CLINICAL OBSTETRICS AND GYNECOLOGY

Volume 48, Number 3, 639647

2005, Lippincott Williams & Wilkins

Etiology of Pelvic
Organ Prolapse
JOSEPH I. SCHAFFER, MD, CLIFFORD Y. WAI, MD, and
MURIEL K. BOREHAM, MD
Department of Obstetrics and Gynecology, University of Texas
Southwestern Medical Center, Dallas, Texas

Introduction
Pelvic organ prolapse is a global health concern affecting adult women of all ages. The
exact prevalence of prolapse is unknown.
The lifetime risk of a woman undergoing
surgery for prolapse or incontinence in the
United States is estimated to be 11%.1 A
study by Swift et al of 1004 women, aged
18 to 83, presenting for routine annual gynecologic examination, revealed the distribution of pelvic organ support by Pelvic Organ
Prolapse Quantication (POPQ) staging to
be: stage 0 = 24%, stage 1 = 38%, stage 2 =
35%, and stage 3 = 3%.2 These data are similar to those found in 27,342 women who
participated in the Womens Health Initiative
Hormone Replacement Therapy Clinical Trial
(WHI), in which approximately 40% were
found to have some form of prolapse.3 The
discrepancy between the percentage of women
undergoing surgery for prolapse and those
found to have it on a routine examination
Correspondence: Joseph I. Schaffer, MD, Associate Professor of Obstetrics and Gynecology, Chief of Gynecology,
Director, Division of Urogynecology and Reconstructive
Pelvic Surgery, University of Texas Southwestern Medical
Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9032.
E-mail: joseph.schaffer@utsouthwestern.edu
CLINICAL OBSTETRICS AND GYNECOLOGY

may be the result of the fact that this condition is often asymptomatic. However, if
increased emphasis is placed on careful
evaluation of symptoms and directed prolapse examination, the practitioner is likely
to identify many symptomatic women who
would benet from nonsurgical or surgical
therapy.
In this chapter, we discuss the etiology of
pelvic organ prolapse with emphasis on risk
factors and mechanisms of prolapse.

Risk Factors
There have been many postulated risk factors for pelvic organ prolapse, including
pregnancy, vaginal childbirth, aging, chronically increased intraabdominal pressure,
menopause, hypoestrogenism, trauma, genetic factors, race, musculoskeletal diseases,
chronic diseases, smoking, and prior surgery. It is likely that the etiology of pelvic
organ prolapse is multifactorial and results
from a combination of risk factors, which
vary from patient to patient. Although women
frequently relate the onset of prolapse to an
inciting event such as an episode of heavy
lifting or a traumatic incident in which they
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felt tissues give way or break, the process of

prolapse development generally occurs over
many years and is usually the result of multiple factors. It is the rare patient whose prolapse can be attributed to 1 independent risk
factor or inciting event.
Vaginal childbirth is the risk factor most
frequently associated with pelvic organ prolapse. In the Pelvic Organ Support Study
(POSST), increasing parity was associated
with advancing prolapse.2 The risk of prolapse increased 1.2 times with each vaginal
delivery. In the Oxford Family Planning
study, women with 2 deliveries were 8.4
times more likely to have surgery for prolapse compared with women with no deliveries.4 A case-controlled study comparing
Turkish women who had surgery for prolapse and/or incontinence with those who
had not found that women with 4 or more
vaginal deliveries had 11.7 times the risk
of experiencing prolapse or incontinence.5
These studies, and multiple other epidemiologic investigations, have denitively shown
that childbirth increases a womans chance
of developing prolapse.
Although vaginal delivery is implicated
in the etiology of prolapse, specic obstetric
risk factors remain controversial. Macrosomia, prolonged second stage of labor, episiotomy, anal sphincter laceration, epidural
analgesia, forceps and oxytocin use have
all been proposed as risk factors but have
not been denitively been proven to be so.
Although each of these factors may turn
out to have importance, it is the sum of all
the events that occur as the fetus travels
through the birth canal that predisposes to
prolapse.
Direct and indirect injury to the muscles,
nerves, and connective tissues of the pelvis
and pelvic oor can occur during vaginal
delivery. The pelvic oor is exposed to compression and extreme pressures from the
fetal head and maternal expulsive efforts.
In a study of 42 women with spontaneous
occiput anterior vaginal deliveries, it was
found that the average peak pressure on
the fetal head and pelvic oor during bearing

down efforts was 238.2 82.4 mm Hg and

the maximum pressure in 1 patient was
403.0 mm Hg.6 Pressures of this magnitude
potentially cause temporary or permanent
stretch and tear injury to maternal tissues.
It is the relationship among the fetal head,
the maternal bony, and soft pelvis, and the
amount of compression and force, which
likely will determine how much injury occurs.
A normal-sized fetal head might cause damage in a small pelvis, whereas a large head
might be able to traverse a large pelvis with
less force and compression, and less potential for injury.
Episiotomy and operative vaginal delivery are potential, but unproven, risk factors
for the development of prolapse. However,
these maneuvers are known to cause direct
injury to the anal sphincter and pelvic oor
musculature, which would logically predispose to the development of prolapse.
Although it has been argued that rapid forceps delivery and episiotomy can protect
the pelvic oor by decreasing compression and maternal expulsive efforts, this has
never been proven. Because elective episiotomy and operative vaginal delivery have not
been shown to be benecial, and the potential harm is great, use of these procedures
should be avoided when possible.
The use of elective cesarean section to
prevent pelvic oor dysfunction is a topic
of much debate. If all women underwent
cesarean section, there would undoubtedly
be less future pelvic oor dysfunction.
However, most women do not develop pelvic oor dysfunction. A policy of elective
cesarean section would subject many
women to a potentially dangerous procedure to prevent a condition that they never
would have developed. Therefore, efforts
should be aimed at identifying which
women are at risk and which factors in
the delivery process can be modied. The
prudent use of elective cesarean section
in high-risk women (those who already
have pelvic oor dysfunction or a pelvic
oor injury, or those with strong family histories, and so on) seems reasonable.

Pelvic Organ Prolapse

Pregnancy itself has been suggested as a
risk factor for prolapse. Possible mechanisms include the stretching of connective
tissue, which occurs to accommodate the
pregnancy, and increased intraabdominal
pressure. OBoyle showed nulliparous pregnant women did have increased prolapse
stage during pregnancy; however, it is unclear whether these ndings were related
to tissue hypertrophy or true prolapse.7 In
a recent magnetic resonance imaging study
of nulliparous women at term, Boreham
showed that 8% had a discontinuous levator
ani muscle.8 These ndings may represent
pregnancy-related changes or normal variation in levator ani morphology.
Age appears to be a risk factor for pelvic
organ prolapse. In the POSST study, there
was a 100% increased risk of prolapse for
each decade of life.2 Olsen found that the
cumulative incidence of primary operations
for prolapse and incontinence increased
from 0.1% in the 20- to 29-age group to
11.1% in the 70- to 79-age group.1 Aging
is a complex process and the increase in prolapse may be the result of the combination of
physiological aging, hypoestrogenism, and
an increased incidence of age-related degenerative and organic diseases. Women who
develop prolapse at an early age can be
postulated to have a more severe form of
the disease than older women. Their condition has arisen without the inuence of
aging and coexistent medical conditions.
This suggests that genetic factors or more
severe childbirth injury are part of the problem. Surgical management should aim to
provide the most durable repair because these
women are at higher risk for recurrence.
Chronically increased intraabdominal
pressure is believed to be a clinically relevant factor in the pathogenesis of prolapse.
This condition is not well dened but may
be the result of obesity, chronic constipation,
chronic coughing, or repetitive heavy lifting.
Numerous studies have identied obesity
as an independent risk factor for stress urinary incontinence.912 However, the association between obesity and the development

641

of pelvic organ prolapse is less clear. In

some studies, increased body mass index
has been associated with pelvic organ prolapse3; however, other studies have failed
to nd a correlation between prolapse and
increased body mass index.13 Heavy lifting
has also been implicated in the pathogenesis
of prolapse. A Danish study found that nursing assistants who were exposed to repetitive
heavy lifting were at increased risk of undergoing surgeries (odds ratio 1.6) for prolapse
when compared with the general population.14 Nonsurgical and surgical management plans for patients with prolapse should
include adjuvant attempts to decrease
chronically increased intraabdominal pressure. Aggressive treatment of chronic constipation and obesity is warranted in most
cases of prolapse. Although this has not
been tested in a randomized, controlled trial,
the potential benets greatly outweigh the
risks. Likewise, therapy should not be withheld in patients who cannot successfully
control these conditions.
Cigarette smoking and chronic obstructive pulmonary disease (COPD) have also
been associated with the development of
pelvic organ prolapse; however, there is little
data to support this proposed relationship.1,15 Although it is postulated that chronic
coughing, ie, chronic repetitive increases in
intraabdominal pressure, might lead to prolapse, no clear mechanism has been determined. It is possible that tobacco abuse with
the inhaled chemical compounds, and not
chronic cough, may cause changes that lead
to pelvic organ prolapse.

Theory of Prolapse
Development
It is postulated that pelvic organ support is
maintained by complex interactions among
levator ani muscles, the vagina, and connective tissue of the pelvic oor. However,
the mechanisms by which the levator ani
supports the vaginal wall and how these
mechanisms fail during the development

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Schaffer et al

of prolapse have not been fully delineated. A

major problem facing researchers is difculty in modeling the complex interactions
among the levator ani, nerves, and connective tissue that contribute to the development
of pelvic organ prolapse.
When the levator ani muscle has normal
tone and the vagina has adequate depth, the
upper vagina lies nearly horizontal in the
standing female. This creates a ap-valve
effect in which the upper vagina is compressed against the levator plate during periods of increased intraabdominal pressure. It
is theorized that when the levator ani muscle
loses tone, it drops from a horizontal to a
semivertical position, causing a widened
or open genital hiatus that predisposes
the pelvic viscera to prolapse.16 Without
adequate levator ani support, the visceral
fascial attachments of the pelvic contents
are placed on tension and are thought to
stretch and eventually fail.

Mechanism of Levator
Ani Damage
Skeletal muscle is a dynamic tissue that is
constantly remodeling and regenerating. A
heterogeneous population of bers with different functions allows skeletal muscle to
adapt to different situations such as stretch
and mechanical load. It is thought that damage to the levator ani muscles occurs as a
result of direct injury to the muscle tissue
or through damage to its nerve supply. Labor
and vaginal delivery has the potential to
cause this type of damage. It is unclear what
affect other pathologic conditions such as
chronically increased intraabdominal pressure has on the levator ani muscle.

Direct Injury
Direct injury to the levator ani muscles is
believed to occur during the second stage
of labor. The muscle undergoes signicant
stretch as the fetal head distends the pelvic
oor. It has been shown through computer-simulated models that the medial

pubococcygeus muscles undergo the most

stretch.17 Tunn et al described the levator
ani muscle after vaginal delivery in 14
women.18 They found the urogenital and
levator hiatus areas to be increased immediately postpartum compared with repeat
scans 2 weeks later. This suggests the levator
ani actually remodels and recovers in some
women after vaginal delivery. This appears
to be true functionally as well, in that
postpartum women have been found to
have decreased pelvic oor muscle strength
after delivery with return of function by
10 weeks.19 However, it is also likely that
in some cases, permanent stretch injury
occurs. Evidence for this is suggested by
the clinical observation that multiparous
women have a widened genital hiatus when
compared with nulliparous women.
In the developing world, prolonged and
obstructed labor causes ischemic injury with
resultant stulas. In a less extreme situation,
it is possible that during second-stage labor,
the vagina and levator ani muscle may be
deprived of oxygen and undergo necrotic
changes. If the injury is severe enough,
the muscle tissue may become so devascularized that it becomes severely atrophied
or nonfunctional. In Tunns small series,
1 woman showed complete unilateral loss
of the iliococcygeal muscle 6 months after
vaginal delivery.18
The levator ani is a skeletal muscle comprised mainly of slow oxidative (type I)
bers. Changes seen in slow twitch muscle
after denervation include muscle necrosis
with resultant atrophy and brosis. A study
of 45 premenopausal cadavers showed
brosis of the levator ani (especially the
ventral portion) increases with increasing
parity, and in nulliparous women, these
changes increased with age. However, there
was no evidence of neurologic damage in
either group.20

Neurologic Injury
In addition to anatomic studies, pudendal
nerve terminal motor latencies (PNTMLs)

Pelvic Organ Prolapse

and electromyography (EMG) have been
used to investigate neural damage after vaginal delivery. There is evidence that pudendal neuropathy is associated with vaginal
delivery.21 In addition, chronic straining to
achieve defecation has been associated with
pelvic muscle denervation.2224 The excess
straining and perineal descent that occurs
can cause stretching of the pudendal nerve
and result in neuropathy.25 However, there
is little proof that pudendal neuropathy is
associated with the development of prolapse.
It is proposed that stretch injury of the
pudendal nerve occurs during the second
stage of labor because the nerve is xed as
it exits Alcocks canal.26 Snooks et al found
evidence of prolonged pudendal nerve
latency in 80% of primigravid women after
childbirth, but most resolved by 6 months
after delivery.24 Although a number of these
women will acquire urinary or fecal incontinence, only a small fraction will actually
develop the clinical problem of prolapse.
In fact, Heit et al did not nd evidence of
denervation when studying ber distribution
in levator ani of women with prolapse.27
This may be explained by understanding
the levator ani nerve supply. The predominant innervation of the levator ani is derived
solely from efferent branches of sacral nerve
roots 2 through 4 through the pelvic nerve
complex with no contribution from the
pudendal nerve.28
EMG is more sensitive to subtle neuropathy than PNTML and has the additional
advantage of allowing distinction between
acute and chronic nerve damage. Weidner
et al established the feasibility of quantitative EMG in the levator ani of nulliparous
women.29 Although quantitative EMG of
the anal sphincter after vaginal delivery
has been performed, postpartum nerve
injury in the levator ani has yet to be investigated with EMG.30
Nerve injury is a suspected risk factor for
pelvic organ prolapse. Further research is
necessary to delineate the role it plays in
the pathophysiology of this condition.

643

Mechanism of Vaginal
Wall Injury
The vaginal wall is comprised of squamous
epithelium, smooth muscle muscularis, and
adventitia. All elements are embedded in an
extracellular matrix that includes collagen
and elastin bers and smooth muscle.
Abnormalities of any of these components
may contribute to vaginal dysfunction and
the development of pelvic organ prolapse.
SITE-SPECIFIC DEFECTS

The site-specic defect theory is based on

the premise that tears in the endopelvic fascia surrounding the vaginal wall allow herniation of the pelvic organs. The association
of pelvic organ prolapse with vaginal delivery is consistent with this theory. However,
study of the microscopic anatomy of the
vaginal wall indicates that endopelvic fascia
does not exist as a specic anatomic tissue,
but rather represents the bromuscular layer
of the vaginal wall (ie, vaginal muscularis
and adventitia).31
Although most researchers agree that
vaginal delivery predisposes women to
pelvic organ prolapse, there is less agreement regarding the changes in the pelvic
musculature and vaginal wall that result
in prolapse. Nichols and Randall proposed
an attenuation of the vaginal wall without
loss of fascial attachments. They term prolapse of this type as distention cystocele or
rectocele.32 Anterior and posterior wall
defects resulting from loss of attachment
of the lateral vaginal wall to the pelvic side
wall are described as displacement (paravaginal) cystocele or rectocele. It is reported that in the distention-type prolapse,
the vaginal wall looks smooth and without rugae as a result of attenuation,
whereas, in the displacement-type prolapse,
vaginal rugae will be visible. Both types of
defects could result from the stretching or
tearing that occurs during the second stage
of labor.

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Schaffer et al

SMOOTH MUSCLE DYSFUNCTION

Abnormalities in the anatomy, physiology,

and cellular biology of smooth muscle in
the vaginal wall may contribute to the pathophysiology of pelvic organ prolapse. For
example, smooth muscle bers arising from
the vaginal wall attach to the levator ani
complex,33 and dysfunction of this smooth
muscle may affect the attachment of the lateral
vagina to the pelvic side wall. Additionally,
it has been shown that the fraction of smooth
muscle in the muscularis of the anterior and
posterior vaginal wall apex in women with
prolapse is decreased compared with women
without prolapse.31 A decreased smooth
muscle content of the round ligament in
women with pelvic organ prolapse has also
been described.34
The cellular processes that effect these
changes in the vaginal wall during the pathogenesis of pelvic organ prolapse are
unknown. Currently, it is not known whether
changes in smooth muscle content are a
result of the mechanical forces imposed
on the prolapsed tissues, or if decreased
amounts of muscularis smooth muscle have
a role in the development of this disorder.
Decreased content of differentiated smooth
muscle in the vaginal wall of women with
pelvic organ prolapse may be secondary to
mechanical forces imposed on prolapsed
vaginal tissues or to denervation of the vaginal tissues during vaginal delivery. Nevertheless, decreased fraction of smooth muscle
in the muscularis of prolapsed vaginal tissues may impair vaginal tone.

Connective Tissue Problems

The connective tissue of the pelvis is comprised of collagen, elastin, smooth muscle,
and microbers, which are anchored in
an extracellular matrix of polysaccharides.
The connective tissue that the pelvic organs
are invested in provides much of the anatomic support of the pelvis and its contents.
There is evidence that suggests abnormalities of connective tissue and connective tissue repair may predispose women to pro-

lapse.35,36 For example, Norton found that

women with joint hypermobility had a
higher prevalence of genital prolapse (cystocele, rectocele, and uterine/vaginal vault
prolapse) compared with women with normal joint mobility. Women with connective tissue disorders such as Ehlers-Danlos
or Marfans syndrome are more likely to
develop pelvic organ prolapse35 and urinary
incontinence.37 In a small case series studying symptoms of prolapse in patients with
connective tissue disorders, one third
women with Marfans syndrome and three
fourths of women with Ehlers-Danlos syndrome reported a history of pelvic organ
prolapse.37
Collagen is one of the main constituents of
pelvic connective tissue. There are many
types of collagen described. However, types
I and III are the most prevalent in pelvic tissues. Type I collagen bers are usually well
organized and are associated with ligamentous tissue. Type III collagen is common in
the loose areolar tissue, which makes up the
vaginal wall adventitia and surrounds the
pelvic organs. Quantitative or qualitative
deciencies in collagen have been associated with the development of pelvic organ
prolapse.
Decreased collagen content is found in
women with stress urinary incontinence and
pelvic organ prolapse. When compared with
women with pelvic organ support, those
with prolapse were found to have less total
collagen in their pubocervical fascia as
well as a weaker type of collagen.38,39 This
may be secondary to increased collagen turnover or breakdown. Site-specic analysis of
collagen in prolapsing tissue has found structural, biochemical, and quantitative differences in collagen content.40,41
The fascia and connective tissues of the
pelvic oor may also lose strength consequent to aging and loss of neuroendocrine
signaling in pelvic tissues.36 Estrogen deciency can affect the biomedical composition, quality, and quantity of collagen. Estrogen inuences collagen content by increasing synthesis or decreasing breakdown.

Pelvic Organ Prolapse

Exogenous estrogen supplementation has
been found to increase the skin collagen
content in postmenopausal women who
are estrogen-decient.42 Estrogen supplementation before prolapse surgery, and/or
postoperatively, is considered essential by
many prolapse surgeons. Although this practice may seem logical and empirically sound,
there is no evidence to suggest improved
surgical outcomes with the use of adjuvant
estrogen.

Conclusions
Pelvic organ prolapse is a common condition that can severely impact on quality of
life. It is likely to become more common
as the population ages in the coming years.
Epidemiologic studies point to vaginal delivery as the strongest risk factor, although
the etiology is often multifactorial. The
pathophysiological mechanisms of prolapse
have not been fully elucidated, but it is likely
that damaged or malfunctioning skeletal
muscle, smooth muscle, connective tissue,
and nerves all play a role in the progression
of this disease.
Much is still unknown regarding the etiology of pelvic organ prolapse. Current theories do not adequately explain why a gravida zero can develop pelvic organ prolapse,
whereas a gravida 9 may have excellent pelvic organ support. Similarly, we cannot
always explain why 1 patient develops recurrence after repair of all support defects,
whereas another patient with the same repair
has a permanent cure.
The most successful approach to pelvic
organ prolapse may ultimately be prevention. Therefore, research and clinical practice should focus on identifying modiable
risk factors. Vaginal delivery is the most
obvious risk factor, which has the potential
to be modied. Future research should try to
identify specic aspects of the birthing
process, which can be modied to decrease
the incidence of prolapse and pelvic oor
dysfunction.

645

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