DOI: 10.1111/j.1744-4667.2012.00133.

x 2012;14:257–66
The Obstetrician & Gynaecologist
Review
http://onlinetog.org

Obstetric pelvic floor and anal sphincter injuries

a b, c
Farah Lone MBBS MRCOG, Abdul Sultan MD FRCOG, * Ranee Thakar MD MRCOG
a
Subspecialty Trainee Urogynaecology, Department of Obstetrics and Gynaecology, Croydon University Hospital, 530 London Road, Croydon,
Surrey CR7 7YE, UK
b
Consultant Obstetrician and Gynecologist, Department of Obstetrics and Gynaecology, Croydon University Hospital, 530 London Road, Croydon,
Surrey CR7 7YE, UK
c
Consultant Obstetrician and Urogynaecologist, Department of Obstetrics and Gynaecology, Croydon University Hospital, 530 London Road,
Croydon, Surrey CR7 7YE, UK
*Correspondence: Abdul H Sultan. Email: abdul.sultan@mayday.nhs.uk

Key content Learning objectives

 Vaginal delivery, especially the first, contributes to the  To review the effect of childbirth on pelvic organ function.
development of pelvic organ prolapse, and urinary and anal  To identify and appropriately manage anal sphincter injuries
incontinence. following childbirth.
 Although the effects of childbirth on the pelvic floor are commonly
Ethical issues
reported within 12 months of delivery, the peak presentation of  There are inadequate long-term data from well-conducted
symptoms occur some 2–3 decades later.
 Vaginal childbirth, advancing maternal age and increasing body
longitudinal studies to make definitive recommendations in many
aspects of pelvic organ dysfunction.
mass index are the most consistent risk factors.
 Diagnosis of obstetric anal sphincter trauma can be improved Key words: anal incontinence / childbirth / pelvic floor
by training and thereby minimising the risk of anal dysfunction / pelvic organ prolapse / urinary incontinence
incontinence.
 Further research, using pelvic floor imaging, may improve our
understanding of the nature of pelvic floor and anal sphincter
injuries.

Please cite this paper as: Lone F, Sultan A, Thakar R. Obstetric pelvic floor and anal sphincter injuries. The Obstetrician & Gynaecologist 2012;14:257–66.

Introduction
The earliest evidence of severe perineal injury sustained
during childbirth is from the mummy of Henhenit, an
Egyptian woman approximately 22 years of age from the
harem of King Mentuhotep II of Egypt in 2050BC.1
Surgical repair of severe perineal injury was first mentioned
in the Arabic book Al Kanoun, but the first recorded case
of perineal suture was by Guillemiau around 1610.1 In
1943, Gainey examined 1000 consecutive women at the
postnatal visit and identified levator damage in 31%, a
cystocele in 26% and a rectocele in 12%.2 In 1955, he
presented data on a second series of 1000 consecutive
women delivered by prophylactic forceps aided by a
mediolateral episiotomy and reported a considerable
reduction in levator damage, cystocele and rectocele to
11.5%, 9.9% and 1.5%, respectively.3 In recent years, with
advances in imaging techniques, the understanding and
management of birth-related trauma to the pelvic floor has
improved dramatically.
Anatomy
The perineum corresponds to the pelvic outlet and is bound
anteriorly by the pubic arch, posteriorly by the coccyx and
laterally by the ischiopubic rami, ischial tuberosities and
sacrotuberous ligaments. The perineum can be divided into
two triangular parts by drawing an arbitrary line transversely
between the ischial tuberosities. The anterior triangle
(urogenital triangle) contains the superficial muscles, which
include the superficial transverse perineal, bulbospongiosus
and ischiocavernosus muscles. The posterior triangle (anal
triangle) contains the anal sphincter complex.
The pelvic floor mainly consists of the musculotendinous
sheet called the levator ani muscle. There is considerable
inconsistency in the literature regarding the anatomy of the
levator ani muscle.4 However, it is broadly accepted that the
levator ani is subdivided into the iliococcygeous,
pubococcygeous and ischiococcygeous. The pubococcygeous
is further subdivided into the pubourethralis, pubovaginalis
and puborectalis. The puborectalis is the most caudal

ª 2012 Royal College of Obstetricians and Gynaecologists 257

 Obstetric pelvic floor and anal sphincter injuries
Figure 1. Schematic representation of obstetric anal sphincter injuries (Reproduced with permission from Springer)6
component of the levator ani complex and is situated
cephalad to the deep component of the external anal
sphincter (EAS), from which it is almost inseparable. The
puborectalis therefore participates in the sphincter
mechanism. Between the two arms of the puborectalis lies
the levator hiatus, through which the rectum, vagina and
urethra pass. The innervation of the pelvic floor is via the
sacral nerves S2–S4 and it is believed that some innervation
also occurs via the pudendal nerve.5
The anal sphincter complex consists of the EAS and
internal anal sphincter (IAS) separated by the conjoint
longitudinal coat (Figure 1).6 The IAS is a continuation of
the circular smooth muscle of the bowel and ends above the
anal margin at the junction of the superficial and
subcutaneous part of EAS. The EAS is innervated by the
inferior rectal branch of the pudendal nerve and contributes
15–30% of the resting anal pressure and 70% of the squeeze
anal pressure.7 The IAS is innervated by the sympathetic (L5)
and parasympathetic nerves (S2–S4) and accounts for
50–85% of the resting pressure.8
Classification of perineal trauma
Adopting uniform definitions/classification for perineal and
anal sphincter injuries during childbirth reduces under-
reporting of true obstetric anal sphincter injury and facilitates
future audits and risk management. The current classification
of perineal trauma9 includes the classification of anal
sphincter tears proposed by Thakar and Sultan (Box 1).10
Incorrect classification and inappropriate repair can have
epidemiological, clinical and medico-legal implications.
258
Box 1. Classification of perineal trauma9,10
First-degree: Laceration to the vaginal epithelium or perineal skin only
Second-degree: Involvement of the perineal muscles but not the anal
sphincter
Third-degree: Disruption of the anal sphincter muscles which should
be further subdivided into:
3a <50% thickness of external sphincter torn
3b >50% thickness of external sphincter torn
3c: Internal sphincter also torn
Fourth-degree: Third-degree tear with disruption of the anal
epithelium
Prevalence
More than 85% of women in the UK sustain some form of
perineal trauma during vaginal delivery.11 However, the
prevalence is dependent on variations in obstetric practice,
including rates and type of episiotomy, which vary not only
between one country and the next but also at a national level
between delivery units and individual practitioners. In the
UK, the episiotomy rate is 8–16%12 compared with 52–82%
in some European countries13 and 39% in the USA.14
The prevalence of third- and fourth-degree tears,
collectively referred to as obstetric anal sphincter injuries
(OASIS), is dependent on the type of episiotomy practised.
In centres where mediolateral episiotomies are practised, the
rate of OASIS is 1.7% (2.9% in primiparae) compared with
12% (19% in primiparae) in centres practising midline
episiotomy.6 A recent (2010–2011) survey of maternity units
in the UK has revealed an OASIS rate of 3% (range of 0–8%)
ª 2012 Royal College of Obstetricians and Gynaecologists

(2.1% in primiparae).15 This wide range suggests that at the
highest extreme there could be an element of overdiagnosis.
However, what is more alarming is that units in the lower
extreme are probably failing to diagnose a large number
of OASIS.
Pelvic floor dysfunction following
childbirth
Although the effects of childbirth on the pelvic floor are
commonly reported within 12 months of delivery, the peak
presentation of symptoms occur some 2–3 decades later.16 In
addition to direct trauma to the anal sphincter, perineal and
levator ani muscles, stretching and possible tearing of the
endopelvic fascia may lead to pelvic floor dysfunction.17 The
much higher prevalence of incontinence and prolapse in later
life may reflect the cumulative effects of covert obstetric
trauma, ageing, progression of neuropathy, weakness of
fascial supports and the hormonal changes at menopause.
Symptoms of obstetric-related pelvic floor dysfunction are
as follows:
 Anal incontinence
 Urinary incontinence
 Pelvic organ prolapse
 Sexual dysfunction.
Anal incontinence
The WHO International Consultation on Incontinence
defines anal incontinence as the involuntary loss of flatus,
liquid or solid stool that is a social or hygienic problem.18
Mechanism
Direct mechanical injury. The processes of continence
and defaecation are complex and hence the understanding of
pathophysiological mechanisms related to childbirth
continues to evolve. Direct mechanical injury to the EAS
and/or IAS resulting from obstetric trauma is a major cause
of anal incontinence.19
Neurological injury. Pudendal neuropathy may be the
result of nerve compression from the fetal head,20 fetal
macrosomia, prolonged pushing during the second stage of
labour and forceps delivery. The pudendal nerve is particularly
susceptible to compression and damage at the point where it
curves round the ischial spine and enters the pudendal canal
enclosed in its tight fibrous sheath (Alcock’s canal). Stretched
or compressed nerves often undergo demyelination but usually
recover with time20 or re-innervation of muscle occurs.21
Combined mechanical and neurological trauma.
Isolated neurological injury, as described above, is believed
ª 2012 Royal College of Obstetricians and Gynaecologists
Lone et al.
to be rare. Neuropathy more commonly accompanies
mechanical damage.
Other mechanisms. Additional factors also play a role in
maintaining anal continence, namely, normal consistency of
stool, normal bowel transit and rectal sensitivity, a functional
rectal reservoir, and intact somatic and autonomic innervation.
Incidence
In a postal questionnaire study of 906 women, 10 months
after vaginal delivery, 4% developed new faecal
incontinence.22 Flatus incontinence is more common and
has been reported in 29% of primiparous women 9 months
after delivery.23 A meta-analysis of five studies (717 vaginal
deliveries) imaging the anal sphincter revealed a 26.9%
incidence of anal sphincter defects in primiparous women
and an 8.5% incidence of new sphincter defects in
multiparous women. Although approximately 35% of
women with a sphincter defect on endoanal ultrasound
were symptomatic, 3.4% of women experienced postpartum
faecal incontinence without a sphincter defect.24
OASIS are clinically detectable in about 3% of vaginal
deliveries in centres practising mediolateral episiotomy but
rates of 7% have been described.25 When endoanal
ultrasound was first performed in a prospective childbirth
study, it was assumed that the OASIS seen on endoanal
ultrasound were occult.26 However, it has been subsequently
shown that genuine occult injuries are a rare entity as
virtually all OASIS can be detected clinically by an
appropriately trained clinician, highlighting the need for
intensive and more focused training in the identification of
OASIS.27 Although Faltin et al.28 have shown that detection
can be improved by performing endoanal ultrasound before
suturing, there were occasions when OASIS diagnosed
by endoanal ultrasound could not be identified and
repaired clinically.
Despite primary repair, anal incontinence occurs in 39% of
women.6 This may be indicative of inappropriate diagnosis
or inadequate repair technique. Sultan et al.20 conducted an
interview of 75 doctors and 75 midwives and reported that
91% and 60%, respectively, indicated inadequate training in
perineal anatomy and 84% and 61%, respectively, reported
inadequate training in identifying third-degree tears.
In a 10-year longitudinal study following OASIS,
deterioration in anal pressures occurred over time and were
greater among women who had experienced complete rather
than partial tears. Flatus and liquid faecal incontinence were
more common among women who had sustained OASIS and
symptoms were most severe after IAS injury.29 Despite
obvious injury to the anal sphincters, symptoms of anal
incontinence may not occur for some time after delivery. Bek
and Laurberg30 found that in women who experienced
transient anal incontinence after a complete tear, 39% had a
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 Obstetric pelvic floor and anal sphincter injuries
(a)
(b)
Figure 2. Endoanal ultrasound of the mid-anal canal. (a) Intact
sphincters. P = probe; SM = submucosa; EAS = external anal
sphincter; IAS = internal anal sphincter. (b) Defects in the internal anal
sphincter (between white arrows) and external anal sphincter
(between black arrows) after inadequate fourth-degree tear repair
relapse of symptoms after the next vaginal delivery. The
major long-term problem seen in these women was
incontinence of flatus. Full-thickness anal sphincter
disruption (Figure 2) was the most significant risk factor in
the development of faecal incontinence.
Risk factors
In a Swedish study of 1336 women, the prevalence of flatus
incontinence was found to be higher among women who had
sustained OASIS.31 The first vaginal delivery confers the
greatest risk of sustaining OASIS, with new injuries occurring
up to 10 times more commonly in primiparous women.32 The
prevalence of faecal incontinence is predominantly associated
with forceps delivery, unassisted delivery at home, large fetal
head circumference, obesity and increasing maternal age.33
Midline episiotomy,34 first vaginal delivery, shoulder dystocia
and a persistent occipito-posterior position have been
identified as the main risk factors for the development of
OASIS.20,27 In a study of 531 consecutive women who had
sustained OASIS,35 the risk factors and outcome of different
grades of OASIS were assessed. The use of epidural analgesia
was found to be the only independent factor predicting a
260
major tear and hence a higher risk of faecal incontinence and
lower anal canal pressures.
Can caesarean section reduce the risk of anal
incontinence?
No significant difference in anal incontinence was seen in a
randomised controlled trial on short and long-term follow-
up.36,37 In a cohort study, first delivery by caesarean section
appeared to reduce significantly the prevalence of faecal
incontinence but not symptoms of severe flatus
incontinence.38 In a 12-year longitudinal study, MacArthur
et al.39 reported that there was no difference in faecal
incontinence among women who had delivered either
exclusively by caesarean section or who had some
spontaneous vaginal births and some deliveries by caesarean
section.39 In the absence of OASIS, delivery by caesarean
section does not reduce the risk of anal incontinence.
Caesarean section protects against new sphincter tears, which
would explain why some studies have found a reduced
prevalence of faecal incontinence after caesarean section.40
Role of imaging
Endoanal ultrasound yields highly detailed images of the
sphincter (Figure 2). Imaging has become essential in the
assessment and management of faecal incontinence
particularly related to obstetric trauma.
Urinary incontinence
Mechanism
The exact mechanism of stress urinary incontinence in
pregnancy and childbirth is not clear and is probably
multifactorial. The development of symptoms of urinary
incontinence during pregnancy, with a rapid postpartum
recovery followed by a steady decline of continence over time
suggests a dual mechanism of nerve and tissue involvement.
Pudendal nerve conduction and electromyography studies
have shown denervation injury after childbirth.41,42
In pregnancy, as a result of a reduction in the total collagen
content and consequent change in the tensile properties of
connective tissue, there is an increase in mobility of the
bladder neck (Figure 3).43–45 Compared with continent
women, those who have postpartum stress urinary
incontinence have been found to have greater bladder neck
mobility during straining before delivery.45
Prospective urodynamic studies performed during
pregnancy and 6 to 9 weeks postpartum revealed a
notable decrease in urethral closure pressure and urethral
length44,46 after vaginal delivery. Women with persistent
urinary incontinence after childbirth were found to have a
shorter urethral length and a lower closure pressure
compared with continent women.47 Subsequent studies
have demonstrated that the midurethral closure pressure
ª 2012 Royal College of Obstetricians and Gynaecologists

(a)
(b)
Figure 3. Translabial ultrasound image. (a) Normal scan in a woman
without prolapse symptoms. B = bladder; SP = symphysis pubis;
U = urethra. (b) Scan of a multiparous woman at best Valsalva. The
woman had symptoms of bulge in the vagina. BSD = bladder–
symphysis distance; C = cystocele. Note the rotation of bladder neck
and short BSD at Valsalva
(above 20 cmH2O) was a contributing factor in
maintaining urinary continence.48,49
Using magnetic resonance imaging (MRI), a two-fold
increase in levator ani injuries has been shown in women
with stress incontinence compared with primiparous
continent women50 but this association was not found
using three-dimensional ultrasound.51
Incidence
Compared with nulliparous women, new urinary
incontinence is more common in parous women. A lower
incidence after planned caesarean section has been shown in
a randomised controlled trial (absolute relative risk [RR]
difference –2.8%, 95% confidence interval [CI] –5.1% to
–0.5%).36 A prospective cohort study of 949 women found
that urinary incontinence was experienced by 22.3% before
pregnancy, 65.1% during the third trimester and 31.1%
after delivery.52
Viktrup et al.53 interviewed 278 primiparae and found that
the prevalence of stress urinary incontinence 5 years after a first
delivery was 30%. Nineteen percent of those without
ª 2012 Royal College of Obstetricians and Gynaecologists
Lone et al.
symptoms after their first delivery had urinary incontinence
in contrast with 92% in those who had symptoms at 3 months
postpartum. At 12 years follow-up, 91% of women who
developed symptoms during the first pregnancy or shortly after
delivery but without remission 3 months postpartum had
stress urinary incontinence compared with 57% in those who
had remission of symptoms at 3 months postpartum.54
Risk factors
The evidence regarding the contribution of obstetric factors
to the development of stress urinary incontinence is
conflicting and it is debatable whether pregnancy or
delivery is the major contributor to postpartum
incontinence. Some investigators found a relationship with
the duration of the second stage of labour (>1 hour)55 and
birthweight,22 while others have found no significant
correlation between stress urinary incontinence and fetal
head circumference, second stage of labour56 or
birthweight.53 There is, however, a group of women at an
inherent increased risk of developing urinary incontinence
because of abnormalities in collagen.57
Rortveit et al.58 reported that the prevalence of any
incontinence was 10% in the nulliparous group, 16% in the
caesarean section group and 21% in the vaginal delivery
group. Thus, pregnancy itself rather than delivery may also be
an important causal factor in the development of urinary
incontinence. Postpartum urinary incontinence was
independently associated with incontinence prior to and
during pregnancy, even among those having a caesarean
section. These studies highlight that antenatal and pre-
pregnancy stress urinary incontinence increases the risk of
future stress urinary incontinence.
Can caesarean section reduce the risk of urinary
incontinence?
The short-term effect of caesarean section on the prevalence
of postpartum urinary incontinence has been seen in four
cohort studies. Two studies52,58 have found a lower
prevalence of urinary incontinence after caesarean section.
Two cohort studies22,26 have reported the long-term effect of
delivery mode: one reported reduced prevalence of urinary
incontinence after first delivery by caesarean section and the
other reduced prevalence of persistent postpartum urinary
incontinence after delivery exclusively by caesarean section.
Women who have never given birth appear to be at lower risk
of urinary incontinence than those who have delivered only
by caesarean section. In a 12-year follow-up study,
MacArthur et al.39 found that after adjustment for parity,
body mass index and age at first birth, women who delivered
exclusively by caesarean section were less likely to have
urinary incontinence than those who only had spontaneous
vaginal births, but not if they had a combination of caesarean
section and spontaneous vaginal births.
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 Obstetric pelvic floor and anal sphincter injuries
(a) (b)
Figure 4. Three dimensional endovaginal ultrasound image. AP = antero-posterior; LA = levator ani; L-R = left to right width; SP = symphysis
pubis. (a) Normal levator hiatus dimensions. (b) Enlarged levator hiatus in a woman with pelvic organ prolapse (1 = AP 59.6 mm; 2 = L-R width
51.7 mm; 3 = area 20.7 cm2). (c) Levator avulsion on left side (marked by an arrow)
Role of imaging
Ultrasound imaging is increasingly being used to study
bladder and urethral anatomy (Figure 3). Three-dimensional
imaging after vaginal delivery shows an enlarged levator
hiatus (Figure 4), a reduction in urethral sphincter volume
and increased bladder neck mobility both in the antenatal
and postpartum period. Other ultrasound studies have
shown that the bladder neck is lower (Figure 3) after
vaginal delivery as compared with nulligravid controls and
women delivered by elective caesarean section.59
Levator avulsion injury (Figure 4) was previously reported
to have a significant association with new stress urinary
incontinence.60 However, recent research by the same group
has demonstrated that puborectalis trauma is not associated
with an increased risk of stress urinary incontinence or
urodynamically proven stress urinary incontinence in a
urogynaecological population.51
Pelvic organ prolapse
Mechanism
Levator ani muscle injury (partial or complete) found in
vaginally parous women increases the chance of a woman
developing pelvic organ prolapse (POP) by 4 to 11 times.58
Large imaging studies50,61 and biomechanical studies62 have
shown that levator avulsion injuries or denervation occurs
during descent of the fetal head and maternal expulsive forces
during the active second stage of labour and crowning.
Consequently, the levator hiatus enlarges and leads to
anterior and central compartment prolapse.63
Incidence
Prolapse is noted to be more common in women after a
vaginal delivery. Fifty percent of parous women have
some degree of POP, of whom 15% are symptomatic
whereas symptomatic prolapse is found in 2% of
nulliparous women.64
262
(c)
Risk factors
O’Boyle et al.65 found that increase in POP quantification stage
was seen in nulliparous pregnant women and also in those who
had a vaginal delivery. Hence, both pregnancy and vaginal
delivery are important risk factors for the development of POP.
Hormonal and mechanical effects associated with the gravid
uterus contribute to changes in pelvic organ support during
pregnancy. Electromyography (EMG) studies have shown that
significant pelvic denervation and reinnervation are associated
with stress incontinence and POP.41,43 Collagen changes in the
pelvic floor that are related to childbirth and endogenous
hormone changes may also predispose to POP.
Role of imaging
Translabial/transperineal ultrasound allows definition of the
presence of POP by demonstrating descent of the vaginal wall
sonographically (Figures 3 and 5). Vaginal childbirth results
in 28% enlargement of the levator hiatus (Figure 4) after a
levator avulsion compared with 6% hiatus enlargement
without avulsion injury.66 Enlarged hiatus is found in
women who have clinically significant POP.67 Dietz et al.60
used translabial ultrasound to demonstrate that pregnancy
and vaginal delivery result in an increased prevalence and size
of a true rectocele (Figure 5).
An MRI study50 has shown that 20% of primiparous
women had a visible defect in the pubovisceral or
iliococcygeal portion of the levator ani muscle. These
defects were not seen in nulliparous women. The most
common morphologic abnormality of the levator ani is
described as an avulsion injury of the pubovisceral muscle
from the pubic ramus (Figure 4). This has been described in
one-third of women and appears to be related to childbirth.60
Sexual dysfunction
Although sexual health problems are common after childbirth,
they are frequently under-reported. Embarrassment and
ª 2012 Royal College of Obstetricians and Gynaecologists

(a)
(b)
Figure 5. Translabial ultrasound image. (a) Normal scan in a woman
without prolapse symptoms. AR = ampulla recti; AC = anal canal; B =
bladder; SP = symphysis pubis. (b) Scan of multiparous woman at best
Valsalva. The woman had symptoms of bulge in the vagina. R =
rectocele
preoccupation with the newborn are some of the reasons why
many women do not seek help. Furthermore, there is a lack of
professional awareness and expertise in recognition of sexual
dysfunction. In the postpartum period, the most common
sexual disorder is sexual pain followed by disorders of sexual
desire, arousal and orgasm.68 These disorders may occur in a
different sequence and may be interdependent.
Mechanism
The evolution from a pre-pregnant state to the postpartum
period is a life-changing event with complex physiological
and psychological sequelae. Perineal pain and dyspareunia
are commonly a result of spontaneous perineal trauma,
episiotomy and instrumental delivery. In a retrospective
cohort of 626 primiparous women over a 6-month period
after delivery, women with second-degree and third or
fourth-degree tears were 80% and 270%, respectively, more
likely to report dyspareunia at 3 months postpartum.69
In a longitudinal survey of 122 married Nigerian
primiparous women, perineal trauma or pre-pregnancy
dyspareunia predicted dyspareunia at 3 months
ª 2012 Royal College of Obstetricians and Gynaecologists
Lone et al.
postpartum.70 This highlights that mechanisms leading to
sexual dysfunction are multifactorial.
Incidence
Sexual health problems, as recalled by women, increase
significantly after childbirth. Healthcare workers need to be
made aware of this silent affliction as sexual morbidity can
have a detrimental effect on a woman’s quality of life,
impacting on her social, physical and emotional wellbeing.
Perineal pain occurs in up to 42% of women immediately
after delivery and significantly reduces to 22% and 10% at 8
and 12 weeks, respectively.71 In a cross-sectional study of 796
primiparous women over a 6-month period after delivery,
Barrett et al.72 found that 62% experienced dyspareunia in the
first 3 months postpartum, decreasing to 31% at 6 months.
Thirty two percent had resumed intercourse within 6 weeks of
giving birth and the majority of respondents (89%) had
resumed intercourse within 6 months.
Risk factors
Compared with normal delivery, perineal pain occurs more
frequently and persists for a longer period after an
instrumental or breech vaginal delivery. In a prospective
study, Barrett et al.72 found that dyspareunia in the first
3 months after delivery was significantly associated with
vaginal delivery and previous experience of dyspareunia.
However, at 6 months there was no association between
dyspareunia and mode of delivery but previous experience of
dyspareunia remained a significant risk factor.72 This suggests
that women with pre-existing dyspareunia prior to pregnancy
may have specific needs or issues that could be identified and
managed antenatally. Further analysis of the same cohort of
women found that depression is another risk factor in
delaying the resumption of sexual intercourse by 6 months.
Glazener71 found that women who reported perineal pain,
depression and tiredness experienced problems related to
intercourse more often than those who did not report
these concerns.
Management
Role of the perineal clinic
The perineal clinic is an ideal setting to offer patients
support, debriefing and focus on health concerns relating to
the delivery including urinary, bowel, sexual, prolapse and
wound problems. A large number of women attending this
clinic will have sustained a third- or fourth-degree tear.
Antenatal women with any of these problems, including
female genital mutilation, are also being seen in the perineal
clinic. As these problems are usually of a sensitive nature,
women should ideally be seen in a dedicated perineal clinic
instead of a busy general clinic approximately 6–8 weeks after
delivery. Furthermore, this environment would facilitate
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 Obstetric pelvic floor and anal sphincter injuries
childcare and breastfeeding. A dedicated one-stop perineal
clinic provides women with an opportunity to be given an
explanation of the circumstances under which the perineal
injury occurred and appropriate counselling regarding mode
of subsequent delivery. However, the best model of care is
dependent on local expertise and resources.
Who should look after these women?
Ideally, a team of healthcare providers with the knowledge and
expertise to care for these women should be available to
mothers. Experienced professionals (such as urogynaecologists
and trained nurses or midwives) who are trained in anal
manometry and endoanal ultrasound scanning, form an
integral part of this clinic. Integration of multidisciplinary
professionals such as physiotherapists, continence nurse
specialists, colorectal nurse specialists, colorectal surgeons
and psychosexual counsellors promote a holistic approach to
pelvic floor and perineal problems.
Delivery after anal sphincter injury
Women who sustain OASIS need counselling regarding
their management in a subsequent pregnancy. The two
major issues following OASIS that concern women most
when contemplating delivery in a subsequent pregnancy are
the risk of recurrence of OASIS and the risk of developing
anal incontinence.
Risk of recurrence of OASIS
While there is evidence that a policy of restrictive episiotomy is
better than routine episiotomy, there are no randomised
studies regarding the use of prophylactic episiotomy in women
who previously sustained OASIS. Most of the published
studies are from centres practising selective midline
episiotomy where the recurrence rate of OASIS is 11%.73 In
centres where the normal practice is to perform selective
mediolateral episiotomy, OASIS recurred in 4.4%25 to 6.8%.74
The authors therefore do not recommend routine
episiotomy following previous OASIS.
Risk of developing anal incontinence after
subsequent vaginal delivery
The data available are limited and retrospective. Poen et al.75
identified 43 women (original cohort of 117 women with
OASIS) who had a subsequent vaginal delivery. The rate of
anal incontinence was 56% compared with 34% in those who
did not subsequently deliver (RR 1.6; 95% CI 1.1–2.5) but
there was no comparable caesarean section group. Sangalli et
al.76 followed up 177 women 13 years after OASIS and found
that only 2.5% of women complained of faecal incontinence
after a third-degree tear compared with 26.5% following a
fourth-degree tear. This could reflect the effect of not
specifically identifying and repairing the IAS. These results
are also supported by Roos et al.35 who did a follow-up study
264
of 531 women 9 weeks after delivery and found that women
with grade 3c/4 tears had significantly worse defaecatory
symptoms and bowel-related quality of life compared with
women with grade 3a/3b tears.
Recommended mode of delivery for subsequent
pregnancy
There are no randomised studies to determine the most
appropriate mode of delivery following OASIS. In order to
counsel women, it is useful to have a symptom questionnaire
as well as anal ultrasound and manometry results.74 If vaginal
delivery is contemplated then these tests should be performed
during the current pregnancy.
Figure 6 shows a flow diagram illustrating management
after a third/fourth-degree tear in subsequent pregnancies
conducted in Croydon University Hospital, Surrey, UK over
the past 10 years.6 Follow-up of these women through a
subsequent pregnancy and delivery revealed that 70% of
women achieved a vaginal delivery without any compromise
of anorectal function.74
Women who sustained OASIS with subsequent severe
incontinence should be offered secondary sphincter repair
provided there is an EAS defect and there is evidence of
contractility in the residual muscle.10 Some women with
faecal incontinence may choose to complete their family
before embarking on anal sphincter surgery. Following
counselling, these women are allowed a vaginal delivery as
the risk of further damage is minimal and should not impact
on the outcome of surgery. This benefit should be weighed
against the risks associated with caesarean section for all
subsequent pregnancies.77
Figure 6. Management of obstetric anal sphincter injuries for
subsequent pregnancies
ª 2012 Royal College of Obstetricians and Gynaecologists

Conclusion
Pelvic floor injuries during a vaginal delivery can be considered
a significant factor in the development of urinary incontinence,
faecal incontinence, pelvic organ prolapse and sexual
dysfunction. About eight out of ten women in the UK sustain
some form of perineal trauma during childbirth. Overall,
although there has been a noticeable increase in the prevalence
of OASIS, this could be largely attributed to improvements in
detection of such injuries. A good understanding of perineal
and anal sphincter anatomy and adherence to sound principles
of management are associated with a better outcome. Increased
body mass index, large fetal head, forceps delivery and first
vaginal delivery have been implicated in the development of
pelvic floor dysfunction. However, a recent study from 201139
has shown that unless women have all their deliveries by
the abdominal route, caesarean section does not protect
from subsequent urinary incontinence. Even among those
who do deliver exclusively by caesarean section, 40% still
report urinary incontinence and caesarean section confers no
benefit in terms of subsequent faecal incontinence. It would
therefore appear that the pregnancy itself rather than mode of
delivery alone may be a contributory factor in the development
of pelvic floor dysfunction.
Only a large randomised controlled trial of elective
caesarean section versus vaginal delivery could determine the
role of elective caesarean section in protecting against pelvic
floor dysfunction without a resultant increase in morbidity
and mortality. In the absence of such information, we need to
focus on making vaginal delivery safer by more focused
training and implementing evidence-based obstetric practice.
Conflict of interest
None declared.
References
1 Magdi I. Obstetric injuries of the perineum. J Obstet Gynecol Br
Commonw 1942;49:687–700.
2 Gainey H. Postpartum observation of pelvic tissue damage. Am J
Obstet Gynecol 1943;45:457.
3 Gainey H. Postpartum observation of pelvic tissue damage: further
studies. Am J Obstet Gynecol 1955;70:800.
4 Kearney R, Sawhney R, Delancey J. Levator ani muscle anatomy
evaluated by origin-insertion pairs. Obstet Gynecol 2004;104:168–73.
5 Barber MD, Bremer RE, Thor KB, Dolber PC, Kuehl TJ, Coates KW.
Innervation of the female levator ani muscles. Am J Obstet Gynecol
2002;187:64–71.
6 Sultan A, Thakar R. Third and fourth degree tears. In: Sultan A, Thakar
R, Fenner D, editors. Perineal and Anal Sphincter Trauma. London:
Springer; 2009. p. 33–51.
7 Sultan AH, Kamm MA, Hudson CN. Pudendal nerve damage during
labour: prospective study before and after childbirth. BJOG
1994;101:22–8.
8 Kaiser A, Ortega A. Anorectal anatomy. Surg Clin N Am
2002;82:1125–38.
ª 2012 Royal College of Obstetricians and Gynaecologists
Lone et al.
9 Royal College of Obstetricians and Gynaecologists. The Management
of Third and Fourth-degree Perineal Tears. Guideline No. 29. London:
RCOG Press; 2007.
10 Thakar R, Sultan A. Management of obstetric anal sphincter injury. The
Obstetrician & Gynaecologist 2003;5:72–8.
11 McCandlish R, Bowler U, van Asten H, Berridge G, Winter C, Sames L,
et al. A randomised controlled trial of care of the perineum during
second stage of normal labour. BJOG 1998;105:1262–72.
12 Department of Health. Statistical Bulletin-NHS Maternity Services.
London: Department of Health; 2003.
13 European Perinatal Health Report. 2008 [www.europeristat.com].
14 Weber A, Meyn L. Episiotomy use in the United States, 1979–1997.
Obstet Gynecol 2002;100:1177–82.
15 Johnson A, Sultan AH, Thiagamoorthy G, Thakar R. A national survey
of incidence of perineal trauma and obstetric practice in the United
Kingdom. Personal communication.
16 Dolan L, Lee R, Hilton P. Prevalence and obstetric antecedents of pelvic
floor dysfunction. Neurourol Urodyn 2006;26:508–9.
17 Kapoor D, Thakar R, Sultan A. Combined urinary and fecal
incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2005;16:321.
18 Norton C, Whitehead W, Bliss DZ, Harari D, Lang J. Conservative and
pharmacological management of faecal incontinence in adults.
In: Abrams P, Cardozo L, Khoury S, Wein A, editors. Incontinence.
Plymouth: Health Publications; 2009. p.1321–1386.
19 Sultan A, Nugent K. Pathophysiology and nonsurgical treatment of
anal incontinence. BJOG 2004;111(Suppl 1):84–90.
20 Sultan A, Kamm M. Hudson C, Bartram I. Third degree obstetric anal
sphincter tears: risk factors and outcome of primary repair. BMJ
1994;308:887–91.
21 South M, Stinnett S, Sanders D, Weidner A. Levator ani denervation
and reinnervation 6 months after childbirth. Am J Obstet Gynecol
2009;200:519.
22 MacArthur C, Glazener C, Wilson P, Lancashire R, Herbison G, Grant A.
Persistent urinary incontinence and delivery mode history: a six-year
longitudinal study. BJOG 2006;113:218–24.
23 Zetterström JP, López A, Anzén B, Dolk A, Norman M, Mellgren A.
Anal incontinence after vaginal delivery: a prospective study in
primiparous women. BJOG 1999;106:324–30.
24 Oberwalder M, Connor J, Wexner SD. Meta-analysis to determine the
incidence of obstetric anal sphincter damage. Br J Surg
2003;90:1333–7.
25 Harkin R, Fitzpatrick M, O’Connell P, O’Herlihy C. Anal sphincter
disruption at vaginal delivery: is recurrence predictable? Eur J Obstet
Gynecol Reprod Biol 2003;109:149–52.
26 Sultan A, Kamm M, Hudson C, Thomas J, Bartram C. Anal sphincter
disruption during vaginal delivery. N Engl J Med 1993;329:1905–11.
27 Andrews V, Thakar R, Sultan A, Jones P. Occult anal sphincter injuries
—myth or reality? BJOG 2006;113:195–200.
28 Faltin D, Boulvain M, Floris L, Irion O. Diagnosis of anal sphincter tears
to prevent fecal incontinence: a randomized controlled trial. Obstet
Gynecol 2005;106:6–13.
29 Fornell E, Matthiesen L, Sjödahl R, Berg G. Obstetric anal sphincter
injury ten years after: subjective and objective long term effects. BJOG
2005;112:312–6.
30 Bek K, Laurberg S. Risks of anal incontinence from subsequent vaginal
delivery after a complete obstetric anal sphincter tear. BJOG
1992;99:724–6.
31 Fornell E, Wingren G, Kjolhede P. Factors associated with pelvic floor
dysfunction with emphasis on urinary and fecal incontinence and
genital prolapse: an epidemiological study. Acta Obstet Gynecol Scand
2004;83:383–9.
32 Sultan AH. Anal incontinence after childbirth. Cur Opin Obstet
Gynecol 1997;9:320–4.
33 Roman H, Robillard PY, Payet E, El Amrani R, Verspyck E, Marpeau L,
et al. Factors associated with fecal incontinence after childbirth.
265
 Obstetric pelvic floor and anal sphincter injuries
Prospective study in 525 women. J Gynecol Obstet Biol Reprod (Paris)
2004;33:497–505.
34 Carroli G, Mignini L. Episiotomy for vaginal birth. Cochrane Database
Syst Rev 2009;(1):CD000081.
35 Roos AM, Thakar R, Sultan A. Outcome of primary repair of obstetric
anal sphincter injuries (OASIS): does the grade of tear matter?
Ultrasound Obstet Gynaecol 2010;36:368–74.
36 Hannah M, Hannah W, Hewson S, Hodnett E, Saigal S, Willan A.
Planned caesarean section versus planned vaginal birth for breech
presentation at term: a randomised multicentre trial. Term Breech Trial
Collaborative Group. Lancet 2000;356:1357–83.
37 Hannah ME, Whyte H, Hannah WJ, Hewson S, Amankwah K, Cheng
M, et al. Maternal outcomes at 2 years after planned cesarean section
versus planned vaginal birth for breech presentation at term: the
international randomized Term Breech Trial. Am J Obstet Gynecol
2004;191:917–27.
38 Dolan L, Hilton P. An epidemiological survey to assess prevalence and
risk factors for PFD in primigravidae delivered 20 years earlier: a
secondary analysis. Neurourol Urodyn 2007;26:717–8.
39 MacArthur C, Glazener C, Lancashire R, Herbison P, Wilson D; ProLong
study group. Exclusive caesarean section delivery and subsequent
urinary and faecal incontinence: a 12-year longitudinal study. BJOG
2011;118:1001–7.
40 Brown S, Wadhawan H, Nelson R. Surgery for faecal incontinence in
adults. Cochrane Database Syst Rev 2010;(9):CD001757.
41 Snooks S, Swash M, Setchell M, Henry M. Injury to the innervation of
pelvic floor sphincter musculature in childbirth. Lancet 1984;2:546–
50.
42 Smith A, Hosker G, Warrell D. The role of partial denervation of the pelvic
floor in the aetiology of genitourinary prolapse and stress incontinence
of urine: a neurophysiological study. BJOG 1989;96:24–8.
43 Deindl F, Vodusek D, Hesse U, Schussler B. Pelvic floor activity patterns:
comparison of nulliparous continent and parous urinary stress
incontinent women. Br J Urol 1994;73:413–7.
44 Meyer S, Schreyer A, De Grandi P, Hohlfeld P. The effects of birth on
urinary continence mechanisms and other pelvic-floor characteristics.
Obstet Gynecol 1998;92:613–8.
45 King J, Freeman R. Is antenatal bladder neck mobility a risk factor for
postpartum urinary and fecal incontinence? Obstet Gynecol
1998;105:1300–7.
46 Van Geelen JM, Lemmens WA, Eskes TK, Martin CB Jr. The urethral
pressure profile in pregnancy and after delivery in healthy nulliparous
women. Am J Obstet Gynecol 1982;144:636–49.
47 Losif S, Ulmsten U. Comparative urodynamic studies of continent and
stress incontinent women in pregnancy and in puerperium. Am J
Obstet Gynecol 1981;140:645–50.
48 Kim K, Ashton-Miller J, Strohbehn K, DeLancey J, Schultz A. The
vesico-urethral pressuregram analysis of urethral function under stress.
J Biomech 1997;30:19–25.
49 Pirpiris A, Shek K, Dietz H. Urethral mobility and urinary incontinence.
Ultrasound Obstet Gynecol 2010;36:507–11.
50 Kearney R, Miller J, Ashton-Miller J, DeLancey J. Obstetric factors
associated with levator ani muscle injury after vaginal birth. Obstet
Gynecol 2006;107:144–9.
51 Dietz H, Kirby A, Shek K, Bedwell P. Does avulsion of the puborectalis
muscle affect bladder function? Int Urogynecol J Pelvic Floor Dysfunct
2009;20:967–72.
52 Eason E, Labreque M, Marcoux S, Mondor M. Effects of carrying a
pregnancy and of method of delivery on urinary incontinence: a
prospective cohort study. BMC Pregnancy Childbirth 2004;4:4.
53 Viktrup L, Lose G. The risk of stress incontinence five years after first
delivery. Am J Obstet Gynecol 2001;185:82–7.
54 Viktrup L, Rortveit G, Lose G. Risk of stress urinary incontinence twelve
years after the first pregnancy and delivery. Obstet Gynecol
2006;108:248–54.
266
55 Chaliha C, Sultan AH, Bland JM, Monga AK, Stanton SL. Anal function:
effect of pregnancy and delivery. Am J Obstet Gynecol
2001;185:427–32.
56 Wilson P, Herbison R, Herbison G. Obstetric practice and the
prevalence of urinary incontinence three months after delivery. BJOG
1996;103:154–61.
57 Keane D, Sims T, Bailey A, Abrams P. Analysis of the pelvic floor
electromyography and collagen status in premenopausal nulliparous
females with genuine stress incontinence. Neurourol Urodyn
1992;11:308–9.
58 Rortveit G, Dalveit A, Hannestad Y, Hunskaar S. Norwegian EPINCONT
study. N Engl J Med 2003;348:900–7.
59 Toozs-Hobson P, Balmforth J, Cardozo L, Khullar V, Athanasiou S. The
effect of mode of delivery on pelvic floor functional anatomy. Int
Urogynecol J Pelvic Floor Dysfunct 2008;19:407–16.
60 Dietz H, Lanzarone V. Levator trauma after vaginal delivery. Obstet
Gynecol 2005;106:707–12.
61 Dietz H. Does delayed childbearing increase the risk of levator injury in
labour? ANZJOG 2007;47:491–5.
62 Lien K, Mooney B, DeLancey J, Ashton-Miller J. Levator ani muscle
stretch induced by simulated vaginal birth. Obstet Gynecol
2004;103:31–40.
63 Dietz H, Steensma A. The prevalence of major abnormalities of the
levator ani in urogynaecological patients. BJOG 2006;113:225–30.
64 Swift S, Woodman P, O’Boyle A, Kahn M, Bland D, Wang W, et al.
Pelvic Organ Support Study (POSST): the distribution, clinical definition
and epidemiologic condition of pelvic organ support defects. Am J
Obstet Gynecol 2005;192:795–806.
65 O’Boyle AL, Woodman PJ, O’Boyle JD, Davis GD, Swift SE. Pelvic organ
support in nulliparous pregnant and nonpregnant women: a case
control study. Am J Obstet Gynecol 2002;187:99–102.
66 Shek K, Dietz H. The effect of childbirth on hiatal dimensions. Obstet
Gynecol 2009;113:1272–8.
67 Majida M, Braekken I, BØ K, Benth J, Engh M. Anterior but not
posterior compartment prolapse is associated with levator hiatus area:
a three- and four-dimensional transperineal ultrasound study. BJOG
2011;118:329–37.
68 Abdool Z, Thakar R, Sultan AH. Postpartum female sexual function. Eur
J Obstet Gynecol Reprod Biol 2009;145:133–7.
69 Signorello L, Harlow B, Chekos A, Repke J. Postpartum sexual
functioning and its relationship to perineal trauma: a retrospective
cohort study of primiparous women. Am J Obstet Gynecol
2001;184:881–8.
70 Oboro V, Tabowei T. Sexual function after childbirth in Nigerian
women. Int J Gynecol Obstet 2002;78:249–50.
71 Glazener C. Sexual function after childbirth: women’s experiences,
persistent morbidity and lack of professional recognition. BJOG
1997;104:330–5.
72 Barrett G, Pendry E, Peacock J, Victor C, Tkakar R, Manyonda I.
Women’s sexual health after childbirth. BJOG 2000;107:186–95.
73 Payne T, Carey J, Rayburn W. Prior third or fourth-degree perineal tears
and recurrence risks. Int J Gynecol Obstet 1999;64:55–7.
74 Scheer I, Thakar R, Sultan A. Mode of delivery after previous obstetric
anal sphincter injuries (OASIS): a reappraisal? Int Urogynecol J
2009;20:1095–101.
75 Poen A, Felt-Bersma R, Strijers R, Dekker G, Cuesta M, Meuwissen S.
Third degree obstetric perineal tear: long-term clinical and functional
results after primary repair. Br J Surg 1998;85:1433–8.
76 Sangalli M, Floris L, Faltin D, Weil A. Anal incontinence in women with
third or fourth degree perineal tears and subsequent vaginal deliveries.
ANZJOG 2000;40:244–8.
77 Sultan A, Stanton S. Preserving the pelvic floor and perineum during
childbirth: elective caesarean section? BJOG 1996;103:731–4.
ª 2012 Royal College of Obstetricians and Gynaecologists