A Urogynecologist’s View of
the Pelvic Floor Effects of Vaginal
Delivery/Cesarean Section for the Urologist
René Genadry, MD
Corresponding author
René Genadry, MD
Johns Hopkins at Greenspring, 10755 Falls Road,
Suite 330, Lutherville, MD 21093, USA.
E-mail: rgenadr@jhmi.edu
Current Urology Reports 2006, 7:376 –383
Current Science Inc. ISSN 1527-2737
Copyright © 2006 by Current Science Inc.
Pregnancy and parturition have been implicated in the
development of pelvic floor dysfunction. These disorders
include urinary incontinence, fecal incontinence, pelvic
organ prolapse, and other pelvic and sexual dysfunctions.
The urologist caring for women with urinary dysfunc-
tion needs to be familiar with the causes of pelvic floor
dysfunction and their implications. Defects of the pelvic
floor have clearly resulted from the traumatic effect of
vaginal delivery. The likely mechanisms of injuries dur-
ing vaginal delivery involve stretching and compression
of the pudendal nerve and peripheral branches, as well
as an additional tearing of muscles and connective tissue.
Optimal management of labor and optimal techniques of
repair of unavoidable sphincteric lacerations, ante- and
postpartum pelvic floor muscle conditioning, and timely
and proper indications for cesarean delivery will mini-
mize the effect of incidental traumatic delivery.
Introduction
“This is the reason why the cure of many diseases
is unknown to the physicians of Hellas, because they
are ignorant of the whole, which ought to be studied
also; for the part can never be well unless the whole
is well.” (Socrates)
The issue of pregnancy and the pelvic floor is very momen-
tous as prophylactic abdominal delivery is discussed and
currently carried out in an attempt to prevent the devel-
opment of pelvic floor disorders (PFD). Pregnancy and
parturition have been implicated in the development of
PFD [1,2]. These disorders include urinary incontinence
(UI), fecal incontinence (FI), pelvic organ prolapse (POP),
and other pelvic and sexual dysfunctions. The absence of
complete, valid, and relevant information limits our abil-
ity to make accurate generalizations. The decisions thus
are based on opinions, anecdotal information, and data
of varying value and significance applied to the particular
situation. The urologist caring for women with urinary
dysfunction needs to be familiar with the causes of PFD
and their implications. Just what is known of the effects
of pregnancy and parturition on the pelvic floor? With
two daughters of reproductive age, the need for an answer
becomes even more pressing and timely.
The focus of this article is primarily on UI, FI, and
POP with regard to the nulliparous pregnant patient.
The development of pelvic floor dysfunction is
multifactorial and depends on genetic, physical, and
environmental factors. Most women deliver without evi-
dent long-term adverse effects [3]. A small proportion
of women develop symptomatic PFD following deliv-
ery. Defects of the pelvic floor also have occurred in the
absence of pregnancy and parturition [4]. It has been
difficult to dissect the critical determinants of an adverse
effect of vaginal delivery (VD) and the possible protective
effect of cesarean delivery (CD) [5,6]. In the meantime,
the rate of CD in this country is at its highest (29.1%).
This represents an increase of 40% from 1996 to 2004.
Clearly, a better understanding of the normal processes
of labor and delivery, the elements of proper recovery,
and the ability to define and identify hazardous factors
before they result in an irremediably traumatic delivery
are warranted. The relevant data are limited, but their
significance is the subject of this review, as is the effect of
pregnancy and vaginal birth and the possible protective
role of cesarean section on the pelvic floor.
Pregnancy and the Pelvic Floor
The pelvic floor includes the levator ani muscle, contribut-
ing to the pelvic diaphragm acting as a sphincter around
the genital hiatus, along with the urethral and anal
sphincters, endopelvic fascia, and its condensations and
connective tissue and neurovascular structures therein
contained. It functions as a unit and its overall efficacy
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry
depends on its weakest component [7]. Thus, any focal
defect is compensated for by its more effective components
until their alteration eventually leads to decompensation
and failure. Facilitating events may occur that will deter-
mine the occurrence of such decompensation.
Anatomical adaptation
During pregnancy, the pelvic floor undergoes adaptive
changes under the influence of hormonal and mechani-
cal effects to accommodate the progressively enlarging
uterus and the need for a competent genital hiatus capable
of enlarging during parturition, with impunity to allow
the delivery of the fetus. The plasticity of these structures
is indeed phenomenal in order to sustain such variations
in size and resilience without more obvious indication of
inadequate recovery. Understanding these processes holds
the key to preventing their failure.
Hormonal effects
There is a remarkable paucity of data on the effect of
pregnancy on the pelvic floor and its components. In addi-
tion to a number of hormones, including progesterone,
which has known smooth muscle-relaxing properties,
the corpus luteum of pregnancy, the deciduae, and later
the placenta produce relaxin, which peaks during the
first trimester and contributes to placental implantation
and growth. In late pregnancy, it facilitates dilation of
the cervix and relaxation of the symphysis pubis. It also
downregulates the estrogen receptors. Such downregula-
tion leads to failure to maintain elastic fiber regeneration
and homeostasis that, in mice, has been shown to lead to
PFD [8]. During pregnancy, higher relaxin activity was
measured in women with PFD compared with asymptom-
atic women [9]. Furthermore, fibroblasts from women
with SUI respond differently to reproductive hormones
than control subjects. Increasing relaxin concentrations
seem to favor increased elastolytic activity [10]. This
deserves close scrutiny as the clinical use of relaxin to
facilitate birth is being investigated [11].
Mechanical effects
The average weight gain during pregnancy is approxi-
mately 28 pounds. This contributes to a variety of
changes, including an increase in the lower back lordosis
to compensate for uterine enlargement along with stretch-
ing of the abdominal wall muscles, occasionally leading
to their separation. At approximately 10 to 12 weeks,
the symphysis pubis widens and there is increased mobil-
ity of the sacroiliac joints and a significant increase of
the anterior tilt of the pelvis to allow easy passage of the
fetus through the birth canal. The constantly increasing
weight and resulting mechanical stress over a softened
pelvic floor leads to progressive weakening of the pelvic
floor support system. Pregnant women have been found
to have increasing stage of prolapse as pregnancy pro-
gresses and compared with age-matched, non-pregnant
377
control subjects [12]. Myogenic alterations seem to be
the most plausible cause of such weakening of the pelvic
floor [13]. When the appearance of the levator ani muscle
in pregnancy was imaged by three-dimensional magnetic
resonance, variation in morphology was common and
recognizable injury was uncommon in asymptomatic nul-
liparous women at term [14]. The effect of high-impact,
high-intensity sport and training on levator ani morphol-
ogy leads to significant differences in the cross-sectional
area and width of the pelvic floor muscles [15]. The pos-
sibility that athletes have longer second-stage labor has
been raised, and predicting the course of labor and the
effectiveness of pelvic floor rehabilitation would certainly
be beneficial. The exact role of biometric indices of the
pelvic floor muscle mass requires elucidation.
Functional adaptation
The functional anatomy of the lower urinary tract has
been investigated during pregnancy. In addition to rec-
ognized racial differences [16], the urethral sphincteric
mechanism and its support also are affected by heredity.
Translabial ultrasonography revealed a diminished ure-
thral sphincteric function induced by pregnancy that also
favors a backward displacement of the bladder neck in
nulliparous women compared with their twin sisters [17].
In a comparative study of pregnant and non-pregnant
women, a decrease in maximal urethral closure pressure
and area of continence at rest and at stress in pregnancy,
as well as a decrease in the pressure transmission ratio
values were demonstrated [18]. There was no correlation
between these parameters and advancing pregnancies.
Compared with antenatal measurements, such displace-
ment during coughing and Valsalva were significantly
increased after delivery, although in some, resolution
occurred. The transient increase in bladder neck displace-
ment seems to relate to a decrease in the resistance of the
pelvic floor. This phenomenon has been dubbed “stress
relaxation” resulting from molecular reorganization and
fiber movement leading to the necessary adaptation of
collagen tissue to permit physiologic stretching during
pregnancy and parturition [19].
Clinical effects of pregnancy
Clinically, it has been estimated that up to 82% of
women report symptoms of stress urinary incontinence
during pregnancy [20–23,24•]. In a recent prospec-
tive, longitudinal cohort study of 515 nulliparous with
singleton pregnancy, urogenital symptoms were found
to occur in almost all of the women during pregnancy
[25]. Although irritative symptoms were prevalent early
on, they remained stable during gestation, whereas the
prevalence of true incontinence symptoms increased with
gestational age. Of note is the fact that most women were
not bothered by their symptoms. What is responsible for
these symptoms? In addition to hormonal effects, uter-
ine enlargement, and increased pressure, the cause of UI
378 Voiding Dysfunction
in pregnancy may be due to a combination of factors,
including an increase in glomerular filtration rate and
bladder irritability and a decrease in strength of fascial
and pelvic floor support system made worse by heredi-
tary and environmental predispositions. These changes
recede over a variable period during the year following
delivery. Aggressive management during that time should
primarily aim at muscle reconditioning.
The reported incidence of anal incontinence (AI)
varies between 1% and 45%. Common causes of AI are
anatomic and functional and usually are unrelated to
pregnancy. Following pregnancy and delivery, AI results
from a recognized or unrecognized sphincter laceration
and/or a neuropathic injury. Pregnancy per se does not
induce any change in pelvic nerve conduction; neverthe-
less, severe AI following elective and pre-labor emergency
CD has been reported [26].
Although incontinence is a more common complaint
than other symptoms of poor support, such weakened
support is a more common physical finding during preg-
nancy [27]. Pregnancy is associated with pelvic relaxation
even before delivery. The anterior compartment seems to
lead to the increase in Pelvic Organ Prolapse Quantifica-
tion staging during pregnancy and does not necessarily
change following delivery [12]. It is higher in women who
deliver vaginally than in those who deliver by cesarean
section, although the latter affords no guaranteed protec-
tion because pelvic floor mobility can follow CD [28] as a
result of pregnancy-induced softening of the tissues of the
pelvic floor. The degree to which this softening recedes has
not been properly evaluated. It is fair to say that it is rare
that a patient who has had a normal pregnancy and a nor-
mal delivery sustains any significant abnormality unless
other factors, such as time, genetics, and circumstances,
have subsequently contributed. This change in organ
mobility implies alterations in the biochemical properties
of the supportive structures in pregnancy. Data on basic
mechanisms are lacking and clinical studies have largely
to rely on statistical acrobatics to attempt a tentative sig-
nificance of reality. No relevant randomized, controlled
study is available to help dissect the causal effect of VD
and the protective effect of cesarean delivery. Basic sci-
ence should further elucidate these properties and allow
beneficial clinical applications.
Vaginal Delivery and the Pelvic Floor
Vaginal delivery is the natural process of birth. When dif-
ficult, assistance or alternatives are required. At times, the
resulting anatomic and physiologic changes eventually lead
to symptomatic dysfunction. Defects of the pelvic floor have
clearly resulted from the traumatic effect of VD. It has been
estimated that one in 10 parous women may develop POP
because of a traumatic delivery, although most women who
delivered vaginally do not seem to present with significant
problems. What are the processes involved in VD?
Normal labor and delivery
In its optimal progression, labor and delivery are clini-
cally divided into three stages. The first stage results in
cervical effacement. It is completed with cervical dilation
that allows the passage of the presenting part through the
birth canal. The second stage begins with complete cervi-
cal effacement and dilatation and results in the expulsion
of the fetus. The third stage is completed by the separa-
tion and expulsion of the placenta. The birth canal is
functionally closed and maintained in proper position by
a number of layers of muscular and connective tissues that
collectively form the pelvic floor. The hydrostatic pressure
of the bulging membranes contributes to cervical dilation.
After the membranes have ruptured, as the presenting part
descends into the birth canal, it leads the way and exerts
most of the direct pressure on the pelvic floor. The median
duration of the second stage is approximately 50 minutes
in nulliparous, but it can be highly variable. However,
it may become dangerously long if there is a contracted
pelvis, inappropriate presentation, or ineffective expulsive
uterine contractions. A second stage lasting more than 2
hours is considered abnormal and usually prompts active
management. The resulting opening of the genital hiatus
to allow the passage of the fetus through the birth canal
is witnessed mostly by stretching the fibers of the leva-
tor ani muscle and connective tissues and by drastically
distending the perineum to a thin membranous structure
that should be protected during the process of delivery.
The role of episiotomy in this process remains controver-
sial and requires further study. The progressive descent
of the presenting part through the birth canal represents
the most critical event, and is potentially damaging in
its aftermath. In the nulliparous patient, such descent is
slowly initiated before the onset of labor. Although such
passage necessarily involves accommodation and stretch-
ing, it is the exaggeration of each that may lead to damage
through compression and tearing. Mechanical damage
is amplified by neurovascular compromise resulting in
devascularization and denervation.
Abnormal labor and delivery
In the event of arrest in the progress of labor, oxytocin
augmentation is used to amplify contractions and increase
the pressure through the pelvis and through the outlet,
with the aid of mechanical devices including forceps or
a vacuum. At times, this results in the relatively forceful
extraction of an otherwise poorly positioned presenting
part. In fact, an outlet forceps has been advocated to
direct the presenting part away from the perineum in an
attempt to minimize trauma to the latter or to hasten deliv-
ery in the presence of fetal distress. An episiotomy also
was meant to provide a similarly protective effect of the
urethral and anal sphincters by avoiding uncontrollable
tearing of tissue. However, the effect of these maneuvers
had not been fully investigated before their implementa-
tion [29]. Thus, whereas the delivery of the presenting
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry
part threatens the anal canal, its descent through the birth
canal during labor is a potential threat to the structures of
the pelvic floor.
Mechanisms of injury
The likely mechanisms of injuries during VD have been
well stated [30]. In essence, they involve stretching and
compression of the pudendal nerve and peripheral branches
as well as an additional tearing of muscles and connective
tissue. Neurophysiologic studies have been widely reported
with varying degrees of accuracy and significance. With
improved imaging, the muscular defects are beginning
to be defined while the connective tissue defects remain
largely speculative. The degree of recovery or permanence
of these changes requires further investigation.
We are just witnessing the emergence of simulated
studies on the biometrics of the pelvic floor muscles. A
three-dimensional computer model based on MRI sug-
gests that the most medial and inferior part of the levator
have to increase its length by a factor of 3.5 in order to
accommodate a fetal head; thus, the lower third of the
pubococcygeus is most at risk during vaginal birth [31].
Furthermore, the nerves to the anal sphincter are stretched
beyond the 15% strain threshold of damage to a degree
influenced by that of perineal descent [32]. Similar stud-
ies are needed for the connective tissue and neurovascular
pedicle; their long-term effect and their biologic proper-
ties of resilience and healing require definition. In the
meantime, a number of neurophysiologic, epidemiologic,
and clinical studies are attempting to define risk factors.
FI after childbirth initially was related to pudendal
nerve injury [33]. Occult pudendal nerve damage was
common, at times reversible but more severe depending
on increased birth weight, forceps delivery, and pro-
longed second stage. After 5 years, changes persisted in
36% of patients, whereas 60% developed flatal inconti-
nence and all developed symptoms of stress incontinence.
Women who delivered by cesarean section did not seem
to be affected.
In addition to these neurophysiologic abnormalities,
occult external anal sphincter defects were detected by
ultrasonography [34]. Eight of 10 patients undergoing
forceps delivery had such lesions and none of the cesarean
patients had any lesions or symptoms. Quantitative elec-
tromyography after a reportedly uncomplicated vaginal
delivery can detect the presence of subtle nerve injuries
that are not detected by conduction studies [35], casting
some doubt on the clinical significance of damage to the
peripheral innervation of the external anal sphincter dur-
ing uncomplicated deliveries.
Clinical effects of parturition
These data were disturbing. AI is a devastating condition.
The anal sphincter is at most risk for direct damage. The
issue of a protective effect of CD was raised. A number
of obstetric factors were suspected, including instrumental
379
delivery and episiotomy [36]. The role of a prolonged sec-
ond stage and macrosomia remains controversial. Forceps
delivery and anal sphincter laceration were responsible
for 3.1% of patients experiencing fecal incontinence and
25.5% of patients experiencing flatal incontinence after
childbirth [37]. Direct anal sphincter laceration was
strongly predicted by first vaginal birth, median episi-
otomy, and the use of forceps or vacuum but not by birth
weight or length of second stage. Anal incontinence at 9
months postpartum predicts persistence [38]. Unrecog-
nized injuries to the internal anal sphincter also play a role.
Denervation is likely operative in a number of cases over
time. Whereas AI resulting from direct and visible trauma
may be immediate, neuropathic pathology requires time to
declare itself. The contribution of inadequate repair of the
external anal sphincter rupture and internal anal sphincter
extension require proper definition. The optimal technique
and timing of repair of the external anal sphincter requires
further investigation. It has been suggested that patients
with previous external anal sphincter rupture undergo a
cesarean section during childbirth [39,40]. A number of
studies have confirmed that women with UI are likely to
also suffer from FI and prolapse [41].
There is good evidence that pregnancy and parturi-
tion contribute to the risk of UI. Although the urethral
sphincter mechanism is affected, and de novo stress incon-
tinence has been reported to be between 3.7% and 19%,
the contribution of independent obstetric factors remains
controversial. Pregnancy and VD increase the degree of
bladder neck descent with cough, but UI, which is common
during pregnancy, occurs less frequently postpartum [42].
When stress urinary incontinence develops during the first
pregnancy, the risk of stress urinary incontinence occurring
15 years later is doubled [43]. Most vaginal damage is done
during the first delivery [44], although a cumulative effect
can be expected with future pregnancies. The main combi-
nation of risk factors for stress urinary incontinence after
pregnancy includes age, previous incontinence, prolonged
labor, and VD [45]. However, in a cross-sectional study of
2625 women, the prevalence of severe stress incontinence
was not associated with the mode of delivery. The risk fac-
tors for severe incontinence included increased body mass
index, diabetes, previous incontinence surgery, parity, and
childbirth before the age of 22 years [46]. VD is a major risk
factor for stress incontinence among mothers of multiples.
In this instance, CD provides an independent protective
effect regardless of age, parity, and body mass index [47].
Control of obesity before pregnancy and regular exercises
involving the pelvic floor before and after birth reduces
the risk of postpartum incontinence [48]. The pelvic floor
muscle weakness is but one of the factors leading to UI.
Genetic factors play a substantial role in the development
of urge and mixed incontinence but a less prominent one in
stress incontinence [49]. Recent studies have attempted to
control for environmental and genetic factors and look at
the mode of delivery and future risk of incontinence. They
380 Voiding Dysfunction
resulted in conflicting reports. No statistically significant
difference was noted in the groups regarding UI when nul-
liparous nuns were compared with their parous sisters. In
this instance, the risk may be due to familial traits and are
unrelated to the mode of delivery [50]. On the other hand,
in comparing UI among identical twin sisters, risk factors
included age, obesity, and mode of delivery. VD increased
the risk by a factor of 2.28 over CD [51].
Modifiable obstetrical practices offer a mean to alter
the effect of VD on the pelvic floor. However, proper
data are lacking. Coached pushing in the second stage
of labor seems to alter the urodynamic indices regarding
first urge to void and bladder capacity, increase the risk
of detrusor overactivity, and result in significant descent
of the posterior vaginal wall [52•]. The contribution of
conduction anesthesia remains controversial. A number
of epidemiologic studies have shown that CD provides
only partial protection. This seemingly fades over time
and with increasing parity [53].
Regarding POP, pregnancy and parturition have been
implicated as major risk factors for prolapse. Vaginal
birth, operative delivery in particular, negatively affects
pelvic organ support. POP is associated more strongly with
birth than urinary or fecal incontinence, as the chance for
developing POP increases by 4 to 11 times [54] and stress
incontinence increases by 2.7 times [55]. Indices of exces-
sive stretching and tearing such as vaginal lacerations and
episiotomy and multiple deliveries are main predisposing
factors for symptomatic POP. A strong protective func-
tion is afforded by CD [56].
Childbirth-related injuries leading to different types of
incontinence may be interdependent of one another. The
effect of altered obstetrical practice on the pelvic floor
requires investigation that is more stringent unless all of
the deliveries bypass labor and VD. The protective effect
of cesarean section also may be altered by epidural anal-
gesia and may not be effective against AI [57]. An unmet
challenge that remains is the ability to identify high-risk
labors early to avoid irremediable damage.
Cesarean Section and the Pelvic Floor
Although arguments for and against the benefits of univer-
sal cesarean section continue, the more or less informed
patients and their treating physicians are struggling with
a difficult decision based on intuitive impression and
anecdotal circumstances. Abdominal delivery presents
surgical risks in addition to VD and in proportion to its
emergency. What is known of the benefits of CD?
Cesarean deliver, urinary incontinence, anal
incontinence, and pelvic organ prolapse
Viktrup and Lose [58] prospectively questioned 305
primiparas about their UI before, during, and after preg-
nancy and noted that in those without antepartum stress
incontinence, 13% developed it postpartum compared
with none of the 35 women who delivered by cesarean
section. After the first year, only 3% of the women expe-
rienced stress incontinence. However, after 5 years, of the
91% who were questioned originally, a prevalence of 30%
was reported; CD was protective. Time, per se, is a risk fac-
tor in the development of post-delivery stress incontinence,
as are increased parity and obesity [59,60]. In the Epide-
miology of Incontinence in the County of Nord-Trøndelag
study, only the increased risk of stress incontinence was
dependent on and associated with the mode of delivery
[61]. No association of incontinence with mode of delivery
was noted in older age groups. Thus, there is some retro-
spective evidence for some protective role of CD in some
circumstances. However, this seems to fade after the third
delivery [62]. A CD following obstructed labor does not
seem protective [63]. It is difficult to assess the role of fetal
descent prior to labor and its implication in prelabor CD.
Using a validated urinary symptom questionnaire,
Chaliha et al. [64] compared 40 women who had three
elective CDs with 80 women who had three VDs. Symp-
toms of incontinence, both fecal and urinary, are reported
following VD and elective cesarean, with a prevalence of
stress incontinence being far greater following multiple
VDs [64]. Elective CD may protect against the develop-
ment of stress incontinence, but the risk of FI and other
urinary symptoms may not be reduced. CD in the first
pregnancy appears to protect against pelvic floor surgery
later [65]. This risk seems to be reduced from 5% to 1%
but not eliminated.
Role of elective cesarean delivery
Culligan et al. [66], using a decision analytic model to
compare standard of care with a policy declaring that
all primigravid patients in the United States undergo an
ultrasound at 39 weeks gestation, followed by an elective
cesarean section for any fetus estimated to be ≥ 4500 g,
calculated that for every 100,000 deliveries, 16.6 fewer
permanent brachial plexus injuries and 185.7 fewer cases
of AI are prevented. They argued a favorable cost analysis
for such a policy [66].
Overall, the evidence that planned elective CD affects
the rate of stress and anal incontinence is relatively weak
in the absence of properly conducted prospective stud-
ies. In essence, more uniform sets of definitions and
outcome measures are required to gain useful informa-
tion. Because of such uncertainties, controversies as to
the benefit of CD on demand will continue. It has been
suggested that CD be more widely available to women,
particularly to nulliparous patients having undergone
pelvic reconstructive surgery.
Cesarean delivery on maternal request was the topic of
a consensus conference in March 2006 [67•]. A review of
reliable evidence suggested that none existed dealing with
this specific area. What exists is significantly limited by its
minimal relevance to primary CD. The only randomized,
prospective study was the breech trial [68]. This was a
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry
prospective trial focusing primarily on neonatal outcomes
following planned VD versus planned CD for breech
presentation. Planned CD significantly reduced the risk
of UI at 3 months; however, in another 2-year postpar-
tum follow-up, the difference was no longer statistically
significant. Two studies followed a prospective cohort
format and were of moderate relevance. One revealed that
the planned elective CD performed during the first stage
of labor seemed protective against UI compared with
spontaneous VD; the risk of postpartum incontinence
at 6 weeks was 35% for forceps, 23% for spontaneous
VD, 9% for spontaneous CD, and 4% for elective CD
[69]. The other moderately relevant study suggested that
incontinence 1 year postpartum was not significantly dif-
ferent among primiparous women who underwent VD or
CD during labor; however, it was significantly lower in
patients who had an elective CD [63].
Regarding anorectal function, six studies assessed
symptoms of AI. Two originated from the breech trial
and used two different measures at two points in time;
there was no significant difference in rates of FI between
planned VD and planned CD. The two moderately rel-
evant studies suggested an increasing risk of FI with
emergency CD and VD compared with elective CD; the
latter was not always protective [70,71]. One study noted
that AI was higher with forceps-assisted delivery than
with spontaneous VD [72].
One low-relevance study examined POP using an
essentially administrative set of data. No evidence for the
association was found between POP and planned VD or
planned CD [73].
Whether and when CD provides protection and for
how long requires further elucidation. During an abnor-
mal VD, an increased risk of damage can be expected.
This in turns leads to an increased risk of pelvic floor dys-
function, which eventually can lead to the development of
pelvic organ and pelvic floor dysfunction with increasing
age and parity, particularly when associated with opera-
tive VD, long second stage, and macrosomia.
Conclusions
The best way to avoid pelvic floor damage is to predict
operative VD and prolonged second stage as well as fetal
weight. Connective tissue injury and repair are not very
well understood. It is assumed that the connective tissue
of repair is weaker than the native connective tissue; over
time, this could be a significant element in the development
of pelvic floor dysfunction, but further research is needed.
However, it is known that immediately after delivery, UI
and decreased strength of the pelvic floor occur less often
following a CD. Likewise, direct trauma of the urethral,
anal, and pelvic sphincters can be avoided by an elective
CD. Once labor is started and the process of delivery is
initiated, it is difficult to prevent the effect of compres-
sion and stretching from having a deleterious effect on the
381
pelvic floor structures. It is important to identify which
factors are most deleterious.
A better definition of the role of the genetic, physical,
and environmental factors in the development of PFD is
warranted. Although it is known that VD increases the
risk by two to three, most patients do well following ideal
VD. Modifiable factors including PFM rehabilitation, con-
trol of obesity, and macrosomia, as well as predictors of
normal labor and uninstrumented delivery, will contribute
to a significant reduction in the morbidity of parturition.
Optimal indications for CD and optimal techniques of
repair of unavoidable sphincteric lacerations will mini-
mize the effect of incidental traumatic delivery. I would
offer nulliparous patients who are predictably at high risk
for pelvic floor damage and dystocia a CD to prevent or
delay pelvic floor morbidity.
With regard to my daughters and while awaiting
more pertinent information, they will have to make their
decisions individually, based on the inherent risks of preg-
nancy and the advice of their obstetrician well attuned to
the long-term effects of VD and the added risks of assisted
VD. Such a partnership with an experienced obstetrician
skilled in the proper identification and reconstruction of
the internal and external anal sphincters in the event a less
than optimal VD is encountered in addition to a healthy
lifestyle, including proper pelvic floor muscle conditioning
before and after delivery, hopefully will result in a healthy
progeny at minimal exposure.
References and Recommended Reading
Papers of particular interest, published recently,
have been highlighted as:
• Of importance
•• Of major importance
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of surgically managed pelvic organ prolapse and urinary
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2. DeLancey JO: The hidden epidemic of pelvic floor
dysfunction: achievable goals for improved prevention and
treatment. Am J Obstet Gynecol 2005, 192:1488–1495.
3. Nygaard I, Bradley C, Brandt D, et al.: Pelvic organ pro-
lapse in older women: prevalence and risk factors. Obstet
Gynecol 2004, 104:489–497.
4. Harris RL, Cundiff GW, Coates KW, et al.: Urinary incon-
tinence and pelvic organ prolapse in nulliparous women.
Obstet Gynecol 1998, 92:951–954.
5. Nygaard I: Should women be offered elective cesarean
section in the hope of preserving pelvic floor function? Int
Urogynecol J 2005, 16:253–254.
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