Best Practice & Research Clinical Obstetrics and Gynaecology

Vol. 19, No. 6, pp. 807–828, 2005

doi:10.1016/j.bpobgyn.2005.08.001
available online at http://www.sciencedirect.com

Female voiding dysfunction

Lawrence O. Olujide* MBBS, MA, MRCOG

Specialist Registrar in Obstetrics and Gynaecology

Suzanne M. O’Sullivan MBBS, MRCOG

Consultant Obstetrician and Gynaecologist
Department of Obstetrics and Gynaecology, Royal Bournemouth Hospital, Castle Lane East,
Bournemouth, Dorset BH7 7DW, UK

Female voiding dysfunction is poorly understood; it lacks standard definitions, and there is no
consensus on diagnostic criteria. In the majority of women who are neurologically intact the
cause is idiopathic. It affects the sufferers’ quality of life, but unfortunately there is a paucity of
published literature on its management. This review examines the current knowledge on the
management of this common problem. Diagnosis is aimed at identifying the underlying
aetiological factors, which are discussed, as well as the importance of a detailed history and
focused physical examination. Investigations essential to management are outlined. Develop-
ments in the medical treatment of voiding dysfunction have been disappointing. The role of
surgery is even more limited except for those with postoperative voiding problems after new-
generation sling procedures. Intermittent self-catheterisation, supervised and supported by a
dedicated nursing specialist, remains the mainstay of management. A multidisciplinary approach is
essential to success. Emerging treatment modalities such as sacral and peripheral neuromodu-
lation and the use of a1-blockers are discussed. Botulinum toxin A injections have been useful in
some cases. There are relatively few publications on the effectiveness of these interventions in
clinical practice. These issues need to be addressed by quality research. Female voiding
dysfunction presents a challenge to urogynaecologists and urologists alike.

Key words: voiding dysfunction; female; Fowlers syndrome; sacral neuromodulation.

Female voiding dysfunction is complex in nature, poorly understood, and difficult to

treat. Voiding disorders in men are relatively common and are usually due to bladder
outlet obstruction secondary to prostatic hyperplasia or hypertrophy; extensive data
on the aetiology and management of this condition exist. In women there is a lack of
standard definition, and data on the prevalence of voiding dysfunction are conflicting.

* Corresponding author. Tel.: C44 1202 2303626x4336.

E-mail address: lawrence@olujide.freeserve.co.uk (L.O. Olujide).

1521-6934/$ - see front matter Q 2005 Elsevier Ltd. All rights reserved.
808 L. O. Olujide and S. M. O’Sullivan

Consensus on the diagnostic criteria for female voiding dysfunction is also poor. The
International Continence Society (ICS) states that ‘normal voiding is achieved by a
voluntarily initiated continuous detrusor contraction that leads to complete bladder
emptying within a normal time span, and in the absence of obstruction’.1 It should
follow that female voiding dysfunction falls outside this definition. Stanton et al defined
voiding dysfunction in women as ‘a condition in which the bladder fails to empty
completely and easily after micturition’, with uroflow studies showing repeated peak
flow rates of !15 mL/seconds and/or 200 mL or more of residual urine.2
The incidence of female voiding dysfunction varies from 6.8 to 61.7% in selected
populations based on symptoms alone, and appears to increase with age.2–4 Lepor et al
studied the prevalence of female voiding dysfunction in the community and showed that
40% of women aged 80 have symptoms of poor stream compared to 10% of 19–29-
year-olds. Interestingly, however, other symptoms such as hesitancy, intermittency,
incomplete emptying and abdominal straining were commoner in younger age groups.5
Asymptomatic patients can have objective urodynamic evidence of suboptimal voiding,
while some patients with a clear history may have no measurable explanation of their
symptoms. Urodynamic evidence of voiding difficulty was confirmed in only 21.2% of
symptomatic patients in a study by Groutz et al in 1999.3 Often there is no correlation
between the subjective and objective evidence of voiding difficulty. Dietz et al, in a study
of the relationship between symptoms and uroflowmetry, demonstrated that only
hesistancy, poor stream and interrupted voiding have a strong association with
objective voiding dysfunction.6
Voiding disorders in women are common and may go unrecognised until the patient
presents with troublesome symptoms such as recurrent urinary tract infections or
overflow incontinence. Little is published on the impact of voiding dysfunction on the
quality of life of sufferers, but one can assume that voiding dysfunction may have a
negative impact on one’s normal activities and state of mind. Das et al showed that
voiding dysfunction can have a serious impact on the physical, social and psychological
aspects of life of the sufferers.7 Possible sequelae of abnormal voiding are far-reaching
and include pelvic discomfort, urinary retention with or without incontinence,
recurrent urinary tract infection and the consequent risk of upper urinary tract
damage, altered sexual function, and the potential need for self-catheterisation. This
chapter will focus on the diagnosis and the management options for women with
voiding dysfunction.

CLASSIFICATION

There is no agreed classification for female voiding dysfunction. Stanton advised that
any classification should consider not only the anatomical, functional and neurological
aspects of micturition but also relaxation of pelvic floor muscles.2 There is no such
classification specific to voiding female dysfunction. The ICS1 has taken a functional
approach to describing the abnormalities of voiding, focusing mainly on bladder and
urethral activity during micturition. Voiding dysfunction, according to the ICS, can be
due to the bladder (detrusor underactivity, acontractile bladder) or can be urethral
(bladder outlet obstruction, intermittent involuntary contractions of peri-
urethral striated muscle during voiding, detrusor sphincter dyssynergia, non-relaxing
urethral sphincter obstruction). Detrusor sphincter dyssynergia and non-relaxing
 Female voiding dysfunction 809

Table 1. Classification of voiding difficulties and retention.

Condition Symptoms Urodynamic data

Asymptomatic Frequency UTI Reduced flow, Elevated, normal or
voiding difficulty reduced voiding pressure with or
without residual urine
Symptomatic Reduced stream, Incomplete emptying, Peak flow !15 mL/seconds, Elevated
voiding difficulty straining, frequency, UTI voiding pressure with or
without residual urine
Acute retention Painful or painless Residual urine
Chronic Reduced sensation, poor stream, Flow !15 mL/seconds Low or elevated
retention incomplete emptying, straining, voiding pressure, residual urine with or
frequency, nocturia, incontinence, UTI without upper tract dilatation
Acute or Painful or painless, frequency, Residual urine with or without low
chronic incontinence voiding pressure
retention

UTI, urinary tract infection.

urethral sphincter obstruction are seen in patients with neurological lesions. Monga8
proposed a working classification for female voiding dysfunction as shown in Table 1.

PATHOPHYSIOLOGY

Normal micturition consists of alternating storage and expulsion phases, and these
depend on the ability of the bladder to serve as a reservoir during filling and as a pump
during voiding. In contrast, the urethra acts as a watertight sphincter during filling and as
a conduit during voiding. The storage phase depends on anatomical integrity of the
bladder, bladder neck and urethra, stability of detrusor muscle, normal urethral
sensation, normal bladder compliance at maximum capacity, and a functional urethral
closure pressure mechanism. The voiding phase requires a sustained, adequate bladder
contraction coordinated with relaxation of the urethral and pelvic floor muscles. The
bladder contraction is mediated by the parasympathetic nerve supply, while urethral
relaxation is mediated by cholinergic inhibition of the a-adrenergic sympathetic input
on urethral smooth muscle and suppression of activities of the striated urethral
sphincter.9–11
Normal micturition requires the complex interaction between somatic and
autonomic nervous systems and neural integration at the peripheral, spinal and central
levels.11 The mechanism of voiding is poorly understood, but it involves activation of
the sacral micturition reflex and coordination of impulses between the cerebral cortex,
pontine micturition and sacral micturition centres. As the bladder distends, there is
low-level firing of afferent neurons from the bladder, and a reflex inhibitory response to
the bladder via the hypogastric nerve, with a stimulatory response to the external
urethral sphincter from the pudendal nerve. With further distension of the bladder,
there is activation of myelinated a–d afferent nerves. Nerve impulses from the bladder
mechanoreceptors, bladder muscle and periurethral striated muscle travel to the
pontine micturition centre (lateral region) via the lateral spinothalamic tract and
posterior column. The medial region of the pontine micturition centre also receives
810 L. O. Olujide and S. M. O’Sullivan

impulses from the pelvic floor, including the anal sphincter. These impulses activate the
spinobulbospinal reflex, which is relayed through the pontine micturition centre.
Barrington’s pontine micturition centre also receives inhibitory impulses from the
cerebral cortex, basal ganglia and cerebellum, and facilitatory impulses from the
anterior pons and posterior hypothalamus.12,13 Nerve impulses are sent from the pons
to the sacral micturition centre, which in turn sends efferent impulses to the bladder via
the pelvic, hypogastric and pudendal nerves. The pelvic nerves carry the
parasympathetic efferent input to the bladder and the hypogastric nerves carry the
sympathetic efferent input to the bladder and the urethra. The somatic nerve supply to
the external urethral sphincter is carried via the pudendal nerves (see Figure 1).
Provided that it is socially acceptable to void, facilitatory impulses from the higher
centre start a cascade of neural transmission resulting in relaxation of the pelvic floor
muscles and the striated urethral sphincter, with contraction of the detrusor, resulting
in opening of the bladder neck and urethra, allowing the flow of urine. The reversal of
these processes terminates voiding. Disturbance to any of these processes—whether
anatomical, neurological, or psychological—at any level of the centre for control can
result in voiding dysfunction.

PAG
Pontine
Storage
Center Pontine +
Micturition
Center

Hypogastric
Nerve
+ contracts Hypogastric
detrusor outlet Nerve
– inhibits detrusor

+
Bladder Pelvic Nerve +

+
Internal Bladder Pelvic Nerve –
sphincter +
Pudendal Nerve + contracts detrusor
External Internal
– inhibits bladder outlet
sphincter sphincter

External Pudendal Nerve

sphincter

Figure 1. Nerve supply to the bladder and urethra. PAG, periaqueductal gray. Reproduced from Sullivan and
Yalla (2002, Urologic Clinics of North America 29:499–514) with permission.
 Female voiding dysfunction 811

Normal voiding therefore involves the complex interaction of voluntary and

involuntary factors which requires an intact spinobulbospinal and sacral micturition
reflex with intact detrusor and urethral sphincter mechanisms. Inability of the bladder
to maintain an effective contraction, failure of urethral relaxation or obstruction of the
urethra can result in voiding dysfunction. Voiding dysfunction may also be secondary to
failure of synchronisation of the bladder and urethral actions.

AETIOLOGICAL FACTORS

Voiding disorders in women may be due to simple urethral kinking caused by prolapse,
or poor detrusor contractility which is more common with advancing age. Surgery for
prolapse or incontinence is also associated with voiding disorders, and neurological
disorders can cause problems as described above. Habit and psychological factors may
also be involved. Identifying aetiological factors is crucial to managing women with
voiding dysfunction and will impact on management decisions and prognosis.

Idiopathic factors

In some patients there is no identifiable aetiological factor for voiding dysfunction, and
this may be a consequence of ageing. Overall, idiopathic factors are the most common
cause of voiding dysfunction in women.

Urethral causes

Urethral causes of voiding difficulties are related to either bladder outlet obstruction or
instability of the urethral sphincter mechanism. Bladder outlet obstruction is less
common in women than in men and may be due to intrinsic or extrinsic blockage of the
urethral lumen. In women with a neurogenic bladder it tends to be caused by detrusor
sphincter dyssynergia. Intrinsic urethral strictures can arise secondarily to scar tissue
formation from inflammation, infection surgical procedures such as urethral dilatation,
urethrotomy or urethral injury during pelvic surgery. Urethral diverticulae can be
difficult to diagnose and should not be forgotten as a cause of urethral compression.
Severe atrophy of the urogenital tissue in the elderly woman may also cause urethral
narrowing, and urethral caruncles may also cause voiding problems.
Genital prolapse, by kinking the urethra, causes bladder outlet obstruction in 2% of
women with grades 1 and 2 prolapse and up to 33% of women with grades 3 and 4
prolapse.14 Uterine fibroids, ovarian cysts, haematocolpos, retroverted gravid uterus
or even faecal impaction can cause bladder outlet obstruction resulting in urinary
retention and/or voiding dysfunction. Gaynor-Krupnick and Kreder reported a case of
leiomyoma of the bladder neck causing outlet obstruction.15
Fowler et al16 described a primary disorder of the external urethral sphincter with
hypertrophy of the muscle fibres which fail to relax during micturition, resulting in
voiding difficulties. Electromyography of the muscle shows characteristic complex
repetitive discharges along with decelerating bursts described as ‘whale noises’. This
disorder - referred to as Fowler’s syndrome—is difficult to treat and is sometimes
associated with polycystic ovaries. Groutz et al in 2001 found that 2% of patients
referred with voiding dysfunction had voluntary contraction of the external urethral
812 L. O. Olujide and S. M. O’Sullivan

sphincter during micturition.17 This functional non-neurogenic bladder outlet disorder

is also referred to as Hinman syndrome.

Bladder causes

Female voiding occurs at a higher flow rate and at a lower voiding pressure than in the
male. It is not unusual to see rapid and efficient voiding during urodynamics or
videocystometry as a result of pelvic floor relaxation with or without abdominal
straining, without a rise in detrusor pressure. Urethral resistance is much lower in the
female, particularly following childbirth, and while we can see efficient contractions
during videocystometry, voiding pressures may be low as that may be all that is required
to void efficiently in a lower outlet-pressure system.
Over-distension of the bladder is more common in women than in men and can
result in voiding dysfunction. It is often due to urinary retention following regional
analgesia, pelvic or abdominal surgery, or childbirth. A single episode of urinary
retention of several hours can lead to a hypo- or acontractile bladder. Acute urinary
retention that is left untreated can cause overstretching of the basal urothelium leading
to ischaemic damage of the bladder muscle, resulting in a proliferative vascular response
and irreversible damage due to laying down of new collagen.18
Detrusor myopathy has been described in patients with chronic abacterial cystitis.19
Histological features of detrusor myopathy include muscle-cell degeneration, fatty
replacement, hydropic cytoplasm, karyopyknosis and karyorrhexis. Electron
microscopy showed a reduced myofibrillar mass and cytoplasmic density. More
recently, Martin et al20 described the presence of lipid inclusion bodies within the
detrusor tissue of patients with a primary myopathy causing urinary retention.

Iatrogenic causes

Any anti-incontinence procedure—such as colposuspension, needle suspension

procedures, tension-free transvaginal tapes (TVTs) or transobturator tapes (TOP),
bladder neck injections or anterior repairs—can result in kinking, compression and
eventual fibrosis of the periurethral tissues.21–25 Various studies have shown voiding
disorders ranging from 1.9 to 24% after bladder neck surgery.25–28,33,38 Ward et al24,
in a randomised controlled trial of Burch colposuspension versus TVT, showed no
significant difference in the rate of voiding disorders (7 and 9%, respectively) after each
procedure. Phillips et al30 reported a case of late allergic reaction to collagen used for
bladder neck injection resulting in voiding difficulties.
The risk of postoperative voiding dysfunction is increased in patients with low
detrusor voiding pressure, peak flow rates of less than 15 mL/seconds, residual urine,
enterocoele or vault prolapse.27,31,32 Table 2 summarises the risk factors identified for
voiding dysfunction after anti-incontinence surgery as highlighted by Wang et al.27
Pelvic surgery—particularly radical hysterectomy—may result in voiding dysfunction
secondary to denervation of the bladder and/or urethra. Severe and untreated
postoperative pain can result in urinary retention and secondary voiding difficulty due
to over-distension. Genital trauma sustained during childbirth, especially following
instrumental delivery and episiotomy, can cause enough pain and periurethral oedema
to result in acute urinary retention. Early detection and appropriate catheter
management can prevent the long-term sequelae of chronic urinary retention.
 Female voiding dysfunction 813

Table 2. Risk factors for postoperative voiding dysfunction.

Age over 65 years

Additional surgical procedures
Type of surgical procedure
Postoperative cystitis
Preoperative acontractile adder
Excessive elevation of the adder neck
Menopausal status
Abnormal preoperative voiding studies
Preoperative enterocoele or vault prolapse

Neurogenic causes

Occasionally, neurological disorders such as multiple sclerosis or spinal cord

compression may present with symptoms of altered voiding. We often see the long-
term sequelae of chronic voiding disorders in patients with neurological lesions. Dwyer
and Desmedt29 identified neurological problems as a cause of voiding dysfunction in 6%
of referred women; 23% of their patients with urinary retention had an identifiable
neurological disorder. Neurological lesions affecting voiding can be unilateral or
bilateral and may be congenital, neoplastic, degenerative, inflammatory, traumatic or
vascular. Acute urinary retention can be due to cerebrovascular accidents or multiple
sclerosis.34 Voiding dysfunction may also be due to Parkinson’s disease or systemic
sclerosis.35
The site and severity of the neurological lesion tends to inform the presenting
features, although symptoms are not always in proportion to the neurological problem.
Interruption of the inhibitory influence of the suprapontine centre can lead to detrusor
hyperreflexia and loss of voluntary control, while interruption of the neural pathways
connecting the pontine micturition centre to the sacral micturition centre results in
loss of coordination of the detrusor and urethral voiding pattern (detrusor sphincter
dyssynergia) in addition to hyperreflexia. The urethra contracts at the same time as the
detrusor, preventing the passage of urine and increasing the intravesical pressure. In
time the repeatedly high bladder pressures may lead to bladder diverticulae and
ureteric reflux with or without nephropathy.
Varying degrees of upper or lower motor neuron bladder symptoms—ranging from
hyperreflexia to areflexia—may be seen in neurological lesions involving the sacral
cord. In this type of lesion the external urethral sphincter may be non-functional or
overactive. Patients with infrasacral cord lesions generally do not have atonic bladders.
Denervation at this level—e.g. following radical pelvic surgery—usually results in
hyperreflexia with poor bladder compliance. Voiding is adversely affected not because
of detrusor sphincter dyssynergia but because of discordant contractility due to
denerration. The reason for this is that the postganglionic neurons are in the bladder
wall, and it is the preganglionic neurons that are damaged, giving an upper
motor neuron type of picture.82 A similar type of lesion may be seen in patients with
myelodysplasia, diabetic neuropathy, lumbar disc prolapse, spina bifida and low spinal
cord tumours.36
Temporary symptoms of voiding difficulties may occur after childbirth due to
stretching or bruising of the pudendal nerve.36 This injury is usually neuropraxic in type
and recovers with time.
814 L. O. Olujide and S. M. O’Sullivan

Pharmacological causes

Drugs such as anticholinergics and ganglion blocking agents that interfere with the
release and action of acetylcholine at bladder neuromuscular junctions may cause
voiding dysfunction. Interestingly, Robinson et al37 presented a case series of 18 women
with proven voiding difficulties who underwent treatment with antimuscarinic
medication. Objective and subjective testing did not show any deterioration in voiding
function during or after treatment. Adrenergic agonists such as duloxetine,
pseudoephedrine, and ephedrine increase urethral resistance and may cause voiding
problems. Anti-psychotics, anti-parkinsonian medications, some antidepressants,
opiates, and some decongestants and antihistamines can also adversely affect
micturition.

Inflammatory causes

Retention may occur due to infective, allergic or chemical reactions of the urogenital
tissues, due to either painful stimuli or contact with urine which can cause increased
pain. Herpetic lesions cause retention by this mechanism, but inflammation of the nerve
roots due to the herpes simplex virus can also lead to voiding problems.39 Shah et al40
described a group of women with bladder hypersensitivity. In this group catheterisation
tended to elicit significant pain, and urodynamic studies showed detrusor overactivity
with objective evidence of voiding dysfunction. The authors suggested that these
findings might be secondary to an inflammatory reaction of unknown origin.

Endocrine causes

Diabetes mellitus is known to cause peripheral neuropathy and this can adversely affect
bladder contractility, resulting in urinary retention or incomplete bladder emptying.
Hypothyroidism may also affect the bladder in the same way, resulting in incomplete
emptying and chronic retention.41

Psychological causes

Psychological problems and stress caused by depression, rape, marital disharmony or

even schizophrenia can result in voiding dysfunction.42 This diagnosis should only be
made after a careful history and examination have ruled out other organic and
neurological causes of voiding dysfunction. The patient may be responsive to
psychotherapy or psychopharmacological drugs.
‘Bad’ voiding habits secondary to poor bladder training in childhood can result in
voiding dysfunction. Bellina et al43 suggested that voiding dysfunction secondary to the
voluntary withholding of urination in individuals who worked long hours could be
compounded by stress.44

CLINICAL EVALUATION

The goal of clinical evaluation is to identify the underlying aetiological factor or

factors in order to initiate treatment that will remove these factors, relieve
symptoms and prevent complications. A targeted history and physical examination
 Female voiding dysfunction 815

should help in identifying the underlying cause of the voiding dysfunction. As well
as obtaining relevant information with regard to bladder function, a full
gynaecological, medical and neurological history should be taken. Previous surgery
and past attempts at treating this condition should be recorded. Symptoms
suggestive of psychiatric illness should prompt a request for a formal evaluation by
an appropriate specialist. The impact of symptoms on quality of life should also be
considered.

Clinical presentation

The presentation of patients with voiding dysfunction varies from the incidental finding
of objective evidence of a voiding problem in asymptomatic patients to those who
present with florid symptoms.
Asymptomatic patients may be found to have high residual urine on ultrasound
scanning done for other indications, abnormal uroflowmetry or voiding cystometry.
The diagnosis of voiding dysfunction in these patients is based on maximum flow rate !
15 mL/seconds or residual urine O150 mL.
Those with overt symptoms may present with a variety of complaints, including
hesitancy, straining to void, poor stream, prolonged and interrupted flow, double
micturition and a feeling of incomplete emptying. Infrequent voiding, manipulation of
voiding position, staying longer in the toilet to ensure complete voiding, terminal
dribbling or even overflow incontinence are also common in women with voiding
dysfunction. The prevalence of these symptoms increases with age.
Acute retention is defined as the sudden onset of painful or painless inability to
void over 12 hours, requiring catheterisation with removal of a volume equal to or
greater than normal bladder capacity.1 Failure of bladder emptying where more than
50% of the bladder capacity is removed during catheterisation is referred to as
chronic retention. Chronic retention is usually painless and tends to develop over a
period of time. The high residual urine associated with chronic retention is often
complicated by recurrent urinary tract infections, which can cause frequency of
micturition, dysuria and lower abdominal pain. Definitions of the symptoms of voiding
dysfunction are given in the publication of the Standardisation Subcommittee of the
ICS.1
General examination should include observation and assessment of the patient’s gait,
mobility and demeanour. Obvious problems with mobility or dexterity may affect
management decisions such as suitability for self-catheterisation. On abdominal
examination, suprapubic fullness, renal angle tenderness, and any palpable masses
should be looked for. Pelvic examination, carried out when the bladder is empty, may
reveal atrophy of the lower genital tract, vulvovaginal inflammation, genital prolapse,
and any pelvic masses or tenderness. A cough test after reduction of any significant
genital prolapse with, for example, a ring pessary may demonstrate occult stress
incontinence. The anterior vaginal wall should be palpated for urethral tenderness,
masses or scarring from previous surgery or trauma. A palpable bladder tends to
contain more than 200 mL residual urine.
Directed sacral nerve evaluation to assess S2–S4 should be performed. This
involves examination of the spine, lower limbs and anal canal to look for normal
muscle tone and normal saddle and lower limb sensation. Peripheral reflexes should
be checked.
816 L. O. Olujide and S. M. O’Sullivan

INVESTIGATIONS

A midstream urine (MSU) will identify or rule out urinary tract infection, which is a
common problem for women with urinary retention. In 2001 Carlson et al, in a study of
26 patients with non-neurogenic voiding dysfunction, showed that 42% of these
patients have a history of urinary tract infection.45 The author emphasised the
importance of diagnosis and treatment of urinary tract infection before proceeding to
further investigation or intervention. If there is a history of recurrent urinary tract
infection it is worth ruling out diabetes mellitus using serum glucose estimation.

Frequency/volume chart

A frequency/volume chart will record a patient’s daily fluid intake and urine output. It
provides objective data on fluid intake, frequency of micturition, urinary incontinence
episodes and volumes voided. This can provide information regarding symptom-limiting
behaviour (e.g. fluid restriction) and assess the impact of symptoms on quality of life.
The normal functional bladder capacity for an adult female is between 350 and 700 mL.
This may be abnormal in women with chronic retention; however, if the voiding
disorder has not led to acute retention the diary may demonstrate normal functional
bladder capacity despite the presence of symptoms of voiding difficulty

Uroflowmetry

This simple, non-invasive test is used to measure the volume of urine voided, assess
maximal and average flow rates, and record the voiding pattern. A normal flow pattern
is classically bell-shaped and is demonstrated in Figure 2. A normal-shaped flow,

UROFLOWMETRY
5 nl/s/Div
Qura

VB MT VE
10 s/Div

Figure 2. Dump-bell-shaped normal flow rate. Maximum flow rate: 28.4 mL/seconds; volume voided:
378 mL. No residual urine.
 Female voiding dysfunction 817

UROFLOWMETRY

5 nl/s/Div
Qura

VB MT VE
38 s/Div

Figure 3. Example of interrupted flow, although patient had a maximum flow rate of 15.9 mL/seconds and no
residual after voiding 591 mL. Patient had vaginal prolapse.

however, does not exclude voiding dysfunction.46–48 The maximal flow rate should be
O15 mL/seconds provided that O150 mL urine is voided, and the residual volume
should not be more than 150 mL. Flow-rate patterns are influenced by vaginal prolapse,
emotional stress, age, and personal habits; therefore at least two flow-rate
measurements should be recorded before confirming a diagnosis. Examples of flow-
rate patterns are shown in Figures 3 and 4. There are many established normograms for
interpreting flow-rate patterns in men, but only the Liverpool normogram has been
advocated in women.49,81 The Liverpool normograms (Figure 5) classify normal and
abnormal flow values and cover a wide range of voided volumes, offering reference
ranges for maximum and average urinary flow rates. A study by Constantini et al of 348
women with voiding disturbances concluded that uroflowmetry has a good specificity
and a high negative predictive value.50 Unfortunately, flow-rate measurement alone
cannot discriminate between poor detrusor function and outlet obstruction. In these
cases further pressure-flow studies may be required.

Subtracted voiding cystometry

Filling cystometry gives information on bladder sensitivity, compliance and detrusor

contractility. It may indicate an upper or lower motor neuron lesion. The voided
volume, post-void residual, pattern of flow, maximum flow rate and maximum detrusor
pressure during micturition are recorded during the voiding phase of the study. The
maximum detrusor pressure should be S15 cmH2O, although this varies with
advancing age, and some older women can void with little or no detrusor activity. One
should, however always consider underlying neurological disease.
Bladder outlet obstruction is uncommon in women. High-pressure detrusor
contractions with low maximum flow rates on pressure-flow studies are diagnostic of
818 L. O. Olujide and S. M. O’Sullivan

UROFLOWMETRY

5 nl/s/Div
Qura

VB MT VE
38 s/Div

Figure 4. Prolonged voiding. The patient voided 443 mL over 109 seconds with a maximum flow rate of
10.6 mL/seconds.

bladder outlet obstruction in men, but this is rarely seen in women. High detrusor
pressure during voiding is seen, however, in female patients with Fowler’s syndrome,
detrusor sphincter dyssynergia, and sometimes genital prolapse. Videocystometry can
image the voiding mechanism and show specific urethral obstruction and bladder wall

70 95th

90th
60
MAXIMUM URINE FLOW RATE (ml/s)

75th
50

50th
40

25th
30
10th
5th
20

10

0
0 100 200 300 400 500 600
VOIDED VOLUME (ml)

Figure 5. Liverpool normogram for maximum urine flow rate in women. From Haylen et al (1989, British
Journal of Urology 64:30–38) with permission.
 Female voiding dysfunction 819

160
140 Severe obstruction (3)
120
Pdet.max (cmH2O) 100
80 Moderate obstruction (2)
60
40 Mild obstruction (1)
20 No obstruction (0)
0
0 10 20 30 40 50
Free Qmax (ml/s)

Figure 6. Female bladder-neck obstruction normogram. From Blaivas and Groutz (2000, Neurourology and
Urodynamics 19:553–564) with permission.

problems—for example, diverticulae—as well as ureteric reflux if present. Nitti et al51

advocated video urodynamics for diagnosing female voiding dysfunction using a set of
criteria for diagnosis even in the absence of clinical symptoms. In this study, patients
with bladder outlet obstruction had significantly higher voiding pressures, lower flow
rates and higher post-void residuals than patients with no obstruction. However, 10.5%
of their patients had a maximum detrusor pressure !20 cmH2O, and 11.8% had a
maximum flow rate O15 mL/second, exposing the limitations of using absolute figures
in diagnosing voiding dysfunction. In order to reduce these limitations, Blaivas and
Grouz proposed a normogram for women with bladder outlet obstruction52 using a
combination of information from free flowmetry and pressure studies (see Figure 6).
There is a paucity of literature, however, on the sensitivity and specificity of this
normogram.

Ultrasound scan

Ultrasound can provide a non-invasive method of assessing residual urine, bladder

thickness, and structural abnormalities of the urinary tract, including urethral
diverticulae. The accuracy of ultrasound may be affected by pelvic masses or the
body habitus of the patient. Recently, ultrasound has been used in the assessment and
treatment of postoperative voiding dysfunction following TVT.53 Ultrasound may also
be used to identify foreign bodies within the bladder, such as intravesical suture
material, mesh, calculi or any retropubic haematomas. Renal ultrasound can be used to
screen for upper renal tract pathology such as hydronephrosis or renal scarring.

Doppler planimetry

Doppler planimetry (bladder scanner) is used routinely in a clinical and postoperative

setting to assess urinary residual volumes. This non-invasive technique is easy to learn
and perform. Up to 12 images are acquired suprapubically using a hand-held transducer
over the bladder area. Several scans are performed until two or three consistent
readings are obtained. The sensitivity of this technique is poor for volumes !100 and
O400 mL. In addition, artefacts may be introduced by the presence of uterine fibroids,
a retropubic haematoma or ovarian cysts.
820 L. O. Olujide and S. M. O’Sullivan

Electromyography

Electromyography (EMG) of the external urethral sphincter or levator ani muscle has
been used in diagnosing Fowler’s syndrome and detrusor sphincter dyssynergia. In
Fowler’s syndrome, EMG produces a typical ‘whale-like’ sound on attempting to void or
during micturition.17 Electromyography has not proven to be useful in distinguishing
between neurogenic and non-neurogenic voiding dysfunction, but can be useful in
providing therapeutic biofeedback54 and in diagnosing pelvic floor denervation and
multiple system atrophy. The latter condition mimics Parkinson’s disease and is
characterised by the atrophy of cells in Onuf’s nucleus in the sacral spinal cord. EMG is
performed by using a single concentric needle placed either into the distal urethral or
external anal sphincter.

Cysto-urethroscopy

Difficulty in inserting a cystoscope may suggest urethral stenosis. Visualising the bladder
may show tumours, stones, foreign bodies, suture material or mesh, or bladder
diverticulae. It is important to visualise the total mucosal surface area, including any
diverticulae, as pathology may be missed.

TREATMENT

Often it is impossible to reverse or cure the underlying cause of voiding disorders,

and treatment is then aimed at compensating and relieving symptoms whilst
minimising long-term complications. Prevention with regard to voiding disorders is
infinitely better than cure. We know that pelvic surgery, epidural and spinal
anaesthesia and childbirth are risk factors for the development of urinary retention.
Training medical and nursing staff to anticipate and rapidly treat suspected urinary
retention in these at-risk patients will reduce the number of cases. This can be simply
achieved using protocols where voided volumes of uncatheterised patients are
measured; if incomplete voiding is suspected, residual volumes can be easily measured,
ideally using a bladder scanner to avoid unnecessary catheterisation. Women with
suboptimal voiding who are considering stress incontinence or extensive prolapse
surgery should be counselled about the significant risk of chronic urinary retention. It
is often useful to teach them self-catheterisation preoperatively so that they can give
fully informed consent.

Intermittent self-catheterisation

Intemittent self-catheterisation was first described as a non-sterile technique in 197255

when it was used to relieve incomplete bladder emptying in patients with spinal injuries.
It is now the primary treatment for chronic urinary retention, obviating the need for
indwelling catheters and drainage bags. Whilst the idea is often daunting to women,
once counselled and supported by specialist staff they usually master it easily and
tolerate it well. Most will notice an improved quality of life, with less or no overflow
incontinence and a reduction in urinary tract infections. There is a large choice of
discreet, lubricated, and easily disposable catheters on the market. The technique can
also be employed by the relatives or carers of severely incapacitated patients.
 Female voiding dysfunction 821

The technique is designed for everyday use, and the patient is taught to use a
mirror to find the urethral meatus while lying down or in the sitting position. They
are then taught to insert a fine-bore catheter. Patients need to have reasonable
dexterity, and most gain proficiency quickly. The number of catheterisations
required depends on whether the patient is able to partially void and also on the
fluid intake and post-void residuals. Antibiotic prophylaxis should be given if
necessary only at the beginning of the programme and for patients with symptoms
of cystitis, as 50% of patients will have asymptomatic bacteriuria. The procedure
has good long-term results.56
If patients are unable or unwilling to self-catheterise, then suprapubic rather than
urethral catheterisation should be considered. Long-term catheters should be silicone-
or Teflon-based to reduce complications such as encrustation and catheter blockage.
Regular washouts may also be required to reduce the latter problem. Local
complications include leakage around the catheter site, granulation tissue, and
occasionally pain secondary to bladder spasm.
The initial catheter may be placed under local, regional or general anaesthetic. The
catheter should be changed every 8 weeks; thereafter this is usually performed by a
community nurse specialist. A flip flow valve may be attached to the catheter and free
drainage performed at night only. This provides better cosmesis for the patient and
allows them to practise voiding through the urethra if appropriate, using the catheter to
measure the residual volume and empty the bladder. Long-term catheterisation is
always associated with bacteriuria, and antibiotics should be given only if patients are
symptomatic. Prophylaxis may be considered in some cases.

Pharmacotherapy

Discontinuing medications known to cause voiding disorders may easily sort out the
problem; however, alternative treatments may need to be instituted for chronic
conditions. Supervision by the patient’s primary care physician is important. Drug
treatment for voiding dysfunction has been largely ineffective and associated with a high
incidence of side-effects.57,58 There has been recent evidence that tamsulosin, an
a1A/a1D-selective adrenergic antagonist, is useful in improving the symptoms, maximum
flow rate and post-void residual volume in some women. However, only 18 women
with functional bladder-neck obstruction were recruited for this study. Further work is
awaited on the clinical usefulness of tamsulosin.59 Table 3 shows the range of medical
treatments that have been tried for voiding dysfunction. Research is required into
medications that might enhance bladder contractility or aid urethral relaxation during
micturition with minimal side-effects. Diazepam has been found to be useful in relieving
psychogenic and immediate postoperative voiding dysfunction caused by anxiety and
pain, although its effectiveness is variable.60
Botulinum toxins A and B have been used in the management of voiding dysfunction.
Phelan et al showed notable improvement in patients’ ability to void after injection of
80–100 units of botulinum toxin A into the external urethral sphincter in 21 patients
(including 13 women) with mainly neurogenic voiding dysfunction.61 Kuo62 achieved an
effective reduction in urethral sphincter resistance among patients with detrusor
overactivity and voiding dysfunction with a dose of 50 units. Botulinum toxin has also
been used successfully to treat urinary retention after pubovaginal sling operations.63
Injected into the detrusor muscle it has improved the quality of life of women
with detrusor sphincter dyssynergia despite the continuing requirement for
822 L. O. Olujide and S. M. O’Sullivan

Table 3. Medical treatment of voiding dysfunction.

Target organ Group of drugs Examples

Stimulation of the bladder
Relaxation of the urethral
sphincter mechanism
Muscarinic agents
Anticholinesterase
a-adrenergic blockers
Prostaglandins
a-adrenergic blocking
agents
Mixed a1- and
a2-adrenergic drugs
a2 stimulants
Striated muscle relaxants
Carbachol 0.25 mg subcutaneously
Bethanechol Cl 25–100 mg qds orally
Distigmine bromide 5 mg po/0.5 mg
intramuscularly
Propanolol
PGE2, PGF2a intravesical
Phenobenzamine 10 mg bd Prazosin
0.5 mg
Isoxsuprine hydrochloride 30 mg qds
Terbutaline sulphate 5 mg tds
Dantrolene 25 mg daily, Baclofen 5 mg
tds–25 mg qds, Diazepam 5 mg tds or
10–15 mg nocte

self-catheterisation. Anticholinergic agents may also be combined with clean

intermittent self-catheterisation in patients with detrusor hyperreflexia for symptom
relief. Botulinum toxin, however, has not been demonstrated to be effective in treating
Fowler’s syndrome.64

Surgery

In cases of voiding dysfunction caused by genital prolapse, correction of the

prolapse using pessaries or surgery should cure the symptoms. Several surgical
procedures have been described for managing voiding dysfunction. Urethral
dilatation with Hagar’s dilators or Otis urethrotomy has been effective in some
cases of urethral stenosis. However, overzealous urethral dilation can lead to
trauma and scarring and a consequent deterioration of voiding function or the
development of stress urinary incontinence due to injury to the urethral sphincter
mechanism. Yang and Huang reported the successful use of dilators in relieving
post-TVT voiding dysfunction.55 Rardin et al28 and Ozel et al65 treated the same
problem with simple vaginal release of the tape after TVT and transobturator tape
procedures respectively. In addition to loosening and cutting of the tape,
urethrolysis has been used to relieve postoperative voiding dysfunction after
tension-free sling operations. There is no consensus on the management of voiding
dysfunction after continence surgery, as shown in a survey of 344 physicians by
Nguyen et al.66 Urethrotomy and bladder-neck incisions are neither appropriate
nor advisable for idiopathic voiding difficulty in present-day practice.
A range of other procedures—including partial cystectomy and substitution
sigmoid colon-cystoplasty—have been suggested as alternatives to self-catheterisa-
tion; however, the results are disappointing in terms of restoration of normal
voiding.67,68 Continent urinary diversion operations such as the Mitrofanoff procedure
may benefit specific patients who are unable to tolerate self- or indwelling
catheterisation.
 Female voiding dysfunction 823

Alternative therapies

Biofeedback and bladder retraining

Learned behaviour may predispose to voiding problems, and bladder retraining with
biofeedback may be useful in this group of patients. There is no proven evidence that
bladder retraining is effective in the management of voiding dysfunction.

Turbine valves
These are replaceable intraurethral prostheses made of a valve and pump placed in a
catheter-like soft casing secured at the bladder neck by soft silicone fins and at the
external meatus by a flange. They are controlled by a battery-operated remote control
placed on the lower abdomen.69 When activated, the valve opens and the pump ‘sucks’
out the urine. Continence is restored after the bladder is emptied by automatic closure
of the valve. Despite encouraging short-term results, long-term complications include
infections, dyspareunia, migration of the device and a high rate of removal.70,71 Mazouni
et al found that 50% of their patients were satisfied with the device, while complications
made it unacceptable for the other 50%.72

Electrical stimulation and neuromodulation

Electrical stimulation using vaginal, anal, intravesical and transdermal devices has been
employed in women with voiding difficulty.5 Segmental sacral neuromodulation using
implantable neural prostheses has also been evaluated, with mixed results. This is a
two-stage procedure aimed at stimulating the S3 sacral nerve roots unilaterally or
bilaterally. A temporary electrode is inserted under local anaesthesia for
percutaneous evaluation. In responders, a permanent implant may be applied. The
exact mechanism of action of neuromodulation is unclear, but Thon et al73
hypothesised that the electrical current modulates reflex pathways involved in the
filling and evacuation phases of the micturition cycle. This technique has been shown
to benefit some patients, including those with Fowler’s syndrome.74 Shaker and
Hassouna75 reported improved voiding in a group of 20 patients with non-obstructive
retention after a mean follow-up of 15 months. In another study by Abosief et al, 18
out of 20 patients were able to void after implantation of a permanent sacral nerve
root stimulator.76 In a study of 33 patients, Scheepens et al77 concluded that bilateral
sacral neuromodulation is not superior to unilateral implantation. However, bilateral
stimulation might be more effective in patients who only partially respond to
temporary devices.
Posterior tibial nerve stimulation (PTNS) is also being used in the treatment of
female voiding dysfunction. The posterior tibial nerve contains L5–S3 fibres and
originates from the same level of the spinal cord as the parasympathetic
innervation to the bladder. Stimulation of the posterior tibial nerve has been
found to be effective in the treatment of female voiding dysfunction.78,79 Treatment
is aimed above the medial malleolus through a percutaneuos needle. Stimulation of
the nerve results in a sensory response which includes a tickling sensation in the
sole of the foot, and a motor response in the form of plantar flexion of the big toe
and fanning of the remaining toes. Treatment is carried out for 30 minutes every
12 weeks. In their study of 29 patients with idiopathic non-obstructive voiding
dysfunction, Vandoninck et al showed that 41% of patients achieved a minimum of
50% reduction in their total catheterised volume over 24 hours.80 After 12
824 L. O. Olujide and S. M. O’Sullivan

sessions of PTNS the detrusor pressure at maximal flow increased significantly,

with a reduced residual volume, while the bladder capacity remained the same.
Unfortunately, none of the patients in this study became free of intermittent
catheterisation. Two patients had no residual volume but still continued to
catheterise at least once a day. This study included both males and females
undergoing treatment over 144 weeks. PTNS may prove a useful tool in the
treatment of voiding disorders, but more studies are required.

SUMMARY

Pre-emptive management in at-risk women and prompt treatment of acute retention

can reduce the incidence of serious voiding disorders in women. Strict management
protocols and the education of medical and nursing staff on labour wards and postnatal,
gynaecological and surgical wards should make this complication a rare one.
Intermittent self-catheterisation remains the most effective therapy for chronic urinary
retention, and new developments in the design and ergonomics of disposable catheters
have been beneficial to patients. Patients should be treated with understanding and
empathy, and a multidisciplinary approach should ensure successful management.
Developments in neuromodulation, surgery and pharmacotherapy have been
disappointing, and their role to date is limited. Further research is needed in these
areas.

Practice points

† prevention is better than cure; peripartum bladder care and postoperative

bladder management should be optimised, particularly following incontinence
and prolapse surgery
† detailed urogynaecological history and focused physical examination are
important in identifying this problem
† the aetiology and management of voiding disorder in women is quite different
from those in men
† frequency/volume charts, free uroflowmetry with residual volume estimation,
with or without subtracted cystometry, are useful not only in establishing
diagnosis but also in monitoring progress
† intermittent clean self-catheterisation remains the mainstay of managing
chronic retention
† identifying women at risk of urinary retention after surgery or childbirth, and
using rigid protocols to diagnose and treat urinary retention, will reduce cases
of chronic retention and bladder over-distention
† new modalities of treating female voiding dysfunction include the use of
tamulosin (a1 blockers), botulium injections, and sacral neuromodulation
 Female voiding dysfunction 825

Research agenda

† consensus on terminology used to describe voiding dysfunction

† voiding dysfunction and quality of life
† international consensus on the diagnostic criteria for female voiding
dysfunction, including the role of nomograms in interpreting flow-rate
parameters
† further research into the medical treatment of female voiding dysfunction
† effectiveness of sacral or peripheral neuromodulation in daily clinical practice
† management of postoperative voiding dysfunction following new generation
sling procedures

REFERENCES

*1. Abrams P, Cardozo L, Fall M, Griffiths D et al. The standardisation of terminology of lower urinary tract
function: report from the standardisation sub-committee of the international continence society.
Neurourology and Urodynamics 2002; 21: 119–167.
2. Stanton S, Ozsoy C & Hilton P. Voiding difficulties in the female: prevalence, clinical and urodynamic
review. Obstetrics & Gynaecology 1983; 61: 144–147.
3. Groutz A, Gordon D, Lessing JB et al. Prevalence and characteristics of voiding difficulties in women: are
subjective symptoms substantiated by objective urodynamics data? Urology 1999; 54: 268–272.
4. Farrar D, Osborne J, Stephenson T et al. A urodynamic view of bladder outflow obstruction in the female:
factors influencing results and treatment. British Journal of Urology 1976; 47: 817.
5. Lepor H & Machi G. Comparison of AUA symptoms index in unselected males and females between fifty-
five and seventy-nine years of age. Urology 1993; 42: 36–41.
*6. Dietz HP & Haylen BT. Symptoms of voiding dysfunction: what do they really mean? International Journal of
Urogynaecology and Pelvic Dysfunction 2004; 16(1): 52–55.
7. Das AK, Carlson AM et al. Improvement in depression and health related quality of life after sacral nerve
stimulation therapy for treatment of voiding dysfunction. Urology 2004; 64(1): 62–68.
8. Monga AK. Non-neurogenic voiding difficulties and retention. In: Cardozo L, Staskin, editors. Textbook of
Urogynaecology. London: Martin Dinitz, 2001, pp. 855–863.
9. Wyndaale JJ. A clinical study on subjective sensations during bladder filling. International Urogynae Journal
1990; 2: 215–218.
10. Vaugh CW & Satchell PM. Urine storage mechanism. Progress in Neurobiology 1995; 46: 215–237.
*11. Sullivan MP & Yalla SV. Physiology of female micturition. Urologic Clinics of North America 2002; 29:
499–514.
12. Carlson CA. The supraspinal control of the urinary bladder. Acta Pharmacology Toxicology 1978;
43(supplement 2): 8–12.
13. Nathan PW, The central nervous connection of the bladder. In Williams DI (ed.) Scientific Foundations of
Urology, vol. 2. Chigaco: Year book Publishers, 1976, pp. 51–58.
14. Chaikin DC, Romanzi L & Rosenthal J. The effects of genital prolapse on micturition. Neurorology
Urodynamics 1998; 17: 426–427.
15. Gaynor-Krupnick DM & Kreder KJ. Bladder neck leiomyoma presenting as voiding dysfunction. Journal of
Urology 2004; 172(1): 249–250.
16. Fowler CJ & Kirby RS. Abnormal electromyographic activity in the striated urethral sphincter in 5 women
with urinary retention. British Journal of Urology 1985; 57: 67–70.
17. Groutz A, Blaivas JG, Pies C & Sassone AM. Learned voiding dysfunction among adults. Neurourology
Urodynamics 2001; 20: 259–268.
18. Tong YC, Monson FC, Erica B & Levin RM. Effects of acute in vitro overdistension of the rabbit urinary
bladder on DNA synthesis. Journal of Urology 1992; 148: 1347–1350.
826 L. O. Olujide and S. M. O’Sullivan

19. Holm-Bentzen M, Larsen S, Hainan B & Hald T. Non-obstructive detrusor myopathy in a group of patients
with chronic abacterial cystitis. Scandinavian Journal of Urology and Nephrology 1985; 124: 1015–1017.
20. Martin J, Sobeh M, Swash C et al. Detrusor myopathy: a cause of detrusor weakness with retention. British
Journal of Urology 1993; 235–236.
21. Copcoat MJ, Shah PJ, Cumming J et al. How does bladder function changes in the early period after
surgical alteration in outflow resistance? Journal of the Royal Society of Medicine 1987; 80: 753–754.
22. Walter S, Olesen KP, Hald T et al. Urodynamics evaluation after vaginal repair and colposuspension.
British Journal of Urology 1982; 54: 377–380.
23. Lose G, Jorgensen L, Mortensen SO et al. Voiding difficulties after colposuspension. Obstetrics and
Gynaecology 1987; 69: 33–38.
24. Ward KL, Hilton P & Browning J. A randomised trial of colposuspension and tension free vaginal tape for
primary genuine stress incontinence. Neurourology Urodynamics 2000; 19: 386–388.
25. Ulmsten U, Johnson P & Rezapour M. A three year follow up of tension free vaginal tape for surgical
treatment of female stress incontinence. British Journal of Obstetrics and Gynaecology 1999; 106: 345–350.
26. Smith RNJ & Cardozo L. Early voiding difficulty after colposuspension. British Journal of Urology 1997; 80:
911–914.
*27. Wang KH, Neimark & Davila GW. Voiding dysfunction following TVT procedure. International
Urogynaecology Journal 2002; 13: 353–358.
28. Rardin CR, Rosenbelt PL, Kohli N et al. Release of tension free vaginal tapes for the treatment of
refractory post operative voiding dysfunction. Obstetrics & Gynaecology 2002; 100(5, Part 1): 898–902.
29. Dwyer PL & Desmedt E. Impaired bladder emptying in women. Australia and New Zealand Journal of
Obstetrics and Gynaecology 1994; 34: 73–78.
30. Phillips C, Robertshaw JR & Monga AK. Late hypersensitivity reaction to periurethral collagen injection.
British Journal of Urology 2001;.
31. Bladder emptying problems. In Wall LL, Norton PA & DeLancey JOL (eds.) Practical Urogynaecolgy.
Baltimore: Williams & Wilkins, 1993, pp. 274–292.
*32. Mutone N, Brizendine E & Hale D. Factors that influence voiding function after the tension-free vaginal
tape procedure for stress urinary incontinence. American Journal Obstetrics & Gynaecology 2003; 188:
1477–1481.
33. Weinberger MW & Ostergard DR. Postoperative catheterization, urinary retention, and permanent
voiding dysfunction after polytetrafluoroethylene suburethral sling placement. Obstetrics & Gynaecology
1996; 87: 50–54.
34. Koldewijn EL, Hommes O, Lemmens W et al. Relationship between lower urinary tract abnormalities and
disease related parameters in multiple sclerosis. Journal of Urology 1995; 154: 169–173.
35. Lazerri M, Beneforti P, Benjamin G et al. Vesical dysfunction in systemic sclerosis(scleroderma). Journal of
Urology 1995; 153: 1184–1187.
*36. Nitti VW. Evaluation of the female with neurogenic voiding dysfunction. International Urogynaecology
Journal and Pelvic Floor dysfunction 1999; 10: 119–129.
37. Robinson . Effect of drug treatment on voiding function ICS-UK, 18–19, March, Abstract No-024 2004.
38. Stanton SL, Cardozo LD. A comparison of vaginal and suprapubic surgery in the correction of
incontinence due to urethral sphincter incompetence. 1979; 51: 497–499.
39. Hemrika DJ, Schutte MF & Bleker OP. Elsberg syndrome: a neurologic basis for acute retention in patients
with genital herpes. Obstetrics and Gynaecology 1986; 68: 37S–39S.
40. Shah PJR, Whiteside CG, Milroy EJG & Turner-Warwick RT. The hypersensitive female bladder—a catheter
diagnosis? Proceeding of the XIIIth Annual Meeting of the International Continence Society 1983 p. 202–3.
41. Anderson LF, Agner T, Walter S & Hansen JM. Micturition pattern in hyperthyroidism and
hypothyroidism. Urology 1987; 29: 223–224.
42. Krane R & Siroky M. Psychogenic voiding dysfunction. In Krane R & Siroky M (eds.) Clinical Neurourology.
Boston: Little, Brown & Co, 1978, pp. 275–284.
43. Bellina JH, Schenck D & Millet AH. Outflow uropathy: occupational disorder? Journal La State Med Soc
1999; 151: 414.
44. Kaplan WE, Firlit CF & Schoenberg HW. The female urethral syndrome: external urethral spasm as
etiology. Journal of Urology 1980; 124: 48.
45. Carlson KV, Rome S & Nitti VW. Dysfunctional voiding in women. Journal of Urology 2001; 165: 143–148.
 Female voiding dysfunction 827

46. Drach GW, Ignatoff J & Layton T. Peak urinary flow rate: observations in female subjects and
comparisons to male subjects. Journal of Urology 1979; 122: 215–219.
47. Griffith DJ, Constatinou CE & van Mastrigt R. Urinary bladder function and its control in healthy female.
American Journal of Physiology 1986; 251: 225–230.
*48. Pauwels E, De Watchter S & Wyndaele J. A normal flow pattern in women does not exclude voiding
pathology. International Urogynecology Journal and Pelvic Floor Dysfunction 2005; 16: 104–108.
49. Haylen BT, Law MG, Frazer M & Schulz S. Urine flow rates and residual urine volumes in urogynaecology
patients. International Urogynaecology and Pelvic Floor Dysfunction 1999; 10: 378–383.
50. Constantini E, Mearini E, Pajoncini C et al. Uroflowmetry in female voiding disturbances. Neurourology and
Urodynamics 2003; 22: 569–573.
51. Nitti VW, Tu LM & Gitlin J. Diagnosing bladder outlet obstruction in women. Journal of Urology 1999; 161:
1535–1540.
52. Blaivas JG & Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract
symptomatology. Neurourology and Urodynamics 2000; 19: 553–564.
53. Yang JM & Huang WC. Sonographic findings in a case of voiding dysfunction secondary to the tension-free
vaginal tape (TVT) procedure. Ultrasound Obstetrics and Gynaecology 2004; 23: 302–330.
54. Maizels M, King L & Firlit C. Urodynamics feedback: a new approach to treat vesical sphincter dyssynergia.
Journal of Urology 1979; 122: 205–209.
55. Laipes J, Diokno c, Silber SJ & Lower BS. Clean intermittent self catheterization in the treatment of lower
urinary tract disease. Journal of Urology 1972; 107: 458–461.
56. Wyndaele J & Maes D. Clean intermittent self catheterization: a 12 year follow-up. Journal of Urology 1990;
143: 906–908.
57. Kumar A, Mandhani A, Gogoi S & Srivastava A. Management of functional bladder neck obstruction in
women: use of alpha- blockers and paediatric resectoscope for bladder incision. Journal of Urology 1999;
162: 2061–2065.
58. Riedl CR, Stephen RL, Daha LK et al. Electromotive administration of intravesical bethanechol and clinical
impact on acontractile detrusor management: an introduction of a new test. Journal of Urology 2000; 164:
2108–2111.
*59. Pischedda A, Pirozzi FF, Madonia M et al. Use of alpha 1-blockers in female functional bladder neck
obstruction. Urology International 2005; 74(3): 256–261.
60. Stanton SL. Drug management of voiding difficulties in the female. In Cardozo L (ed.) Update on Durgs and
Lower Urinary Tract. London: Royal Society of Medicine, 1988, pp. 21–24.
61. Phelan M, Franks M, Somogyi G et al. Botulinum toxin urethral sphincter injection to restore bladder
emptying in men and women with voiding dysfunction. Journal of Urology 2005; 165: 1107–1110.
*62. Kuo HC. Effect of Botulinum A toxin in the treatment of voiding dysfunction due to detrusor
underactivity. Urology 2003; 61: 550–554.
63. Smith CP, O’Leary M, Erickson J et al. Botulinum toxin urethral sphincter injection resolves urinary
retention after pubovaginal sling operation. International Urogynaecology Journal and Pelvic Floor
Dysfunction132002;: 185–186.
64. Fowler CJ, Betts CD, Christmas TJ et al. Botulinum toxin in the treatment of chronic urinary retention in
women. British Journal of Urology 1992; 70: 387–389.
65. Ozel B, Minaglic S et al. Treatment of voiding dysfunction after transobturator tape procedure. Urology
2004; 64(5): 1030.
66. Nguyen JK. Diagnosis and treatment of voiding dysfunction caused by urethral obstruction after anti-
incontinence surgery. Obstetrics & Gynaecology Survey 2002; 57(7): 468–475.
67. Klarskov P, Anderson JT, Asmussen CF et al. Acute urinary retention in women: a prospective study of
18 consecutive cases. Scandinavian Journal of Urology and Nephrology 1987; 21: 29–31.
68. Taguchi Y. Augmentation and replacement sigmoid colocystoplasy. A review of 10 patients. British
Journal of Urology 1987; 60: 231–235.
69. Monga AK, Beyar M, Nativ O & Stanton SL. A new intraurethral sphincter prosthesis for retention:
preliminary clinical results. Neurology and Urodynamics151996;: 406–407.
70. Madjar S, Halachmi S, Wald M et al. Long term follow up of the In-Flow intraurethral inset for the
treatment of women with voiding dysfunction. European Urology 2000; 38: 161–168.
71. Krishna NS & Glen ES. Re: A remote controlled intraurethral insert for artificial voiding: a new concept
for treating women with voiding dysfunction(letter). Journal of Urology 2000; 163: 1258.
828 L. O. Olujide and S. M. O’Sullivan

72. Mazouni et al. Urethral device in women with chronic urinary retention: an alternative to self
catheterisation. European Journal of Obstetrics & Gynaecology Reproductive Biology 2004; 115(1): 80–84.
73. Thon WF, Baskin LS, Jonas U et al. Neuromodulation of voiding dysfunction and pelvic pain. World
Journal of Urology 1991; 9: 38.
74. DasGupta R, Apostolidis A & Fowler C. Urodynamics results following successful sacral neuromodulation
in women with urinary retention. European Urology 2003; 2: 70.
75. Shaker HS & Hassouna M. Sacral root neuromodulator in ididopathic nonobstructive chronic urinary
retention. Journal of Urology 1998; 159: 1476–1478.
*76. Abosief S, Tamaddon K, Chalfin S et al. Sacral neuromodulation in functional urinary retention: an
effective way to restore voiding. British Journal of Urology 2002; 90: 662–665.
77. Scheepens WA, De Bie RA, Weil EHJ & Van Kerrebroeck EV. Unilateral versus bilateral sacral
neuromodulation in patients with chronic voiding dysfunction. Journal of Urology 2002; 168: 2046–2050.
78. van Balken MR, Vandoninck V, Gisof KW et al. Posterior tibial nerve stimulation as neuromodulative
treatment of lower urinary tract dysfunction. Journal of Urology 2001; 166: 914–918.
79. Vandoninck V, van Balken MR, Finazzi Agor E et al. Posterior tibial nerve stimulation in the treatment of
idiopathic non-obstructive dysfunction. Urology 2003; 61(3): 567–572.
80. Vandoninck V, Balken MR, Finazzi Agor E, Heesakkers JPFA et al. Posterior tibial nerve stimulation in the
treatment of voiding dysfunction:urodynamic data. Neurourology and Urodynamics 2004; 23: 246–251.
81. Haylen BT, Ashby D, Sutherst JR et al. Maximum and average urine flow rates in normal male and female
populations- the Liverpool normograms. British Journal of Urology 1989; 64: 30–38.
*82. O’Callaghan D & Dwyer PL. Clinical and urodynamic follow-up of women with established urinary
dysfunction after radical hysterectomy. Australia NZ Journal of Obstet Gynaecology 1994; 34: 557–561.