CLINICAL AND SYSTEMATIC REVIEWS
nature publishing group
521
Pregnancy and Postpartum Bowel Changes: Constipation and Fecal Incontinence Grace Hewon Shin, MD1, 2, Erin Lucinda Toto, MD1, 2 and Ron Schey, MD, FACG1
Pregnancy and the postpartum period are often associated with many gastrointestinal complaints, including nausea, vomiting, and heartburn; however, the most troublesome complaints in some women are defecatory disorders such as constipation and fecal incontinence, especially postpartum. These disorders are often multifactorial in etiology, and many studies have looked to see what risk factors lead to these complications. This review discusses the current knowledge of pelvic floor and anorectal physiology, especially during pregnancy, and reviews the current literature on causes and treatments of postpartum bowel symptoms of constipation and fecal incontinence. Am J Gastroenterol 2015; 110:521–529; doi:10.1038/ajg.2015.76; published online 24 March 2015
INTRODUCTION Constipation and fecal incontinence are common disorders associated with pregnancy and the postpartum period, and are a cause for significant patient stress as well as health-care burden. The main muscles that function primarily in the process of defecation are the levator ani muscle along with the anal sphincter complex. These muscles also have a major role in urination and support of the pelvic viscera. Their structure and function may be affected by chronic straining, older age, physical conditioning, and conditions of increased intraabdominal pressure, such as obesity and pregnancy. Maclennan et al. (1) demonstrated that 46% of women acknowledge some form of pelvic floor dysfunction that increases after pregnancy according to parity and age. It was felt, however, that the main insult to the pelvic floor is the pregnancy itself, rather than the mode of delivery (1). However, other studies indicated that the mode of delivery also may have a role, as women undergoing cesarean sections have slightly less postpartum pelvic floor dysfunction and organ prolapse than their counterparts who had vaginal deliveries (2,3). Given that many prior studies showed that the pelvic floor injury during pregnancy and the mode of delivery have been implicated as the main causes of defecation disorders in postpartum women, much research has sought to further demonstrate its validity. This review will discuss the physiology of the pelvic floor and how it is affected by pregnancy, as well as expand on the current diagnosis and management of postpartum defecatory disorders.
PELVIC FLOOR AND ANORECTAL ANATOMY AND PHYSIOLOGY: EFFECT OF PREGNANCY Anatomy of the pelvic floor
The levator ani muscle complex is a thin, broad muscle that forms much of the floor of the pelvis (Figure 1). The levator ani complex consists of three muscles: (i) the iliococcygeal, (ii) the pubococcygeal, and (iii) the puborectalis muscles. It supports the viscera of the pelvic cavity, aids in continence/defecation via creating the anorectal angle, and has a role in sexual function. It attaches to the posterior surface of the superior pubic rami anteriorly, the medial surfaces of the ischium posteriolaterally, and the coccyx posteriorly. The puborectalis component attaches to the pubic rami anteriorly and loops posteriorly around the rectum. The levator ani complex works in concert during defecation and is innervated by branches of the pudendal, inferior rectal, perineal, and sacral (S3 and S4) nerves (4). This complex, in conjunction with the internal and external anal sphincters, determines continence, and any perturbation in the structure or function of these muscles may predispose toward constipation or incontinence. The female pelvic floor is divided into anterior and posterior components by the urogenital tract (the vaginal canal and urethra). Injury to the anterior pelvic floor results primarily in urinary incontinence, and injury to the posterior floor results primarily in problems with anal continence and defecation. Physiology of continence and defecation
The physiology of the maintenance of continence and defecation is a highly complex, coordinated process. The pressure of the anal
1
Section of Gastroenterology, Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania, USA; 2These authors contributed equally to this work. Correspondence: Ron Schey, MD, FACG, Neurogastroenterology and Esophageal Disorders Program, Temple University Physicians/Section of Gastroenterology, 3401 North Broad Street, 8th Floor Parkinson Pavilion, Philadelphia, Pennsylvania 19140, USA. E-mail: [email protected] Received 29 October 2014; accepted 10 February 2015
© 2015 by the American College of Gastroenterology
The American Journal of GASTROENTEROLOGY
REVIEW
CME
522
Shin et al.
Anterior
REVIEW
Levator ani
Symphysis pubis
Pubococcygeus Iliococcygeus
(Urogenital diaphragm) Urethra Vagina Anal canal
(Obturator internus)
Coccyx
(Piriformis) Posterior
Levaor ani Coccygeus
Pelvic diaphragm
Figure 1. The levator ani muscle complex forms much of the floor of the pelvis.
sphincter is maintained mainly by the internal anal sphincter, which is tonically contracted at rest, and to a much less extent by the external anal sphincter, which is under volitional control (5). The musculature of the pelvic floor also has constant resting tone, with the levator ani complex creating an acute anorectal angle and the internal anal sphincter involuntarily contracted. This angle and sphincter act as mechanical barriers to stool flow. This tone is typically maintained except during voluntary urinary voiding, defecation, and performing a Valsalva maneuver. The process of defecation is best described in four physiological phases: (i) the basal/resting phase; (ii) a predefecatory phase that leads to generation of the urge to defecate; (iii) the expulsive phase; and finally the (iv) termination of defecation. Propulsive forces generated by the migrating motor complexes in the colon transfer stool into the rectum. Arrival of stool in the rectum leads to distension of the rectum and activation of the rectoanal inhibitory reflex. It is this distension that is perceived by the brain and leads to the urge to defecate. Anal sampling differentiates stool from flatus and allows the stool to enter the anal canal. If defecation is not appropriate at that time, the pelvic floor and external anal sphincter will contract, preventing the passage of stool. When the appropriate social situation arises, the act of defecation is undertaken that involves the relaxation of the muscular sling created by the puborectalis muscle that widens the anorectal angle, straightening the anorectal canal. The external anal sphincter is then relaxed and the anterior abdominal musculature, diaphragm, and rectum contract, leading to expulsion of the stool from the anal canal via increased intraabdominal pressure. After this, the internal anal sphincter and puborectalis return to their resting contracted state (6). Maintenance of continence is affected by many factors, including mental function, stool volume and consistency, colonic transit, rectal distensability, anal sphincter function, anorectal sensation, and anorectal reflexes. For this review, only the factors associated with pregnancy and postpartum pelvic floor dysfunction will be discussed. Effects of pregnancy
During pregnancy, the hormone progesterone acts to relax smooth muscle globally. This is important to maintain the pregnancy and The American Journal of GASTROENTEROLOGY
to prevent premature uterine contractions. This also leads to other sequelae in the gastrointestinal tract, including decreased whole gut motility (leading to delayed gastric emptying and constipation), as well as diminished tonic contractions of sphincters (including the lower esophageal sphincter leading to esophageal reflux and heartburn), and possibly the anal sphincters (7–9). Mapping of androgen, estrogen, and progesterone receptors indicate that these receptors are also found in the stratified squamous epithelium of the anal canal, undoubtedly affecting sphincter function (10). Progesterone also causes ligamentous laxity (11,12), leading to stretching of the pubic symphysis. This, combined with the increased abdominal pressure and weight associated with the gravid uterus, induces conformational changes in the pelvic floor, leading to altered defecatory patterns, such as pelvic organ prolapse, excessive perineal descent, and feelings of obstructed defecation. Postpartum incontinence is usually attributed to injury to the anal sphincters and the pudendal nerve during childbirth, either through a naturally occurring tear or an iatrogenic episiotomy. Injury can also be exacerbated by instrument-assisted delivery methods, such as forceps and vacuum. The muscles of the pelvic floor can be injured by excessive weight gain during pregnancy, a prolonged second stage of labor (pushing), and large gestational size of the infant moving through the birth canal. The latter often improves postpartum, as the weight is lost and the pelvic floor muscles heal and tighten again.
BOWEL SYMPTOMS Constipation
Epidemiology. Approximately 40% of pregnant women suffer from constipation at some point during or after their pregnancies. In a prospective study by van Brummen et al. (13), constipation was more common at 12 than at 36 weeks of gestation (8.9% vs. 4.5%), and then it remained roughly stable at 3 and 12 months postpartum (4.6% and 4.2%, respectively). Symptoms suggestive of difficult defecation (painful defecation, feeling of incomplete evacuation) were found to be equally common at 12 and 36 weeks. One in three women complained of a pain before, during, or VOLUME 110 | APRIL 2015 www.amjgastro.com
Pregnancy and Postpartum Bowel Changes
523
Table 1. Causes of constipation in pregnancy
REVIEW
Dehydration (nausea/vomiting, poor oral intake) Hormonal (progesterone, hypothyroidism) Mechanical (gravid uterus, pelvic floor conformational changes) Drugs (antiemetics, iron, tocolytics) Parity Preexisting disease Chronic idiopathic constipation Irritable bowel syndrome Congenital or acquired megacolon
Pubic bone
Chronic idiopathic intestinal pseudoobstruction
Vaginal opening
after defecation. All of these bowel symptoms, with the exception of a feeling of incomplete evacuation, became less prevalent 12 months postpartum than at any stage during pregnancy. Another study conducted by Derbyshire et al. showed that the prevalence of both straining (21–39%) and incomplete evacuation (12.5– 22%) were high in all trimesters, with the prevalence of incomplete evacuation and the time to complete the act of defecation falling markedly when evaluated 6 weeks postpartum (15). Rates of constipation were found to be highest in the first two trimesters (35 and 39%), and then declined to 21% in the third trimester and to 17% postpartum (13). Rates of constipation symptoms vary markedly from study to study, possibly based on the definition of constipation used and the method of reporting. Further studies using a standardized definition are needed to better elucidate the rates of constipation in this subset of the population. Pathophysiology. The pathophysiology of constipation varies over the course of the gestation. During the first trimester, progesterone effects cause decreased small bowel and colonic motility and subsequent slow transit constipation, often exacerbated by poor fluid intake from nausea and lack of dietary fiber. Later in the pregnancy, pressure on the rectosigmoid colon from the gravid uterus can cause an obstructive constellation of constipation symptoms (Table 1 and Figure 2). The prevalence of incomplete evacuation is highest in the first trimester, arguing against the “mechanical hypothesis” of constipation in pregnancy, as the uterus has not yet grown large enough to cause obstructive symptoms (14). Furthermore, the fact that rates of constipation are highest in the first two trimesters lends credence to a hormonal etiology of constipation in this subset of patients (15). Interestingly, in vivo studies have shown that progesterone stimulates, rather than diminishes, colonic motility, although it is unclear whether this stimulation is actually propulsive. Hence, it may be a lack of gastrointestinal responsiveness to progesterone, rather than the excess progesterone itself, that leads to constipation in pregnant women (16,17). Levator ani dysfunction can occur as a sequelae of chronic straining or increased abdominal pressure, as in the case of pregnancy. Multiple or subsequent pregnancies may further augment © 2015 by the American College of Gastroenterology
Pelvic floor muscles Figure 2. Effect of gravid uterus causing obstructive symptoms.
this effect. In levator ani dysfunction at rest, there is sagging of the levator plate, as well as subluxation of the suspensory sling and hiatal ligament. The levator hiatus is widened and lowered, thus exposing the anal canal to increased intraabdominal pressure. On straining, contraction of both the sagging levator plate and the subluxated suspensory sling is too weak to induce opening of the anal canal for the descending fecal mass. The increased intraabdominal pressure dissipates through the abnormally wide levator hiatus closing the anal canal, resulting in fecal obstruction. Analysis of levator ani muscle by electromyography and manometry in 100 women showed that levator dysfunction occurs most frequently in multiparous as compared with primiparous and nulliparous women. Insult to the levator muscle as measured by electromyography was most significant in multiparous women with a history of prolonged second stage of labor (pushing). This is thought to be a result of pudendal neuropathy and the development of pudendal canal syndrome (18). Risk factors. There are conflicting data regarding whether the mode of delivery has any association with subsequent constipation. One study showed no association between the method of delivery (spontaneous vaginal delivery, instrumented vaginal delivery, or cesarean section delivery) and the rate of constipation reported at 3, 6, and 12 months postpartum. However, another study found that after adjusting for age and parity, the mode of delivery was associated with an increased odds of having obstructed defecation (19,20). Further studies are needed to better understand the relationship between mode of delivery and rates of obstructed or dyssynergic defecation. Other factors to consider with regard to constipation during pregnancy are preexisting functional bowel disorders, especially irritable bowel syndrome (IBS), as well as medication side effects. The hallmark of IBS is abdominal pain or discomfort associated The American Journal of GASTROENTEROLOGY
REVIEW
524
Shin et al.
with a change in bowel habits. Women of child-bearing age are the main demographic of all IBS diagnoses in the community, and the incidence of undiagnosed IBS is quite high. Unfortunately, there is a dearth of studies looking at the course of IBS during pregnancy. Anecdotal reports have shown IBS to remit during pregnancy, only to relapse postpartum (14). On the other hand, pregnancy has been shown to exacerbate other colonic motility disorders such as Hirshsprung’s disease, idiopathic megarectum/megacolon, and pseudo-obstruction. In addition, hypothyroidism is always something to consider in any patients who suffer from constipation, including during pregnancy. Along with preexisting functional bowel disorders, pregnant women are frequently prescribed antiemetic medications such as ondansetron, promethazine, and prochlorperazine, and antihistamines such as doxylamine, diphenhydramine, and meclizine, all of which cause constipation as a known side effect. In addition, iron supplementation formulations often prescribed in pregnancy for anemia can cause further constipation (21). The degree of constipation is directly proportional to the amount of elemental iron ingested, with some formulations reporting an estimated 50% rate of treatment-related constipation. This effect can be mitigated by switching to a formulation containing a lower amount of elemental iron (22–25). Finally, the use of magnesium sulfate as a tocolytic to prevent preterm labor or to treat preeclampsia is also associated with significant constipation. Treatment. Therapy for pregnancy-associated constipation is similar to that of the general population. It is aimed at reassuring the patient, encouraging adequate fluid intake, using fiber supplementation (20–35 g/day), and osmotic laxatives such as polyethylene glycol (8–25 g/day) and lactulose (15–30 ml/day). These interventions are safe during pregnancy; however, polyethylene glycol is not approved by the Food and Drug Administration for use in pregnancy and carries a pregnancy category C rating (26). Polyethylene glycol causes water retention in the stool and has minimal systemic absorption; therefore, it is unlikely to cause any fetal malformations. Lactulose carries a pregnancy category B; it creates an osmotic effect within the colon with resultant distension promoting colonic peristalsis and is also minimally absorbed. Despite their widespread use and presumed safety, patients should be counseled with regard to the theoretical risks associated with these medications, and a risk/benefit analysis should be discussed. Hemorrhoids. Hemorrhoids are common during pregnancy and during the postpartum period, especially in patients suffering from constipation. Straining during defecation in constipated patients and pressure from pushing during the second stage of labor may contribute to hemorrhoid development. The main manifestations of internal hemorrhoids are anal discomfort and bleeding, whereas external hemorrhoids primarily cause external anal pain and pruritus. The main pathogenesis is increased intraabdominal pressure by the enlarging gravid uterus causing vascular engorgement and venous stasis. The primary treatment for both types of hemorrhoids is initially conservative with increasing dietary fiber and water intake, as well as the use of stool softeners. The American Journal of GASTROENTEROLOGY
Table 2. Grades of hemorrhoids Grade I
Internal hemorrhoids that do not prolapse
Grade II
Internal hemorrhoids that prolapse with defecation but reduce spontaneously
Grade III
Internal hemorrhoids that prolapse with defecation and require manual reduction
Grade IV
Internal hemorrhoids that are prolapsed and cannot be reduced manually
Hydrocortisone suppositories and sitz baths may reduce the swelling, discomfort, and pruritus associated with external hemorrhoids. If conservative therapy fails and symptomatic internal hemorrhoids persist, surgical or endoscopic therapy may be indicated in the postpartum period. Endoscopic band ligation, injection sclerotherapy, infrared coagulation, and surgical hemorrhoidectomy are all safe options in the postpartum period (27). The preferred treatment modality depends on the grade of hemorrhoids (Table 2). Grade I hemorrhoids typically respond to conservative therapy. Medically refractory grade I or II hemorrhoids can best be addressed with endoscopic modalities, with rubber band ligation showing 80% success rates (28). Symptomatic grade III hemorrhoids can be treated with either rubber band ligation or surgical excision, and grade IV hemorrhoids or grade III hemorrhoids with significant prolapse are best addressed surgically. One evaluation of stapled hemorrhoidopexy shows a 90% patient satisfaction rating postoperatively, despite a recurrence rate of approximately 18% (29). If possible, any procedure requiring sedation or prone positioning should be avoided during the first and third trimesters. Fecal incontinence
Epidemiology. Between 3 and 4% of women report new symptoms related to altered anal continence after pregnancy. Altered fecal continence has been reported in as many as 25% of primiparous women at 6 weeks postpartum (30). Fecal incontinence was found to be prevalent in 3.9% of women as early as at 12 weeks of gestation, and it increases to 5.7% at 3 months postpartum (13). Knowing that this problem may be underappreciated is emphasized by the finding in one study that only 14% of symptomatic women sought medical attention (31). However, one cannot underestimate the emotional, physical, social, and mental effects that this disorder causes. The median age of onset is in the seventh decade, at a time when these patients often cannot adequately take care of themselves, causing increased health-care costs and decreased quality of life (32). Pathophysiology. Fecal incontinence results from a complex interplay of insults to the structure and functions of the anal sphincter and the richly innervated anorectum along with the loss of the anal endovascular cushions (33). Each mechanism of maintaining continence has an important role. After pregnancy, the main mechanism of fecal incontinence is thought to be secondary to sphincter weakness and loss of stool awareness that are further VOLUME 110 | APRIL 2015 www.amjgastro.com
Pregnancy and Postpartum Bowel Changes
Risk factors. A recent study found that factors leading to postpartum anal incontinence several days after delivery included forceps delivery, prolonged second stage of labor >5 hours, expulsion phase >20 minutes, uterine revision, and first-degree perineal lacerations, whereas long-term incontinence between 6 and 8 weeks postpartum identified risk factors such as shoulder dystocia, anuvulvar distance 105 mm (34). A third- or fourth-degree sphincter tear was significantly associated with fecal incontinence 12 months postpartum (Table 3 and Figure 3). Previous theories noted that elective cesarean section, before any pushing, possibly had protective effects. However, urgent or emergent cesarean performed during the second stage of labor was thought to increase risk owing to prolonged pushing. A metaanalysis of 18 studies showed that symptoms of anal incontinence in the first year postpartum are associated with mode of delivery. Women having any type of vaginal delivery compared with a cesarean section had an increased risk of developing symptoms of solid, liquid, or flatus anal incontinence (35). However, a large prospective cohort study—“The Childbirth and Pelvic Symptoms study”—performed by the Pelvic Floor Disorders Network was done to prospectively estimate the prevalence of postpartum fecal and urinary incontinence in primiparous women. Women with and without clinically recognized anal sphincter tears during vaginal delivery and women delivered by cesarean before labor were analyzed. Compared with the vaginal control group, women in the sphincter tear cohort reported more fecal incontinence, fecal urgency, increased flatus incontinence, and greater fecal incontinence severity at 6 weeks and 6 months postpartum. At 6 months postpartum, 22.9% of women delivered by cesarean reported urinary incontinence, whereas 7.6% reported fecal incontinence. This highlights an important point that although women © 2015 by the American College of Gastroenterology
Table 3. Classification of third- and fourth-degree tears First degree
Limited to vaginal mucosa and skin of introitus
Second degree
Extends to the fascia and muscles of the perineal body
Third degree
Fourchette, perineal skin, vaginal mucosa, muscles, and the anal sphincter are torn
3a
Partial tear of the external anal sphincter involving 50% Tear of the external anal sphincter
3c
Internal sphincter is torn
Fourth degree
Fourchette, perineal skin, vaginal mucosa, muscles, anal sphincter, and rectal mucosa are torn
Rectum (torn) Anal sphincter (torn)
Perineal muscles (torn)
Anal sphincter (torn)
Figure 3. Classification of clinically significant perineal tears: (a) third degree and (b) fourth degree.
with clinically recognized anal sphincter tears during vaginal delivery are more likely to report postpartum fecal incontinence than women without sphincter tears, cesarean delivery before labor is not entirely protective against pelvic floor disorders (36). Similarly, other studies showed that there was no evidence of lower risk of subsequent fecal incontinence for exclusive cesarean section deliveries (37–39). A recent large cohort study—The Maternal Health Study—showed that the mode of delivery really did not alter the likelihood of fecal incontinence beyond the first 3 months postpartum (40). Despite the common belief that an elective cesarean section may be protective against the subsequent development of fecal incontinence (36), the current literature does not support this theory (Table 4). Many studies continue to look at the risk factors associated with fecal incontinence after pregnancy. In a large-scale study of 4,002 women, the prevalence of both flatal and fecal incontinence increased with age (P
nature publishing group
521
Pregnancy and Postpartum Bowel Changes: Constipation and Fecal Incontinence Grace Hewon Shin, MD1, 2, Erin Lucinda Toto, MD1, 2 and Ron Schey, MD, FACG1
Pregnancy and the postpartum period are often associated with many gastrointestinal complaints, including nausea, vomiting, and heartburn; however, the most troublesome complaints in some women are defecatory disorders such as constipation and fecal incontinence, especially postpartum. These disorders are often multifactorial in etiology, and many studies have looked to see what risk factors lead to these complications. This review discusses the current knowledge of pelvic floor and anorectal physiology, especially during pregnancy, and reviews the current literature on causes and treatments of postpartum bowel symptoms of constipation and fecal incontinence. Am J Gastroenterol 2015; 110:521–529; doi:10.1038/ajg.2015.76; published online 24 March 2015
INTRODUCTION Constipation and fecal incontinence are common disorders associated with pregnancy and the postpartum period, and are a cause for significant patient stress as well as health-care burden. The main muscles that function primarily in the process of defecation are the levator ani muscle along with the anal sphincter complex. These muscles also have a major role in urination and support of the pelvic viscera. Their structure and function may be affected by chronic straining, older age, physical conditioning, and conditions of increased intraabdominal pressure, such as obesity and pregnancy. Maclennan et al. (1) demonstrated that 46% of women acknowledge some form of pelvic floor dysfunction that increases after pregnancy according to parity and age. It was felt, however, that the main insult to the pelvic floor is the pregnancy itself, rather than the mode of delivery (1). However, other studies indicated that the mode of delivery also may have a role, as women undergoing cesarean sections have slightly less postpartum pelvic floor dysfunction and organ prolapse than their counterparts who had vaginal deliveries (2,3). Given that many prior studies showed that the pelvic floor injury during pregnancy and the mode of delivery have been implicated as the main causes of defecation disorders in postpartum women, much research has sought to further demonstrate its validity. This review will discuss the physiology of the pelvic floor and how it is affected by pregnancy, as well as expand on the current diagnosis and management of postpartum defecatory disorders.
PELVIC FLOOR AND ANORECTAL ANATOMY AND PHYSIOLOGY: EFFECT OF PREGNANCY Anatomy of the pelvic floor
The levator ani muscle complex is a thin, broad muscle that forms much of the floor of the pelvis (Figure 1). The levator ani complex consists of three muscles: (i) the iliococcygeal, (ii) the pubococcygeal, and (iii) the puborectalis muscles. It supports the viscera of the pelvic cavity, aids in continence/defecation via creating the anorectal angle, and has a role in sexual function. It attaches to the posterior surface of the superior pubic rami anteriorly, the medial surfaces of the ischium posteriolaterally, and the coccyx posteriorly. The puborectalis component attaches to the pubic rami anteriorly and loops posteriorly around the rectum. The levator ani complex works in concert during defecation and is innervated by branches of the pudendal, inferior rectal, perineal, and sacral (S3 and S4) nerves (4). This complex, in conjunction with the internal and external anal sphincters, determines continence, and any perturbation in the structure or function of these muscles may predispose toward constipation or incontinence. The female pelvic floor is divided into anterior and posterior components by the urogenital tract (the vaginal canal and urethra). Injury to the anterior pelvic floor results primarily in urinary incontinence, and injury to the posterior floor results primarily in problems with anal continence and defecation. Physiology of continence and defecation
The physiology of the maintenance of continence and defecation is a highly complex, coordinated process. The pressure of the anal
1
Section of Gastroenterology, Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania, USA; 2These authors contributed equally to this work. Correspondence: Ron Schey, MD, FACG, Neurogastroenterology and Esophageal Disorders Program, Temple University Physicians/Section of Gastroenterology, 3401 North Broad Street, 8th Floor Parkinson Pavilion, Philadelphia, Pennsylvania 19140, USA. E-mail: [email protected] Received 29 October 2014; accepted 10 February 2015
© 2015 by the American College of Gastroenterology
The American Journal of GASTROENTEROLOGY
REVIEW
CME
522
Shin et al.
Anterior
REVIEW
Levator ani
Symphysis pubis
Pubococcygeus Iliococcygeus
(Urogenital diaphragm) Urethra Vagina Anal canal
(Obturator internus)
Coccyx
(Piriformis) Posterior
Levaor ani Coccygeus
Pelvic diaphragm
Figure 1. The levator ani muscle complex forms much of the floor of the pelvis.
sphincter is maintained mainly by the internal anal sphincter, which is tonically contracted at rest, and to a much less extent by the external anal sphincter, which is under volitional control (5). The musculature of the pelvic floor also has constant resting tone, with the levator ani complex creating an acute anorectal angle and the internal anal sphincter involuntarily contracted. This angle and sphincter act as mechanical barriers to stool flow. This tone is typically maintained except during voluntary urinary voiding, defecation, and performing a Valsalva maneuver. The process of defecation is best described in four physiological phases: (i) the basal/resting phase; (ii) a predefecatory phase that leads to generation of the urge to defecate; (iii) the expulsive phase; and finally the (iv) termination of defecation. Propulsive forces generated by the migrating motor complexes in the colon transfer stool into the rectum. Arrival of stool in the rectum leads to distension of the rectum and activation of the rectoanal inhibitory reflex. It is this distension that is perceived by the brain and leads to the urge to defecate. Anal sampling differentiates stool from flatus and allows the stool to enter the anal canal. If defecation is not appropriate at that time, the pelvic floor and external anal sphincter will contract, preventing the passage of stool. When the appropriate social situation arises, the act of defecation is undertaken that involves the relaxation of the muscular sling created by the puborectalis muscle that widens the anorectal angle, straightening the anorectal canal. The external anal sphincter is then relaxed and the anterior abdominal musculature, diaphragm, and rectum contract, leading to expulsion of the stool from the anal canal via increased intraabdominal pressure. After this, the internal anal sphincter and puborectalis return to their resting contracted state (6). Maintenance of continence is affected by many factors, including mental function, stool volume and consistency, colonic transit, rectal distensability, anal sphincter function, anorectal sensation, and anorectal reflexes. For this review, only the factors associated with pregnancy and postpartum pelvic floor dysfunction will be discussed. Effects of pregnancy
During pregnancy, the hormone progesterone acts to relax smooth muscle globally. This is important to maintain the pregnancy and The American Journal of GASTROENTEROLOGY
to prevent premature uterine contractions. This also leads to other sequelae in the gastrointestinal tract, including decreased whole gut motility (leading to delayed gastric emptying and constipation), as well as diminished tonic contractions of sphincters (including the lower esophageal sphincter leading to esophageal reflux and heartburn), and possibly the anal sphincters (7–9). Mapping of androgen, estrogen, and progesterone receptors indicate that these receptors are also found in the stratified squamous epithelium of the anal canal, undoubtedly affecting sphincter function (10). Progesterone also causes ligamentous laxity (11,12), leading to stretching of the pubic symphysis. This, combined with the increased abdominal pressure and weight associated with the gravid uterus, induces conformational changes in the pelvic floor, leading to altered defecatory patterns, such as pelvic organ prolapse, excessive perineal descent, and feelings of obstructed defecation. Postpartum incontinence is usually attributed to injury to the anal sphincters and the pudendal nerve during childbirth, either through a naturally occurring tear or an iatrogenic episiotomy. Injury can also be exacerbated by instrument-assisted delivery methods, such as forceps and vacuum. The muscles of the pelvic floor can be injured by excessive weight gain during pregnancy, a prolonged second stage of labor (pushing), and large gestational size of the infant moving through the birth canal. The latter often improves postpartum, as the weight is lost and the pelvic floor muscles heal and tighten again.
BOWEL SYMPTOMS Constipation
Epidemiology. Approximately 40% of pregnant women suffer from constipation at some point during or after their pregnancies. In a prospective study by van Brummen et al. (13), constipation was more common at 12 than at 36 weeks of gestation (8.9% vs. 4.5%), and then it remained roughly stable at 3 and 12 months postpartum (4.6% and 4.2%, respectively). Symptoms suggestive of difficult defecation (painful defecation, feeling of incomplete evacuation) were found to be equally common at 12 and 36 weeks. One in three women complained of a pain before, during, or VOLUME 110 | APRIL 2015 www.amjgastro.com
Pregnancy and Postpartum Bowel Changes
523
Table 1. Causes of constipation in pregnancy
REVIEW
Dehydration (nausea/vomiting, poor oral intake) Hormonal (progesterone, hypothyroidism) Mechanical (gravid uterus, pelvic floor conformational changes) Drugs (antiemetics, iron, tocolytics) Parity Preexisting disease Chronic idiopathic constipation Irritable bowel syndrome Congenital or acquired megacolon
Pubic bone
Chronic idiopathic intestinal pseudoobstruction
Vaginal opening
after defecation. All of these bowel symptoms, with the exception of a feeling of incomplete evacuation, became less prevalent 12 months postpartum than at any stage during pregnancy. Another study conducted by Derbyshire et al. showed that the prevalence of both straining (21–39%) and incomplete evacuation (12.5– 22%) were high in all trimesters, with the prevalence of incomplete evacuation and the time to complete the act of defecation falling markedly when evaluated 6 weeks postpartum (15). Rates of constipation were found to be highest in the first two trimesters (35 and 39%), and then declined to 21% in the third trimester and to 17% postpartum (13). Rates of constipation symptoms vary markedly from study to study, possibly based on the definition of constipation used and the method of reporting. Further studies using a standardized definition are needed to better elucidate the rates of constipation in this subset of the population. Pathophysiology. The pathophysiology of constipation varies over the course of the gestation. During the first trimester, progesterone effects cause decreased small bowel and colonic motility and subsequent slow transit constipation, often exacerbated by poor fluid intake from nausea and lack of dietary fiber. Later in the pregnancy, pressure on the rectosigmoid colon from the gravid uterus can cause an obstructive constellation of constipation symptoms (Table 1 and Figure 2). The prevalence of incomplete evacuation is highest in the first trimester, arguing against the “mechanical hypothesis” of constipation in pregnancy, as the uterus has not yet grown large enough to cause obstructive symptoms (14). Furthermore, the fact that rates of constipation are highest in the first two trimesters lends credence to a hormonal etiology of constipation in this subset of patients (15). Interestingly, in vivo studies have shown that progesterone stimulates, rather than diminishes, colonic motility, although it is unclear whether this stimulation is actually propulsive. Hence, it may be a lack of gastrointestinal responsiveness to progesterone, rather than the excess progesterone itself, that leads to constipation in pregnant women (16,17). Levator ani dysfunction can occur as a sequelae of chronic straining or increased abdominal pressure, as in the case of pregnancy. Multiple or subsequent pregnancies may further augment © 2015 by the American College of Gastroenterology
Pelvic floor muscles Figure 2. Effect of gravid uterus causing obstructive symptoms.
this effect. In levator ani dysfunction at rest, there is sagging of the levator plate, as well as subluxation of the suspensory sling and hiatal ligament. The levator hiatus is widened and lowered, thus exposing the anal canal to increased intraabdominal pressure. On straining, contraction of both the sagging levator plate and the subluxated suspensory sling is too weak to induce opening of the anal canal for the descending fecal mass. The increased intraabdominal pressure dissipates through the abnormally wide levator hiatus closing the anal canal, resulting in fecal obstruction. Analysis of levator ani muscle by electromyography and manometry in 100 women showed that levator dysfunction occurs most frequently in multiparous as compared with primiparous and nulliparous women. Insult to the levator muscle as measured by electromyography was most significant in multiparous women with a history of prolonged second stage of labor (pushing). This is thought to be a result of pudendal neuropathy and the development of pudendal canal syndrome (18). Risk factors. There are conflicting data regarding whether the mode of delivery has any association with subsequent constipation. One study showed no association between the method of delivery (spontaneous vaginal delivery, instrumented vaginal delivery, or cesarean section delivery) and the rate of constipation reported at 3, 6, and 12 months postpartum. However, another study found that after adjusting for age and parity, the mode of delivery was associated with an increased odds of having obstructed defecation (19,20). Further studies are needed to better understand the relationship between mode of delivery and rates of obstructed or dyssynergic defecation. Other factors to consider with regard to constipation during pregnancy are preexisting functional bowel disorders, especially irritable bowel syndrome (IBS), as well as medication side effects. The hallmark of IBS is abdominal pain or discomfort associated The American Journal of GASTROENTEROLOGY
REVIEW
524
Shin et al.
with a change in bowel habits. Women of child-bearing age are the main demographic of all IBS diagnoses in the community, and the incidence of undiagnosed IBS is quite high. Unfortunately, there is a dearth of studies looking at the course of IBS during pregnancy. Anecdotal reports have shown IBS to remit during pregnancy, only to relapse postpartum (14). On the other hand, pregnancy has been shown to exacerbate other colonic motility disorders such as Hirshsprung’s disease, idiopathic megarectum/megacolon, and pseudo-obstruction. In addition, hypothyroidism is always something to consider in any patients who suffer from constipation, including during pregnancy. Along with preexisting functional bowel disorders, pregnant women are frequently prescribed antiemetic medications such as ondansetron, promethazine, and prochlorperazine, and antihistamines such as doxylamine, diphenhydramine, and meclizine, all of which cause constipation as a known side effect. In addition, iron supplementation formulations often prescribed in pregnancy for anemia can cause further constipation (21). The degree of constipation is directly proportional to the amount of elemental iron ingested, with some formulations reporting an estimated 50% rate of treatment-related constipation. This effect can be mitigated by switching to a formulation containing a lower amount of elemental iron (22–25). Finally, the use of magnesium sulfate as a tocolytic to prevent preterm labor or to treat preeclampsia is also associated with significant constipation. Treatment. Therapy for pregnancy-associated constipation is similar to that of the general population. It is aimed at reassuring the patient, encouraging adequate fluid intake, using fiber supplementation (20–35 g/day), and osmotic laxatives such as polyethylene glycol (8–25 g/day) and lactulose (15–30 ml/day). These interventions are safe during pregnancy; however, polyethylene glycol is not approved by the Food and Drug Administration for use in pregnancy and carries a pregnancy category C rating (26). Polyethylene glycol causes water retention in the stool and has minimal systemic absorption; therefore, it is unlikely to cause any fetal malformations. Lactulose carries a pregnancy category B; it creates an osmotic effect within the colon with resultant distension promoting colonic peristalsis and is also minimally absorbed. Despite their widespread use and presumed safety, patients should be counseled with regard to the theoretical risks associated with these medications, and a risk/benefit analysis should be discussed. Hemorrhoids. Hemorrhoids are common during pregnancy and during the postpartum period, especially in patients suffering from constipation. Straining during defecation in constipated patients and pressure from pushing during the second stage of labor may contribute to hemorrhoid development. The main manifestations of internal hemorrhoids are anal discomfort and bleeding, whereas external hemorrhoids primarily cause external anal pain and pruritus. The main pathogenesis is increased intraabdominal pressure by the enlarging gravid uterus causing vascular engorgement and venous stasis. The primary treatment for both types of hemorrhoids is initially conservative with increasing dietary fiber and water intake, as well as the use of stool softeners. The American Journal of GASTROENTEROLOGY
Table 2. Grades of hemorrhoids Grade I
Internal hemorrhoids that do not prolapse
Grade II
Internal hemorrhoids that prolapse with defecation but reduce spontaneously
Grade III
Internal hemorrhoids that prolapse with defecation and require manual reduction
Grade IV
Internal hemorrhoids that are prolapsed and cannot be reduced manually
Hydrocortisone suppositories and sitz baths may reduce the swelling, discomfort, and pruritus associated with external hemorrhoids. If conservative therapy fails and symptomatic internal hemorrhoids persist, surgical or endoscopic therapy may be indicated in the postpartum period. Endoscopic band ligation, injection sclerotherapy, infrared coagulation, and surgical hemorrhoidectomy are all safe options in the postpartum period (27). The preferred treatment modality depends on the grade of hemorrhoids (Table 2). Grade I hemorrhoids typically respond to conservative therapy. Medically refractory grade I or II hemorrhoids can best be addressed with endoscopic modalities, with rubber band ligation showing 80% success rates (28). Symptomatic grade III hemorrhoids can be treated with either rubber band ligation or surgical excision, and grade IV hemorrhoids or grade III hemorrhoids with significant prolapse are best addressed surgically. One evaluation of stapled hemorrhoidopexy shows a 90% patient satisfaction rating postoperatively, despite a recurrence rate of approximately 18% (29). If possible, any procedure requiring sedation or prone positioning should be avoided during the first and third trimesters. Fecal incontinence
Epidemiology. Between 3 and 4% of women report new symptoms related to altered anal continence after pregnancy. Altered fecal continence has been reported in as many as 25% of primiparous women at 6 weeks postpartum (30). Fecal incontinence was found to be prevalent in 3.9% of women as early as at 12 weeks of gestation, and it increases to 5.7% at 3 months postpartum (13). Knowing that this problem may be underappreciated is emphasized by the finding in one study that only 14% of symptomatic women sought medical attention (31). However, one cannot underestimate the emotional, physical, social, and mental effects that this disorder causes. The median age of onset is in the seventh decade, at a time when these patients often cannot adequately take care of themselves, causing increased health-care costs and decreased quality of life (32). Pathophysiology. Fecal incontinence results from a complex interplay of insults to the structure and functions of the anal sphincter and the richly innervated anorectum along with the loss of the anal endovascular cushions (33). Each mechanism of maintaining continence has an important role. After pregnancy, the main mechanism of fecal incontinence is thought to be secondary to sphincter weakness and loss of stool awareness that are further VOLUME 110 | APRIL 2015 www.amjgastro.com
Pregnancy and Postpartum Bowel Changes
Risk factors. A recent study found that factors leading to postpartum anal incontinence several days after delivery included forceps delivery, prolonged second stage of labor >5 hours, expulsion phase >20 minutes, uterine revision, and first-degree perineal lacerations, whereas long-term incontinence between 6 and 8 weeks postpartum identified risk factors such as shoulder dystocia, anuvulvar distance 105 mm (34). A third- or fourth-degree sphincter tear was significantly associated with fecal incontinence 12 months postpartum (Table 3 and Figure 3). Previous theories noted that elective cesarean section, before any pushing, possibly had protective effects. However, urgent or emergent cesarean performed during the second stage of labor was thought to increase risk owing to prolonged pushing. A metaanalysis of 18 studies showed that symptoms of anal incontinence in the first year postpartum are associated with mode of delivery. Women having any type of vaginal delivery compared with a cesarean section had an increased risk of developing symptoms of solid, liquid, or flatus anal incontinence (35). However, a large prospective cohort study—“The Childbirth and Pelvic Symptoms study”—performed by the Pelvic Floor Disorders Network was done to prospectively estimate the prevalence of postpartum fecal and urinary incontinence in primiparous women. Women with and without clinically recognized anal sphincter tears during vaginal delivery and women delivered by cesarean before labor were analyzed. Compared with the vaginal control group, women in the sphincter tear cohort reported more fecal incontinence, fecal urgency, increased flatus incontinence, and greater fecal incontinence severity at 6 weeks and 6 months postpartum. At 6 months postpartum, 22.9% of women delivered by cesarean reported urinary incontinence, whereas 7.6% reported fecal incontinence. This highlights an important point that although women © 2015 by the American College of Gastroenterology
Table 3. Classification of third- and fourth-degree tears First degree
Limited to vaginal mucosa and skin of introitus
Second degree
Extends to the fascia and muscles of the perineal body
Third degree
Fourchette, perineal skin, vaginal mucosa, muscles, and the anal sphincter are torn
3a
Partial tear of the external anal sphincter involving 50% Tear of the external anal sphincter
3c
Internal sphincter is torn
Fourth degree
Fourchette, perineal skin, vaginal mucosa, muscles, anal sphincter, and rectal mucosa are torn
Rectum (torn) Anal sphincter (torn)
Perineal muscles (torn)
Anal sphincter (torn)
Figure 3. Classification of clinically significant perineal tears: (a) third degree and (b) fourth degree.
with clinically recognized anal sphincter tears during vaginal delivery are more likely to report postpartum fecal incontinence than women without sphincter tears, cesarean delivery before labor is not entirely protective against pelvic floor disorders (36). Similarly, other studies showed that there was no evidence of lower risk of subsequent fecal incontinence for exclusive cesarean section deliveries (37–39). A recent large cohort study—The Maternal Health Study—showed that the mode of delivery really did not alter the likelihood of fecal incontinence beyond the first 3 months postpartum (40). Despite the common belief that an elective cesarean section may be protective against the subsequent development of fecal incontinence (36), the current literature does not support this theory (Table 4). Many studies continue to look at the risk factors associated with fecal incontinence after pregnancy. In a large-scale study of 4,002 women, the prevalence of both flatal and fecal incontinence increased with age (P
