Urinary and Bowel Complications After Stroke

 

Recommendations

Acute phase

A. All wards and stroke units should have established assessment and management protocols for both urinary and faecal incontinence, and for constipation in stroke patients

B. Patients should not have an indwelling [urethral] catheter inserted unless indicated to relieve urinary retention or where fluid balance is critical

Rehabilitation phase

A. All wards and stroke units should have established assessment and management protocols for both urinary and faecal incontinence, and for constipation in stroke patients

B. Patients with stroke who have continued loss of bladder control 2 weeks after diagnosis should be reassessed to identify the cause of incontinence and have an ongoing treatment plan involving both patients and carers. The patient should:

 Have any identified causes of incontinence treated

 Have an active plan of management documented

 Be offered simple treatments such as bladder retraining, pelvic floor exercises, and external equipment first

 Only be discharged with continuing incontinence after the carer [family member] or patient has been fully trained in its management and adequate arrangements for a continuing supply of continence aids and services are confirmed and in place

C. All stroke patients with a persistent loss of control over their bowels should:

 Be assessed for other causes of incontinence, which should be treated if identified

 Have a documented, active plan of management

 Be referred for specialist treatments if the patient is able to participate in treatments only be discharged with continuing incontinence after the carer [family member] or patient has been fully trained in its management and adequate arrangements for a continuing supply of continence aids and services are confirmed and in place

D. Stroke patients with troublesome constipation should:

 Have a prescribed drug review to minimise use of constipating drugs

 Be given advice on diet, fluid intake, and exercise

 Be offered oral laxatives

 Be offered rectal laxatives only if severe problems remain


Adapted from Intercollegiate Stroke Working Party [1]



The National Sentinel Stroke Clinical Audit 2010 [2] found that only 63 % of stroke patients with persistent bowel and bladder complaints had a documented plan to promote continence. The audit also revealed the inappropriate use of urinary catheterisation in acute stroke patients: 20 % of patients were catheterised in the first week following stroke, and in 10 % of these cases there was no clear rationale for the insertion. These results demonstrate a failure by healthcare professionals to adequately assess and manage a significant number of stroke patients with continence problems. This may be the consequence of multiple factors such as inadequate education on bowel and bladder management amongst nurses and doctors, nursing staff shortages, time constraints, inadequate toilet facilities, and a lack of moving and handling aids. It is vital that these factors are acknowledged as barriers to providing good continence care and are adequately addressed to improve the quality of care provided.



Post-stroke Urinary Incontinence



Epidemiology


The International Continence Society has attempted to standardise the terminology of lower urinary tract dysfunction. It has established the definition of urinary incontinence as “the involuntary loss of urine that is a social or hygienic problem”, which has been further subdivided according to the patient’s symptoms [3]. This terminology has been universally accepted for use in international consultation documents and National Institute for Health and Care Excellence (NICE) guidelines [3, 4].

It is widely recognised that post-stroke urinary incontinence is common, but there is considerable variation in the reported prevalence rates; this is due to several factors:

1.

The use of different definitions of urinary incontinence

 

2.

Different population samples (hospital versus community)

 

3.

Measurement of prevalence at varying time intervals following acute stroke (at admission, 1 week, 1 year)

 

4.

Different study designs

 

5.

Failures to account for the presence of premorbid incontinence

 

In a review of nine hospital-based studies published between 1985 and 1997, Brittain et al. reported rates of post-stroke urinary incontinence at admission between 32 % and 79 % of patients [5]. In a population-based study conducted in 2001, Patel et al. found rates of post-stroke urinary incontinence of 40 % at 7–10 days following admission [6]. Data from the UK collected between 1998 and 2004 have also demonstrated urinary incontinence rates of 39–44 % at 1 week post-admission [7].

Comparatively, epidemiological trials such as the Leicestershire MRC Incontinence Study found that 34.2 % of adults over the age of 40 had urinary incontinence at times, with severity increasing with age [8]. This suggests that many stroke patients may have already experienced bladder problems prior to their stroke.


Natural History of Post-stroke Urinary Incontinence


Post-stroke urinary incontinence is a persistent condition, with significant numbers of patients remaining incontinent at discharge [6, 9]. Patel et al. explored the natural history of post-stroke urinary incontinence in 235 patients over a 2-year period [6]. Data for this study was acquired from the South London Stroke Register, a population-based register covering a population of over 230,000. Follow-up data was obtained using personal interviews with patients and their carers and through postal questionnaires [10]. The study reported urinary incontinence prevalence rates of 19 % at 3 months, 15 % at 1 year, and 10 % at 2 years [6]. Three further studies have demonstrated the persistence of urinary incontinence at 1 year, reporting prevalence rates ranging from 9 to 27 % [1113]. Although all of these studies excluded patients with premorbid bladder problems, the definitions of urinary incontinence and assessment methods varied, which may account for the variation in prevalence rates reported.

Certain factors have been identified as independent predictors of persistent post-stroke urinary incontinence [1317]:

1.

Increasing age

 

2.

Female sex

 

3.

Stroke severity and size

 

Patients suffering from total anterior circulation infarcts were found to be less likely to regain continence at 3 months. Comparatively, patients who suffered a lacunar infarct had an odds ratio of 3.65 [95 %, CI: 1.1–12.2] for regaining continence [14]. These finding were supported by a prospective study investigating the association of bladder function with unilateral hemispheric stroke [15], which identified a significant positive correlation between large infarct size and the development of post-stroke urinary incontinence. The authors of this study concluded that such infarcts involving both cortical and subcortical regions of the brain were more likely to result in damage to neuro-micturition pathways (spinothalamic) and result in communication difficulties, both directly and indirectly contributing to incontinence.

Currently, there is no data to support a correlation between either the location of the stroke lesion or the aetiology of the stroke (haemorrhagic versus ischaemic) and the development of urinary incontinence, and further research is required in this area.


Effects of Urinary Incontinence on Stroke Outcomes


It is widely recognised that urinary incontinence following stroke is a strong and independent predictor of poor outcome [6, 11, 12, 14, 18, 19]. Persistent urinary incontinence at 3 months following stroke has been reported to be the single best predictor of moderate to severe disability in patients under the age of 75 [20]. A prospective observational study of 324 patients was conducted in 2001 investigating the impact of persistent urinary incontinence at 3 months on stroke outcome [14]. On multiple logistic regression analysis, persistent post-stroke urinary incontinence was independently associated with a greater rate of institutionalisation of 27 % compared to 9 % in the group who regained continence. They also investigated the impact on post-stroke disability using the Barthel Index and the Frenchay Activities Index [FAI] and found disability to be significantly worse in those patients who remained incontinent at 3 months. Another population-based study reported even higher rates of institutionalisation—45 % at 1 year, which was four times greater than in those who regained continence [11].

Post-stroke urinary incontinence is also independently associated with higher mortality rates [12, 21]. A study in 2011 reported significantly higher mortality rates in the incontinent group at time intervals of 1 week, 6 months, and 1 year [12]. The authors highlighted that regaining continence within the first week following stroke was associated with a better prognosis, which was similar to those with normal bladder control.

There are many reasons why persistent urinary incontinence is associated with worse outcomes:

1.

Interference with the ability to participate in stroke rehabilitation. Physical and psychological factors may impact on the patient’s ability to participate in rehabilitation [22]. Urinary incontinence may lead to low morale and poor self-esteem, resulting in apathy and a reduced desire to participate in rehab. Stroke patients who have a poor response to rehabilitation are more likely to have a poor functional outcome, increased length of hospitalisation, and a greater mortality rate [22, 23].

 

2.

Psychological impact. Urinary incontinence may be extremely distressing for both the patient and their carer. This condition may result in a significant impact on the patient’s quality of life, interfering with social activities, sleep patterns, and personal relationships, resulting in feelings of embarrassment and guilt. On multivariate analysis, Brittain et al. demonstrated that depression after stroke was more than twice as likely in patients suffering from incontinence compared to those without bladder problems [24].

 

3.

Marker of stroke severity. Persistent urinary incontinence is associated with larger strokes and has been related to coma states [14, 25]. Extensive brain damage may impair toileting skills due to altered sensorium.

 

4.

Increased risk of falls. Patients suffering from urge incontinence may attempt to ambulate to the bathroom in a rush, and this has been associated with an increased risk of falls, which may lead to fractures and subsequent increased hospitalisation [26].

 

Pre-existing urinary incontinence has also been associated with poor outcomes following stroke. Studies analysing this relationship have found higher mortality rates amongst this group. Jawad et al. reported that 79 % of patients who died prior to their 6-month functional review suffered from premorbid urinary incontinence [27]. Similar findings were demonstrated in another study, which reported that of the 16 patients with pre-existing incontinence, 19 % died within the first week, 44 % died within 3 months, and 25 % died within 2 years [7].


Neural Control of Micturition


In order to determine the cause of urinary incontinence following a stroke, it is important to consider the factors controlling normal micturition. Complex neural mechanisms located in the brain, spinal cord, and peripheral ganglia are responsible for ensuring bladder filling and voiding occurs in a coordinated manner [28]. These mechanisms control smooth and striated muscle activity of the following anatomical structures:



  • Urinary bladder and bladder neck


  • Urethra


  • Urethral sphincter


  • Pelvic floor muscles

Figure 8.1 illustrates the different structures and neural mechanisms involved. The spinobulbospinal pathway mediates the voiding reflex and it is believed that this reflex operates as a switch, being either completely “off” during bladder filling or “on” during voiding [28, 29].

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Fig. 8.1
The neural control of micturition (From Mehdi et al. [80]. © 2013 John Wiley & Sons Ltd. With permission from John Wiley and Sons)


Bladder-Filling Cycle


During the filling cycle, stretch receptors within the bladder detrusor muscle signal low intensity afferent impulses to the spinal cord via the pelvic nerves (S2–S4) and then via the spinal cord (lateral spinothalamic tracts) to the pontine micturition centre and the frontal cortex. This results in three processes:

1.

Inhibition of the parasympathetic innervation of the detrusor muscle of the bladder via the pelvic nerves, resulting in bladder relaxation.

 

2.

Stimulation of the sympathetic outflow in the hypogastric nerve, resulting in contraction of the bladder outlet (bladder neck and urethra).

 

3.

Stimulation of the sympathetic outflow in the pudendal nerve via neurons in the Onuf’s nucleus, resulting in contraction of the external urethral sphincter.

 

These spinal reflexes are collectively known as the “guarding reflex” allowing one to remain continent. Furthermore, several studies have suggested that a region within the lateral pons of the brain known as the “pontine storage area” may contribute to this process by stimulating striated urethral sphincter activity [2830].


Bladder-Voiding Cycle


The bladder is usually able to hold approximately 500 ml of urine before needing to empty. At a critical level of bladder distention, the afferent impulses in the pelvic nerves intensify to the spinal cord, switching the spinobulbospinal pathway to maximal activity [28]. These signals are relayed from the spinal cord to the pontine micturition centre of the brain via the periaqueductal grey. Activation of the pontine micturition centre results in the following:

1.

Inhibition of sympathetic outflow in the hypogastric and pudendal nerves, resulting in bladder outlet and urethral sphincter relaxation.

 

2.

Stimulation of parasympathetic outflow to the bladder, resulting in detrusor muscle contraction.

 


Voluntary Control


Voluntary voiding is under strict control from higher brain centres, which have been identified using functional magnetic resonance imaging. These include the prefrontal cortex—in particular the right inferior prefrontal gyrus—the anterior cingulate cortex, the thalamus, the caudal hypothalamus, and the insula [28, 30]. The periaqueductal grey plays a pivotal role in relaying signals to and from these higher brain centres to control primary input into the pontine micturition centre. This process ensures that voiding only takes place when it is considered to be socially desirable to do so and effectively suppressed at all other times [2831].


Types of Post-stroke Urinary Incontinence


Several different processes may account for the development of post-stroke urinary incontinence. Figure 8.2 illustrates the various types of urinary incontinence that may occur following a stroke.

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Fig. 8.2
Schematic diagram representing the causes and types of post-stroke urinary incontinence (From Mehdi et al. [80]. © 2013 John Wiley & Sons Ltd. With permission from John Wiley and Sons)


Direct Damage to the Neuromicturition Pathways: Urge Incontinence


This is the most frequently reported cause of post-stroke urinary incontinence [15, 32, 33]. The stroke lesion itself may directly disrupt the neuromicturition pathways within the brain, resulting in uninhibited detrusor contractions. The consequence of detrusor overactivity is often a sudden urge to void that is difficult to postpone, and subsequently may result in the involuntary leakage of urine. The strength of the contractions will determine the degree of urinary leakage, with stronger ones resulting in complete bladder emptying. Conversely, weaker contractions lead to frequent small-volume leakages and ineffective bladder emptying, which results in large residual volumes of urine [>100 ml]. Thus, patients with urge incontinence also complain of symptoms of urinary frequency and nocturia [33]. Detrusor overactivity is also referred to as detrusor hyper-reflexia and can be demonstrated using urodynamic studies; however, this investigation is not routinely required. Studies using urodynamic evaluation of stroke patients have reported a wide variation in prevalence rates of this condition, ranging from 37 to 90 % [15, 34, 35]. There is inconclusive data associating the site of the stroke lesion and the development of urge incontinence; however, lesions in the frontal lobe have been suggested [34, 36].


Detrusor Hyporeflexia with Overflow Incontinence


This type of post-stroke incontinence has been reported in various studies, with prevalence rates ranging from 21 % to 35 % [15, 17, 32, 37]. It has been postulated that detrusor hyporeflexia may occur after an acute stroke because of an initial loss of bladder tone. However, in most of these studies, non-stroke factors were also present such as use of anticholinergic medications or diabetic polyneuropathy, which can affect bladder tone and result in overflow incontinence [15]. Detrusor hyporeflexia results in the incomplete bladder emptying, resulting in large post-void residual urine volumes (>100 ml) and subsequent symptoms of dribbling and/or continuous leakage of urine. The resultant urinary retention may occur acutely, and is usually very painful, or it may be chronic, developing over a longer period of time, in which case it is usually painless. In all cases of urinary retention, constipation must be excluded as a causative factor.


Impaired-Awareness Urinary Incontinence


A few prospective hospital-based trials have explored the concept of impaired awareness of urinary incontinence in acute stroke patients [36, 38, 39]. This type of incontinence has been defined as “Urinary incontinence with reduced ability to be aware of bladder signals before leakage, to take notice of eventual leakage, or both” [39]. In a cohort of 65 patients, more than half were found to have impaired awareness of their symptoms, ranging from slight unawareness to anosognosia. The authors reported that this type of incontinence appeared to be an independent risk factor for poor outcome both at 3 months and 1 year following stroke [38, 39]. When compared to patients with urge incontinence, it was found that those with impaired awareness had a greater frequency of parietal stroke lesions and, less frequently, frontal lesions. This finding was consistent with the known role of the parietal and temporal lobes in correctly identifying and validating signals in a given social circumstance, compared to the volitional role of the frontal lobe structures in the conscious recognition of afferent bladder signals.


Functional Incontinence


Stroke-related factors, such as cognitive, communicative, or mobility difficulties, may impact indirectly on the patient’s ability to maintain effective toileting skills despite normal bladder function [5, 7, 15]. The resulting “functional” incontinence has been significantly associated with aphasia and/or cognitive impairment [15]. In another study, the following stroke-related factors were reported on multivariate analysis to be significantly associated with initial urinary incontinence: visual field defects, dysphagia, motor weakness, and age over 75 years.


Stress Incontinence


This type of incontinence does not occur as a direct consequence of stroke; however, stroke-related factors might aggravate a pre-existing condition. Stress incontinence occurs upon exertion (standing, coughing, and sneezing) and it is primarily the consequence of weakness of the pelvic floor muscles [4]. Reduced pelvic muscle tone and motor weakness resulting from an acute stroke can lead to greater exertional efforts in toileting, exacerbating pre-existing stress incontinence. Acute stroke can also be complicated by aspiration pneumonia, and the resulting cough may also aggravate this type of incontinence [40].


Transient Causes of Urinary Incontinence


These transient causes are potentially reversible and, if present, it is imperative that they are adequately addressed. The pneumonic “DIAPPERS” illustrates these causes [41]:



  • Delirium


  • Infection—urinary tract or chest infections


  • Atrophic urethritis/vaginitis—thin, sore skin may be contributing to the incontinence


  • Pharmaceuticals—antimuscarinics, diuretics, sedatives


  • Psychiatric


  • Excess urine output—large fluid intake, caffeinated drinks


  • Restricted mobility—arthritis pains, fear of falling


  • Stool impaction


Assessment of Post-stroke Urinary Incontinence



Initial Assessment at Admission


All stroke units should have an agreed protocol for the assessment of urinary incontinence. Firstly, all patients admitted to hospital following an acute stroke should undergo a basic assessment of their bladder function to identify any problems. This initial assessment can be carried out by nursing staff and should include a urine dipstick to identify the presence of a urinary tract infection. If bladder problems are identified, then a full continence assessment should be undertaken to identify the type of urinary incontinence and any contributing factors.


Comprehensive Assessment of Continence


This should be undertaken as soon a bladder problem such as urinary incontinence is identified. It is important to appreciate that this is a personal assessment regarding a potentially sensitive topic, which requires both time and privacy. Although there are very few studies evaluating the different assessment processes used, Table 8.2 outlines a framework for the assessment of urinary incontinence. This assessment should guide the development of a suitable treatment strategy tailored to the individual patient’s needs.


Table 8.2
Assessment strategy to identify and evaluate post-stroke urinary incontinence









































Assessment

Rationale

Basic nursing assessment within 24 h of admission

To identify those patients who are incontinent of urine

History taking

Onset and duration of symptoms? Urgency? Dribbling?

Are symptoms related to a specific activity? e.g. coughing, sneezing

Pre-existing incontinence?

Associated bowel symptoms?

Medications (diuretics, anticholinergics, oestrogens, sedatives, antidepressants)

Fluid intake?

Medical history—diabetes, recurrent urinary tract infections, and dementia

Cognitive abilities?

Functional capacity: dexterity, mobility, and aids

Effect on quality of life?

To determine the type of urinary incontinence

To plan appropriate management strategies

To determine problems caused by UI and/or contributing to it

Clinical assessment

Clinical examination: neurological and abdominal examination, rectal and pelvic examinations

Urinary frequency and volume charting for 5–7 days

Fluid intake charting

Bowel chart

To assess for a palpable bladder suggestive of urinary retention, constipation and/or any prolapse, atrophy, or signs of infection

To assess current pattern of voiding and bladder capacity

To determine if symptoms are worse at particular times of the day—to plan schedule for prompted voiding

To assess number and types of drinks

To assess for constipation

Functional capacity of toilet skills [17]

To assess ability to get to a toilet or request for help

To assess ability to manage clothing and maintain appropriate posture to allow micturition

Initial Investigations

Urinalysis

Post-void residual volumes using a bladder scanner

Evidence of urinary tract infection

Evidence of incomplete emptying and urinary retention

Transient causes of UI

Pneumonic: DIAPPERS [58]

Delirium

Infection

Atrophic urethritis/vaginitis

Pharmaceuticals

Psychiatric

Excess urine output

Restricted mobility

Stool impaction

To identify and address any reversible causes

Consideration of non-neurological causes of UI

Consider causes such as chronic chest infections leading to continual strain on the urethral sphincter due to coughing, or polyuria in diabetes, for example


Reprinted from Mehdi et al. [80]. © 2013 John Wiley & Sons Ltd. With permission from John Wiley and Sons


Detailed Bladder History


Table 8.2 illustrates the key components of the clinical history, which must be ascertained in all patients with urinary incontinence. It is essential to establish whether there were any pre-existing bladder problems prior to the stroke. Any previous gynaecological or urological procedures undertaken must also be noted, as they may impact on the current bladder complaints. Co-existing conditions such as diabetes, multiple sclerosis, spinal injuries, and dementia may also contribute to urinary incontinence. A full medication history must also be sought, as several drugs have been associated with bladder problems, including the following: antimuscarinic agents (urinary retention and constipation), diuretics (polyuria), sedatives (mobility problems and confusion), calcium channel antagonists (urinary retention and constipation), opiates (urinary retention, constipation, confusion, and reduced mobility), and cholinesterase inhibitors (increase bladder contractility). In addition to the questions outlined in Table 8.2, specific bladder-related questions should be included in the history to identify the presence of the following symptoms:



  • Urgency: is there an insuppressible desire to void and difficulties reaching the toilet in time?


  • Frequency: how often does the patient need to urinate in a period of 24 h?


  • Nocturia: how often does the patient need to urinate overnight?


  • Hesitancy: is there any difficulties initiating urine flow?


  • Poor stream: is the flow of urine weak and slow or intermittent?


  • Straining: does the patient need to strain to empty their bladder?


  • Symptoms of incomplete bladder emptying: any dribbling of urine or a continuous leakage?


  • Dysuria: any pain on passing urine?


  • Leakage of urine on exertion: any incontinence upon coughing, sneezing, laughing?

These questions will help to determine the type of urinary incontinence, the severity, and pattern of the symptoms and will enable the healthcare professional to plan an appropriate treatment strategy.

Finally, social and environmental factors must also be assessed, although this could be done in the latter stages of the patient’s admission, closer to the time of discharge. These factors include the impact of incontinence on the patient’s social activities, work life, and sexual relationships.


Clinical Assessment


Clinical assessment of a patient with urinary incontinence should include the following:

1.

Abdominal examination: to assess for the presence of a palpable bladder, indicating urinary retention, masses, and relevant surgical scars.

 

2.

Neurological examination: to assess the severity of functional impairment resulting from the stroke and how this will impact on the patient’s toileting abilities.

 

3.

Pelvic examination: to assess for the presence of any vaginal prolapse, the general skin condition of the groin/perineum, and the presence of any atrophy.

 

4.

Rectal examination: to assess for faecal loading suggesting constipation, which may contribute to incomplete bladder emptying and subsequent urinary retention.

 


Functional Assessment of Toileting Skills


A patient’s ability to actually use a toilet may be affected by stroke, and therefore an evaluation of this is imperative as part of the continence assessment. Both physical and cognitive difficulties may contribute, and these should be formally assessed using validated standardised tests such as the Mini Mental State Examination [42]. Key components of this assessment should include the following information:



  • Ability to physically mobilise to and locate the toilet or use hand-held urinals


  • Ability or motivation to request for assistance to use the toilet if this is required


  • Ability to independently remove clothing once toilet is reached


  • Ability to maintain an appropriate posture to allow micturition to occur


Frequency and Volume Charting (Bladder Diaries)


This assessment method is very important for all patients suffering from urinary incontinence. It involves recording the frequency and volume of all fluid intake and of all urine output over a minimum of 3 days. The optimum duration that a bladder diary should be kept is unclear from clinical studies; however, this assessment method is useful in determining the best schedule for bladder training strategies [4]. The chart should inform the healthcare professional regarding the following:
Jun 27, 2017 | Posted by in NEUROLOGY | Comments Off on Urinary and Bowel Complications After Stroke

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