Pelvic floor trauma following va

ginal deliveryHans Peter Dietz

Purpose of review

Recent years have seen a steady increase in the information

available regarding pelvic floor trauma in childbirth. A review

of this information is timely in view of the ongoing discussion

concerning elective caesarean section.

Recent findings

In addition to older evidence regarding pudendal nerve

injury, it has recently been shown that inferior aspects of the

levator ani and fascial pelvic organ supports such as the

rectovaginal septum can be disrupted in childbirth. Such

trauma is associated with pelvic organ prolapse, bowel

dysfunction, and urinary incontinence. Elective caesarean

section seems to have a limited protective effect that

appears to weaken with time. Older age at first delivery may

be associated with a higher likelihood of trauma and

subsequent symptoms.

Summary

Pelvic floor trauma is a reality, not a myth. It is currently not

possible, however, to advise patients as to whether

avoidance of potential intrapartum pelvic floor trauma is

worth the risk, cost, and effort of elective caesarean section.

In some women this may well be the case. The identification

of women at high risk for delivery-related pelvic floor trauma

should be a priority for future research in this field.

Keywords

childbirth, delivery, levator muscle, pelvic floor, prolapse,

ultrasound

Curr Opin Obstet Gynecol 18:528–537. � 2006 Lippincott Williams & Wilkins.

Nepean Campus, Western Clinical School, University of Sydney, Penrith, Australia

Correspondence to H.P. Dietz, PhD, 193 Burns Rd, Springwood 2777 NSW,AustraliaTel: +61 2 4751 8140; fax: +61 2 4734 1817; e-mail: hpdietz@bigpond.com

Current Opinion in Obstetrics and Gynecology 2006, 18:528–537

Abbreviations

MRI m

528

agnetic resonance imaging

POP-Q p elvic organ prolapse quantification system

� 2006 Lippincott Williams & Wilkins1040-872X

IntroductionObstetrics is currently undergoing its most major change

since the introduction of antenatal ultrasound. At times

one wonders whether in the long run vaginal childbirth is

destined to become a practice limited to fringe groups

and resource-poor settings. Not surprisingly, the issue

often elicits emotional responses as any change in the

status quo would have major implications for the relative

role of healthcare providers and require significant redis-

tribution of scarce resources. Inevitably, discussion of

pelvic floor trauma in childbirth is seen as partisan,

due to the fact that a growing awareness of potential

negative effects of vaginal childbirth, such as urinary and

faecal incontinence and pelvic organ prolapse, is very

likely to contribute to rising caesarean section rates, even

if other factors may currently predominate [1,2]. There is

no doubt, however, that caesarean section, whether

primary or secondary, can lead to significant and occasion-

ally major morbidity and even mortality. For now we have

no means of determining whether this risk outweighs the

risk of attempted vaginal childbirth in a given patient,

and this must be reflected in the advice that we provide to

our patients.

For some forms of pelvic floor morbidity, it is not clear

whether pregnancy or childbirth is to blame [3,4], and

long latencies between the presumptive cause (child-

birth) and effect (incontinence and prolapse) further

complicate research. Despite all this, we now have rela-

tively firm epidemiologic evidence on the association

between vaginal childbirth and urinary incontinence

and prolapse [4,5��,6], as summarized in Fig. 1 first

published in a review article by DeLancey [5��].

Regarding prolapse, pregnancy and childbirth are well

documented as major risk factors [3,6]. Caesarean deliv-

ery is associated with less need for surgical correction of

incontinence or prolapse [3] and seems protective against

symptomatic prolapse [7]. Regarding urinary inconti-

nence, several large epidemiologic studies have shown

that caesarean section provides partial protection from

stress incontinence [4,8,9��]. The one randomized con-

trolled trial that may shed light on the degree of protec-

tion to be expected from elective caesarean section is the

Term Breech Trial. It showed a relative risk of 0.62 in the

elective caesarean section group 3 months after childbirth

[8], but of course these data are of limited use due to the

special nature of breech delivery. Any protective effect

appears to fade over time [9��] as congenital factors and

changes related to ageing will increasingly outweigh the

Trauma following vaginal delivery Dietz 529

Figure 1 The effect of vaginal parity on the prevalence of urinary

incontinence and pelvic organ prolapse

10

8

6

4

2

00 1 2 3 >4

Parity

Prolapse

1

2

4

89

10.7

2.42.6 2.8

Urinary incontinence

Relative risk

Parity and associated relative risks. Originally adapted from [6] and [4];reproduced with permission from [5��].

effects of traumatic childbirth as women grow older. One

may contend, however, that any protective effect will

apply during the most active decades of a woman’s life

and therefore be desirable, even if this protection is lost

later in life.

Paradoxically, the situation seems less clear as regards

faecal incontinence, despite its being associated with

the one type of pelvic floor trauma that is often clearly

evident at the time of delivery, i.e. anal sphincter

trauma. Epidemiologic evidence generally does not

support a protective effect of caesarean section in

comparison with normal vaginal delivery [9��,10],

although much of the data is diluted by caesarean

section performed in labour. The risk of anal incon-

tinence seems significantly higher after forceps deliv-

ery [9��,10–12], however, and older age at first delivery

is another risk factor [9��].

Our knowledge base regarding the impact of vaginal

childbirth on the anatomy and function of the female

pelvic floor has increased markedly over the past two

decades. While it was established in the 1980s and

1990s that vaginal childbirth (or even just the attempt

at vaginal delivery) may significantly change pudendal

nerve conduction patterns [13,14], the limited useful-

ness of tests of nerve function in clinical practice [15]

has cast doubts on the relevance of denervation as a

major aetiologic factor in pelvic floor disorders. Con-

centric needle electromyography may provide more

accurate information but is technically difficult and

unlikely to attract many volunteers. It is not surprising

therefore that little recent electrophysiologic work

has been reported, although what there is tends to

confirm previous findings of electromyographic altera-

tions in parous women [16–18]. This review therefore

focuses on imaging evidence accumulated over the past

5 years.

Recent investigations using techniques such as magnetic

resonance imaging (MRI) and three-dimensional or four-

dimensional ultrasound have focused on pelvic organ

support, the integrity of fascial support structures, func-

tion and morphology of the levator ani muscle, and the

external and internal anal sphincter. While the relative

roles of muscle and fascia for pelvic organ support con-

tinue to be debated, both seem to be subject to delivery-

related trauma.

Pelvic organ supportClinical studies of pelvic organ support were until

recently limited by a lack of sufficiently sensitive tools

for prolapse assessment. This has changed with the

introduction of the pelvic organ prolapse quantification

system (POP-Q) [19]. Vaginal parity seems to be a risk

factor for pelvic organ prolapse as defined by the POP-Q

assessment [20] and is associated with higher degrees of

pelvic organ mobility as shown by POP-Q in young

women [21], but studies comparing antepartum with

postpartum findings are scarce due to the fact that even

such a simple assessment is invasive and less well toler-

ated in pregnancy and puerperium.

Several authors have demonstrated increased pelvic

organ mobility in parous women on using real-time

ultrasound imaging, whether in cohorts of symptomatic

older patients presenting to urogynaecology clinics [22] or

in the puerperium. There are few data on the effect of

pregnancy itself [23], but several authors have observed

the effect of labour and delivery, examining women both

before and after childbirth [24–27]. From this evidence,

it seems clear that prelabour caesarean section and

caesarean section in first stage result in little change

in bladder neck support. Vaginal delivery, conversely,

in particular operative vaginal delivery, is associated with

a highly significant increase in bladder neck mobility. An

example of markedly increased bladder and urethral

mobility after a vacuum extraction for failure to progress

in second stage is shown in Fig. 2 [27].

There seems to be sufficient proof for the hypothesis that

pelvic organ support can be impaired by vaginal child-

birth. It is unclear whether this effect is due to stretching

or avulsion of structures and whether the observed

changes are primary (i.e. directly due to childbirth) or

the medium-term or long-term consequence of levator

impairment. Several mechanisms may well coexist in one

individual. Risk factors are operative vaginal delivery,

prolonged second stage, and possibly high birth weight.

The extent of such trauma, however, clearly varies from

one person to the next.

Furthermore, it has recently been shown that any deliv-

ery-related changes occur against the background of

marked variations in pelvic organ support in young

530 Urogynecology

Figure 2 Bladder neck mobility on Valsalva manœuvre at 37 weeks (a) and 3 months postpartum (b)

Markedly increased bladder and urethral mobility after a vacuum extraction for failure to progress in second stage. Reproduced with permission from[27].

nulliparous women [28]. As the most significant changes

are observed in those with the least organ mobility

antenatally [29], the effect of childbirth may be a partial

equalization of those interindividual differences. We are

not currently able to distinguish between preexisting or

postpartum (postdelivery) prolapse, but recent develop-

ments hold out promise that this may soon change.

Direct evidence of fascial traumaSeveral attempts have been made to define fascial trauma

after vaginal delivery. In the anterior compartment it

has long been assumed that childbirth may result in dis-

ruption of the ‘endopelvic fascia’, in particular of para-

urethral and paravaginal structures. To date, such attempts

have generally been unsuccessful, although transrectal

three-dimensional or four-dimensional ultrasound using

Figure 3 Comparison of posterior compartment imaging (midsagit

vaginal delivery (b), on maximal Valsalva manœuvre

The anorectal junction appears normal on the left.On the right, there is a rectocoele of a depth ofabout 2 cm, filled with stool. Reproduced withpermission from [30�].

high-frequency transducers may be able to identify the

subvesical part of the endopelvic fascia. Contrary to what

has been surmised in the past, such defects may be

multiple and, analogous to striae gravidarum, too complex

to invite surgical reconstruction.

As opposed to the situation regarding the anterior compart-

ment, posterior compartment prolapse commonly provides

indirect evidence of fascial trauma, due to the distinct

appearances of a ‘true’ rectocoele, which is thought to

represent a defect of the rectovaginal septum or Denon-

villier’s fascia. Analogous to increased bladder descent

after childbirth, there is a highly significant increase in

caudal displacement of the rectal ampulla after childbirth

[27]. In addition, however, it has recently been shown that

vaginal childbirth also results in an increased prevalence of

tal plane) in the third trimester (a) and 3 months after normal

Trauma following vaginal delivery Dietz 531

true rectocoele, i.e. presumptive defects of the rectovagi-

nal septum, and that existing defects seem to grow larger

[30�]. Such defects are strongly associated with symptoms

of pelvic organ prolapse and obstructed defecation [31].

Figure 3 [30�] shows a case of de-novo true rectocoele 3

months after vaginal delivery.

Levator traumaWhat clinicians and physiotherapists call ‘the pelvic floor’

is, for practical purposes, the pubococcygeus–puborecta-

lis complex. This muscle complex forms a V-shaped or

U-shaped sling around the anorectal junction, inserting

on the pelvic sidewall from the pubic rami to the ischial

spine. The levator hiatus, i.e. the space bordered by this

sling, contains the urethra anteriorly, the vagina centrally,

and the anorectum posteriorly (see Fig. 4 [32��] for a

comparison of MRI and ultrasound imaging of the hiatus

in the axial plane).

The area of the levator hiatus in young nulliparous

women varies from 6 to 36 cm2 on Valsalva manœuvre

[33�]. The area of the average fetal head in the plane of

minimal diameters measures 70–90 cm2 (equivalent to a

head circumference of 300–350 mm), requiring marked

distension and deformation of the levator complex. Lien

et al. [34] in Ann Arbor, Michigan, have been able to show

with the help of MRI-based computer modelling that the

most inferior and medial parts of the levator complex may

have to increase in length by a factor of 3 or more during

crowning of the fetal head. Given this degree of acute

distension, it is remarkable that many women seem to go

through childbirth without sustaining major soft tissue

trauma.

Evidence on the effects of childbirth on levator structure

and function is available both from clinical research on

Figure 4 A comparison of magnetic resonance (a) and three-dime

muscle in a 23-year-old nulliparous volunteer

The pelvic floor consists of the pubococcygeus–puborectalis complex, which forms a V-shaped orU-shaped sling around the anorectal junction,inserting on the pelvic sidewall from the pubicrami to the ischial spine. The levator hiatus, i.e. thespace bordered by this sling, contains the urethraanteriorly, the vagina centrally, and the anorectumposteriorly. Reproduced with permission from[32��].

pelvic floor function, usually obtained by physiotherapists,

and from imaging. Several papers over the past decade

have described patterns of injury observed on MRI,

although no comparative study of antepartum and post-

partum levator anatomy has been published to date. From

studies in parous women [35,36], it has been speculated

that the change in the typical H-shaped appearance of the

vagina may be due to traumatic loss of paravaginal supports

unilaterally or bilaterally. Hoyte et al. [37] have shown a

significant decrease in levator muscle volume and

increase in levator hiatus width in women with stress

incontinence and prolapse. Other authors [38] have

attributed abnormalities in density and structure of the

levator ani to childbirth-related trauma.

With the advent of sonographic three-dimensional

imaging techniques, pelvic floor ultrasound is now also

capable of demonstrating both the normal pubococcy-

geus–puborectalis complex and abnormalities seen in

parous women [32��,39,40��]. Recent technologic devel-

opments such as speckle reduction algorithms and tomo-

graphic or multislice imaging have markedly increased

resolutions and now allow quantification of levator trauma

in all dimensions [41] (Figs. 5–8). As a result, four-

dimensional pelvic floor ultrasound now achieves spatial

resolutions similar to or better than MRI in all three

dimensions, while temporal resolutions are markedly

superior to MRI, allowing the real-time observation of

manœuvres.

Presence and extent of levator defects seem to be associ-

ated with symptoms and signs of pelvic organ prolapse,

especially of the anterior and central compartment

[32��,40��,41]. While levator avulsion was observed in

11% of women with normal uterine support, it was found

in 25% of all women with uterine descent and in about

nsional pelvic floor ultrasound (b) imaging of the pubovisceral

532 Urogynecology

Figure 5 A comparison of magnetic resonance (a) and ultrasound (b) imaging in patients with a typical right-sided avulsion injury

(arrows) to the pubovisceral muscle

Reproduced with permission from [40��].

half of those with second-degree or third-degree uterine

prolapse [40��]. There appears to be a link between

levator trauma and worsened or de-novo stress incon-

tinence 3 months postpartum [32��], although this asso-

ciation seems to disappear later in life [40��], an

observation that accords with the fact that epidemiologic

evidence demonstrates much stronger associations

between childbirth and prolapse than between parity

and stress incontinence (Fig. 1). Avulsion of the pubo-

rectalis may be the cause of stress incontinence, or it

may just be a marker for (currently undetectable) trauma

to fascial supports of the urethra and anterior vaginal

wall.

Figure 6 Small unilateral trauma to the left anterior aspect of the

translabial three-dimensional/four-dimensional ultrasound

(a) Image obtained at 37 weeks; (b) 4 monthspostpartum.

Major trauma to the levator ani, as described in Fig. 5

[40��] and Figs 6–8, is palpable and was first described in

1943 [42]. Palpation of the levator ani by physiotherapists

and gynaecologists or urogynaecologists does not cur-

rently include a morphologic assessment, however, and

the digital diagnosis of such defects may require signifi-

cant teaching. In a recent study comparing three-

dimensional ultrasound and levator palpation by a

conventionally trained physiotherapist, agreement bet-

ween the two methods was very poor [43], but another

paper comparing digital assessment by a specifically

trained physician and MRI showed better agreement

[44�].

pubovisceral muscle (asterisk), as seen in the axial plane on

Trauma following vaginal delivery Dietz 533

Figure 7 Major bilateral trauma to the pubovisceral muscle (asterisks), as imaged on translabial three-dimensional/four-dimen-

sional ultrasound

Both insertions of the pubovisceral muscle havebeen avulsed from the pelvic sidewall. (a) Imageobtained at 36 weeks; (b) 3 months postpartum.

There seems to be an association between age at first

delivery and levator trauma [32��,45,46��]. This obser-

vation agrees with recent epidemiologic data from Nor-

Figure 8 Bilateral avulsion injury to the pubovisceral muscle 4 yea

third-degree cystocoele and second-degree uterine prolapse, as

dimensional/four-dimensional ultrasound

The figure shows a coronalreference plane (top left) and eightsuccessive axial planes from 5 mmcaudal to the hiatus to 15 mmcranial to the hiatus, showing thebulk of the pubovisceral muscleavulsed from the pelvic sidewallon both sides.

way. Rortveit and Hunskaar [47] showed in a reanalysis

of the EPINCONT study (Epidemiology of Inconti-

nence in the County of Nord-Trøndelag) that stress

rs after rotational forceps delivery (asterisks), associated with

seen on tomographic ultrasound imaging, translabial three-

534 Urogynecology

Figure 9 Hiatal dimensions before (a) and 4 months after vaginal delivery (b) as seen on maximal Valsalva manœuvre in the axial

plane

These images were obtained by translabial four-dimensional ultrasound, with the plane of minimaldimensions identified in the midsagittal plane androtated through 908 to obtain a representation ofthe hiatus in the axial plane. It is evident that hiataldimensions – both diameters and area – areincreased in the postpartum image on the right.

incontinence was more likely in women who had had

their first baby at an older age, a finding that has since

been confirmed by others [48��]. These observations

may have significant public health implications, as in

Western societies the age of primiparae has risen by

about 10 years over the past two generations.

Childbirth does not just affect morphology or macro-

anatomic appearances, it seems to have an effect on

biomechanics as well. Childbirth clearly changes both

dimensions and distensibility of the hiatus [32��,49], as

Figure 10 Appearances on translabial ultrasound, coronal plane, in t

anal sphincter tears

Scars or defects are indicated byasterisks.

shown in Fig. 9, but it is currently unclear whether this is

due to functional or morphologic change.

Anal sphincter traumaAnal sphincter injury is a form of pelvic floor trauma

familiar to all practising obstetricians, and (since it is

generally obvious to the naked eye) there seems little

scope for debating a causal link with childbirth. While

primary repair is undertaken at delivery as a matter of

course, the quality of both detection and repair of

such trauma seems to vary significantly. Anal sphincter

hree women (a–c) 6–8 weeks after primary repair of third-degree

Trauma following vaginal delivery Dietz 535

Figure 11 Appearances on translabial ultrasound of a major fourth-degree tear

(a) Coronal plane and (b) midsagittal plane. EAS,external anal sphincter, IAS, internal anal sphincter.Image courtesy of Dr A. Steensma, Rotterdam.

injuries may well occur more frequently than previously

reported, in up to one-quarter of vaginal deliveries, with

lower estimates due to ineffective intrapartum detection

rather than covered ‘occult’ defects [50�]. The main risk

factor is considered to be instrumental vaginal delivery

[51]. Anal incontinence is common after third-degree

and fourth-degree tears, even if they are recognized and

repaired at the time of injury, and can have a major effect

on a woman’s quality of life. As in other pelvic floor

disorders, however, the condition may be influenced by

several other aetiologic factors such as chronic diarrhoea,

anorectal surgery, cognitive impairment, and neuro-

pathy (either as a result of traumatic childbirth or due

to other causes). Not surprisingly, the strength of the

association between obstetric factors and faecal incon-

tinence varies with the age of the population under

scrutiny [9��]. It seems that many if not most women

remain asymptomatic after anal sphincter injury [52].

Conversely, evidence of old sphincter trauma is found in

more than 70% of women with late-onset faecal incon-

tinence [53].

The anal sphincter is generally imaged by endoanal

ultrasound, using high-resolution probes with a field of

vision of 3608. This method is firmly established as one of

the cornerstones of a colorectal diagnostic workup for anal

incontinence and is covered extensively in the colorectal

and radiologic literature [54–56]. Due to the limited

availability of such probes, obstetricians and gynaecolo-

gists have taken to using high-frequency curved array

probes placed exoanally, i.e. transperineally [57,58,59�] in

the coronal rather than the midsagittal plane.

On exoanal or translabial ultrasound, the external

sphincter appears as an isoechoic to hyperechoic ring

structure, while the internal anal sphincter is hypo-

echoic. Anal sphincter defects appear as a discontinuity

of these ring structures (Figs 10 and 11). In the coronal

plane, defects are conveniently described using a clock

face notation. In the longitudinal plane, sphincter

defects can be described by measuring defect length

relative to total sphincter length.

After repair of third-degree and fourth-degree tears,

ultrasound commonly demonstrates residual defects,

and the extent of such incompletely or inadequately

repaired defects seems associated with decreased

sphincter pressures and an increased risk of anal incon-

tinence [60�]. Figure 10 shows the degree to which

appearances in the coronal plane may vary after primary

repair of third-degree anal sphincter trauma, and Fig. 11

illustrates the potential cranial extent of such trauma.

ConclusionThere is little doubt that some women suffer significant

trauma to pelvic floor structures as a consequence of

(successful or unsuccessful) attempts at vaginal child-

birth. Trauma may affect the pudendal nerve or its

branches, the anal sphincter, the puborectalis–pubococ-

cygeus complex, or pelvic fascial structures. The more

protracted a delivery is and the longer the duration of

second stage, the higher seems the likelihood of ana-

tomic or functional alteration, although some forms of

trauma may also occur as a result of precipitate labour.

Vaginal operative delivery seems to be a risk factor for all

forms of impairment mentioned above, whether inde-

pendently or due to its association with prolonged second

stage. Changes in demographics and obstetric practice

may influence the likelihood of pelvic floor trauma

and future incontinence or prolapse. Ever-increasing

caesarean section rates may ultimately prevent the need

for pelvic floor surgery in some women, but for the next

few decades we are likely to see an increase in the

prevalence of pelvic floor morbidity, especially pelvic

organ prolapse, due to delayed childbearing.

Delivery-related pelvic floor trauma is a reality, not a

myth. It is an entirely different question, however, as to

whether such trauma is common or severe enough to

require a change in clinical practice. Currently, we cannot

536 Urogynecology

be sure whether avoidance of potential intrapartum pel-

vic floor trauma is worth the risk, cost, and effort of

performing an elective caesarean section. In order to

make preventive intervention feasible, we may first have

to learn to identify women most at risk of delivery-related

pelvic floor trauma, and this should be a priority topic for

future research. Ultimately, however, only randomized

controlled trials of planned vaginal birth versus planned

caesarean section, whether in high-risk patients or in an

unselected population, will eventually provide meaning-

ful information to women and their healthcare providers.

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�Dietz HP, Steensma AB. The role of childbirth in the aetiology of rectocele. Br JObstet Gynaecol 2006; 113:264–267.

First direct evidence on the role of childbirth in the aetiology of rectocoele.

31 Dietz HP, Korda A. Which bowel symptoms are most strongly associated witha true rectocele? Aust N Z J Obstet Gynaecol 2005; 45:505–508.

32

��Dietz H, Lanzarone V. Levator trauma after vaginal delivery. Obstet Gynecol2005; 106:707–712.

This small observational study in women 2–4 weeks before and 2–6 months afterchildbirth provides direct proof for the hypothesis that childbirth is responsible forcertain morphologic abnormalities observed in parous women and suggests thatolder age at first delivery is a risk factor for such trauma.

33

�Dietz H, Shek K, Clarke B. Biometry of the pubovisceral muscle and levatorhiatus by three-dimensional pelvic floor ultrasound. Ultrasound ObstetGynecol 2005; 25:580–585.

First description of translabial three-dimensional pelvic floor ultrasound as a tool toassess biometric indices of the levator ani muscle and hiatus.

34 Lien KC, Mooney B, DeLancey JO, Ashton-Miller JA. Levator ani musclestretch induced by simulated vaginal birth. Obstet Gynecol 2004; 103:31–40.

35 Klutke C, Golomb J, Barbaric Z, Raz S. The anatomy of stress incontinence:magnetic resonance imaging of the female bladder neck and urethra. J Urol1990; 143:563–566.

36 Huddleston H, Dunnihoo D, Huddleston P, Meyers P. Magnetic resonanceimaging of defects in DeLancey’s vaginal support levels I, II, and III. Am JObstet Gynecol 1995; 172:1778–1782.

37 Hoyte L, Schierlitz L, Zou K, et al. Two- and 3-dimensional MRI comparison oflevator ani structure, volume, and integrity in women with stress incontinenceand prolapse. Am J Obstet Gynecol 2001; 185:11–19.

38 Tunn R, DeLancey JO, Howard D, et al. MR imaging of levator animuscle recovery following vaginal delivery. Int Urogynecol J 1999; 10:300–307.

39 Dietz H. Ultrasound imaging of the pelvic floor: 3D aspects. UltrasoundObstet Gynecol 2004; 23:615–625.

40

��Dietz H, Steensma A. The prevalence of major abnormalities of the levatorani in urogynaecological patients. Br J Obstet Gynaecol 2006; 113:225–230.

First ultrasound study to estimate the prevalence of levator avulsion injury insymptomatic women and the first to show an association between such traumaand pelvic organ prolapse.

41 Dietz HP. The classification of major morphological abnormalities of thepubovisceral muscle. Neurourol Urodyn; 2006; 25 In press.

Trauma following vaginal delivery Dietz 537

42 Gainey HL. Postpartum observation of pelvic tissue damage. Am J ObstetGynecol 1943; 46:457–466.

43 Dietz H, Hay-Smith E, Hyland G. Vaginal palpation and 3D pelvic floorultrasound in the diagnosis of avulsion defects of the levator ani. NeurourolUrodyn. 2006; 25 In press.

44

�Kearney R, Miller JM, Delancey JO. Interrater reliability and physical examina-tion of the pubovisceral portion of the levator ani muscle: validity comparisonsusing MR imaging. Neurourol Urodyn 2006; 25:50–54.

This paper demonstrates that levator trauma identified on imaging can be palpatedvaginally, although palpation requires significant training and may underestimatethe extent of trauma.

45 Dietz HP. Does delayed childbearing increase the risk of levator injury inlabour? Neurourol Urodyn. 2006;25 In press.

46

��Kearney R, Miller J, Ashton-Miller J, Delancey J. Obstetric factors associatedwith levator ani muscle injury after vaginal birth. Obstet Gynecol 2006;107:144–149.

This paper investigates obstetric risk factors for levator trauma and confirms thatolder age at first delivery seems to be a risk factor.

47 Rortveit G, Hunskaar S. The association between the age at the first and lastdelivery and urinary incontinence. Neurourol Urodyn 2004; 23 (5/6):562–563.

48

��S Glazener CM, Herbison GP, MacArthur C, et al. New postnatal urinaryincontinence: obstetric and other risk factors in primiparae. BJOG 2006;113:208–217.

Another outstanding paper that has arisen from the study mentioned in MacArthuret al. (Br J Obstet Gynaecol 2005; 112:1075–1082).

49 Steensma AB, Dietz H. 3D pelvic floor ultrasound in the assessment of thelevator ani muscle complex [abstract]. Ultrasound Obstet Gynecol 2004;24:258.

50

�Andrews A, Sultan A, Thakar R, Jones P. Occult anal sphincter injuries: mythor reality? Br J Obstet Gynaecol 2006; 113:195–200.

A very interesting study suggesting that ‘occult’ anal sphincter injuries are gen-erally visible on diligent examination and that previous low prevalence estimates foranal sphincter injuries are due to our failure to detect sphincter trauma.

51 Sultan AH, Kamm MA, Hudson CN, et al. Anal sphincter disruption duringvaginal delivery. N Engl J Med 1993; 329:1905–1911.

52 Oberwalder M, Connor J, Wexner SD. Meta-analysis to determine theincidence of obstetric anal sphincter damage. Br J Surg 2003; 90:1333–1337.

53 Oberwalder M, Dinnewitzer A, Baig MK, et al. The association between late-onset fecal incontinence and obstetric anal sphincter defects. Arch Surg2004; 139:429–432.

54 Williams AB, Bartram CI, Halligan S, et al. Alteration of anal sphinctermorphology following vaginal delivery revealed by multiplanar anal endo-sonography. Br J Obstet Gynaecol 2002; 109:942–946.

55 Gold DM, Bartram CI, Halligan S, et al. Three-dimensional endoanal sono-graphy in assessing anal canal injury. Br J Surg 1999; 86:365–370.

56 Frudinger A, Bartram CI, Halligan S, Kamm M. Examination techniques forendosonography of the anal canal. Abdom Imaging 1998; 23:301–303.

57 Peschers UM, DeLancey JO, Schaer GN, Schuessler B. Exoanal ultrasound ofthe anal sphincter: normal anatomy and sphincter defects. Br J ObstetGynaecol 1997; 104:999–1003.

58 Timor-Tritsch IE, Monteagudo A, Porges RF, Santos R. Simple ultrasoundevaluation of the anal sphincter in female patients using a transvaginaltransducer. Ultrasound Obstet Gynecol 2005; 25:177–183.

59

�Yagel S, Valsky DV. Three-dimensional transperineal sonography for evalua-tion of the anal sphincter complex: another dimension in understandingperipartum sphincter trauma. Ultrasound Obstet Gynecol 2006; 27:119–123.

Interesting paper describing the use of three-dimensional pelvic floor ultrasoundfor the assessment of anal sphincter tears.

60

�Starck M, Bohe M, Valentin L. The extent of endosonographic anal sphincterdefects after primary repair of obstetric sphincter tears increases over timeand is related to anal incontinence. Ultrasound Obstet Gynecol 2006;27:188–197.

Important longitudinal study showing that most women show evidence of residualsphincter defects after repair and that the extent of such defects is associated withcontractile function and symptoms of anal incontinence.