CLINICAL AND SYSTEMATIC REVIEWS

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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 oor 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; 110:521529; 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 oor

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

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: Ron.schey@tuhs.temple.edu
Received 29 October 2014; accepted 10 February 2015

2015 by the American College of Gastroenterology

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Anterior

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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 oor 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
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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 (79).
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
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Table 1. Causes of constipation in pregnancy

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Dehydration (nausea/vomiting, poor oral intake)

Hormonal (progesterone, hypothyroidism)
Mechanical (gravid uterus, pelvic oor 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 (2139%) 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
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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 Hirshsprungs 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 (2225). 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 (2035 g/day), and osmotic laxatives such as polyethylene glycol (825 g/day) and lactulose (1530 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.
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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
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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 <2 cm, perineal scars, and transverse abdominal
diameter >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 studyThe Childbirth and
Pelvic Symptoms studyperformed 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. Classication 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% thickness

3b

>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. Classication of clinically signicant 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 (3739). A recent large cohort studyThe
Maternal Health Studyshowed 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<0.001) and parity (P<0.001). Flatal
incontinence was reported by 11.4% of nulliparous woman, 18.9%
of women who delivered by cesarean only, 23.2% of women with
vaginal delivery, and 24.4% of women with mixed type of delivery, representing a significant impact of the mode of delivery
(P<0.001). Fecal incontinence was reported by 1.2% of nulliparous
women, 1.1% of women who delivered by cesarean only, and 2.9%
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aggravated by aging. Sphincter weakness is caused by structural

injuries to the anal sphincter musclesboth internal and external
sphinctersinjury to the pudendal nerve, or a combination of
the two. Loss of stool awareness arises from damage to the nerves
allowing anorectal sensation, resulting in inability to differentiate formed stool, liquid stool, or flatus, not to mention losing the
warning signs of imminent defecation. The mechanism of how
humans perceive stool in the anorectum is unknown. However,
various studies looking at continence with balloon distention and
rectal sensitivity are pointing to what is likely the parasympathetic
sensory innervation of the sacral nerves S2, S3, and S4.
Acutely after a complicated delivery with high-degree tears,
women may experience fecal incontinence secondary to the acute
structural injury, requiring surgical intervention. Acute-onset
fecal incontinence is not frequently seen, as most women of childbearing age have enough reserve in the other mechanisms of continence to compensate for the acute structural or neurologic injury.
However, a majority of the patients present later in life as discussed
in this review, and the treatment options are mainly geared toward
those who present with delayed-onset fecal incontinence. The
delayed-onset disease is likely multifactorial, as each mechanism
of continence starts to lose its competency.

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Table 4. Causes of incontinence in pregnancy

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Vaginal delivery
Forceps
Emergency cesarean section
Epidural anesthesia
Perineal laceration
Obstetric genital stula

of women with vaginal delivery (P=0.005), but the association

between fecal incontinence and the mode of delivery again did not
persist after adjusting for age (20).
Evaluation of anatomical damage of the anal sphincter showed
that it is less common following vacuum extraction than forceps
deliveries, and that operative vaginal deliveries may contribute to
unrecognized vaginal trauma, and the degree of injury directly
correlates to symptoms of incontinence (4143). A recent study
demonstrated that the prevalence of anal incontinence was highest among women with a previous delivery complicated by obstetric anal sphincter injury (24.4%), followed by risk factors such as
increasing parity (44,45).
Several studies had shown that the severity of pelvic organ
prolapse does not have a major role for pelvic organ prolapse in
defecatory disorders, reinforcing the prevailing notion that these
symptoms are predominantly attributable to disordered anorectal
structure and/or function, including anal sphincter injury (4648).
Kearney et al. (48) 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 22 of 160 patients: the use of forceps, the occurrence of an anal
sphincter tear, and an episiotomy were significant risk factors.
McKinnie et al. (49) found that although parous women were
twice as likely to experience fecal incontinence as their nonparous
counterparts, this risk was not reduced by cesarean section. Complete rupture of the anal sphincter, however, was associated with
increased fecal incontinence compared with both the cesarean and
normal delivery groups, and these patients frequently wished to
postpone or avoid further deliveries, or often chose to go directly
into cesarean delivery for the subsequent pregnancies (50). They
did detailed analysis of multiple birth-related factors, and failed
to identify any significant differences between women who had
vaginal or cesarean deliveries. Hence, it suggests that parity is an
important factor in the etiology of incontinence, with the mode of
delivery possibly adding to this risk.
Treatment. Given the multiple mechanisms that maintain continence, treatments are more likely to be successful if several of
these deficits are addressed instead of just one.
Treatments of fecal incontinence range from conservative
management, such as dietary modification and fiber supplementation, to pharmacologic intervention with agents such as
loperamide, all the way to pelvic floor muscle training and surgical management. Surgical intervention is typically reserved
for those women refractory to nonsurgical options. Both pelvic
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floor muscle training and surgery can be used for the prevention
and treatment of urinary and fecal incontinence for the pregnant
and postpartum women. A recent Cochrane review of 22 trials
involving over 8,000 women showed that there was some efficacy
in pelvic floor muscle training for the prevention and treatment
of urinary incontinence in patients who were continent during
pregnancy at 6 and 12 months postpartum. However, the data are
unclear in women who were already experiencing incontinence
during pregnancy. In addition, there are little data regarding the
long-term effects of pelvic floor muscle training for either urinary
or fecal incontinence (5153).
These studies were mainly questionnaire based, and they bring
up an important concern for recall bias, selection bias, a lack of
detail on the type of cesarean section performed (whether elective
or emergency), or on complications of vaginal delivery (instrumentation, tears, episiotomy). On the basis of these study limitations,
no specific recommendations regarding the mode of delivery in the
prevention of fecal incontinence can be given (54). Several small
studies have evaluated the changes in anal sphincter physiology and
morphology owing to pregnancy, and concluded that without evidence of tears, there have been documented changes in sphincter
morphology that are nonsignificant and not sufficient enough to
predict symptom development (5558). In addition, a recent study
showed that in women sustaining third-degree tears, early biofeedback with pelvic floor muscle training had no additional value (59).
Recent studies have attempted to evaluate methods to prevent clinical complaints of incontinence. Hayes et al. (60) found
that residual sphincter defects were found in as much as 61% of
women after sphincter repair, which was associated with higher
rates of abnormal resting and squeeze anal pressures. The use of
three-dimensional transperineal ultrasound to evaluate the repair
of third- or fourth-degree intrapartum tears have shown that
although many of these patients did complain of incontinence
initially, 42% showed no sonographic evidence of previous injury
when examined several months after the repair, and their symptoms of incontinence did not differ from the control groups. However, the rate of complaints was higher in patients with abnormal
follow-up ultrasounds, and 25% of these patients had clinical deterioration of incontinence symptoms after the second delivery (61).
This brings up the question of whether or not we should be using
ultrasound assessment of the anal sphincter to screen high-risk
individuals as part of clinical counseling before subsequent trial of
labor or elective cesarean delivery.
Numerous developments have been made in the surgical therapies available to treat fecal incontinence. Neosphincter creation
(muscle or artificial) is more invasive and associated with considerable morbidity, although some patients will experience substantial improvements in their continence.
Previous studies have reported that injection therapy of bulking
agents into the anal canal seems to be safe and leads to a reduction in the number of incontinence episodes in the short term,
and it seems to improve symptoms and quality of life regardless
of the material used. However, definitive conclusions could not
be drawn owing to study heterogeneity (62). A recent study by
Graf et al. (63) reported that injection therapy of the bulking agent
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CONCLUSION
Pelvic floor disorders, including constipation and fecal incontinence, are very common during and after pregnancy. The etiology of the disorders are often multifactorial. Constipation may be
caused by dehydration and poor fiber intake from nausea/vomiting, hormonal changes during pregnancy causing gastrointestinal
hypomotility, conformational changes of the pelvic floor owing to
increased intraabdominal pressure, luminal obstruction from the
weight of the gravid uterus, drug effects from antiemetics, tocolytics, and iron supplementation, or exacerbations of preexisting irritable bowel syndrome or chronic idiopathic constipation.
Although troublesome, it is important for the patient to know that
pregnancy-associated constipation usually improves after delivery
and it can be managed with diet and medications. Complications
associated with pregnancy-induced constipation include hemorrhoids and pelvic floor laxity, managed with improved bowel regimens, hemorrhoid-directed endoscopic or surgical interventions,
and pelvic floor muscle training.
Postpartum fecal incontinence studies continue to show that
despite the troublesome effects on the patients in both short
and long term, the exact etiology is multifactorial and difficult to
predict. Prolonged and complicated labor and delivery, along with
sphincter tears, appear to increase the risk of postpartum incontinence severity. Many of these patients suffer incontinence in the
short-term postpartum period and, thankfully, the symptoms do
appear to improve in many after 1236 months, although studies
are lacking with regard to how many of these patients are showing
up in our primary care and subspecialty offices with these symptoms decades later. Currently, there are new methods to treat fecal
incontinence including the sacral nerve stimulation and the lessinvasive percutaneous tibial nerve stimulation techniques. The
goal in these patients refractory to more conservative management would be to decrease the symptom scores, and further investigation on these treatments are needed to determine whether the
symptoms can be eliminated altogether. Future research is needed
to see how these treatments really alter a patients overall quality
of life.
2015 by the American College of Gastroenterology

CONFLICT OF INTEREST

Guarantor of the article: Ron Schey, MD, FACG.

Specific author contributions: Grace H. Shin and Erin L. Toto:
review of previous and current information, drafting of manuscript,
and critical revision of the manuscript for important intellectual
content. Ron Schey: review of previous and current information,
drafting of the manuscript, critical revision of the manuscript for
important intellectual content, review supervision, and guarantor for
submission.
Financial support: None.
Potential competing interests: None.

Study Highlights
WHAT IS CURRENT KNOWLEDGE

Constipation and fecal incontinence are common disorders

associated with pregnancy and the postpartum period and
can cause signicant patient stress as well as health-care
burden.

Approximately 40% of pregnant women suffer from constipation at some point during and after their pregnancy, and
there are conicting data regarding whether the mode of
delivery has any association with subsequent constipation.

Altered fecal continence has been reported in as many as

25% of primiparous women at 6 weeks postpartum, and
anatomical damage of the anal sphincter is less common
after vacuum extraction than after forceps deliveries.

Operative vaginal deliveries may contribute to unrecognized

vaginal trauma, and the degree of injury directly correlates
to symptoms of incontinence.

WHAT IS NEW HERE

Therapy for pregnancy-associated constipation is similar

to that of the general population. It is aimed at reassuring

the patient, encouraging adequate uid intake, using ber
supplementation, as well as osmotic laxatives (such as
polyethylene glycol (PEG) or lactulose).

PEG is not approved by the Food and Drug Administration

(FDA) for use in pregnancy, and although minimally absorbed,

it does carry a pregnancy category C rating.

Despite the common belief that an elective cesarean

section may be protective against the subsequent development of fecal incontinence, the current literature does not
support this theory.

Numerous developments have been made in the surgical

therapies available to treat fecal incontinence: Neosphincter

creation (muscle or articial), injection therapy of bulking
agents into the anal canal, sacral nerve stimulation (SNS),
and recently a percutaneous tibial nerve stimulation (PTNS).

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Pregnancy and Postpartum Bowel Changes