Incontinence and retention--how the bladder misfunctions.
Article Type: Disease/Disorder overview
Subject: Urinary incontinence (Diagnosis)
Urinary incontinence (Care and treatment)
Bladder (Physiological aspects)
Urethra (Physiological aspects)
Urine (Retention)
Urine (Diagnosis)
Urine (Care and treatment)
Author: Casey, Georgina
Pub Date: 08/01/2011
Publication: Name: Kai Tiaki: Nursing New Zealand Publisher: New Zealand Nurses' Organisation Audience: Trade Format: Magazine/Journal Subject: Health; Health care industry Copyright: COPYRIGHT 2011 New Zealand Nurses' Organisation ISSN: 1173-2032
Issue: Date: August, 2011 Source Volume: 17 Source Issue: 7
Geographic: Geographic Scope: New Zealand Geographic Code: 8NEWZ New Zealand
Accession Number: 266344847
Full Text: The control of bladder function is a fascinating interaction between the somatic and visceral motor nervous systems. Continence and micturition rely on co- ordinated activity of these systems, along with adequate skeletal muscle function, intact sensory nerve pathways and the input of higher brain centres. Disruption to nervous function by injury or drugs, or loss of muscle function, can lead to incontinence or retention.

With the ageing of the population, the occurrence of urinary incontinence and retention are expected to rise. Nurses in all professional settings will be increasingly involved in the prevention, identification, treatment and support of men and women with actual or potential incontinence or retention issues. In aged care, an understanding of the underlying causes of incontinence can assist with the management of incontinence for those patients who cannot be successfully treated.

INTRODUCTION

The International Continence Society defines urinary incontinence as any involuntary leakage of urine. (1) It is estimated that 30 percent of older adults in the community and 50 percent of those in residential care are affected by urinary incontinence. Up to the age of 80 years, incontinence affects women two times more often than mates. But over 80 years, men and women are affected equally. (2) Incontinence may cause social isolation and embarrassment. It is believed to be consistently under-reported and sufferers may take up to 10 years to seek help for their condition. (3) Incontinence is a significant risk factor for entry into residential care in older adults.

In New Zealand, 1.1 million people over the age of 15 are believed to suffer from urinary and/or faecal incontinence. The cost of this in terms of health care, incontinence products, drugs and Lost productivity is estimated at $8 billion per annum. (4)

Urinary retention is the inability to voluntarily pass urine. There may be complete lack of voiding, incomplete emptying of the bladder or overflow incontinence. (5) The most common cause of retention is obstruction due to an enlarged prostate gland, thus this condition occurs most frequently in males: more than one third of New Zealand men over the age of 60 experience moderate to severe symptoms. (6)

Nurses working in the surgical field commonly encounter post-operative urinary retention. While this is normally transient, it can increase the risk of developing urinary tract infection, detrusor dysfunction or renal damage. In addition, the discomfort associated with retention in the post-operative period can increase the need for analgesics and decrease mobilisation.

An understanding of the mechanisms controlling the storage and passing of urine allows assessment of the causes of incontinence and retention. Knowledge of these mechanisms helps the nurse provide care for clients who are experiencing incontinence from whatever source. For many sufferers, support and conservative (nonsurgical) interventions will be sufficient to treat incontinence. The role of nurses in providing these is essential For some older adults, interventions to restore continence may be inappropriate. In these situations an understanding of normal processes of micturition can assist nurses in the delivery of optimum care, reducing adverse consequences for this group of patients.

FUNCTIONAL ANATOMY OF THE LOWER URINARY TRACT

Bladder

The bladder (or urinary vesicle) is a hollow organ formed by an inner epithelial layer (the urothetium), connective tissue and the detrusor muscle. The detrusor is composed of smooth muscle fibres arranged in coarse bundles, interspersed with collagen and elastin fibres. The ureters insert into the bladder low in the posterior wall, forming a triangle with the bladder outlet called the trigone.

The bladder functions as a passive storage vesicle for urine and is very compliant. During fitting, the detrusor actively relaxes white the bladder neck remains contracted so that intravesicular pressure does not exceed outlet resistance. (7) The average bladder can comfortably hold 300-500ml of urine. A sensation of bladder fullness occurs around 200ml but the pressure generated by the detrusor muscle remains low until micturition is triggered or maximum capacity is reached.

Urethra

The urethra is composed of epithelial tissue surrounded by a thin layer of circular smooth muscle and a thicker layer of longitudinal smooth muscle. The smooth muscle forms an internal sphincter for the urethra, close to the bladder neck. In mates this is enhanced by the presence of the prostate gland. (7) An external sphincter composed of a layer of skeletal muscle ties along the tower two-thirds of the urethra. This horseshoe-shaped thick band of skeletal muscle tissue kinks the urethra when contracted. (7) The external sphincter arises from the puborectatis muscle and is mainly composed of type I fibres (stow, prolonged contractions), although composition varies with ethnicity. (8)

The epithelial layer of the urethra ties in folds that, together with secreted mucus, provide a natural watertight seat mechanism during bladder filling. The folds of epithelium "stick" to each other and are maintained by the presence of circulating oestrogen. After menopause, urethral (and vaginal) epithelium undergoes a degree of atrophy that may contribute to toss of continence. (9)

[FIGURE 1 OMITTED]

The pelvic floor

The pelvic floor supports the organs of the pelvic cavity. It is a three-layered structure composed of connective tissue fascia and pelvic floor muscles. These extend from the symphisis pubes at the front, around the sides of the bony pelvis and attach to the coccyx at the rear. (10) Contraction of these muscles results in an inward lift and squeeze around the anus, vagina and urethra. (10) The key muscles are the levator and group, made up of the pubococcygeus, iliococcygeus and puborectatis muscles. The pubococcygeus surrounds the urethra, vagina and anus and contributes to active closure of these when contracted.

An important rote of the pelvic floor in relation to continence is maintenance of the angle between the bladder and posterior urethra, which ensures that any increase in intra-abdominal pressure (eg with coughing) is transmitted equally to all sides of the urethra, as well as the bladder. The relaxation of the pelvic floor during the first stage of micturition causes complete toss of the posterior urethrovesical (PUV) angle. Pelvic floor weakness reduces the PUV angle and affects the transmission of increased intra-abdominal pressure to the urethra, contributing to stress incontinence.

NERVOUS CONTROL OF MICTURITION

Motor control in the body occurs via three pathways of the peripheral nervous system: somatic (under conscious control), and the sympathetic and parasympathetic branches of the autonomic nervous system. The urinary tract is innervated by all three motor systems which interact to maintain continence and ensure appropriate micturition.

Somatic motor inputs

Somatic fibres travel in the pudendal nerve from the sacral spinal cord to the external urethral sphincter and pelvic floor (figure 1). Stimulation of this nerve causes contraction of the sphincter and assists with the maintenance of continence. Inhibition of this somatic nerve pathway is required for normal micturition.

Parasympathetic motor inputs

Parasympathetic innervation occurs throughout the bladder watt, particularly in the dome (fig 1). Release of acetylcholine (ACh) from parasympathetic nerve endings triggers muscurinic (M) receptors on the smooth muscle of the detrusor. Binding of ACh to M3 receptors directly triggers contraction of the detrusor, white binding of ACh to M2 receptors blocks the relaxation effects of the sympathetic system (described below). Contraction of the detrusor increases intravesicular pressure above that of the outlet and micturition occurs. (11)

Adenosine triphosphate (ATP) is released from parasympathetic postganglionic fibres, as well as ACh. In a normal bladder, this secondary neurotransmitter is broken down before reaching receptors in the detrusor. For some people with overactive bladders, ATP is either released in excess or not broken down and triggers detrusor contraction, independent of ACh mechanisms. (12)

Sympathetic motor inputs

The sympathetic nerves supplying the bladder exit the spinal cord between T10-L2 (fig 1). The majority of sympathetic fibres end in the bladder neck, trigone and upper urethra. Noradrenaline acting on alpha-1 adrenoreceptors causes contraction of smooth muscle in these regions. This maintains closure of the bladder outlet during filling and also prevents reflux of urine into the ureters.

Activation of beta-2 (and possibly beta-3) adrenoreceptors in the bladder dome causes active relaxation of the detrusor during the filling phase. This increases the compliance of the bladder, allowing filling to occur without a corresponding increase in pressure. (12)

Sensory innervation and control

Sensory pathways in control of micturition arise in the suburothelial and detrusor layers of the bladder and in the bladder neck and upper urethra (fig 1). These lightly myelinated A-delta fibres transfer action potentials to the sacral and thoracolumbar spinal cord. (13)

When the uroepithelium is stretched, the cells release ATP and this triggers action potentials by binding to muscarinic and/or vanilloid receptors on the sensory nerve endings. (13) C-fibres are also present in the bladder wall and are activated by irritant stimuli or excessive stretching. (7)

Some sensory fibres travel to the thoracolumbar spine, where they may trigger sympathetic stimulation that induces relaxation of the detrusor and increased closure of the bladder outlet during the filling phase. The majority of sensory fibres travel to the S2 to S4 segments of the sacral spinal cord. Here they trigger both reflex and ascending pathways (fig 1). Spinal cord processing of signals involves a variety of neurotransmitters including ATP, endogenous opioids, and 5-hydroxytryptamine (5HT or serotonin). (8)

Ascending pathways travel up the spinal cord to the micturition centre in the pons of the brainstem and to higher centres, where the need to pass urine is interpreted and behavioural decisions made. Dopamine is a key neurotransmitter here. Conscious control of micturition occurs via action potentials sent down to the micturition centre, which co-ordinates motor activity to maintain continence or to trigger micturition, as appropriate.

There is, however, a micturition reflex that operates purely at the Level of the sacral spinal cord. This is evident where there is a spinal cord injury above the sacral level: once the initial spinal shock has resolved, fitting of the bladder results in reflex detrusor contraction and emptying. A similar reflex occurs when, during normal micturition, urine enters the bladder outlet and upper urethra: sensory signals from these areas trigger the reflex arc that stimulates further detrusor contraction, making voiding more forceful, (13) an unhelpful reflex in the presence of stress or urge incontinence.

NORMAL SEQUENCE OF MICTURITION

Inhibition or filling phase

Contraction of the external sphincter and pelvic floor muscles and sympathetic activation of the internal sphincter maintain outlet pressure higher than intravesicle pressure. At this stage, outlet pressure is around 45-65 centimetres of water (cm H20), white bladder pressure will only increase to 5-10cm H20. Parasympathetic input to the detrusor is inhibited by descending pathways from the micturition centre. (8) The bladder fills with urine. Sympathetically mediated contraction of the bladder neck prevents reflux of urine through the ureters (vesicoureteral reflux).

Once bladder volumes reach 15D-250ml, watt tension begins to increase. Sensory receptors are activated when detrusor pressure reaches about 15-20cm H20 (welt below outlet closure pressure).

This pressure will be reached more rapidly when there is reduced bladder watt compliance. Ascending sensory pathways give rise to an initial conscious sensation of bladder fullness. If socially inappropriate to urinate, the higher centres wilt signal to the micturition centre and inhibitory signals will be relayed down the spinal cord to maintain the bladder in the inhibitory phase.

Micturition or emptying phase

If micturition is possible, the micturition centre co-ordinates the change from inhibition to stimulation of detrusor activity. Parasympathetic fibres are stimulated, sympathetic and somatic activity suppressed. The pelvic floor relaxes and the PUV angle increases. Urethral closure pressure drops and detrusor pressure increases so that urine begins to flow.

As explained above, the vesicourethral reflex is stimulated as urine enters the upper urethra and detrusor contraction becomes more forceful Urine normally flows at a rate of 18ml/sec for adult females. In males, flow rate decreases with age from around 21ml/sec up to age 45, down to about 9ml/sec over the age of 65 years. A urinary flow rate of less than 10ml/sec is regarded as indicative of bladder outflow obstruction or impaired detrusor function. (14)

On completion of micturition, there is normally only a very small volume of urine remaining in the bladder. Normal residual volume is less than 50-100mL. (14)

Residual volumes greater than 180ml significantly increase the risk of developing urinary tract infection and detrusor dysfunction. (15)

PHARMACOLOGY AND MICTURITION

The key rote of neurotransmitters in micturition means that it is vulnerable to drugs that alter neurotransmission. Pharmacological adverse effects on micturition may be overlooked in the evaluation of incontinence and retention. Table 1 (p24) gives key classes of drugs and outlines their effects.

Many of the drugs in Table 1 are psychotropics or used for treatment of neurological disorders. In older adults, use of psychotropic drugs is high, particularly in tong-term care facilities. It is important to understand that these drugs may be contributing significantly to incontinence issues for this client group. (16) The effect of caffeine on continence has been Long understood, although supporting research is sparse and conflicting, (17) and the mechanisms poorly understood. However, in symptomatic women, there is evidence to suggest that decreasing caffeine intake will lead to an improvement in incontinence episodes. (18)

Duloxetine is a combined serotonin and norepinephrine re-uptake inhibitor used in Europe for treatment of incontinence. (17) It acts by suppressing parasympathetic activity during the filling phase and increasing sympathetic and somatic outputs from the spinal cord, increasing activity in the internal and external sphincters. (19) It is the only pharmacological therapy for stress incontinence but failed to gain approval for this use in the United States due to high risk of suicidality and Liver toxicity. (17) Dutoxetine is not funded in New Zealand or licensed for this use.

THE NEUROGENIC BLADDER

Injury or disruption to nerve pathways controlling micturition will have distinct effects on bladder function, depending on the location of the injury. Sensory or motor pathways between the bladder and spinal cord, ascending and descending pathways within the central nervous system, the micturition centre or higher brain centres may all be affected.

Disruption to control systems above the level of the micturition centre in the brainstem Leads to development of a spastic bladder: the person experiences frequency, urgency and urge incontinence. The filling phase of bladder function is impaired as the micturition centre operates without inhibitory control from the cerebral cortex, so small volumes of urine are voided frequently and incompletely. Stroke, Parkinson's disease, cerebral patsy or brain tumours may all cause development of these tower urinary tract symptoms. (20)

Damage to the spinal cord above the sacral spine affects spinal control pathways. There is spasticity of the bladder but spasticity may also arise in the internal and external sphincters. This condition, termed detrusorsphincter dyssynergia, can lead to retention of urine. (21)

People with multiple sclerosis may exhibit similar symptoms or may have a flaccid bladder.

Of special note is the effect of spinal cord injury above the Level of T6. Stimulation of sympathetic outflow, due to bladder distension, insertion of a urinary catheter or urinary tract infection (among other causes), can Lead to autonomic dysreflexia, evidenced by sudden onset of hypertension, sweating, headache and reflex bradycardia. This is a Life-threatening event and will usually resolve once the triggering stimulus is removed. (22)

Injury at the level of the sacral spine or to peripheral nerves supplying the bladder and sphincters may occur due to diabetes (peripheral neuropathy), Lesions of the sacral spinal cord and its nerve roots, or Lumbar disc herniation.

The bladder becomes flaccid with toss of sensation and urinary retention. Weak micturition pressure occurs with large residual volumes following voiding. Often the first symptom is Loss of bladder sensation. (21) Major pelvic surgery often results in toss of detrusor reflexes, but most patients wilt recover function spontaneously.

STRESS INCONTINENCE

Involuntary leakage of urine may be acute or chronic (see table 2). Acute causes of incontinence may also cause an increase in symptoms in a person with chronic incontinence, so a sudden onset or increase of incontinence should always be investigated.

The majority (50 percent) of chronic urinary incontinence in women is classified as stress incontinence. (3) Stress activities increase intra-abdominal pressure and this is transferred to the pelvic organs. When coughing and sneezing, the bladder wall pressure can increase as high as 150cm [H.sub.2]O. (23) In a well-supported pelvis, increases in intra-abdominal pressure are transferred equally to the bladder wail and the bladder outlet or upper urethra. If the PUV angle is displaced, pressure is not transmitted equally, causing leakage of urine.

Ageing contributes significantly to the development of stress incontinence in both men and women via a number of mechanisms: (23,24)

(1.) Loss of sex hormones (oestrogen, androgen) can cause atrophy of the urethral epithelium. This decreases the ability of the urethra to remain sealed against leakage of urine.

(2.) Benign prostatic hyperplasia in males increases risk of surgery and this can cause loss of smooth muscle function in the upper urethra.

(3.) Ageing results in loss of muscle fibres in both the external and internal urethral sphincters. They are less responsive to stimulation, slower to contract and contractions are weaker.

(4.) Composition of the pelvic floor and external sphincter is altered with ageing. The number of type I fibres (slow, sustained contractions) increases, while type II fibres (rapid, forceful contractions) decrease. The ability to counteract increases in intra-abdominal pressure with a quick tightening of the pelvic floor is reduced.

Pelvic floor injury also causes weakness and a change to the muscle fibre composition. Pregnancy and vaginal delivery (particularly prolonged labour) can cause damage to the pelvic floor. Other types of activity increase the risk of developing stress incontinence for vulnerable populations. The New Zealand Continence Association has adopted the Australian "Pelvic Floor First" approach to exercise, designed to limit increases in intra-abdominal pressure and injury to the pelvic floor. (4) Stress incontinence is amenable to conservative treatment in many instances. Conservative therapy has numerous advantages: low cost, low risk of adverse effects, client autonomy and access through primary care services. (18) With increasing incidence of urinary incontinence, cost and accessibility issues are becoming more important.

Interventions to reduce stress incontinence include: (3,10,18)

* Weight loss.

* Smoking cessation (reduced coughing).

* Avoiding constipation.

* Pre-emptive contraction of pelvic floor muscles during increases in intra-abdominal pressure (the "knack").

* Pelvic floor muscle training. Effectiveness is increased if:

--Programme supervised (at least initially) by a health professional.

--Correct contraction is confirmed.

--Basic principles of muscle training are followed (specificity, overload, progression and maintenance).

--An intense programme is followed.

--Training is sustained.

* Electrical or magnetic field stimulation of pelvic floor muscles may be effective but Lack good research support.

URGE INCONTINENCE

Urge incontinence accounts for about 11 percent of incontinence in women (a mix of urge and stress incontinence affects 36 percent). (3) Here the urge to urinate is immediately followed by involuntary loss of urine. The underlying mechanisms involve overactive detrusor muscle or poor bladder compliance. Overactive bladder (OAB) can occur without incontinence and is characterised by urgency, frequency and nocturia. (17)

Overactive detrusor arises as a consequence of numerous factors. Some of these have been described above in relation to the neurogenic bladder. (25) Drugs, including caffeine, may also cause OAB via interference with neurological controls (table 1). Outlet obstruction, eg due to enlarged prostate, will cause an increase in detrusor activity as the bladder pressure tries to overcome the blockage. Activation of other neurotransmitters such as ATP and C-fibres occurs through unknown causes. (21)

Detrusor activity increases with age. This is due to changes in neuronal activity and also to structure and function of the detrusor. Spontaneous contraction of the muscle occurs and impulses travel more readily from cell to cell, triggering uncontrolled contractions. (11,12,25) Loss of muscle tissue and its replacement by connective tissue due to ageing or injury (eg following retention) causes loss of compliance so the detrusor is less able to relax and expand during the filling phase. Urge incontinence is the most common form of incontinence in older men.

Unlike stress incontinence, urge incontinence can be treated successfully with medication. However, it is recommended treatment for urge incontinence begin with six weeks of bladder retraining before moving on to drug therapy. In care settings or for the cognitively impaired, prompted or timed voiding programmes have been demonstrated to improve continence. (3)

Drug therapy for urge incontinence is associated with adverse effects, more relapse and similar outcomes to bladder retraining. The first line drug therapy for OAB is oxybutynin, an anticholinergic drug that blocks detrusor contractility. (3)

Adverse effects of this drug include dry mouth and blurred vision. It may also cause cognitive impairment in older adults and those with Parkinson's disease. Many people discontinue use of the drug despite continued OAB because of the side effects. (26) Other anticholinergics are available but all have an adverse effect profile. For post-menopausal women, intravaginal, but not systemic, oestrogen may assist with urge incontinence by reducing urethral atrophy.

URINARY RETENTION

The inability to voluntarily pass urine can occur as an acute condition or as a painless chronic state. Retention may present as complete lack of voiding, incomplete bladder emptying or with overflow incontinence. The most common obstructive form of urinary retention is that seen with benign prostatic hyperplasia but other causes may have infectious, inflammatory, neurological or pharmacological origins. (5)

Neurological conditions that cause retention are described above in relation to neurogenic bladder. Pharmacological therapies that cause retention include anticholinergic drugs and alpha-adrenergics (see table 1). Urinary tract infections, urethritis and prostatitis may all cause retention through a combination of urethral oedema and pain. (5)

Post-operative urinary retention occurs in five to 13 percent of general surgical cases. (27) Incidence increases with epidural anaesthesia and pelvic, hip or abdominal surgery. (5) Risk of retention is increased with age, male sex, lack of pre-operative voiding, prolonged anaesthesia and use of opioid analgesics (table 1). Opioids induce retention in a dose-dependent manner; pethidine is particularly associated with post-operative urinary retention. (27)

People with post-operative urinary retention are more likely to be catheterised, have increased length of stay in hospital and are less likely to be discharged home. Retention in older adults may cause confusion and restlessness. Discomfort and pain can reduce post-operative mobilisalion and increase the need for analgesics; in turn, these may increase the incidence of post-operative complications. (27)

Consequences of urinary retention

Acute retention can cause severe pain. Over-distension of the detrusor, even for a single episode, can lead to ongoing abnormal detrusor function with further risk of retention and flaccid bladder. Chronic retention, aside from causing overflow incontinence, can cause reflux of urine through the ureters and eventually renal damage. Damage to the bladder wall may lead to the development of diverticuli and pouching. These, in turn, predispose the development of bladder calculi and infection. The need for repeated catheterisation increases the risk of urinary tract infection, urethral damage and development of strictures. (28)

NON-THERAPEUTIC INTERVENTIONS FOR INCONTINENCE

For some people, return to full continence through conservative therapy or surgery is not possible. In these cases, the aim of therapy becomes contained incontinence. (26) This should not be considered for any patient until the causes of incontinence have been thoroughly investigated and therapeutic interventions considered.

Disposable absorbent pads and pants contain cores that hold urine in a gel form and prevent skin irritation. The degree of absorption required and the size of the pad are determined by the frequency and volume of urine lost during incontinence episodes and how often the pad is changed. Reusable pads with cotton or polyester cores require more frequent changing as they are not as efficient at sequestering the urine away from the skin and cannot absorb as much volume. (29)

Frequent inspection of the skin is required to monitor for irritation and excoriation of the perineum and surrounds. Protective skin care using gentle cleansers, dimethicone or zinc oxide, should be instituted, if there is any sign of irritation or infection. (29)

Catheterisation

Intermittent catheterisation is appropriate for those with urinary retention accompanied by overflow incontinence, where the person themselves or caregivers can be trained in the technique.

Indwelling urethral catheters (IDCs) are appropriate in the following circumstances: (3)

* Chronic urinary retention where intermittent catheterisation is not appropriate.

* Where urine is causing skin irritation or contamination of wounds.

* If bed and clothing changes are causing discomfort or distress.

* Where the person requests catheterisation.

Long-term IDCs are associated with increased risk of infection. They are not recommended for urge incontinence, as the detrusor over-activity causes leakage of urine. Leakage around an IDC occurs when there is obstruction or irritation causing stimulation of the detrusor (table 3). (29)

The UK's National Institute for Health and Clinical Excellence (NICE) guidelines recommend suprapubic catheterisation over IDCs as causing fewer infections and leakage issues. However they carry separate risks and should not be considered unless in a care setting where there is knowledge and expertise available. (3)

CONCLUSION

The incidence of incontinence and retention is increasing as our population ages. Many people with incontinence issues are slow to seek help. Nurses are ideally placed to identify and address the possibility of incontinence or retention in sensitive and culturally appropriate ways. Early intervention increases quality of life and may delay or prevent entry into tong-term care for older adults.

Specialist nursing roles are recognised as increasingly important to best practice, providing support to both nurses and clients in continence care. Understanding the normal controls of micturition and the factors that interfere with these is essential to best practice in the support of clients in the community, acute care and tong-term care facilities.

LEARNING OUTCOMES

* On completion of this article and the accompanying online learning activities you should be able to:

* Describe the anatomy of the lower urinary tract, identifying key structures in maintenance of continence.

* Describe the role of the somatic and visceral nervous systems in control of continence and micturition.

* Describe the role of drugs in micturition and continence.

* Outline key risk factors for incontinence.

* Discuss the rationale for nonsurgical interventions in maintenance of continence.

* Outline factors and risks associated with retention of urine.

Georgina Casey, RN, BSc, PGDipSci, MPhil (nursing), is the director of CPD4nurses.co.nz. She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
Table 1. Classes of drugs affecting micturition

(a) = promotes micturition

(b) = promotes retention

Class of drug          Examples                   Key Effects

                       * drugs used in
                       therapeutic treat-
                       ment of incontinence
                       or retention

Cholinergics/          Muscarine (magic       (a) Stimulate muscarinic
Muscarinic agonists    mushrooms)                 receptors [right
                       Pilocarpine.               arrow] increased
                       Bethanechol *              tone and contrac-
                                                  tion of detrusor.

Anticholinesterases    Neostigmine            (a) Inhibit breakdown of
                       Organophosphate            Ach [right arrow]
                       insecticides               increased tone and
                                                  contraction of
                                                  detrusor.

Anticholinergics/      Oxybutynin *           (b) Block
Antimuscarinics        Tolterodine *              parasympathetic
                       Solifenacin *              transmission
                       Scopolamine                [right arrow]
                       Atropine                   decreased
                       Tricyclic                  contraction of
                         antidepressants          detrusor.

Beta-adrenergic        Adrenaline             (b) Activate beta-2
agonists               Salbutamol                 receptors [right
                                                  arrow] detrusor
                                                  relaxation.

Beta-adrenergic        Propanalol             (a) Block sympathetic
antagonists                                       relaxation of de-
                                                  trusor [right arrow]
                                                  decreased
                                                  compliance.

Calcium channel        Diltiazem              (b) Block smooth muscle
Mockers                Nifedipine                 contraction [right
                                                  arrow] reduced
                                                  detrusor
                                                  contractility.

Alpha-1 adrenergic     Ephedrine              (b) Activate alpha-1
agonists               Pseudoephedrine *          receptors on
                       Tricyclic                  internal sphincter
                         antidepressants *        [right arrow]
                       Amphetamines               contraction.

Alpha-1 receptor       Prazosin *             (a) Block alpha-1
antagonists            Doxazosin *                receptors [right
                       Terazosin *                arrow] re-taxation
                                                  internal sphincter
                                                  and prostate.

Skeletal muscle        Benzodiazepines        (a) Decreased tone
relaxants              Baclofen                   external sphincter.
                       Clonazepam

Dopamine antagonists   Chlorpromazine         (a) Inhibit cortical
                       Haloperidol                control of detrusor
                       Prochlorperidine           [right arrow]
                       Thioridizine               increased reflex
                                                  activity.

Dopaminergics          Levodopa/carbidopa     (b) Enhanced cortical
Dopamine agonists      Bromocriptine              inhibition

Methylxanthines        Caffeine               (a) Thought to increase
                                                  detrusoractivity
                                                  and inhibit internal
                                                  sphincter

Opioid analgesics                             (a) Inhibition
                                                  parasympathetic
                                                  trans mission
                                                  increase bladder
                                                  compliance

Table 2. Causes of urinary incontinence

ACUTE

Urinary tract infection        Bacterial
Inflammation                   Atrophic urethritis or vaginitis

Bladder outlet obstruction     Enlarged prostate
                               Constipation/ Faecal impaction
                               Pelvic organ prolapse

Increased urine production     Diuretic drugs
                               Diabetes

Cognitive impairment           Dementia or Delirium
                               Depression
                               Disorientation in new environment
                               Hypnotic, sedative or other
                               psychoactive drug therapy

Reduced mobility               Accessing toilet
                                 --Illness, surgery or injury
                                 --Gait disorder
                                 --Physical restraint
                               Removing clothing
                               Reduced night-time vision

Acute injury to pelvic floor   Vaginal delivery
                               Pelvic surgery

CHRONIC

Stress                         Pelvic floor weakness
                               Impaired internal sphincter
                               function

Urge                           Overactive detrusor muscle

Mixed

Overflow                       With retention

Table 3. factors contributing to leaking
indwelling urethral catheters

Bladder or bladder   Large catheter (>18Fr)
neck irritation      Overinflated balloon (30mL+)
                     Traction on catheter
                     Symptomatic urinary tract infection
                     CAB

Obstruction          Faecal impaction/constipation
                     Catheter kinking
                     Pelvic organ protapse
                     Bladder calculi
                     Catheter encrustation
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