Voiding difficulty

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CHAPTER 54 Voiding difficulty

L. Bombieri, Robert Freeman

Chapter Contents

INTRODUCTION 836
DEFINITIONS 836
INCIDENCE 837
SYMPTOMS AND CLINICAL EFFECTS 837
CAUSES 838
INVESTIGATIONS 841
MANAGEMENT 843
PREVENTION 845
KEY POINTS 846

Introduction

Normal voiding occurs when tension receptors in the bladder sense fullness and stimulate a sacral reflex of somatically mediated relaxation of the pelvic floor and urethra, and parasympathetically mediated detrusor contraction. In the adult, this simple reflex is under voluntary control via a set of complex pathways which run from the cerebral cortex to the pontine micturition centre and the sacral spinal cord via the lateral spinothalamic tracts and the posterior columns. The sacral micturition centre is located at S2–4 level. Peripheral innervation to the bladder and urethral sphincter is supplied by the pelvic, hypogastric and pudendal nerves.

Imaging studies on normal women have shown that the bladder base and the upper urethra move downwards, the lower urethra remains fixed, the bladder as a whole becomes more ovoid in shape, the posterior urethrovesical angle becomes obliterated, funnelling occurs at the bladder neck, and the whole urethra dilates as the fluid passes.

Studies on detrusor pressure during voiding in normal women suggest that most void with a detrusor contraction greater than 15 cmH2O (mean detrusor pressure at maximum flow 23–28 cmH2O, maximum detrusor pressure 20–36 cmH2O) (Figure 54.1). Detrusor pressure during voiding is generally lower in women than in men. A few normal women have been reported to void with a low pressure detrusor contraction of less than 15 cmH2O, but no normal women void with no contraction at all; such an event may indicate low urethral closure pressure.

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Figure 54.1 Normal voiding.

There are variations in the way that women void. Some women, in addition to pelvic relaxation and detrusor contraction, may strain by an unconscious but sustained Valsalva manoeuvre (Figure 54.2). The contribution of abdominal pressure to the voiding process varies considerably between individuals and within the same individual during consecutive voids.

image

Figure 54.2 Voiding with detrusor contraction supplemented with abdominal straining.

The ‘normal’ voiding curve in women has a single peak, with a fast crescendo and a relatively slow diminuendo, with minimal fluctuations. However, an interrupted pattern can be seen repeatedly in a minority of normal women. Studies of flow rates suggest that most normal women void with a peak flow rate greater than 15 ml/s, with mean values of 23–27 ml/s (Figure 54.1). Peak flow rate values are generally higher in women than in men. The main variable affecting flow rates in normal women is bladder volume, with greater flow rates seen with increasing volumes. Parity, weight and height have no influence on flow rates.

In this chapter, deviations from this pattern of normality will be presented and discussed, particularly with reference to clinical situations relevant to urogynaecological practice.

Definitions

Voiding difficulty

A joint International Urogynecological Association/International Continence Society (ICS) Report on terminology for female pelvic floor dysfunction defines ‘voiding difficulty’ as ‘abnormally slow and/or incomplete micturition’ (Haylen et al 2010). The diagnosis is obtained by symptoms (see below) and urodynamic investigations, and should be based on repeated measurements to confirm abnormality.

Abnormally slow urine flow rates, as determined by uroflowmetry, are best referenced to nomogram charts which provide a range of normality for urinary flow rates in relation to volume voided; abnormal flow is defined as flow under the 10th centile (Haylen et al 1989). To encourage the use of these charts, a larger version of the original charts has been republished recently (Haylen et al 2008a).

Abnormally high postvoid residuals (i.e. volume left in the bladder at the completion of micturition) depend on the method used for measurement and the timing of the measurement after micturition, taking into account renal input of 1–14 ml urine/min (Haylen et al 2010).

Upper limits of postvoid residuals of 30 ml (using immediate ultrasound assessment) and 50–100 ml (using urethral catheterization) have been proposed (Haylen et al 2010).

Acute retention of urine

This is defined as a generally, but not always, painful, palpable or percussable bladder, when the patient is unable to pass any urine when the bladder is full (Haylen et al 2010).

Chronic retention of urine

This is defined as a non-painful bladder where there is a chronic high postvoid residual (Haylen et al 2010).

Incidence

Depending on definition and type of clinic, voiding difficulty in women presenting to a urology or urogynaecology clinic has a variable prevalence ranging from 14% (when using a strict definition based on multiple variables including low flow, high pressure and increased postvoid residual) (Massey and Abrams 1988) to 39% (using a postvoid residual of 30 ml or more) (Haylen et al 2007).

Symptoms and Clinical Effects

When present, symptoms of voiding difficulty are non-specific and include hesitancy, slow stream, straining to void, feeling of incomplete bladder emptying, spraying, need to immediately revoid, position-dependent micturition (e.g. leaning forwards or backwards, semi-erect), and dysuria.

Women with voiding dysfunction may present with urinary incontinence; this is often unconscious leakage due to ‘overflow incontinence’, although this term lacks a precise definition. Recurrent urinary tract infections (UTI) and ‘irritative’ bladder symptoms such as frequency and urgency, with and without coexistent detrusor overactivity, may be reported.

Inability to void usually leads to prolonged use of urinary catheters and an increased incidence of UTI. The risk of acquiring bacteriuria relates to the duration of catheterization, and ranges from 4% to 7.5%/day over the first 10 days of catheterization (Schaeffer 1986). The majority of patients on long-term clean catheterization have bacteriuria, and about one-third of them require intermittent treatment with antibiotics due to symptomatic infection (Lapides et al 1976). Catheter-related UTI is an important cause of hospital-acquired infections, morbidity (e.g. pyelonephritis) and, in the elderly, mortality.

When voiding difficulty develops after surgery, hospital stay is often prolonged. When patients are discharged with a catheter, daily nursing care in the community is required. This can lead to an escalation in costs.

In the long term, inability to void may lead to profound alterations in quality of life and have serious psychological effects.

Causes

The causes of voiding difficulty are shown in Box 54.1.

Box 54.1 Causes of voiding difficulty

• Age
• Postoperative: pelvic surgery, incontinence surgery, prolapse surgery
• Post partum
• Neurological disease
• Psychogenic
• Pelvic organ
• Prolapse
• Idiopathic bladder neck obstruction
• Bladder overdistension/infrequent voiding
• Drugs
• Infection
• Pelvic mass
• Urethral or bladder pathology
• Detrusor myopathy/acontractility
• Iatrogenic

Effects of age on voiding function

The incidence of voiding dysfunction in women increases with age (Haylen et al 2008b), and the process of ageing may decrease detrusor contractility and increase urethral rigidity.

Urodynamic studies have shown that both peak flow rate and detrusor pressure during voiding decrease with advancing age. Older women are also more likely to strain abdominally during voiding and to have higher residual urine volumes (Malone-Lee and Wahedna 1993).

With advancing age, anatomical changes occur in the bladder wall leading to reduced bladder contractility (e.g. increased collagen content in the detrusor muscle, reduction in the number of cholinergic nerves, dedifferentiation of detrusor muscle cells). Changes leading to urethral atrophy and increased rigidity also occur (e.g. reduced striated muscle and vessel content, increased connective tissue).

While it is not clear whether voiding dysfunction is due to ‘normal’ ageing of the lower urinary tract or to the presence of disease processes, age is the only risk factor that has been consistently associated with the development of postoperative voiding dysfunction after anti-incontinence surgery. Increased urethral rigidity may increase the likelihood of causing obstruction, and reduced detrusor contractility may reduce the ability to cope with it.

It is not clear whether the menopause has an effect on voiding which is distinct from age. There are no studies showing that the menopause per se has a deleterious effect on voiding function. However, the distal urethra is oestrogen dependent and therefore susceptible to postmenopausal atrophic changes; the reduction in urethral functional length seen after the menopause is likely to be a manifestation of this process. There is evidence that these changes are more pronounced in a minority (18%) of postmenopausal women (Smith 1972). These women may have increased urethral rigidity and may be predisposed to the development of voiding dysfunction should they undergo pelvic or anti-incontinence surgery.

Postoperative voiding dysfunction

Pelvic surgery

Temporary voiding difficulty is commonly observed after pelvic surgery. In the immediate postoperative period, many reversible factors are likely to play a role. Atropine and other anaesthetic reversal agents with anticholinergic effects (some with a half-life of 3–4 days) may reduce detrusor contractility. Opiates might reduce bladder sensation, pain might inhibit perineal relaxation, and bladder overfilling might depress detrusor contractility. In addition, bruising and oedema can also depress bladder contractility and cause temporary obstruction. Spinal anaesthesia depresses voiding function for up to 4–8 h, depending on whether short- or long-acting agents are used. Epidural anaesthesia may depress voiding function for 14–16 h, especially when supplemented by opioids in the epidural space.

With regards to specific procedures, clinical and urodynamic studies have found no evidence of increased voiding dysfunction in the short term after vaginal hysterectomy with anterior colporrhaphy performed at the same time (Stanton et al 1982), and after abdominal hysterectomy (Wake 1980). Also, no differences in bladder function were observed in a randomized study comparing total with subtotal hysterectomy (Thakar et al 2002). However, a history of previous hysterectomy has been associated with increased risk of voiding difficulty, possibly due to nerve dysfunction (Dietz et al 2002).

Extensive pelvic surgery might lead to denervation and prolonged or permanent voiding difficulty. Radical hysterectomy has been shown to lead to prolonged voiding difficulty in one-quarter of patients (Scotti et al 1986) due to neuropathic dysfunction.

Surgery for stress incontinence

Surgery for stress incontinence is an important cause of impaired bladder emptying in women. There is no universally accepted definition of voiding dysfunction after incontinence surgery, and voiding function is often reported empirically in studies (e.g. as ‘time required for resumption of voiding’ or ‘time of catheter removal’). In most cases, postoperative voiding problems are short term, but they can persist in the long term and lead to profound alterations in quality of life. Prolonged or ‘late’ voiding dysfunction after incontinence surgery may also affect patients who did not have ‘early’ dysfunction in the immediate postoperative period. This may be due to failure to obtain an early diagnosis, progressive effects of scarring or onset of new pathology.

Women with stress incontinence may already have some impairment of voiding function, which may make them more vulnerable to the obstructive effects of surgery. This is suggested by differences in several urodynamic (voiding) variables noted in these women. For example, in contrast with normal women, women with stress incontinence are more likely to strain during voiding, and to initiate voiding with a Valsalva manoeuvre as opposed to pelvic relaxation. They also void with significantly lower detrusor pressures, and up to 15% have been shown to void without a contraction (Figure 54.3; Karram et al 1997). It is not clear whether this is due to the lower mean urethral pressure of women with urodynamic stress incontinence, or whether there is a real impairment of detrusor muscle function in these women.

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Figure 54.3 Voiding without detrusor contraction (pelvic relaxation alone).

Postoperative voiding disorders have been reported to occur after most operations for stress incontinence. Prolonged voiding dysfunction is uncommon after urethral injectables, although an incidence of 5% has been reported (Khullar et al 1997). The colposuspension operation leads to postoperative voiding dysfunction in a mean of 12.5% of patients (Jarvis 1994). Laparoscopic and open colposuspension have the same incidence of postoperative voiding difficulty (Carey et al 2006). Results of a randomized study comparing the tension-free vaginal tape (TVT) procedure with colposuspension suggest that the incidence of voiding difficulty at 6 months is similar after both operations (7%), although patients experience earlier voiding in the immediate postoperative period after the TVT procedure (Ward and Hilton 2002). After the TVT procedure, 11% of women have been reported to need a catheter for more than 24 h (Vervest et al 2007), with only 2% needing tape release for prolonged difficulty (Kuuva and Nilsson 2002, Karram et al 2003, Vervest et al 2007). The transobturator tape (TOT) procedure has been shown to have a lower incidence of postoperative voiding difficulty than the TVT, possibly as it is less obstructive (Latthe et al 2007).

Voiding difficulty after incontinence surgery is multifactorial. In addition to temporary factors, as detailed above, permanent factors might be relevant from the outset. Some factors are obstructive and relate to the operative technique (e.g. excessive tape tension when using midurethral slings, or excessive bladder neck elevation at colposuspension), while others relate to the patient and her capacity to deal with obstruction (e.g. age and poor detrusor contractility). An intrinsically weak detrusor may be unable to cope with even the slightest increase in outflow resistance.

Prolapse surgery

Short-term voiding difficulty is common after vaginal surgery for prolapse. In a large series of women undergoing such surgery, urinary retention (defined as a postvoid residual of ≥200 ml after removal of the catheter the day after the operation) occurred in 29% of women, with 9% experiencing retention for more than 3 days (Hakvoort et al 2009). In another study, 11% of women required catheterization at home after discharge from hospital (Vierhout 1998). However, no patients experienced long-term voiding difficulty (Vierhout 1998, Hakvoort et al 2009). Performing a levator muscle plication (as part of a posterior colporrhaphy) and a Kelly suburethral plication (as part of an anterior colporrhaphy) can increase the risk of postoperative retention (Hakvoort et al 2009).

A policy of early catheter removal, the day after vaginal surgery seems preferable to routine prolonged catheterization (4 days) as it is associated with a lower incidence of UTI and a shorter duration of hospital stay (Hakvoort et al 2004). However, early catheter removal increases the risk of recatheterization: 40% in the ‘early’ removal group vs 9% in the ‘late’ removal group (Hakvoort et al 2004). Prolonged catheterization may therefore be preferable in individual cases when there is an increased risk of postoperative voiding difficulty.

Postpartum voiding difficulty

Prolonged voiding difficulty in the postpartum period requiring self-catheterization is uncommon and has been reported to occur after less than 1% of deliveries (Glavind and Bjørk 2003). However, when using strict criteria [similar to those proposed recently by the International Urogynecological Association/International Continence Society (2010)], up to 43% of women have been shown to have some degree of voiding difficulty after delivery (Ramsay and Torbet 1993). Recognized risk factors for voiding difficulty in the immediate postpartum period are primiparity, instrumental delivery, epidural analgesia, prolonged labour, perineal trauma and poor bladder management resulting in overdistension. In addition to temporary factors (e.g. epidural, morphine, anaesthetic), other factors causing prolonged voiding dysfunction may be present (e.g. trauma to the bladder, pelvic floor muscles and nerves).

Neurological disease

The effects of neurological disease on bladder function and the upper renal tracts depend on the site of the lesion(s). Interruption of the mainly inhibitory pathways from the cerebral cortex to the pontine micturition centre (e.g. stroke, tumour, trauma, Parkinson’s disease) is likely to result in uninhibited detrusor contraction and incontinence. Interruption of the neural pathways from the pontine to the sacral centres [e.g. spinal cord injury, multiple sclerosis (MS)] may also lead to uninhibited contractions (neurogenic detrusor overactivity) with or without failure of relaxation of the urethral sphincter (detrusor sphincter dyssynergia). Interruption of the sacral reflex arc (e.g. diabetic neuropathy, low spinal cord tumours, lumbar disc prolapse) may lead to acontractility of the detrusor muscle (atonic bladder), with voiding difficulty and retention.

Impaired voiding function (e.g. detrusor sphincter dyssynergia) can potentially lead to high detrusor pressure, reflux and upper tract changes (e.g. hydronephrosis), resulting in renal failure.

Specific neurological conditions are discussed below.

Lumbar intervertebral disc prolapse

Lumbar disc prolapse is extremely common, with approximately 30% of adults without back pain having evidence of a protruded disc on magnetic resonance imaging (MRI) (Jarvik and Deyo 2007). In patients with symptomatic lumbar disc prolapse, urodynamic studies have shown voiding difficulty due to reduced detrusor contractility in approximately one-quarter of cases (Bartolin et al 1998). The most common sites of lumbar disc prolapse are L4–5 and L5–S1. Compression occurs more often in a posterolateral direction but may also be central. Patients may report a long history of low back pain, or voiding difficulty may be the first or only symptom. Compression of the sacral nerves can lead to cauda equina syndrome, characterized by voiding difficulty, saddle anaesthesia, bilateral sciatica and low back pain. Physical examination in these cases shows reduced sensation in the saddle and perianal area. If nerve compression is seen on MRI, urgent surgical treatment, usually laminectomy, is indicated. Despite this, voiding function often fails to improve after surgery (Bartolin et al 1999).

The lithotomy position commonly used to perform gynaecological procedures can potentially precipitate lumbar disc prolapse (Choudhari et al 2000). It has been suggested that flexion and hyperabduction of the hips may stretch nerve roots already compromised by a partial ‘occult’ disc prolapse (Choudhari et al 2000). When no other explanation can be found, this possibility should always be considered and investigated by MRI should a patient develop prolonged voiding difficulty after a gynaecological procedure.

Parkinson’s disease

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