many women with IBS describe fluctuations in symptom severity and type in relation to the phase of the menstrual cycle, a careful comparison of both gastrointestinal and gynecological symptoms over the various phases of the cycle between IBS and normal age-matched women failed to reveal any significant differences between the two groups; while the IBS subjects certainly had more symptoms and more severe symptoms at all times, the pattern of symptom flux and variation throughout the cycle was identical to that of those who did not have IBS.15 Interestingly, in this same study it was observed that oral contraceptive use was associated with less severe symptoms among IBS patients throughout the menstrual cycle.15 In contrast to the plethora of studies relating IBS to the menstrual cycle, there is little or no information on the behaviour of IBS during pregnancy. On an anecdotal basis, I have cared for several women whose IBS appeared to remit during pregnancy, only to relapse shortly thereafter. Pregnancy may also exacerbate the course of pre-existing colonic and intestinal motor disorders, such as idiopathic megarectum and megacolon, Hirschsprung’s

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disease and pseudo-obstruction. A case describing the successful management of megarectum associated with severe constipation by the use of large volumes of a polyethylene glycol solution, has been reported.16 INCONTINENCE DURING PREGNANCY While faecal incontinence is, typically, regarded, first and foremost, as a complication of child birth, incontinence has also been reported during pregnancy, per se. In their prospective study, van Brummen and colleagues found that 3–9% of their cohort of 487 women reported faecal incontinence by the 12th week of their first pregnancy; 3% reported incontinence at 36 weeks gestation.4 OTHER ANORECTAL PROBLEMS Haemorrhoids Several factors conspire to render haemorrhoids more common during pregnancy, including, the effects of circulating progesterone on the vasculature, pressure on the superior rectal veins by the gravid uterus and increased circulating volume. Large haemorrhoids can affect anal sphincter function by generating a non-relaxing high-pressure zone at the site of the engorged venous cushions; sphincter function per se is unaffected.17 While a conservative approach to the management of haemorrhoids is traditionally advocated during pregnancy; here, as in so many other areas in relation to medical problems in pregnancy, there is little evidence base.18 Prolapse and or thrombosis of haemorrhoids may prove painful and, thereby, exacerbate constipation. Thrombosed haemorrhoids were described among 13 of 165 consecutive pregnant females during the third trimester in one study19 and in 33 of the same population within two months of delivery. Difficult defaecation and late or traumatic delivery were the most important risk factors for thrombosed haemorrhoids. Fissures In the abovementioned study by Abrahamovitz and colleagues, two instances of anal fissure were detected during the last trimester of pregnancy and 25 instances postpartum; here again, difficult defaecation was the main risk factor.19 Whereas the vast majority of instances of thrombosed haemorrhoids were detected in the immediate post-partum period, fissures tended to be equally common throughout the two months of post-partum observation. Pain related to fissures will exacerbate constipation and further promote fissure formation. The primary goal in management, accordingly, is to prevent and alleviate constipation. POST-PARTUM PROBLEMS Incontinence Pregnancy and parturition, in particular, have long been regarded as major risk factors for the development of urinary and anal (incorporating incontinence for flatus, stool or both) incontinence. Two principal intra-partum events have been traditionally invoked to explain the development of faecal incontinence (to stool, flatus or both)

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post-partum: direct injury to the anal sphincter and traction neuropathy of the pudendal nerve. The former was thought to be most relevant to the development of incontinence in primiparous, the latter in multiparous females. A careful review of the literature indicates that the relationships between pregnancy, parturition and anal incontinence are far more complex. At the outset, one needs to clearly differentiate between the development of faecal incontinence in the immediate aftermath of childbirth, on the one hand, and attempts to relate past obstetric history to the occurrence of faecal incontinence in later life. Post-partum incontinence Turning firstly to the new onset of incontinence, it is abundantly clear that there is an increased prevalence of anal and faecal incontinence following delivery. Data from a large number of studies indicate that between 3 and 4% of women will report new symptoms related to altered anal continence following pregnancy. That this problem may be under-appreciated is emphasised by the finding, in one study, that only 14% of symptomatic women sought medical attention.20 Table 2 summarises the principal risk factors for the development of faecal incontinence in the post-partum period.21–26 While an elective caesarean section is not completely protective against the subsequent development of faecal incontinence,23 it is clear that the risk for this complication is highest following a vaginal delivery; altered faecal continence being reported in as many as 25% of primiparous women at six weeks post-partum.24 In contrast to the possible, though disputed, protective effects of an elective caesarean section, an emergency section, performed in a late stage of labour increases risk. By prolonging the second stage of labour, epidural anesthesia may predispose to pudendal nerve compression and traction injury; the increased use of forceps and episiotomy among women who have received an epidural may also be relevant to the increased prevalence of incontinence noted among those who have received an epidural. Anal sphincter injury Damage to the anal sphincters at the time of delivery looms large in the etiology of faecal incontinence. Studies which have objectively assessed the integrity of the anal sphincters post-partum have revealed a high prevalence of anal sphincter defects; as high as 35–41% when assessed between five and six weeks post partum following a first delivery.27,28 However, it must be pointed out that the majority of such defects are asymptomatic and remain so. In contrast, third or fourth degree tears, recognised at the time of delivery, are associated with a high risk of symptomatic faecal incontinence29,30 which has been

Table 2. Risk factors for the development of incontinence post-partum. a. Vaginal delivery b. Instrumental delivery c. Emergency caesarean section d. Epidural anaesthesia e. Perineal laceration f. Obstetric genital fistula

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documented, in one study, to persist for up to 20 years later.30 Faltin and colleagues followed up a large cohort of women for up to 18 years following delivery; while severe faecal incontinence was, indeed, much more common among those who had sustained tears (13.1% vs 7.8%), they also concluded that in only 6.4% of those who were incontinent could their symptoms be solely attributed to the tear.31 Similarly, Van Brummen and colleagues in assessing symptoms at 12 months post-partum and describing the new onset of faecal incontinence following a first pregnancy among 2.6% of their 487 women, found that the most important predictor was the occurrence of a third or fourth degree tear.4 Given the risk factors associated with the occurrence of third degree tears (first delivery, instrumental delivery, foetal macrosomia, prior tear, mid-line vs medio-lateral episiotomy) it is likely that this event may be fundamental to the pathogenesis of altered faecal continence following delivery, especially among primiparous women. More recently, with the advent of superior clinical tools, attention has focused on the significance of occult sphincter damage. A recent meta-analysis concluded that occult sphincter injury was, indeed, a very clear predictor of risk for faecal incontinence.32 Sultan and colleagues completed a detailed clinical, ultrasonographic, electrophysiological and manometric assessment of 202 women before delivery, six weeks later and at six months following delivery.27 They documented new anal sphincter defects in 35% of primiparous women, of which only 3% were apparent on clinical examination; new defects were far less common among multiparous women. Anal sphincter pressures were lower following delivery and both perineal descent and pudendal nerve terminal motor latency were prolonged. Sphincter defects were especially common among those who had a forceps-assisted delivery (rather than Ventouse extraction); none were observed in those who had been delivered by caesarean section. Sphincter defects were associated with the new onset of bowel symptoms, and urgency and incontinence, in particular. It was notable, however, that only a minority developed either of these symptoms (13% and 23% of primips and multips, respectively). When re-assessed six months, later though urgency and incontinence had improved somewhat, there was no change in the sphincter defects or anorectal manometry; pudendal nerve terminal latency had normalised, however, in 8 of the 12 women in whom it had been abnormal six weeks post-partum. Faltin and colleagues went on to demonstrate, in a randomised, controlled clinical trial, that the detection and repair of such occult defects halved the prevalence of faecal incontinence.33 A tear in a prior pregnancy increases the risk of sustaining a tear in subsequent pregnancies and of developing faecal incontinence21,34 even if the defect was occult.27 Debate continues regarding the protective effect, if any, of episiotomy against subsequent incontinence; Sultan and colleagues, for example, found no evidence of a protective effect. Pudendal nerve injury Electrophysiological studies have documented the occurrence of pudendal nerve injuries in 42% of women following vaginal delivery.35 Again, many instances will remain asymptomatic and 60% were found to have recovered within two months. Role of pregnancy and parturition in the etiology of anal incontinence in later life While, as described above, pregnancy and injuries sustained during childbirth predispose to the new onset of anal incontinence post-partum and longitudinal studies indicate that this problem may persist in the long term, and even deteriorate36 over time,

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studies exploring the contributions of pregnancy and birth trauma to the pathogenesis of faecal incontinence, in general, have been far less conclusive.37 In a population study among 2800 females among whom they described a prevalence of faecal incontinence which ranged from 7.3% in those aged between 20 and 29 to 21.7% in those aged between 50 and 59, Bharucha and colleagues identified the symptom of rectal urgency and a history of anorectal conditions as the strongest independent risk factors for incontinence.38 In contrast, obstetric history was not an independent risk factor and caesarean sections were not apparently protective. Among those women who were classified as having severe faecal incontinence, age and rectal urgency were, again, clear risk factors. With regard to obstetric issues, a history of a vaginal delivery which involved forceps and the placement of sutures to repair a tear was significant only when combined with the additional insult of anorectal surgery. They went on to develop the ‘multiple hit’ concept of faecal incontinence: obstetric injury on its own may not be sufficient, in most cases, to result in incontinence but when combined with rectal urgency, anorectal surgical interventions and in the context of an older individual with a tendency to diarrhoea, problems with continence arise. This concept is in keeping with the disappointing results, in general, of surgical repairs and of biofeedback approaches which focus on the pelvic floor.39 Attention may be better directed to the colon and rectum! Others have also addressed the relationship between parity and incontinence. In general, there does appear to be a weak association between parity and incontinence; some have related this to pelvic floor descent,40 others have actually described pelvic floor descent as protective against incontinence.41 Kearney and colleagues used magnetic resonance imaging to assess the impact of delivery on the levator ani muscles and detected a major defect in the pubovisceral component of this muscle group in 14% of 160 patients; use of forceps, the occurrence of an anal sphincter tear and an episiotomy were significant risk factors.42 McKinnie and colleagues found that while parous females were twice as likely to experience faecal incontinence as their non-parous counterparts, this risk was not reduced by caesarean section.43 Indeed, in their analysis of multiple birth-related factors, they could not identify any difference in risk between those who had vaginal or caesarean deliveries. These studies suggest that some factor related to parity per se, other than the mode of delivery, may play a role in the subsequent development of incontinence. The interpretation of this literature is complicated by several factors; recall bias in retrospective questionnaire-based studies, selection bias and a lack of detail on the type of caesarean section (whether elective or emergency) performed, or on complications of vaginal delivery (instrumental, tears, episiotomy); indeed, a recent critical review concluded that such were the limitations of available evidence that no recommendations could be made in regard to mode of delivery in the prevention of faecal incontinence.44 There is some data on the effects of parturition on anal sphincter physiology and morphology; in the absence of a tear, some changes in sphincter pressures and in sphincter morphology have been documented but these have been relatively minor and not predictive of symptom development.45–48

Management What of the management of incontinence related to birth trauma? Mahony and colleagues demonstrated that biofeedback therapy, based on intra-anal electromyography, was effective.49 Others have failed to document benefit for pelvic floor exercises in the prevention or management of faecal incontinence, in this context.50,51

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Constipation The fact that, in the general population, constipation is two to three times more common in women than in men52,53 has led to an exploration of factors that could explain this dramatic discrepancy. Various mechanisms may be operative. Thus gender, per se, may be relevant, some studies demonstrating slower colon transit54 and an impaired (gastro-colonic) response to a caloric load55 among females. However as outlet-type constipation, a phenomenon that one might expect to result from distortions or disruptions of the pelvic floor during child-birth, is an especially female preserve,53 obstetric history has received close scrutiny among such patients. While not identified, in one study, as an independent risk factor for constipation, in general,37 parity, as well as a history of hysterectomy, has long been considered an important risk factor for the development of disordered defaecation. Furthermore, it has been assumed that disruption of the anatomy of the pelvic floor during parturition is of fundamental importance to the subsequent development of perineal descent, rectocoeles and pelvic floor prolapse and to lead to difficulty with defaecation. However, while there is some evidence for an effect of pelvic floor prolapse on defaecatory performance, the relationship has been far from perfect or consistent. Thus, while constipation and other bowel symptoms are certainly common among patients with perineal descent and vaginal prolapse,56 a cause and effect relationship has not been established, as exemplified by a failure to establish any correlation between the severity of prolapse and the prevalence of bowel dysfunction.57 In one study of 1004 women in the US, no association could be developed between the extent of vaginal wall or pelvic descent and constipation whether expressed as the passage of hard or lumpy stools, a sense of incomplete evacuation or infrequent bowel movements. Straining at stool was associated with more anterior vaginal and perineal descent.58 The perils of identifying correlations between prolapse and any symptom were dramatically illustrated by Klingele and colleagues who could demonstrate prolapse, of at least stage II, in 55% of their healthy control population.41 42% of their patients with obstructed defecation had prolapse. Furthermore, there was no association between the severity of prolapse and the prevalence of obstructed defaecation, though this symptom did relate to the presence of perineal descent. They concluded that, while a subset of subjects with defaecatory disorders, and obstructed defaecation, in particular, have evidence of perineal descent their findings overall, ‘argue against a major role for pelvic organ prolapse in defaecatory disorders’.41 The interpretation of the literature is also hampered by a lack of clarity and consensus on terminology and definitions. Various interpretations of the extant literature on this topic remain tenable: a. perineal decent and vaginal prolapse cause defaecatory dysfunction; b. constipation and straining at stool cause perineal descent and prolapse, and; c. another factor, such as trauma sustained at parturition, leads, independently, to both pelvic floor descent and difficult defaecation causing the two entities to coexist as epiphenomena in the same individual. It is clear that factors, in any event, other than the effects of parturition on the pelvic floor, contribute to defaecatory difficulty in most cases.56

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CONCLUSIONS The effects of pregnancy and parturition on the anal sphincters and pelvic floor are complex and incompletely understood; likewise while anal sphincter tears are a definite risk factor for the development of anal incontinence in the immediate aftermath of childbirth, their role in the development of incontinence later in life may have been overemphasised. Practice points  constipation is common in pregnancy and is primarily due to the hormonal changes that accompany pregnancy and not the effects of the gravid uterus  third and fourth degree tears are a major risk factor for incontinence immediately after pregnancy; many will be missed by usual clinical assessments  the early detection of significant tears by endoanal ultrasonography and their subsequent repair will reduce the likelihood of incontinence  multiple factors contribute to the development of anal incontinence in later life among females; the contribution of injuries sustained during parturition may have been exaggerated in the past  while pregnancy is a risk factor for the later occurrence of difficult defaecation, associations between events during labour and parturition, changes in the anatomy of the pelvic floor and these symptoms is unclear

Research agenda  large prospective studies on the true prevalence and risk factors for anal sphincter injury  careful dissection, using modern technology, of the changes in the anal sphincters and pelvic floor during childbirth and their association with subsequent incontinence and disturbed defaecation in longitudinal follow-up studies  randomised controlled trials of interventions in the management of constipation during pregnancy and incontinence and difficult defaecation following pregnancy REFERENCES 1. DeLancey JO. Anterior pelvic floor in females. In Pemberton JH, Swash M & Henry MM (eds.). The pelvic floor. Its functions and disorders. London: WB Saunders, 2002, pp. 13–28. 2. Quigley EMM. Colonic motility and colonic function. In Pemberton JH, Swash M & Henry MM (eds.). The pelvic floor. Its functions and disorders. London: WB Saunders, 2002, pp. 84–93. 3. Marshall K, Thompson KA, Walsh DM et al. Incidence of urinary incontinence and constipation during pregnancy and postpartum: survey of current findings at the Rotunda Lying-in Hospital. Br J Obstet Gynaecol 1998; 105: 400–402. 4. van Brummen HJ, Bruinse HW, van de Pol G et al. Defecatory symptoms during and after the first pregnancy: prevalences and associated factors. Int Urogynecol J Pelvic Floor Dysfunct 2006; 17: 224–230. 5. Derbyshire EJ, Davies J & Detmar P. Changes in bowel function: pregnancy and the puerperium. Dig Dis Sci 2007; 52: 324–328.

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