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Neurogenic Bladder October 2015 Neurogenic Bladder October 2015

Neurogenic Bladder October 2015 - PowerPoint Presentation

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Neurogenic Bladder October 2015 - PPT Presentation

Normal micturition Normal micturition involves proper function of both bladder amp urethra A detrusor of normal compliance amp a physiologically competent urethral sphincter are both necessary ID: 1007190

amp bladder urology volume bladder amp volume urology detrusor advances 2012 article 816274 pages urinary neurogenic sphincter pressure voiding

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1. Neurogenic BladderOctober 2015

2. Normal micturitionNormal micturition involves proper function of both bladder & urethraA detrusor of normal compliance & a physiologically competent urethral sphincter are both necessary to maintain urinary continenceAny increase in abdominal pressure, which inherently produces an increase in bladder pressure, is normally counteracted by an even greater increase in urethral pressureDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

3. Normal micturitionNormal micturition involves passive, low pressure filling of bladder during urine storage phase while voiding requires coordination of detrusor contraction with internal & external urinary sphincter relaxationThis micturition process is controlled by central nervous system, which coordinates sympathetic & parasympathetic nervous system activation with somatic nervous system to ensure normal micturition with urinary continenceDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

4. Components of nervous system & neural pathways governing function of bladder Robert C. McDonough. Hospital Physician. 2007; 14 Part1.

5. Neurogenic bladder dysfunctionVoiding dysfunction can result from any mechanical or physiologic defects in micturition system  Inability of urinary sphincter to appropriately increase (or decrease) its pressure in response to increased bladder pressureDamage or diseases of central, peripheral & autonomic nervous systems may result in neurogenic bladder dysfunctionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.Neurogenic bladder dysfunction may complicate a variety of neurologic conditions

6. Neurogenic bladder can lead to…Lower urinary tract infectionsUrinary retentionUrinary tract obstructionsUpper urinary tract infectionsSerious systemic illnesses including septicemia & acute renal failureNeurogenic bladder with detrusor overactivity may cause incontinence, which not only leads to embarrassment, depression & social isolation but also may lead to skin decubiti, urethral erosions & upper urinary tract damageDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

7. Classification of Neurogenic BladderMany classifications have been used to group neurogenic bladder dysfunctionEach has their merits and clinical utilityThese classifications may be based on urodynamic findings (e.g., Lapides, Krane & Siroky), neurourologic criteria (Hald and Bradley, Bors and Comarr), or on bladder & urethral function (International Continence Society, WeinDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

8. Classification (Madersbacher)

9. Classification of Neurogenic BladderA popular classification of neurogenic bladder dysfunction based on location of neurologic lesion can help guide pharmacologic & surgical therapies, with voiding abnormalities seen clinically following from disruptions of normal urinary physiologyIn this classification, neurogenic bladder arises from:Lesions above pontine micturition center (e.g. stroke or brain tumor) producing uninhibited bladderLesions between pontine micturition center & sacral spinal cord (e.g., traumatic spinal cord injury or multiple sclerosis involving cervicothoracic spinal cord) producing an upper motor neuron bladderDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

10. Classification of Neurogenic BladderSacral cord lesions that damage detrusor nucleus but spare pudendal nucleus producing a mixed type A bladderSacral cord lesions that spare detrusor nucleus but damage pudendal nucleus producing mixed type B bladderLower motor neuron bladder from sacral cord or sacral nerve root injuriesDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

11. Anatomy & physiology of micturition with potential injury sites to urologic systemDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

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14. Uninhibited neurogenic bladderIn uninhibited neurogenic bladder dysfunction, there is usually reduced awareness of bladder fullness & a low capacity bladder due to reduction of inhibition of pontine micturition center (PMC) by cortical & subcortical structure damageUrinary incontinence may occur with brain lesions occurring above pontine micturition center, especially with bilateral lesionsSince PMC is intact, normal opposition of detrusor & internal/external sphincter tonus is maintained so there are no high bladder pressures developed that can lead to upper urinary tract damageDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

15. Upper motor neuron neurogenic bladder dysfunctionUpper motor neuron neurogenic bladder dysfunction is characterized by detrusor-sphincter dyssynergia (DSD) wherein simultaneous detrusor & urinary sphincter contractions produce high pressures in the bladder (up to 80–90 cm H2O) leading to vesicoureteral reflux (VUR) that can produce renal damageDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

16. Emergence of segmental reflex (resulting in detrusor hyperreflexia), afferent limb of which is subserved by unmyelinated c-fibres following disruption of spinobulbar pathways by spinal cord lesion. Administration of intravesical vanilloids can alleviate symptoms through desensitization of c-fibres

17. DSD: DefinitionKarsenty G, et al. Urology. 2005; 66: 763-8.Involuntary detrusor contractions concurrent with involuntary contraction of urethral striated muscle &/or periurethral striated muscle

18. Mixed type A neurogenic bladderThe more common of the mixed type bladders: Detrusor nucleus damage renders detrusor flaccid (also referred to as detrusor areflexia), while intact pudendal nucleus is spastic producing hypertonic external urinary sphincterBladder is large & has low pressure, so spastic external sphincter produces urinary retentionDetrusor pressure is low so upper urinary tract damage from VUR does not occur & incontinence is uncommonDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

19. Mixed type B neurogenic bladderCharacterized by a flaccid external urinary sphincter due to pudendal nucleus lesion while bladder is spastic due to disinhibited detrusor nucleusThus, bladder capacity is low but vesicular pressures are usually not elevated since there is little outflow resistanceThis leads to problems with incontinence, howeverDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

20. Lower motor neuron neurogenic bladderSacral micturition centers or related peripheral nerves are damaged though thoracic sympathetic nervous system outflow to lower urinary tract is intactBladder capacity is large since detrusor tone is low (detrusor areflexia) & internal urinary sphincter innervation is intactDespite low detrusor pressure, overflow urinary incontinence & urinary tract infections are not uncommonDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

21. Detrusor hyperactivity with impaired bladder contractility (DHIC)Another type of bladder dysfunction was 1st described in nursing home residentsFrequent but weak involuntary detrusor contractions causing incontinence despite incomplete bladder emptying (Resnick)DHIC is associated with bladder trabeculation, slow bladder contraction velocity & elevated urinary residual volume after voiding attemptsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

22. Neurourological EvaluationThis evaluation is essential to assess lower urinary tract functionA full patient history should be obtained including prior genitourinary conditions/surgeries, voiding history, voiding complaints (dysuria, recurrent infections, hesitancy, nocturia, incontinence, urgency, and/or frequency) & medicationsSedative/hypnotic, antidepressant, antipsychotic, antihistamine, anticholinergic, antispasmodic, opiate, alpha adrenergic agonists/antagonists & calcium channel blocking medications may affect voiding functionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

23. Neurourological EvaluationOptimally, a patient urinary diary with voiding pattern, fluid intake & voiding issues can help with patient evaluation and formulation of treatment recommendationsA physical examination focusing on pelvic anatomy & neurologic system is essentialNeurological examination should include mental status, reflexes, strength & sensation (including sacral dermatomes) to determine if there are neurologic conditions present that may contribute to voiding dysfunctionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

24. EAU guidelines 2013.

25. Neurourological EvaluationMechanical issues such as prostate enlargement or bladder prolapse can be found on urologic exam that may impact voiding functionIssues with cognition, hand strength & coordination, joint contractures, mobility, sexuality, social/medical support & other factors may impact type of bladder rehabilitation that is feasible for a given patientFor spinal cord injured patients: Motor level of spinal lesion, whether injury is complete or incomplete, extremity tone, rectal sensation/tone, presence/absence of voluntary rectal tone & bulbocavernosus reflex should be determinedDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

26. Lab EvaluationLaboratory evaluation of neurogenic bladder patients should include:UrinalysisUrine culture & sensitivitySerum BUN/creatinine &Creatinine clearanceDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

27. Postvoid residual (PVR) urinePVR urine volume involves transurethral catheterization to measure residual urine volume in bladder immediately after voiding to determine ability of the bladder to empty completelyPVR determination should always be performed after discontinuing Foley catheterization or before instituting intermittent catheterization as part of a bladder retraining programDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

28. Postvoid residual (PVR) urinePVRs are necessary to prevent overdistension of bladder & determine frequency of catheterization that is needed to keep residual urinary volumes under approximately 400 ccAbnormal residual volumes have been defined by volumes greater than 100 cc or greater than 20% of voided volume & residual urine volumes under 100 cc are associated with reduced risk of development of bacterial cystitisDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

29. UltrasoundNoninvasive means of determining urine post-void residual volumes, especially if precise measurement is not requiredDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

30. Renal clearance tests24-hour urine creatinine clearance & several isotope studies can be used to evaluate and sequentially follow renal function in neurogenic bladder patientsA commonly used test measures GFR via short renal clearance test using 125 I-iothalamateDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

31. Urodynamic evaluationUrodynamic evaluation should be completed to assess urinary function, including:Urinary flowmetryBladder cystometrogram/electromyogram (CMG/EMG)Valsalva leak point pressure (LPP) measurement &Urethral pressure profile (UPP)Urodynamic studies are most definitive & objective means to determine abnormalities in bladder and urethra in filling/storage phase as well as voiding phase in neurogenic bladder dysfunctionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

32. Robert C. McDonough. Hospital Physician. 2007; 14 Part1.Urodynamic study demonstrating detrusor instability

33. Robert C. McDonough. Hospital Physician. 2007; 14 Part1.Urodynamic study: Detrusor–external sphincter dyssynergia

34. Urinary flow rate evaluationNon-invasive way to quantify urinary flow, defined as volume of urine voided per unit of timeUrine flow is dependent on force of detrusor contraction as well as urethral resistanceNormal urine flow curves are bell-shaped with rapid rise to peak flow, a short duration of peak flow & then rapid falloff of urine flowUrine flow rate patterns are not diagnostic, but high flow rates are often seen with neurogenic detrusor overactivity & poor flow rates may reflect weak detrusor pressure and/or urinary outlet obstructionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

35. Other testsBladder cystometrogram/electromyogramUrethral pressure profile (UPP)Dorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

36. Neurogenic Bladder ManagementManagement of neurogenic bladder conditions requires patient education and may include interventions such as:Timed voidingManual expressionMedicationsIntermittent catheterizationIndwelling urinary catheter &Bladder and/or urethral surgical proceduresDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

37. Nonpharmacologic InterventionsBladder retraining & fluid scheduleUse of incontinence pads or external urinary collection devicesIndwelling Foley catheter placement for neurogenic bladder management is an option for uncontrollable incontinence or for urinary retention when intermittent catheterization is not practicalSuprapubic catheters have some advantages over urethral catheters including elimination of those urethral erosion risksIndividualized patient education regarding management of their neurogenic bladder via specialized nursing is important for achieving successful neurogenic bladder managementDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

38. Nonpharmacologic InterventionsNurses can monitor patient compliance with fluid schedule & teach patients how to perform timed voids as well as manual techniques including:Self-catheterizationCrede technique (manual pressure over suprapubic region to increase vesicular pressure to promote bladder emptying)Tapping (over suprapubic area to trigger detrusor contraction in hyperreflexic bladders) &/orValsalva maneuver (which increases vesicular pressure and may also trigger detrusor contraction)Dorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

39. Pharmacologic InterventionsThere are many different classes of drugs that are used to treat neurogenic bladder dysfunction as part of comprehensive bladder management programTricyclic Antidepressant DrugsAnticholinergic (Antimuscarinic) MedicationsCholinergic AgonistsAlpha-2 Adrenergic AgonistsAlpha-1 Adrenergic AntagonistsBenzodiazepinesGABA-B AgonistsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

40. Anticholinergic (Antimuscarinic) MedicationsThis class of medication reduces reflex (involuntary) detrusor activity by blocking cholinergic transmission at muscarinic receptors & is 1st-line option for treating neurogenic detrusor overactivity (NDO)Though available anticholinergic agents have similar efficacy, these drugs differ in terms of side effects & tolerability based on their muscarinic receptor selectivity and rate of drug distributionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

41. Anticholinergic (Antimuscarinic) MedicationsAnticholinergic drugs that bind M1, M2, and M3 muscarinic receptors (nonselective) have more side effects than newer agents that are more selective for M2 and/or M3 receptorsSustained release drug preparations also improve antimuscarinic drug tolerability by attenuating peak drug serum concentrationsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

42. EAU guidelines 2013.

43. Botulinum ToxinBotulinum toxin blocks neuromuscular junction presynaptic vesicle fusion, which prevents acetylcholine release & thus blocks signal transmission across neuromuscular junctionIt also acts on sensory afferent neurons & prevents excitatory effects of nerve growth factor (NGF) on bladder function, which may contribute to its beneficial clinical effects in treating neurogenic bladderInjection of botulinum toxin A into bladder detrusor or external urinary sphincter produces dose-dependent weakening of those muscles, which have a high concentration of cholinergic nerve endingsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

44. Effects of BoNT‑A on detrusor smooth muscle contraction Jiang YH, et al. Nat Rev Urol. 2015; 12(9): 519-33.

45. Botulinum ToxinBotulinum toxin A injections can produce long-lasting improvements in neurogenic detrusor overactivity, incontinence & quality of life in spinal cord injury individualsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

46. Botulinum ToxinDykstra et al. 1st reported using botulinum toxin to successfully treat urinary symptoms by injection of external urinary sphincter of spinal cord injured patients having detrusor sphincter dyssynergiaInjection of botulinum toxin A into bladder detrusor muscle to treat neurogenic incontinence was described a decade laterBotulinum toxin A injection in detrusor & suburothelial regions of bladder body can produce beneficial effects for up to 9 months, though up to 70% of neurogenic detrusor overactivity patients may require catheterization after botulinum toxin injections due to urinary retentionDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

47. Botulinum ToxinSide effects of botulinumtoxin injections are low, with a <1% risk of developing antibodies to toxin & about 1% incidence of temporary distant muscle weaknessApproximately 10% of patients do not obtain desired clinical benefit from botulinum toxin injectionsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

48. Botulinum ToxinA large, retrospective trial of 200 neurogenic bladder patients receiving detrusor botulinum toxin injections demonstrated >50% increase of mean bladder volume to 1st reflex detrusor contraction & maximum cystometric capacity, with a proportional decrease in maximum detrusor pressureThese benefits lasted more than 6 months & could be more cost effective than bladder augmentation surgery over a 5-year period if a 40% early and late complication rate of that surgery is assumed and the botulinum toxin effect lasted at least 5 months (P. Padmanabhan, et al. World Journal of Urology. 2011; 29(1): 51–57)Dorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

49. Ahmed HU, et al. Nat Clin Pract Urol. 2006; 3(7): 368-80.

50. Ahmed HU, et al. Nat Clin Pract Urol. 2006; 3(7): 368-80.

51.

52. Other drugsOpioidsVanilloidsNerve Growth FactorNitrous Oxide AgonistsDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

53. Surgical interventionsWhen nonpharmacologic and pharmacologic treatments fail to control neurogenic detrusor overactivity, then surgical options including neuromodulation are appropriate treatment optionsProcedures to Enhance Detrusor Storage:Neuromodulation for Neurogenic Detrusor OveractivityEnterocystoplastyDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

54. Surgical interventionsProcedures to Control Detrusor Emptying:Urinary DiversionBladder Sphincter Procedures to Enhance EmptyingSphincterotomyUrethral Stents and Balloon DilatationBladder Sphincter Procedures to Restrict EmptyingArtificial Urinary SphincterSling ProceduresDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

55. Other treatmentsLumbar to Sacral Nerve ReroutingSpinal Cord RegenerationDorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.

56. THANK YOU!