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Neurogenic Bladder

  3. 3. INTRODUCTION • Attracting considerable interest in neurorehabilitation practice • importance of this problem to patients’ health and quality of life is now recognized • Bladder symptoms are common and distressing but also potentially amenable to treatment.
  4. 4. THE BLADDER IN HEALTH AND NEUROLOGICAL DISEASE • two roles: storage of urine and voiding at appropriate times • a complex neural control system acts like a switching circuit to maintain a reciprocal relationship between the reservoir function of the bladder and sphincteric function of the urethra
  5. 5. • PMC controls this system and it in turn receives input from higher centers, particularly the medial aspects of the frontal lobes. • Disruption of the spino-bulbo-spinal micturition pathway results in impaired storage and voiding.
  6. 6. Efferent pathways of the lower urinary tract
  7. 7. Storage Dysfunction • results from lesions affecting the spinal or suprapontine micturition pathways • resultsin symptoms such as frequency, urgency, and urgency incontinence
  8. 8. Voiding Dysfunction • typically seen in patients with spinal cord lesions • symptoms such as hesitancy, straining, slow and interrupted stream, or urinary retention
  9. 9. Detrusor Sphincter Dyssynergia • characterized by simultaneous contraction of the external urethral sphincter and detrusor • loss of coordinated activity • void within minutes of having supposedly emptied their bladder (double voiding)
  10. 10. CLASSIFICATIONS • Several classification systems have been proposed to better distinguish types of neurogenic LUTD • Bradley loop classification - Described in 1982, organizes the types of neurogenic bladder by level of injury to different “loops” in the neurologic control mechanism
  11. 11. • Current classifications have been based on • Neurourologic - Bors-Comarr, Hald and Bradley, Gibbons • Functional - Wein • Urodynamic – Lapides, Krane and Siroky, Chancellor and Blaivas • Combination of bladder and urethral function based on urodynamics - International Continence Society
  12. 12. Neuro-Urologic Classifications • Bors and Comarr Classification (1971) –SENSORY NEURON LESION –MOTOR NEURON LESION –LMN NEURON LESION –MIXED LESION • Gibbons classification (1976) –Suprasacral –Sacral: Motor / sensory / Mixed
  13. 13. Urodynamic Classifications • Lapides classification (1970) – Sensory neurogenic bladder – Motor paralytic bladder – Autonomous neurogenic bladder – Uninhibited neurogenic bladder – Reflex neurogenic bladder
  17. 17. Incontinence In The Neurologicalpatient • Multifactorial • Neurological lesion affecting bladder control - detrusor overactivity • Behavioural and cognitive impairment - memory loss, apraxia, visuospatial disorientation, language dysfunction, loss of social inhibitions
  18. 18. • Urological causes - bladder outlet obstruction, urinary tract infection, genuine stress incontinence • Functional incontinence - reduced mobility, poor toilet access • Medication-induced
  19. 19. Transient Causes of Urinary Incontinence “DIAPPERS” • D - delirium • I - infection (asymp. UTI does not cause UI) • A - atrophic urethritis or vaginitis • P - pharmaceuticals • P - psychologic factors (depression, etc) • E - endocrine disorders, excess urine output • R - restricted mobility • S - stool impaction NEJM 1989;320:1
  20. 20. Suprapontine causes • Stroke • Traumatic brain injury • Degeneration: Parkinson disease, Alzheimer disease, dementia with Lewy bodies • Hydrocephalus, normal pressure hydrocephalus • Cerebral palsy • Neoplasm
  21. 21. Infrapontine–suprasacral causes • Demyelination: multiple sclerosis, transverse myelitis, NMOSD • Trauma - SCI • Vascular: arteriovenous malformations, spinal cord infarction • Neoplasm: metastasis, primary • Hereditary: hereditary spastic paraparesis • Infections: tropical spastic paraparesis (HTLV- I)
  22. 22. Infrasacral causes • Spina bifida • Intervertebral disk prolapse • Arachnoiditis • Diabetes mellitus • Pelvic surgery and nerve injury
  23. 23. EVALUATION
  24. 24. History-taking • History-taking forms the cornerstone of evaluation • should assess both the storage and voiding phases of micturition • important also to enquire about bowel, gynaecological and sexual functions as they often coexist • Medication history should be reviewed – opiates, anticholinergic properties (eg, antipsychotic drugs, antidepressant ) and α-adrenoceptor agonists
  25. 25. • storage dysfunction - frequency for micturition, nocturia, urgency and urgency incontinence. • Urgency, frequency and nocturia, with or without incontinence - called the overactive bladder syndrome, urge syndrome or urgency- frequency syndrome
  26. 26. • voiding dysfunction - hesitancy for micturition, a slow and interrupted urinary stream, the need to strain to pass urine, and double voiding, complete urinary retention • functional incontinence - inability to reach the toilet in a timely manner due to their neurological deficits or to poor toilet accessibility
  27. 27. Bladder Diary • supplements the history taking • records the frequency for micturition, volumes voided, episodes of incontinence, and fluid intake over the course of a few days • provides a realtime objective patient-reported measure of LUT symptoms, which might not be obtained through history taking or questionnaires
  28. 28. Physical Examination • critical in deciding whether a patient’s urogenital complaints are neurological in origin • bladder disturbances generally have been shown to correlate with lower limb deficits • Exceptions - lesions of the conus medullaris and cauda equina, where findings may be confined to saddle anesthesia and absence of sacral cord mediated reflexes such as the anal reflex or bulbocavernosus reflex
  29. 29. Physical Examination • CNS – e/o paraparesis, impaired DTR in lower limbs, peripheral neuropathy, assess urogenital sensations, sacral cord mediated reflexes (bulbocavernosus reflex, anal reflex), • inspection of the lumbosacral spine • L/E – bladder distention, suprapubic tenderness in overflow incontinence • P/R – prostate, impacted stool, anal sphincter tone and squeeze response • Functional assessment of mobility to go to toilet and dexterity to remove clothes
  30. 30. Laboratory evaluation • Urine routine , Urine culture and sensitivity – screening for UTI’s • RFT’s, Uric acid • Serum electrolytes • Input-Output chart
  31. 31. Bladder Scan - PVR • extent of incomplete bladder emptying cannot be predicted from history or clinical examination • pertinent to estimate the PVR • Ultrasonography - portable bladder scanner • Catheterization - “in-out” catheterization, especially in patients who perform intermittent self-catheterization
  32. 32. • Done within 5 min of intentional voiding • >100ml is significant • single measurement often not representative and if possible, a series of measurements should be made over the course of 1 or 2 weeks • raised PVR volume – voiding dysfunction, however, it cannot be used to discern whether this is caused by poor detrusor contractility or by obstruction, for which urodynamics would be required
  33. 33. Ultrasound Scan • patients known to be at risk of upper tract disease • performed periodically (at least every 6 months) to evaluate for evidence of damage such as upper urinary tract dilatation or renal scarring. • also detect complications of neurogenic bladder dysfunction such as bladder stones.
  34. 34. • Bladder/detrusor wall thickness and ultrasound estimated bladder weight are being investigated as noninvasive alternatives to assess neurogenic LUT dysfunction • but are not yet established diagnostic options
  35. 35. Urodynamic Studies • examine the function of the lower urinary tract • divided into noninvasive investigations and those requiring urethral catheterization
  36. 36. Noninvasive Bladder Investigations Uroflowmetry • is a valuable, noninvasive investigation to detect voiding dysfunction • combined with an ultrasound measurement of the PVR • should be done before any treatment and can be used to monitor treatment outcomes • important that the patient performs the test with a comfortably full bladder, containing if possible a volume of at least 150 mL
  37. 37. • privacy is essential and a spurious result may be obtained if the subject is not fully relaxed • significant neurogenic bladder disorder is unlikely if a patient has good bladder capacity and normal urine flow rate, and empties to completion
  38. 38. Disadvantage • flow rate and PVR volume depend on both detrusor function and bladder outlet resistance • uroflowmetry is unable to discriminate between the underlying mechanisms
  40. 40. Cystometry • evaluates the pressure–volume relationship during nonphysiological filling of the bladder and during voiding • detrusor overactivity - main abnormality sought during filling cystometry • characterized by involuntary detrusor contractions, which may be spontaneous or provoked
  41. 41. Urodynamics Lab
  42. 42. Filling cystometry demonstrating detrusor overactivity
  43. 43. Videocystometry • cystometry is carried out using a contrast filling medium and the procedure visualized radiographically • gives additional information about morphological changes that are consequent to neurogenic bladder dysfunction in the presence of vesicoureteric reflux • opportunity to inspect the outflow tract during voiding is of great value in patients with suspected obstruction
  44. 44. • valuable in demonstrating the underlying pathophysiology of a patient’s urinary tract • provides information about the safety and efficiency of bladder filling and emptying • valuable for assessing risk factors for upper urinary tract damage and planning management • helpful in identifying concomitant urological conditions such as bladder outflow obstruction or stress incontinence
  45. 45. Indications • spinal cord injury, spina bifida, and advanced MS should undergo complete urodynamic study • significant risk of upper tract involvement and renal impairment • Valuable for demonstrating the underlying pathophysiology of LUTD, detecting risk factors for upper urinary tract damage(high detrusor pressures) and planning management
  46. 46. • Other conditions such as early MS, stroke, and PD - some authors have recommended to restrict the initial evaluation to noninvasive tests • risk for upper urinary tract damage is less
  47. 47. Urethral pressure profile • measured using a catheter mounted transducer that is run slowly through the urethra by a motorized armature • can be performed in men or women • found to be helpful in the assessment of women with obstructed voiding or urinary retention, some of whom have abnormally high urethral pressures
  48. 48. Overactive bladder Pdet cmH2O 0 50 100 150 Pves cmH2O 0 50 100 150 Pabd cmH2O 0 50 100 150 Qura ml/s 0 5 10 15 Uro - Voiding Cystometry#1 20 s 00:00 00:40 01:20 02:00 02:40 03:20 04:00 75 leak2 82 ST c CC CB1 VB MP MF VE
  49. 49. Sphincter Dyssynergia Pdet cmH2O 0 30 60 90 120 150 180 210 Pves cmH2O 0 30 60 Pabd cmH2O 0 30 60 Qura ml/s 0 5 10 EMG uV 0 10 20 Uro - Voiding Cystometry#2 10 s 09:04 09:24 09:44 10:04 10:24 MP MF VE
  51. 51. Pelvic floor Electromyography • first introduced for assessing the extent of relaxation of the urethral sphincter during voiding, with the aim of recognizing detrusor– sphincter dyssynergia • now rarely recorded • technically difficult to obtain a good quality EMG signal from urethral sphincter
  52. 52. • evaluation of men with suspected dysfunctional voiding • Recording electrical silence from the urethral sphincter during voiding would exonerate the external sphincter as the cause of voiding dysfunction
  53. 53. Sphincter EMG • demonstrate changes of reinnervation in the urethral or anal sphincter in neurogenic disorders • Diagnosis of MSA - anterior horn cells in the Onuf nucleus are selectively lost, results in changes in the sphincter muscles that can be identified by EMG
  54. 54. • Evaluation of Suspected Cauda Equina Lesions - investigating innervation of the sacral second, third, and fourth nerve roots • Investigation of Urinary Retention in Young Women - Fowler syndrome ,characteristic abnormality on urethral sphincter EMG, consisting of complex repetitive discharges, akin to the “sound of helicopters” and decelerating bursts, akin to the “sound of underwater recording of whales.”
  55. 55. Pudendal Somatosensory Evoked Potentials. • recorded from the scalp following electrical stimulation of the dorsal nerve of penis or clitoral nerve • abnormal when a spinal cord lesion is the cause of sacral sensory loss or neurogenic detrusor overactivity
  56. 56. Pudendal Nerve Terminal Motor Latency (PNTML). • only test of motor conduction for the pelvic floor • stimulated either per rectally or vaginally using the St Mark electrode, records from the external anal sphincter • Prolongation was initially considered evidence for pudendal nerve damage • This test has not proved contributory in the investigation of patients with suspected pudendal neuralgia.
  57. 57. Penilo-Cavernosus Reflex. • formally known as the “bulbo cavernosus” reflex • assesses the sacral root afferent and efferent pathways • dorsal nerve of penis (or clitoris) is electrically stimulated and recordings are made from the bulbo cavernosus muscle • of value in patients with bladder dysfunction suspected to be secondary to cauda equina damage or damage to the lower motor neuron pathway
  59. 59. • Lesions of the nervous system result in characteristic patterns of bladder dysfunction, depending upon the level of the lesions in the neurological axis • storage function - affected following suprapontine or infrapontine/suprasacral lesions • voiding function - affected by infrapontine lesions
  60. 60. Suprapontine lesions • detrusor overactivity and storage dysfunction • Patients present with urgency, frequency, nocturia and urgency incontinence (collectively known as overactive bladder symptoms)
  61. 61. Infrasacral lesions • reduced detrusor contractility and voiding dysfunction, nonrelaxing urethral sphincters • patients present with hesitancy, slow and interrupted stream, feeling of incomplete emptying, and are often in retention
  62. 62. Infrapontine–suprasacral lesions • resulting in both storage and voiding dysfunction • detrusor overactivity and detrusor sphincter dyssynergia (simultaneous contraction of the external urethral sphincter and detrusor muscle) • results in incomplete bladder emptying and abnormally high bladder pressures
  63. 63. Patterns of LUTD following neurological disease
  64. 64. Diagnostic Findings in Patients with Suspected Neurogenic Bladder Dysfunction
  65. 65. Detrusor Overactivity • Different mechanisms • Suprapontine - Damage to the suprapontine neural circuitry results in removal of the tonic inhibition of the PMC, spontaneous involuntary detrusor contractions occur • spinal cord lesions - due to the emergence of a segmental reflex at the level of the sacral cord, mediated by capsaicin-sensitive C-fibre afferents, which drive involuntary detrusor contractions
  66. 66. Risk of upper urinary tract complications • Detrusor overactivity in combination with DSD - result in high intravesical pressures • morphological changes in the bladder wall - trabeculations and (pseudo-)diverticula • Increased risk of upper urinary tract complications such as vesico-uretero-renal reflux, hydronephrosis, renal impairment, and eventually ESRD
  67. 67. • SCI or spina bifida have a substantially higher risk of developing renal failure compared with the general adult population • low in patients with slowly progressive non- traumatic neurological disorders, such as MS and IPD • Duration of MS and severity of disability are risk factors for upper urinary tract complications
  69. 69. Dementia • Incontinence is often a prominent symptom • occur at variable times during the natural history of dementia • early in NPH, DLB, vascular dementia, and FTD • late in the course of Alzheimer’s disease or Parkinson’s disease with dementia • also from cognitive and behavioural problems, urological causes, and immobility
  70. 70. • treatment of incontinence can exacerbate the dementia • Antimuscarinic medications (detrusor overactivity), can block central muscarinic M1 receptors, resulting in altered cognition • mitigated by using medications with low selectivity for the M1 receptor, such as darifenacin or restricted permeability across the bloodbrain barrier, such as trospium chloride.
  71. 71. Stroke • More than 50% of stroke patients may have urinary incontinencen during the acute phase • Approximately 70% of survivors of hemispheric strokes suffer transient urinary incontinence. • Risk factors for incontinence include lesion diameter, presence of comorbid illnesses such as diabetes, and age
  72. 72. • Incontinence is significantly associated with severe neurological disability, institutionalization and increased mortality • Lesions in the anteromedial frontal lobe, paraventricular white matter, and putamen are more commonly associated with bladder symptoms • small-vessel disease of the white matter - associated with urgency incontinence, important cause of incontinence in functionally independent people older than 60 years
  73. 73. PD • LUTS are common in Parkinson disease - Thirty-eight to 71% • correlation between bladder dysfunction, neurological disability and Hoehn and Yahr stage • suggesting a relationship between dopaminergic degeneration and bladder dysfunction • bladder dysfunction does not occur until some years after the onset of motor symptoms
  74. 74. • Storage symptoms are the most common • Nocturia (56.7%) is the most common symptom, followed by urinary urgency and these together are the commonest nonmotor symptoms in PD
  75. 75. • nocturnal polyuria (NP) - significant cause of nocturia • related to loss of circadian rhythm in PD • NP does not improve with anti-muscarinics directed to help OAB symptoms • Other causes - prostatic enlargement, pelvic floor weakness, stress incontinence, and bradykinesia of pelvic floor muscles causing “pseudo-dyssynergia”
  76. 76. Multiple System Atrophy • bladder symptoms dominate the clinical picture at onset • 41% of present with LUTS and 97% have LUTS during the disease course • incontinence usually arises from detrusor overactivity and external sphincter weakness • more likely to have a high (>100 mL) PVR, DSD, an open bladder neck at the start of bladder filling on videocystometrogram, and a neurogenic EMG of the anal sphincter
  77. 77. Spinal Cord Lesions • most common cause of neurogenic bladder dysfunction • acute SCI there is initially a phase of spinal shock - detrusor is hypocontractile / acontractile and associated with complete urinary retention • duration of this phase varies - about 6 weeks
  78. 78. • Gradually over the course of weeks, new reflexes emerge to reinitiate bladder emptying and cause detrusor contractions in response to low filling volumes • C fibers emerge as the major afferents, forming a spinal segmental reflex • abnormally overactive, small-capacity bladder
  79. 79. Multiple sclerosis • LUTS are common in MS - 75% • strong association - recognized between bladder symptoms and the presence of clinical spinal cord involvement • Most commonly, patients report storage symptoms such as urgency and frequency, and voiding symptoms depending upon spinal cord involvement • 90 % percent of patients have bladder symptoms if the duration is greater than 10 years and symptoms occur on average 6 years into the illness
  80. 80. Spinal cord injury • initially in urinary retention during the spinal shock • develop symptoms as spinal reflexes return • DSD and DO are the hallmarks of spinal cord injury • Sustained high intravesical pressures can ensue, increasing the risk of upper urinary tract damage • Autonomic dysrefl exia can occur after lesions at or above the T6 spinal cord level, triggered by urinary tract infections (UTIs)
  81. 81. Videocystometrogram spinal cord injury
  82. 82. Spina bifida • more than 90% of children with spina bifida have bladder dysfunction • Symptoms generally start in infancy or childhood • Videourodynamic studies have demonstrated a variety of findings: there may be detrusor overactivity, detrusor underactivity, or low compliance with ineffective contractions
  83. 83. • Bladder outlet may show detrusor sphincter dyssynergia, or may be incompetent with a static or fixed distal sphincter • The incidence of upper urinary tract damage tends to increase with age • Adults with spina bifida have eight times the age-standardized risk of renal failure compared to the adult population
  84. 84. Cauda Equina Lesions • Damageto the cauda equina leaves the detrusor decentralized, rather than denervated • postganglionic parasympathetic innervation is unaffected • bladder dysfunction after a cauda equina lesion is unpredictable, even detrusor overactivity has been described
  85. 85. Peripheral neuropathy • LMN disturbance in patients with polyradiculopathy or peripheral neuropathy results in reduced or absent detrusor contractions • Patients have reduced sensation of bladder fullness, inability to initiate micturition voluntarily and bladder distension to the point of overflow incontinence
  86. 86. Diabetic Neuropathy • onset of the bladder dysfunction is insidious, with progressive loss of bladder sensation and impairment of bladder emptying over years, eventually culminating in chronic low pressure urinary retention • Urodynamics - impaired detrusor contractility, reduced urine flow, increased postmicturition residual volume, and reduced bladder sensation • vesical afferent and efferent fibers are involved, causing reduced awareness of bladder filling and decreased bladder contractility
  87. 87. Fowler’s syndrome • young woman in complete urinary retention, no underlying urological or neurological disease, a diagnosis of Fowler’s syndrome should be considered • primary disorder of urethral sphincter relaxation • results in an inhibition of detrusor contractions • Urethral sphincter electromyography (EMG) shows a characteristic pattern of activity and the urethral pressures are usually raised • respond particularly favorably to sacral neuromodulation
  88. 88. TREATMENT
  89. 89. Principles Of Management • goals of management are to achieve urinary continence, improve quality of life, prevent UTIs, and preserve upper urinary tract function • should address both voiding and storage dysfunction • determined by the severity of symptoms and risk of developing upper urinary tract damage • multidisciplinary approach between neurology, urology, and primary care is essential
  90. 90. General Measures • Nonpharmacological measures - effective in the early stages when symptoms are mild • fluid intake of around 1 to 2 liters a day • Caffeine reduction • Bladder retraining - patients void by the clock and voluntarily “hold on” for increasingly longer periods, aims to restore the normal pattern of micturition • Pelvic floor exercises and neuromuscular stimulation
  92. 92. Physical treatments • Behavioural therapy - incontinence is associated with cognitive deficits, and motor deficits • correcting faulty habits such as frequent voiding • Timed voiding - separating toilet visits by fixed intervals of time • Habit retraining - identifying the natural voiding pattern of a patient and the development of an individualised toileting schedule • Verbal prompts and positive reinforcement • Pelvic floor exercises
  93. 93. Anti-Muscarinic Medications • mainstay of treatment for detrusor overactivity • Detrusor relaxation, lower intravesical pressures, and reduced storage symptoms • M3 - widely distributed throughout the detrusor, urothelium, and suburothelium • M2 receptor is functionally the most relevant subtype in the bladder
  94. 94. Adverse events • nonspecific anticholinergic - dry mouth, blurred vision for near objects, tachycardia, and constipation • block central M1 receptors and cause impairment of cognition and consciousness • mitigated by medications which have low selectivity for the M1 receptor, such as Darifenacin, or restricted permeability across the blood brain barrier, such as Trospium
  95. 95. Commonly used antimuscarinic drugs
  96. 96. • Measurement of the PVR should be done before antimuscarinic treatment is started • judicious combination of anti muscarinic treatment plus intermittent self- cathetersation provides the most effective management for neurogenic LUT dysfunction
  97. 97. • Desmopressin - reduces urine production and volume-determined detrusor overactivity • Nocturia, nocturnal polyuria • β3-Adrenoceptor agonists – mirabegron • does not cause anticholinergic s/e and cognitive impairment
  98. 98. Intradetrusor Botulinum toxin • revolutionised the management of neurogenic overactive bladder • type A that is generally used for urological indications • several different preparations, only onabotulinumtoxinA is licensed for treatment of detrusor overactivity incontinence • highly effective, safe, and well tolerated • 20 to 30 injections are made into the bladder wall, requiring a cystoscopy, effect lasts 8 to 11 months
  99. 99. Neuromodulation • Electrical stimulation of peripheral nerves such as the sacral nerve roots, tibial nerve, pudendal nerve, and dorsal genital nerves • overall quality of the evidence is low • mechanism of action is uncertain, modulation of sacral afferent nerves and spinal cord- mediated reflexes through inhibitory interneurons is key
  100. 100. Percutaneous tibial nerve stimulation (PTNS) • safe and effective minimally invasive treatment - mild or moderate overactive bladder symptoms • typical treatment course consists of stimulating the nerve through a fine gauge stainless steel needle using a fixed frequency electrical signal, once weekly for 30 minutes, over an 8–12-week period • effect is fairly short lived • Transcutaneous tibial nerve stimulation (TTNS) is an alternative that can be done at home
  101. 101. Sacral Neuromodulation • extra dural sacral nerve stimulator • mainstay of treatment in Fowler syndrome • highly effective in detrusor overactivity refractory to anti-muscarinic medications • does not increase the PVR volume and its effect is not temporally limited • early bilateral SNM during the phase of spinal shock seems to prevent the subsequent development of neurogenic detrusor overactivity and urinary incontinence in patients with complete SCI • progressive neurological disease are not candidates
  102. 102. Surgery
  103. 103. • best solution for long-term bladder management • however, does not apply to patients with progressive neurological disease causing incontinence
  104. 104. Nerve Root Stimulators • patients who have suffered a complete spinal cord transection, but in whom the caudal section of the cord and its roots are intact • stimulating electrodes are placed around the lower sacral roots (S2 to S4) • activated by an external switching device. • applied intrathecally to the anterior roots, the posterior roots are cut at the same time
  105. 105. Permanent Indwelling Catheters • patient is no longer able to perform self- catheterization • incontinence is refractory to management • indwelling Foley catheter • major problems is catheter bypassing, occurs when strong detrusor contractions produce a rapid urine flow that cannot drain sufficiently quickly
  106. 106. • common response - to use a wider caliber catheter • with the effect that the bladder closure mechanism becomes progressively stretched and destroyed • detrusor contraction may be of sufficient intensity to extrude the 10- or 20-mL balloon of the catheter from the bladder, causing further damage to the bladder neck and resulting in a totally incompetent outlet
  107. 107. • Bladder stones and recurrent infections are also more likely • preferred alternative - suprapubic catheter • better long-term alternative to a urethral catheter • preserves urethral integrity, and helps to promote perineal hygiene and sexual functions
  109. 109. Intermittent catheterisation • best time to begin intermittent catheterisation • PVR volume - related to the overall bladder capacity, consistently more than 100 mL has been advocated if the patient is symptomatic/or more than one-third of bladder capacity • risk of upper urinary tract damage • Catheterisation four to six times per 24 h is recommended to manage complete urinary
  110. 110. Other interventions • Triggered reflex voiding - provoking a bladder contraction through stimulation of sacral and lumbar dermatomes (eg, suprapubic tapping and thigh scratching) • most successful in patients with a suprasacral spinal cord lesion • Bladder expression using Valsalva or Crede manoeuvres (manual compression of the lower abdomen) is not usually recommended because these could be associated with a rise in intravesical pressures
  111. 111. Algorithm for the management of neurogenic LUTD
  112. 112. Management of lower neurologic LUTDS
  113. 113. Stepwise Approach to Neurogenic Bladder Dysfunction • treatment options offered to a patient should reflect the severity of bladder dysfunction, which generally parallels the extent of neurological disease • beyond a certain point, incontinence may become refractory to all treatment options • at this stage a long-term indwelling catheter should be offered.
  114. 114. Stepwise approach
  115. 115. Early Referral To A Urology Service • Symptoms refractory to treatment • Recurrent urinary tract infections • Suspicion of concomitant pathologies such as bladder outlet obstruction due to prostate enlargement, stress incontinence • Renal impairment • Demonstrated hydronephrosis
  116. 116. • Presence of haematuria • Pain suspected to be originating from the urinary tract • Consideration of suprapubic catheterization • Consideration of urological procedures such as intradetrusor injections of botulinum toxin A or surgeries such as augmentation cystoplasty or urinary diversion
  117. 117. REFERENCES • Panicker JN, Fowler CJ, Kessler TM. Lower urinary tract dysfunction in the neurological patient: clinical assessment and management. Lancet Neurol. 2015 Jul;14(7) • Panicker JN, De Sèze M, Fowler CJ. Neurogenic lower urinary tract dysfunction. Handb Clin Neurol. 2013 • Bradley’s Neurology in Clinical Practice 7th

Notas do Editor

  • Red trace (Pabd) is the intra-abdominal pressure recorded by the rectal catheter; dark blue trace (Pves) is the intravesical pressure recorded by the bladder catheter. Pink trace (Pdet) is the subtracted detrusor pressure (Pves-Pabd). Green traces represent volume infused (Vinf) during the test and volume voided (Vura); orange trace represents urinary flow (Qura).
    Black arrow demonstrates detrusor overactivity, and black arrowhead indicates associated incontinence
  • Concentric needle electromyography (EMG) of external anal sphincter from a 64-year-old male presenting with parkinsonism and urinary retention
    Duration of the motor unit is 17.9 msec (normal < 10 msec); prolonged motor units suggest chronic reinnervation. Mean duration of motor unit potentials (MUPs) during study was 22.9 msec; EMG is compatible with a diagnosis of multiple system atrophy.
  • classical features of neurogenic bladder: anteroposterior projection showing diverticuli and “fir tree appearance” (arrow).