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 dysfunction 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 during 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
minimize 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
momentous as prophylactic abdominal delivery is discussed
and currently carried out in an attempt to prevent the
development 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 ability 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 evident
long-term adverse effects [3]. A small proportion of women
develop symptomatic PFD following delivery. 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, contributing
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 depends on its
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry 377
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 determine the
occurrence of such decompensation.
Anatomical adaptation
During pregnancy, the pelvic floor undergoes adaptive
changes under the influence of hormonal and mechanical
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 addition
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 downregulation 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 asymptomatic 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 approximately
28 pounds. This contributes to a variety of changes, including
an increase in the lower back lordosis to compensate for
uterine enlargement along with stretching of the abdominal
wall muscles, occasionally leading to their separation. At
approximately 10 to 12 weeks, the symphysis pubis widens
and there is increased mobility 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
progresses and compared with age-matched, non-pregnant
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
nulliparous women at term [14]. The effect of high-impact,
high-intensity sport and training on levator ani morphology
leads to significant differences in the cross-sectional area and
width of the pelvic floor muscles [15]. The possibility 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 recognized
racial differences [16], the urethral sphincteric mechanism
and its support also are affected by heredity. Translabial
ultrasonography revealed a diminished urethral 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
displacement during coughing and Valsalva were
significantly increased after delivery, although in some,
resolution occurred. The transient increase in bladder neck
displacement 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 prospective, 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, uterine enlargement, and increased pressure, the
cause of UI 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 hereditary and
environmental predispositions. These changes recede over a
variable period during the year following delivery.
378 Voiding Dysfunction
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; nevertheless, 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 pregnancy [27].
Pregnancy is associated with pelvic relaxation even before
delivery. The anterior compartment seems to lead to the
increase in Pelvic Organ Prolapse Quantification 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 protection 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 normal 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 significance 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 science 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
difficult, 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 clinically
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 cervical effacement and
dilatation and results in the expulsion of the fetus. The third
stage is completed by the separation 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 levator 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 controversial 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
stretching, 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 delivery 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 implementation [29]. Thus, whereas the delivery of the
presenting 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
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry 379
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 suggests 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 studies are needed for the connective tissue and
neurovascular pedicle; their long-term effect and their
biologic properties 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 prolonged second stage.
After 5 years, changes persisted in 36% of patients, whereas
60% developed flatal incontinence 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 electromyography
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 during 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
delivery and episiotomy [36]. The role of a prolonged second
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 episiotomy, 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]. Unrecognized 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 parturition
contribute to the risk of UI. Although the urethral sphincter
mechanism is affected, and de novo stress incontinence 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
combination 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 factors 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
resulted in conflicting reports. No statistically significant
difference was noted in the groups regarding UI when
nulliparous 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
380 Voiding Dysfunction
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 excessive
stretching and tearing such as vaginal lacerations and
episiotomy and multiple deliveries are main predisposing
factors for symptomatic POP. A strong protective function 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 analgesia
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 universal
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 pregnancy 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 experienced 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 factor in the development of post-delivery
stress incontinence, as are increased parity and obesity
[59,60]. In the Epidemiology 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
retrospective 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. Symptoms
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 development 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 studies. In
essence, more uniform sets of definitions and outcome
measures are required to gain useful information. 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
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 postpartum 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 different 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 relevant studies
suggested an increasing risk of FI with emergency CD and
VD compared with elective CD; the latter was not always
 A Urogynecologist’s View of the Pelvic Floor Effects of Vaginal Delivery/Cesarean Section Genadry 381
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 abnormal VD, an
increased risk of damage can be expected. This in turns leads
to an increased risk of pelvic floor dysfunction, which
eventually can lead to the development of pelvic organ and
pelvic floor dysfunction with increasing age and parity,
particularly when associated with operative 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 compression and stretching from having
a deleterious effect on the 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, control 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 minimize 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 pregnancy 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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