BJOG: an International Journal of Obstetrics and Gynaecology
December 2004, Vol. 111, Supplement 1, pp. 5– 9
Pathophysiology of urinary incontinence and
pelvic organ prolapse
Paul Hilton, Lucia M. Dolan
INTRODUCTION
NORMAL PELVIC FLOOR FUNCTION
Stress urinary incontinence and pelvic organ prolapse are
common, often debilitating conditions, necessitating surgical correction in 11% of women by the age of 80 years.1 A
common pathophysiology may be implied as aetiological
and aggravating factors are similar and both arise from
failure of pelvic floor support.
The fascial and muscular components within the pelvic
floor and its neural pathways create a dynamic support
mechanism that facilitates storage and voiding of urine and
faeces, and normal sexual function. Stress urinary incontinence and pelvic organ prolapse arise through abnormality
in pelvic floor architecture, at cellular or gross morphological levels, leading to mechanical failure of this support.
Normal functioning of the lower urinary tract depends on
the balance between the powers of urethral resistance and
the forces of urinary expulsion.7 A low pressure reservoir
and a high pressure sphincter are essential for maintenance
of urinary continence. Mechanical support of the vagina has
been proposed to be reliant on three mechanisms: closure of
the vagina at its introitus (by pelvic floor contraction),
vertical suspension of the vagina by the utero-sacral ligaments, and the flap valve effect created from the near
horizontal position of the vagina on the pelvic floor.8
CLASSIFICATION
Stress urinary incontinence
Stress urinary incontinence is the complaint of involuntary leakage of urine on effort or exertion, or on sneezing or
coughing.2 In urodynamic terms, stress continence is maintained when the maximum urethral pressure exceeds the
intravesical pressure.3 In the McGuire classification system,
type 1 and 2 stress incontinence occur because of urethral
hypermobility and type 3 because of intrinsic sphincter deficiency (ISD).4 More recently it has been suggested that there
is a spectrum of urethral characteristics in women with stress
urinary incontinence and ‘delineation into categories may
be simplistic and arbitrary and requires further research’.2
Pelvic organ prolapse
Several descriptive systems have been developed to
classify pelvic organ prolapse. However, few epidemiological studies have examined the distribution of pelvic floor
support within a female population.5 The Pelvic Organ
Prolapse Quantification system (POP-Q) has been formally
accepted by three international societies, although not yet
widely adopted into clinical practice in many areas.6
The pathophysiology of both these conditions might be
considered to represent a function of the mechanisms that
maintain a low pressure urinary reservoir, a high pressure
sphincter, and urethral and vaginal support.
Royal Victoria Infirmary, Newcastle upon Tyne, UK
Correspondence: Mr P. Hilton, Directorate of Women’s Services 3rd
Floor, Leazes Wing Royal Victoria Infirmary, Newcastle upon Tyne, NE1
4LP, UK.
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology
The reservoir function of the bladder
Maintenance of a low pressure reservoir is dependent on
hydrostatic pressure acting at the bladder neck and transmitted pressures from adjacent intra-abdominal viscera, and
tension in the bladder wall9 (see Fig. 1). When there is
adequate urethral support the first of these factors is insignificant. However, when urethral support is inadequate they
may become relevant especially during stress provocation.
Tension in the bladder wall is in part a passive phenomenon related to the distensibility or visco-elastic properties
of the bladder wall itself, and in part an active phenomenon
due to the contractility of the detrusor muscle and its
neurological control.
The neurological control of detrusor contractility is
dependent on a sacral spinal reflex under the control of
several higher centres. This basic reflex arc is best considered as a loop extending from sensory receptors within the
bladder wall through the pelvic plexus and via visceral
afferent fibres travelling with the pelvic splanchnic nerves;
it enters the spinal cord in the S2 –S4 levels synapsing with
cell bodies in the intermedio-lateral grey area of the same
sacral levels, and then via pelvic splanchnic nerves to the
smooth muscle cells of the detrusor (see Fig. 2). Higher
control over the basic reflex arc is mediated through
descending pathways from the pontine reticular formation,
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6
P. HILTON & L.M. DOLAN
and is primarily inhibitory; the normal influence is therefore to prevent contraction of the detrusor and thus to
encourage the maintenance of a low intravesical pressure
during the filling phase of the micturition cycle.
Urethral closure mechanisms
The usual level of continence in the female is at the level
of the bladder neck where passive elastic tension is the
most important factor leading to urethral closure.10,11 In the
mid-urethra at rest, closure is largely maintained through
the intrinsic striated muscle of the rhabdosphincter; however, the extrinsic striated muscles of pubo-coccygeus and
compressor urethrae may be significant in maintaining
urethral closure with increased intra-abdominal pressure.
Although an open bladder neck at rest does not distinguish
stress continent from incontinent women, stress continent
women who have an incompetent bladder neck on coughing might be at risk of developing urodynamic stress
incontinence should the distal sphincter mechanism fail.12
The plasticity of the urethra or its ability to act as a
watertight seal is also important in maintaining continence.
There has been much debate over the morphological components that contribute to the softness, compression and
tension in the urethra. Urethral pressure studies have shown
that approximately one-third of the resting urethral pressure is due to striated muscle effects, one-third to smooth
muscle effects and one-third to the vascular supply.13 With
increasing age both morphological and functional changes
are observed, which may predispose to the development
of stress incontinence.14 These include an increase in
intravesical pressure and a reduction in both mid-urethral
vascular pulsations and maximum urethral closure pressure10,13; the latter starts early and becomes significant
after 36 years.13
Fig. 1. Factors determining intravesical pressure. Reproduced from Hilton,9
with permission of author and publisher.
Fig. 2. The basic visceral reflex arc concerned with detrusor contractility.
Reproduced from Hilton,9 with permission of author and publisher.
Urethral and vaginal support
Support and suspension of the pelvic organs is dependent
on pelvic floor striated muscle and connective tissue, and the
attachments between muscle and connective tissue and the
bony pelvis. The levator ani comprises diaphragmatic and
pubovisceral components,15 and contains type 1 (slowtwitch) fibres that provide resting tone, and type 2 (fasttwitch) fibres that can respond to stress and thus maintain
urethral closure and prevent stretching of the pelvic
ligaments. Pelvic connective tissue facilitates organ displacement and volume changes and functions more as a
mesentery, unlike connective tissue in other parts of the body
where its function is to facilitate locomotion. Both of these
structures are damaged after delivery with tears in the
endopelvic fascia and thinning of the levators seen on MRI.16
The common action of the muscular and the fascial
components in providing pelvic floor support and their role
in the development of pelvic organ prolapse has been
recognised from the beginning of the last century. Paramore used the analogy of a ‘boat in a dry dock’ to explain
the loss of support provided by the levators, and the
suspensory role of the ligaments and fascia.17 Using levator
myography, Berglas and Rubin showed that in normal
nulliparous women the vaginal axis is almost horizontal
and is supported by the levator plate. In genital prolapse,
however, the levator support is lost and as a consequence
the vaginal axis inclines towards the vertical, the levator
hiatus widens and fascial supports are placed under strain.18
On the basis of cadaveric studies, DeLancey has described pelvic floor support at three levels.19 The cervix,
and upper third of the vagina are suspended almost vertically by a sheet of connective tissue from the pelvic wall;
this may be termed the paracolpium, and includes the uterosacral ligaments (level I). The middle third of the vagina is
attached laterally to the pelvic side walls by fascial sheets
extending transversely between the bladder and rectum, and
compromising the pubo-cervical fascia and prerectal fascia
attaching laterally to the arcus tendineus fasciae pelvis and
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology 111 (Suppl. 1), pp. 5 – 9
PATHOPHYSIOLOGY OF URINARY INCONTINENCE AND PELVIC ORGAN PROLAPSE
superior fascia of the levator ani (level II). In the lower
third of the vagina the wall is directly attached to surrounding structures. Anteriorly it fuses with the urethra, posteriorly with the perineal body and laterally with the levator
ani muscles (level III).19 Loss of support at level I leads to
uterine and vault prolapse whilst loss of level II support
results in cystocele and rectocele. During rises in intraabdominal pressure in continent women, the urethra is
supported through its lateral attachments and is compressed by the downward force of intra-abdominal pressure
against the resistance offered by the anterior vaginal wall
and endopelvic fascia below.20 When compression is inadequate because of a failure in suburethral support arising
from a defect in the endopelvic fascia or its attachments,
stress urinary incontinence will occur.
ABNORMAL PELVIC FLOOR FUNCTION
7
Table 1. Factors contributing to the development of urinary incontinence
and prolapse.
Pelvic floor muscle trauma and denervation
Congenital
Age related
Obstetric trauma
Pelvic fracture or surgery
Connective tissue disorders
Congenital or acquired CT disorders
Racial factors
Age related
Pregnancy related
Hormonal status and oestrogen deficiency
Lifestyle factors increasing pressure on the pelvic floor
Smoking, respiratory disease
Obesity
Recreational exercise
Occupational
Neuromuscular injury
The pudendal nerve, which arises from the anterior rami
of S2, S3 and S4, provides somatic innervation to the
striated muscle of levator ani and to the striated muscle
within the external anal and urethral sphincters.
Neuromuscular injury has been proposed as an important
factor in predisposing to pelvic floor dysfunction (see
Table 1). Interest in this area was first stimulated when
histochemical evidence of denervation was observed in the
external anal sphincter in those with faecal incontinence.21
Since then several neurophysiological studies have used
pudendal nerve latency or single fibre or concentric needle
pelvic floor electromyography (EMG) to investigate the
role of nerve injury in pelvic floor dysfunction. Reinnervation, which occurs in response to denervation, is
taken as a marker for injury,22,23 and both prolapse and
stress incontinence are found in association with denervation. Progressive pelvic floor denervation is thought to lead
to sagging of the levators, widening of the levator hiatus
with loss of urethral and vaginal support leading to stress
urinary incontinence and genital prolapse.
Ageing and childbearing are often considered as the two
major factors predisposing to pelvic floor denervation.23,24
Other factors include chronic straining at stool and congenital neurological conditions such as spina bifida and
muscular dystrophy. A gradual increase in denervation of
the pelvic floor has been observed with increasing age,23 as
is observed in striated muscle elsewhere in the body.
During childbirth, the pudendal nerve might be damaged
by compression or by traction within Alcock’s canal.
Snooks et al. using pudendal nerve latency and single fibre
EMG of the external anal sphincter found evidence of
denervation following vaginal delivery which persisted
2 months after delivery.22 Subsequent follow-up in a small
group of women at 5 years showed denervation to have
persisted or become worse.25 In a much larger prospective
study, Allen et al. found that 80% of women had evidence
of partial denervation to the pelvic floor after delivery.24
Longitudinal follow-up of this cohort 7 and 15 years later
indicated that denervation had progressed and the numbers
with stress incontinence had increased from the postnatal
period.26 Although there is much evidence to suggest an
association between these conditions and denervation injury, the relationship between neurogenic injury at childbirth
and long-term risk of stress urinary incontinence remains
unresolved.26
Connective tissue injury
Connective tissue is composed of collagen, elastin,
smooth muscle, fibroblasts and blood vessels. However,
collagen is the main constituent of endopelvic fascia,27 and
abnormalities in the quantity, type and quality of collagen
have been observed in both stress incontinence and in
genitourinary prolapse. Several studies have reported a
decrease in the total collagen content in women with stress
urinary incontinence.28 – 30 A reduction in total collagen and
increased turnover of collagen has been identified in
women with genitourinary prolapse.31 Endopelvic fascial
defects are associated with genitourinary prolapse and
urodynamic stress incontinence.23 Different sites of defect
have been identified in genital prolapse.32 In stress urinary
incontinence a defect in endopelvic fascia is also likely to
be of functional significance given that the urethra is
indirectly attached to the levators by endopelvic fascia
and an intact arrangement assists in urethral positioning.33
Qualitative and quantitative changes in collagen have
been observed in nulliparous women with stress urinary
incontinence.30 Women with stress incontinence and prolapse have an increase in abdominal striae,27 and increased
incidence of joint hypermobility has been observed in
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P. HILTON & L.M. DOLAN
women with genitourinary prolapse.34 However, prolapse
and stress incontinence may be acquired through conditions causing changes in connective tissue. Genitourinary
prolapse is more common with increasing age. With
increasing age connective tissue to muscle ratio is reduced,
and although the formation of collagen cross-links stabilizes the molecule it prevents remodelling and flexibility.
Stress incontinence and prolapse are more common in
multiparous women. We have discussed that there is
evidence to suggest that trauma during childbirth may
cause neuromuscular injury. However, changes in connective tissue also occur during pregnancy.35 Fascia becomes more elastic and vulnerable and women who have
antenatal stress incontinence might have a greater degree
of fascial weakness compared with those who remain
continent.35 Women who develop antenatal stress incontinence even when it resolves in the post natal period, are
twice as likely to develop it again in the future compared
with those without antenatal stress incontinence.26 The
hormonal changes during pregnancy or abnormal remodelling of collagen may be important in the development of
these conditions.
CONCLUSION
There would seem to be two major factors determining
the proneness of the human female to problems of stress
urinary incontinence and prolapse. Firstly, changes in
pelvic floor anatomy resulting from the change from the
pronograde to orthograde posture has meant that the pelvic
floor has had to adapt from its largely muscular function (of
moving the tail) in four legged animals, to a supportive role
in the human. This has been associated with a decrease in
muscle bulk and an increase in connective tissue. Secondly,
the human reproductive process results in a relatively large
fetus with a large bony cranium that has to pass through the
pelvic floor during the processes of labour and delivery. As
a consequence there is a certain inevitability to the problems of prolapse and incontinence as the increasingly
tenuous pelvic floor muscles, and persistently vulnerable
pelvic floor connective tissues are subjected to this degree
of trauma.
The complex aetiology of stress urinary incontinence
and pelvic organ suggests that greater attention should be
given to studying the natural history of these conditions.
Although there is much debate as to the exact site and
mechanism of injury during childbirth, the intimate arrangement of connective tissue and striated muscle within
the pelvic floor suggests that injury to one or other structure is likely to impact on their co-ordinated function.
Further understanding of the biomechanics of the pelvic
floor and dynamic imaging may improve knowledge of
how and when structural abnormalities occur and perhaps
ultimately guide more site-specific treatment. In future
family studies may allow the identification of those women
who may be genetically predetermined to develop these
conditions, and allow timely intervention to prevent the
development of symptoms.
References
1. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL.
Epidemiology of surgically managed pelvic organ prolapse and
urinary incontinence. Obstet Gynecol 1997;89:501 – 506.
2. Abrams P, Cardozo L, Fall M, et al. Standardisation of terminology
of lower urinary tract function: report from the Standardisation
Sub-committee of the International Continence Society. Neurourol
Urodyn 2002;21:167 – 178.
3. Enhorning G. Simultaneous recording of the intravesical and intraurethral pressure. Acta Obstet Gynecol Scand 1961;276s:1 – 69.
4. McGuire EJ. Urodynamic findings in patients after failure of stress
incontinence operations. Prog Clin Biol Res 1981;78:351 – 360.
5. Swift S. The distribution of female pelvic organ support in a population of women presenting for routine gynaecologic healthcare.
Am J Obstet Gynecol 2000;183:277 – 285.
6. Bump RC, Mattiasson A, Bo K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction.
Am J Obstet Gynecol 1996;175:10 – 17.
7. Barnes A. The method of evaluating the stress of urinary incontinence.
Am J Obstet Gynecol 1940;40:381 – 390.
8. DeLancey JOL. Pelvic floor dysfunction: causes and prevention.
Contemp Obstet Gynecol 1993;38:68 – 79.
9. Hilton P. Mechanism of continence. In: Stanton S, Monga A, editors.
Clinical Urogynaecology, 2nd edition. London: Churchill Livingstone, 2000:31 – 40.
10. Hilton P, Stanton SL. Urethral pressure measurement by microtransducer: the results in symptom-free women and in those with
genuine stress incontinence. Br J Obstet Gynaecol 1983;90:919 – 933.
11. Turner-Warwick RT, Brown ADG. A urodynamic evaluation of
urinary incontinence in the female and it’s treatment. Urol Clin N Am
1979;6:203 – 216.
12. Versi E. The significance of an open bladder neck in women. Br J
Urol 1991;68:42 – 43.
13. Rud T. Urethral pressure profile in continent women from childhood
to old age. Acta Obstet Gynecol Scand 1980;59:331 – 335.
14. Carlile A, Davies I, Rigby A, Brocklehurst JC. Age changes in the
human female urethra: a morphometric study. J Urol 1988;139:532 –
535.
15. Lawson J. Pelvic anatomy, I. pelvic floor muscles. Ann Roy Coll Surg
Eng 1974;54:244 – 252.
16. DeLancey JOL, Strohnbehn K, Peschers UM, Quint LE. MRI imaging
of the urethral support mechanism; anatomic considerations.
Neurourol Urodynam 1996;15:362 – 363.
17. Paramore R. The Statics of the Female Pelvic Viscera. London: H.K.
Lewis, 1918.
18. Berglas B, Rubin IC. The study of the supportive structures of
the uterus by levator myography. Surg Gynecol Obstet 1953;97:
677 – 692.
19. DeLancey JOL. Anatomic aspects of vaginal eversion after
hysterectomy. Am J Obstet Gynecol 1992;166:1717 – 1728.
20. DeLancey JOL. Structural support of the urethra as it relates to stress
urinary incontinence: The hammock hypothesis. Am J Obstet Gynecol
1994;170:1713 – 1723.
21. Parks AG, Swash M, Urich H. Sphincter denervation in anorectal
incontinence and rectal incontinence and rectal prolapse. Gut
1977;18:656 – 665.
22. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of
pelvic floor sphincter musculature in childbirth. Lancet 1984;2:546 –
550.
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology 111 (Suppl. 1), pp. 5 – 9
PATHOPHYSIOLOGY OF URINARY INCONTINENCE AND PELVIC ORGAN PROLAPSE
23. Smith AR, Hosker GL, Warrell DW. The role of partial denervation
of the pelvic floor in the aetiology of genitourinary prolapse and
stress incontinence of urine. A neurophysiological study. Br J Obstet
Gynaecol 1989;96:24 – 28.
24. Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage
and childbirth: a neurophysiological study. Br J Obstet Gynaecol
1990;97:770 – 779.
25. Snooks SJ, Swash M, Henry MM, Setchell M. Risk factors in
childbirth causing damage to the pelvic floor innervation. Int J
Colorectal Dis 1986;1:20 – 24.
26. Dolan LM, Hosker GL, Mallett VT, Allen RE, Smith AR. Stress
incontinence and pelvic floor neurophysiology 15 years after the first
delivery. Br J Obstet Gynaecol 2003;110:1107 – 1114.
27. Sayer TR, Dixon JS, Hosker GL, Warrell DW. A study of paraurethral
connective tissue in women with stress incontinence of urine.
Neurourol Urodyn 1990;9:319 – 320.
28. Ulmsten U, Ekman G, Giertz G, Malmstrom A. Different biochemical
composition of connective tissue in continent and stress incontinent
women. Acta Obstet Gynecol Scand 1987;66:455 – 457.
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29. Falconer C, Ekman G, Malmstrom A, Ulmsten U. Decreased collagen
synthesis in stress-incontinent women. Obstet Gynecol 1994;84:583 –
586.
30. Keane DP, Sims TJ, Abrams P, Bailey FJ. Analysis of collagen status in
premenopausal nulliparous women with genuine stress incontinence.
Br J Obstet Gynaecol 1997;104:994 – 998.
31. Jackson SR, Avery NC, Tarlton JF, Eckford SD, Abrams P, Bailey AJ.
Changes in metabolism of collagen in genitourinary prolapse. Lancet
1996;347:1658 – 1661.
32. Shull B. Clinical evaluation of women with pelvic support defects.
Clin Obstet Gynecol 1993;36:939 – 951.
33. DeLancey JOL. Structural aspects of the extrinsic continence
mechanism. Obstet & Gynecol 1988;72:296 – 301.
34. Norton P, Baker J, Sharp H, Warenski J. Genitourinary prolapse: its
relationship with joint mobility. Neurourol Urodynam 1990;9:321 – 322.
35. Landon CR, Crofts CE, Smith ARB, Trowbridge EA. Mechanical
properties of fascia during pregnancy: a possible factor in the development of stress incontinence of urine. Contemp Rev Obstet Gynaecol
1990;2:40 – 46.
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology 111 (Suppl. 1), pp. 5 – 9