Urological problems in pregnancy

C. CHALI HA and S. L. STANTON*

East Surrey Hospital, Redhill, and *St George's Hospital, London, UK
Summary
During pregnancy the urinary tract undergoes extensive
anatomical and physiological changes. These changes
can result in many symptoms and pathological con-
ditions that may affect the mother and fetus. It is well
documented that childbirth may result in urinary tract
damage which may predispose to postpartum symptoms.
This review describes the physiological and pathological
consequences of pregnancy and delivery on the urinary
tract, and how these may be minimized.
Introduction
During pregnancy the urinary tract undergoes extensive
anatomical and physiological changes. These changes
may be further inuenced by alteration in renal function
and intercurrent pathology in pregnancy, and changes
resulting from labour and delivery.
Anatomical and physiological changes
The upper urinary tract
In normal pregnancy the kidneys elongate by <1 cm
because of the increase in vascular volume and inter-
stitial space. Dilatation of the renal pelvis and hydro-
ureter can be seen as early as 7 weeks of gestation and
is thought to be secondary to a muscle-relaxant effect
of progesterone and mechanical obstruction from the
gravid uterus. It is more marked on the right than the
left side, because of dextrorotation of the uterus and
a protective effect of the sigmoid colon on the left ureter.
There is a 4050% increase in GFR and a 6080%
increase in the effective renal plasma ow [1]. Because
of this the plasma creatinine, urea and urate values
are lower than the normal ranges for nonpregnant
women.
The lower urinary tract
The elevated levels of oestrogen and progesterone cause
the bladder and urethral mucosa to become hyperaemic
and congested, and the urethral transitional epithelium
more squamous. The detrusor muscle hypertrophies
under the elevated levels of oestrogen but the increased
levels of progesterone lead to a relative bladder hypotonia
and increased bladder capacity.
The bladder is drawn upwards anteriorly as the uterus
enlarges, becoming more of an abdominal than a pelvic
organ by the third trimester. The base of the bladder
enlarges and the trigone becomes more convex than
concave. Radiological studies in pregnancy show that
the bladder is distorted by the fundus, and in labour the
bladder neck is displaced forwards and becomes more
funnelled [2].
Iosif et al. [3] performed urethral pressure prolometry
and simultaneous urethrocystometry in 14 healthy con-
tinent primiparae in the rst and late third trimester,
and again 57 days postpartum, and reported an
increase in total and functional urethral length, with
an increase in intravesical pressure from 9 to 20 cmH
2
O,
and a corresponding increase in urethral closure
pressure.
Problems in pregnancy
The upper urinary tract
UTI/pyelonephritis: UTIs are a common complication in
pregnancy and the standard denition is a colony count
of >10
5
c.f.u./mL of urine; however, counts as low as
10
2
may represent active infection in pregnancy [4].
The prevalence of asymptomatic bacteriuria is similar to
that in a nonpregnant population, at 510%, but there is
a 34-fold higher progression rate, with <30% develop-
ing symptomatic infection [5]. Acute pyelonephritis com-
plicates 12% of pregnancies. The development of acute
pyelonephritis is associated with maternal and fetal
morbidity and mortality. This typically presents with
fever, costovertebral angle tenderness, cystitis symptoms
and feeling systemically unwell. In severe cases sepsis
and respiratory distress occur. Other reports of obstetric
problems include preterm labour, pre-eclampsia and low
birthweight, so it is advisable that all pregnant women
should be screened frequently in pregnancy for asymp-
tomatic bacteriuria and if positive, treated. Factors that
increase the risk of pathogenicity of bacteriuria in
pregnancy include the decrease in bladder tone and
increased ureteric volume, as well as a facilitatory effect
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2002 BJU International 469
of oestrogen on upper tract infection, especially with the
main pathogenic organism, Escherichia coli. Treatment
should be aggressive, consisting of rehydration, analgesia
and intravenous antibiotics.
Recommended antibiotics for use in pregnancy for
asymptomatic bacteriuria include amoxycillin, an oral
cephalosporin, nitrofurantoin, or nalidixic acid. Sulphon-
amides can also be used, but not in late pregnancy when
they can cross the placenta and increase the risk of
kernicterus by displacing bilirubin bound to albumin.
Tetracyclines cause bone and teeth dysplasia and dis-
coloration, and should be avoided. The antifolate agent
trimethoprim should not be used in early pregnancy as it
may affect neural tube development. Pyelonephritis
should be treated with a second- or third-generation
cephalosporin or a short course of an aminoglycoside.
Prolonged courses of the latter may result in eighth nerve
damage to the fetus.
Postpartum bacteriuria is twice as common in women
who have been catheterized in labour (9.1% vs 4.7%).
This risk increases to 25% where an indwelling catheter
is used, and so ideally all women should be encouraged
to void spontaneously in labour. This bacteriuria also
needs treatment.
Urinary calculi: Despite the increase in urinary stasis,
infection and obstruction in pregnancy, which generally
predisposes to the formation of calculi, the incidence of
renal calculi is <0.3% and similar to that in a
nonpregnant population [6]. Pregnancy also does not
increase the risk of stones in known `stone formers'.
Presentation is usually after 20 weeks' gestation when
ureteric dilatation is most marked. These stones are
mainly composed of calcium, with an increase in struvite
stones also reported. They may present with pain and
tenderness, mimicking acute pyelonephritis, but without
fever. Haematuria and colic may be absent because of
the physiological hydroureter. Ultrasonography should
be used and occasionally a plain abdominal X-ray may be
required; renal function assessment and urine micro-
scopy should also be undertaken. Initial treatment
should be conservative, as 60% of stones will pass
spontaneously. Denitive surgery should be delayed until
at least 4 months postpartum if possible. The safety of
lithotripsy in pregnancy has not been fully validated and
drugs used to prevent stone formation, e.g. thiazides,
xanthine oxidase inhibitors and D-penicillamine, are
best avoided.
Renal failure: Acute renal failure may occur secondary to
complications in pregnancy from pre-eclampsia, uterine
sepsis, pyelonephritis and acute fatty liver of pregnancy.
With improvements in the management of obstetric
haemorrhage and pre-eclampsia, acute renal failure is
seen less often in the West. Effective management of these
clinical situations will often result in a return to normal
renal function.
In women with chronic renal disease, pregnancy may
have an adverse effect on renal function, which is linked
to the degree of functional impairment before pregnancy
and the presence of hypertension. With severe renal
disease patients are often infertile and if pregnancy
occurs, a live birth is uncommon. In those with
moderate or severe renal insufciency (serum
creatinine >133 mmol/L) further loss of function
will occur in half, with 10% of women progressing to
end-stage renal failure [7].
The lower urinary tract
LUTS are very common in pregnancy; there are several
large epidemiological studies which have assessed the
prevalence of dysfunctional urinary symptoms in preg-
nancy, most focusing on the symptom of stress incon-
tinence. Most of these symptoms may be a consequence
of the normal anatomical and physiological changes
that occur in pregnancy, but superimposed on these
changes may be further pathological changes as a con-
sequence of tissue damage either from pregnancy or
labour, resulting in persistent symptoms. The distinction
between normal physiological changes and transient or
permanent pathophysiology is often not clear.
Frequency and nocturia: These are the commonest and
earliest symptoms to develop in pregnancy. Normal non-
pregnant women void four to six times per day and rarely
at night. Francis [8], using a denition of frequency as
at least seven daytime voids and one night-time void,
studied the voiding habits in 400 healthy women during
and after an uncomplicated pregnancy, and compared
them with 50 normal nonpregnant patients of a similar
age. Frequency was reported by 59% in early pregnancy,
61% in mid-pregnancy and 81% in late pregnancy.
Parboosingh and Doig [9], dening nocturia as at least
three night-time voids, questioned 873 healthy antenatal
patients and found that nearly 66% experienced nocturia
by the third trimester. Stanton et al. [10] reported that
frequency was the commonest symptom. The onset of
frequency may be as early as the rst trimester. Cutner
[11] assessed LUTS in 47 women undergoing termi-
nation of pregnancy at 615 weeks gestation, and found
that 40% complained of frequency and 23% of nocturia.
The cause of frequency was unrelated to bladder capacity
or the effect of posture, but ascribable to the polydypsia
and polyuria of pregnancy [8]. Both uid intake
and output increase in the rst trimester, remaining
constant until the third trimester, when a decrease
in sodium output leads to a decrease in urine output.
However, despite this, frequency persists, related to the
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2002 BJU International 89, 469476
pressure on the bladder by the uterus. Cutner [12] found
a correlation between the maximum voided volumes,
rst sensation to void and maximum bladder capacity,
which was in turn related to the presence of low
compliance. There was no correlation between the
maximum voided volumes and diurnal frequency and
nocturia. Parboosingh and Doig [9] measured mean
urine ow and solute excretion in 24-h and overnight
collections, in 100 normal and nonpregnant women.
An increase in sodium excretion was the major reason
for increased night-time voiding, as well as the mobiliza-
tion of dependant oedema at night when in the
recumbent position.
Voiding difculties: Urinary hesitancy may occur in up to
27% of patients in the rst two trimesters [10]. Fischer
and Kittel [13] assessed ow rates in 290 women during
pregnancy and found that there were signicantly higher
peak ow rates in the second and third trimester than in
controls and early pregnancy, but these higher ow rates
were associated with larger voided volumes. Nomograms
have been produced to assess ow rates according to
volumes voided, as low volumes may result in an
articially low peak ow rate [14]. Cutner [12] assessed
ow rates in pregnancy, adjusted for volume voided, and
found no difference in women complaining of hesitancy
or incomplete emptying compared with pregnant women
with normal voiding.
Urinary retention can occur in pregnancy, associated
with the enlargement of a retroverted uterus with
subsequent entrapment of the fundus below the sacral
promontory [15]. Other causes include an enlarging
broid, or a pelvic mass. This retention usually resolves
by 16 weeks' gestation as the uterus grows out of the
pelvis, and can be managed meanwhile with either
bladder drainage or intermittent self-catheterization.
Alternatively, the uterus can be reduced manually,
or a Hodge pessary may be inserted to maintain
uterine position and relieve the obstruction on the
bladder neck.
Postpartum urinary retention is common, with a
reported incidence of 1.717.9% [16]. Risk factors
include a rst labour, instrumental delivery and epidural
analgesia, and a longer duration of labour (o800 min)
[17,18]. Khullar and Cardozo [19] found that the bladder
can take up to 8 h to regain sensation after the last dose
of an epidural, and during this period overdistension of
the bladder may occur, leading to permanent detrusor
dysfunction. Tapp et al. [20] reported that in a group of
six women with acute retention postpartum, two had
permanent voiding difculties, two required intermittent
self-catheterization and two had altered bladder sensa-
tion. Because of this, women with these risk factors
should be watched carefully after delivery to ensure that
voiding is adequate, and if necessary catheterized to avoid
overdistension.
Urgency and urge incontinence also increase in pregnancy;
Cutner et al. [21] found that 62% of women complained
of urgency and 18% complained of urge incontinence in
pregnancy. In another study of 549 nulliparae, 2.2%
reported urgency before pregnancy, with 22.9% and
7.8% reporting urgency in pregnancy and 12 weeks
postpartum, respectively. In this same group of women,
0.5%, 8.0% and 2.2% reported urge incontinence before
pregnancy, in pregnancy and 12 weeks postpartum,
respectively [22].
Cutner et al. [21] reported that 23% of patients had
detrusor instability, lower than the prevalence of women
with irritative urinary symptoms. Chaliha et al. [23], in a
prospective study of 161 nulliparae investigated by
urodynamics in the third trimester, and then 12 weeks
postpartum, found a prevalence of detrusor instability of
8.1% and 6.8%, respectively. In this group of women,
only 4.9% reported urge incontinence postpartum.
This suggests that the aetiology of irritative urinary
symptoms is only partly explained by the development of
detrusor instability and may be also a consequence of low
compliance, as shown by Cutner et al. [21], or urethral
instability.
Stress incontinence is a common symptom associated
with pregnancy and has been reported in up to 85% of
women [8,24,25]. Francis [8] found that in the rst
trimester of pregnancy 16% of women complained of
stress incontinence, with 34% doing so in the second
half of pregnancy. Stanton et al. [10] assessed the prev-
alence of both stress and urge incontinence at 32 weeks'
gestation and found an incidence of 36% and 13%,
respectively. Both studies found that stress incontinence
rarely appears for the rst time after birth without
previous antenatal symptoms, and is commoner in
multiparae than nulliparae.
Viktrup et al. [25] interviewed 305 primiparae and
found that 39% had stress incontinence before, during or
after pregnancy, and 7% developed de novo stress
incontinence after delivery. In those with onset of stress
incontinence in pregnancy only 3% had persisting
symptoms at 1 year after delivery, whereas in those
with onset after delivery, 24% had symptoms at 1 year.
In the 120 patients who had onset of stress incontinence
before, during or after pregnancy, 21 (18%) had new
onset of symptoms postpartum. There was no relation-
ship between the presence of symptoms at 1 year and
obstetric risk factors. In another study by Viktrup and
Lose [26], there was a signicant correlation between
the length of the second stage of labour and the
development of stress incontinence. Wilson et al. [27],
in a postal questionnaire study of 2134 women 3 months
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2002 BJU International 89, 469476
after delivery, found that 34.3% admitted to some degree
of urinary incontinence, with 3.3% having daily or more
frequent leakage. The risk was signicantly less in those
women, especially primiparae, who had a Caesarean
section, whether elective or in labour, suggesting it is
vaginal delivery not pregnancy that predisposes to stress
incontinence. The prevalence of incontinence was similar
in those women having three or more Caesarean sections
(38.9%) to those delivered vaginally (37.7%). Some have
proposed that in this situation incontinence may be
secondary to nerve damage from bladder dissection
during Caesarean section. This is supported by a study of
women who had undergone elective Caesarean section,
of whom 17% reported stress incontinence and 51% had
severe symptoms that occurred for the rst time in
pregnancy or the puerperium [28].
Chaliha et al. [22] interviewed 549 nulliparous women
to assess the prevalence of urinary incontinence before,
during and after delivery. Pregnancy and delivery
resulted in a signicant increase in symptoms of urinary
frequency, incontinence and urgency. Stress inconti-
nence was the most common form of incontinence and
reported by 17 (3.1%), 196 (35.7%) and 68 (12.4%)
women before, during and after pregnancy, respectively
(Table 1). The low prevalence of incontinence before
pregnancy in nulliparous women agrees with previous
data linking parity to incontinence [27,29,30].
Changes in the lower urinary tract and
pelvic oor related to stress incontinence
The exact causes of stress incontinence are unclear and
probably multifactorial, related to nerve damage, and/or
physiological and structural changes of the lower urinary
tract. There also may be a group of women at increased
risk of postpartum incontinence because of abnormalities
of collagen.
Functional changes
Urethral pressure prolometry has been used to evaluate
urethral sphincter function in normal pregnancies and
those complicated by incontinence. Iosif and Ulmsten
[31] compared urethral pressure prole measurements in
pregnant women with stress incontinence with continent
healthy women from an earlier study [3]. The absolute
urethral length increased by a mean of 6.7 mm and the
functional urethral length by 4.8 mm. The maximum
urethral closure pressure increased to 93 cmH
2
O at
38 weeks and then decreased to 69 cmH
2
O (the
value before pregnancy) after delivery. These changes
were not apparent in women complaining of inconti-
nence and are postulated to be a mechanism whereby
continence is maintained despite an increase in intra-
vesical pressure in pregnancy. This agrees with other
studies showing evidence of low urethral pressure in
nonpregnant women with stress incontinence [32,33].
Van Geelen et al. [34] reported similar work in 43
pregnant women; they found an increase in maximum
urethral pressure, urethral length and bladder pressure,
but no signicant differences in maximum urethral
closure pressure or functional urethral length. However
the lack of difference may be because their study group
included continent and stress incontinent women. After
delivery the urethral length and pressure were signi-
cantly lower in those women who had vaginal deliveries
but not in those delivered by Caesarean section. These
changes after vaginal delivery were unrelated to the
duration of the second stage of labour, episiotomy, or
fetal birthweight. This increase in urethral closure
pressure may be a result of an increase in urethral
sphincter volume from increased blood ow, and there is
an increase in the amplitude of vascular pulsations
recorded from the urethral wall, especially in the rst
16 weeks of pregnancy, which may be related to an
increase in blood volume in pregnancy. Pregnant women
with genuine stress incontinence had a lower amplitude
of vascular pulsations in the periurethral plexus than had
continent women, suggesting that this affects urethral
closure pressure [35].
Further work suggesting that childbirth may lead to
permanent damage to the urethral sphincter mechanism
was reported by Tapp et al. [36], who assessed two groups
of women, one with competent urethral sphincter
mechanisms and one with genuine stress incontinence.
The latter group had a negative correlation between
the number of vaginal deliveries and the pressure
transmission ratios in the distal quarter of the urethra;
more vaginal deliveries were associated with poor
function of the distal urethral sphincter mechanism.
As continence is thought to be maintained by the
action of the proximal and not distal sphincter
Table 1 Urinary symptoms in 549 women before, during and after
pregnancy
Symptom Before During After
Urinary frequency 154 (28.0) 445 (81.1) 123 (22.4)*
Nocturia 28 (5.1) 371 (67.6) 24 (4.4)
Urgency 12 (2.2) 126 (22.9) 43 (7.8)*
Stress incontinence 17 (3.1) 196 (35.7) 68 (12.4)*
Urge incontinence 3 (0.5) 44 (8.0) 12 (2.2)*
Incontinence (total) 20 (3.6) 240 (43.7) 80 (14.6)*
Incontinence frequency
< once per week 20 (3.6) 137 (24.9) 53 (9.7)
f daily o once/week 52 (9.5) 14 (2.6)
o Daily leakage 51 (9.3) 13 (2.4)
Protection 56 (10.2) 8 (1.5)
*P<0.05, McNemar's test, compared with values before pregnancy.
472 C. CHALIHA and S. L. STANTON
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2002 BJU International 89, 469476
mechanism, the authors concluded that damage to
the distal sphincter mechanism may result in stress
incontinence in women with impaired proximal sphinc-
ter function.
Cystometry in pregnancy has been used by several
groups; Cutner et al. [21] used cystometry in early preg-
nancy and found a normal rst sensation and bladder
capacity. Kerr-Wilson et al. [37] assessed women uro-
dynamically immediately after delivery and then again
4 weeks afterward, nding a signicant decrease in
maximum cystometric capacity at 4 weeks, and a signif-
icant decrease in primiparae. However, all values were
within normal limits and there was no evidence of
bladder hypotonia. In a large prospective study of 161
nulliparous women in the third trimester and then again
at 12 weeks postpartum, Chaliha et al. [23] found a high
prevalence of genuine stress incontinence and detrusor
instability; 8.7% and 8.1%, respectively, in the ante-
natal period and 5.0% and 6.8%, respectively, after
delivery. The mean values for urodynamic variables
in the third trimester and after delivery were lower
than values dened in a nonpregnant population and
unrelated to obstetric or neonatal variables (Table 2).
After delivery there was an increase in rst sensation and
strong sensation to void, and maximum bladder capacity.
However, despite the high prevalence of symptoms, there
was a poor correlation between symptoms and urody-
namic ndings, which agrees with data in nonpregnant
women [38]. Therefore, these observed changes in
bladder function were consistent with a pressure effect
of a gravid uterus and unrelated to the mode of delivery
and neonatal factors.
Nerve damage
Patients with genuine stress incontinence have been
shown to have abnormal conduction in the perineal
branch of the pudendal nerve which innervates
the periurethral striated muscle and pubococcygeus
muscle [3941]. Several reports also show injury to
the nerve supply after childbirth, but these studies
often do not relate objective damage to symptoms.
Snooks et al. [42] found prolongation of pudendal
nerve terminal motor latencies 4872 h after delivery
in 42% of those delivered vaginally, but not those
delivered by Caesarean section. The degree of pudendal
nerve damage was greater in multiparous women and
correlated with the use of forceps and a longer second
stage of labour. In 60% of women with evidence of nerve
damage, the pudendal nerve latency had returned to
normal at 2 months after delivery. The authors suggested
that vaginal delivery results in pudendal nerve damage
probably from a combination of direct and traction injury
during delivery, and that this may lead to the develop-
ment of stress incontinence. However, that study was not
prospective and included multiparous women who may
have sustained previous nerve damage. Furthermore, the
study assessed innervation of the striated anal sphincter,
which may not reect striated urethral sphincter
innervation, and there was a poor correlation between
abnormal latencies and symptoms. Allen et al. [43], using
concentric needle EMG and pudendal nerve conduction
tests, found evidence of denervation injury in 80% of
women after delivery. Those women with a long (active)
second stage of labour (>56.7 min) and a large baby
(>3.41 kg) showed greater nerve damage.
EMG of the right and left pubococcygeus muscle has
shown that childbirth induces both qualitative and
quantitative changes, such that sphincter weakness
was caused by not only loss of motor units but also
asynchronous activity in those that remained [44].
Structural changes
Trauma from vaginal delivery may result in muscular
and connective tissue damage. Gainey [45] examined
1000 women after delivery, nding evidence of urethral
detachment in 18% and damage to the pelvic oor
Table 2 Urodynamic variables before and after delivery in 161 women who returned for postnatal investigations, and according to the mode
of delivery
Urodynamic
variable, mean (SD) Before After
After/before
(95% CI)* P*
Vaginal
(n=89)
Instrumental
(n=41)
Caesarean
(n=31) P
Sit FDV 111 (70.1) 148 (83.0) 1.34 (1.171.54) <0.001 150 (83) 138 (87) 153 (80) 0.5
Sit SDV 188 (91.3) 217 (94.3) 1.17 (1.071.28) <0.001 225 (96) 203 (96) 214 (87) 0.3
Sit MXCC 301 (146.1) 299 (114.4) 1.03 (0.961.12) 0.4 300 (114) 309 (126) 281 (101) 0.8
Stand FDV 96 (69.3) 139 (90.2) 1.48 (1.301.69) <0.001 96 (68) 162 (115) 140 (75) 0.2
Stand SDV 167 (102.0) 209 (105.0) 1.29 (1.181.42) <0.001 200 (93) 231 (131) 205 (98) 0.7
Stand MXCC 239 (136.4) 271 (123.6) 1.17 (1.081.27) 0.001 264 (14) 290 (146) 265 (119) 0.9
MVP [n] 38 (22.0) [125] 32 (17.2) [118] 0.85 (0.711.01) 0.07 33 (19) [70] 30 (13) [27] 33 (17) [28] 0.7
Peak ow rate [n] 28 (16.3) [153] 23 (14.4) [157] 0.83 (0.750.92) <0.001 24 (18) [85] 22 (8) [38] 23 (9) [30] 0.8
FDV, rst desire to void (mL); SDV, strong desire to void (mL); MXCC, maximum cystometric capacity (mL); MVP, maximum voiding pressure
(cmH
2
O); Peak ow rate (mL/s); *Paired t method on log-transformed data; F-test on log-transformed data, adjusted for antenatal values.
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2002 BJU International 89, 469476
muscles in 31%. More recently, Peschers et al. [46]
evaluated bladder neck position and mobility using peri-
neal ultrasonography at 8 weeks after delivery. Bladder
neck position was signicantly lower and bladder
neck mobility greater after vaginal delivery than in
women who had an elective Caesarean section and
in nulligravid controls. This agrees with Meyer et al.
[47] who reported a signicant increase in bladder
neck mobility after vaginal delivery in primiparae,
but the bladder neck position was only lowered
after forceps delivery. Thus vaginal delivery seems to
alter urethral support, which may result in stress
incontinence.
It has been suggested that there may be a group of
women at an inherent increased risk of developing
incontinence because they have abnormalities in col-
lagen [48], as it is the collagenous component of the
connective tissue that contributes to structural support of
the bladder neck. In pregnancy the tensile properties of
the connective tissue are reduced with a decrease in total
collagen content and increase in glycosaminoglycans
[49]. Changes in collagen may result in greater mobility
of the bladder neck, resulting in stress incontinence. This
was suggested by King and Freeman [50] who used
perineal ultrasonography in 128 primigravidae ante-
natally and then again 1014 weeks after delivery. They
found an increase in bladder neck mobility antenatally in
those women who subsequently developed postpartum
stress incontinence. If collagen abnormalities increase
the risk of incontinence, and if these can be detected
antenatally to dene women at risk of pelvic oor dys-
function, this will allow them to be counselled and
preventative measures instituted if appropriate, e.g.
offering elective Caesarean section. Chaliha et al. [22]
evaluated the role of antenatal history and physical
markers suggestive of collagen weakness, e.g. striae,
hernia, varicose veins and joint mobility, in predicting
postpartum incontinence. In the third trimester,
549 nulliparae were interviewed using a standardized
urinary and bowel symptom questionnaire, and exam-
ined physically to assess these markers of collagen
weakness. Postnatal anal and urinary incontinence
was not related to race, antenatal body-mass index, the
presence of striae, hernia, varicose veins, piles or a family
history of incontinence, prolapse or collagen weakness.
Higher joint mobility scores were associated with
incontinence of atus but not fecal urgency or urinary
symptoms. Therefore, although collagen weakness has
been implicated in the pathogenesis of incontinence,
physical markers of collagen weakness as used in that
study could not predict postpartum incontinence.
Perhaps these markers were not representative of
collagen weakness, or a larger study with a longer
follow-up is required.
Urinary tract trauma during delivery
During labour and delivery the bladder is particularly
vulnerable to trauma. Cystoscopy after delivery shows
changes such as mucosal congestion, submucosal
haemorrhage and capillary oozing, particularly around
the trigone [51]. Even Caesarean delivery does not
eliminate the risk of bladder trauma, as the position of the
bladder as an abdominal organ exposes it to risk at
the time of surgery. The incidence of bladder trauma
at Caesarean section is <1% [52] but increases in
situations where a Pfannenstiel incision, lower seg-
ment incision, previous Caesarean section, prolonged
second stage of labour and Caesarean hysterectomy
have occurred. The dome of the bladder is the site
most frequently injured and should be repaired in
two layers, whereas injuries extending into the trigone
or ureteric orices may require ureteric implantation or
stenting. The incidence of ureteric injuries is <0.1%
[53]. The diagnosis of bladder injury is usually imme-
diate, whereas that of ureteric injury is often delayed,
and should be suspected if the patient presents with
ank tenderness and unilateral hydronephrosis [54].
Urinary tract injury has also been reported after
instrumental deliveries, particularly mid-pelvic forceps,
but even after ventouse delivery [55].
Vesicovaginal stulae as a result of delivery are
reported in 0.7% of patients undergoing Caesarean
section [56]. Currently this complication is rarely seen
in the West, but is common in developing countries in
obstructed labour where there is necrosis of the anterior
vaginal wall and the bladder. These stulae typically
present with continuous incontinence 714 days after
delivery and if suspected should be investigated with
cystoscopy and IVU.
Conclusions
Pregnancy and delivery is a time of major anatomical
and physiological changes to the urinary tract
which may result in an alteration in urinary tract
function, most commonly manifested by the develop-
ment of urinary symptoms. It is well documented
that vaginal delivery results in anatomical, neural
and structural damage to the pelvic oor, and these
changes may result in permanent urinary tract dysfunc-
tion. However, Caesarean section may not totally
prevent postpartum urinary incontinence and overall
may subject a woman to greater morbidity and
mortality. Further work is required to determine the
pathophysiology of childbirth-related injuries to the
urinary tract, and how labour can be managed to
minimize them.
474 C. CHALIHA and S. L. STANTON
#
2002 BJU International 89, 469476
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Authors
C. Chaliha, MA, MD, MRCOG, Registrar in Obstetrics &
Gynaecology.
S.L. Stanton, FRCS, FRCOG, Professor of Pelvic Surgery &
Urogynaecology.
Correspondence: C. Chaliha, East Surrey Hospital, Redhill,
Surrey, UK.
e-mail: charlotte.chaliha@virgin.net
476 C. CHALIHA and S. L. STANTON
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2002 BJU International 89, 469476