Disclosures. Geriatric Incontinence and Voiding Dysfunction. Agenda. Agenda. UI: a Geriatric Syndrome. Geriatric Syndromes 9/7/2018.

Transcription

1 Disclosures Geriatric Incontinence and Voiding Dysfunction None Shachi Tyagi MD, MS Assistant Professor Division of Geriatric Medicine University of Pittsburgh Medical Center UI: a Geriatric Syndrome Geriatric Syndromes Afflicts 15% to 30% of those in community over a third of those in acute setting half of those in nursing home It is abnormal at any age Disease Severity Symptomatic Compensatory Mechanism Asymptomatic 1

2 UI: a Geriatric Syndrome Lower urinary tract changes with age: Bladder sensation, contractility, and the ability to postpone voiding declines Prevalence of involuntary detrusor contractions increases Postvoid residual volume increases (no more than ml) Geriatric Incontinence In the elderly, continence generally results not from normal lower urinary tract but despite abnormal lower urinary tract Compensatory role of factors beyond the lower urinary tract is immensely important These compensatory factors are often impaired in older patients These factors should be identified and addressed in all incontinent older adults Reversal of these factors can resolve or improve incontinence Improve efficacy of lower urinary tract therapy UI: a Geriatric Syndrome Identifying Etiology of UI Transient incontinence Transient Incontinence Incontinence is transient in up to one-third of community-dwelling elderly and up to half of acutely hospitalized Although termed transient, the causes may persist if left untreated Geriatric incontinence is rarely due to just one of these cause 2

3 D: delirium I: infection A: atrophic urethritis/vaginitis P: pharmaceuticals E: excess urine output R: restricted mobility S: stool impaction Delirium: confusional state with waxing and waning attention Results from any underlying illness or medication Incontinence is secondary, abates once underlying cause has been corrected Infection: urinary Symptomatic when dysuria and urgency are so prominent that patient is unable to reach bathroom Asymptomatic bacteriuria does not cause incontinence New onset incontinence or worsening of urinary symptoms with increased confusion in elderly with dementia Atrophic urethritis/ vaginitis Up to 80% of elderly women with incontinence may have atrophic vaginitis Urgency with scalding dysuria that mimics UTI Responds well to low-dose estrogen Pharmaceuticals: prescribed and over-thecounter Most common cause of geriatric incontinence Transient Incontinence: Pharmaceutical Causes Sedative/ hypnotics: long-acting benzodiazepines (diazepam, flurazepam) Alcohol Anticholinergics: dicyclomine, antihistamines (Benadryl) Antidepressants: tricyclics- amitrptyline Narcotic analgesics α-adrenergic antagonists: prazocin, terazocin, doxazocin 3

4 Transient Incontinence: Pharmaceutical Causes α-adrenergic agonists: nasal decongestants Calcium channel blockers: amlodipine Diuretics: furosemide NSAIDS: indomethacin, COX-2 inhibitors Anticonvulsants/nalagesics: gabapentin, pregabalin Thiazolidinediones: rosiglitazone, pioglitazone Excess urine output Large fluid intake/ caffeinated beverages Diuretic agent Metabolic disorder- hyperglycemia, hypercalcemia Mobilization of peripheral edema Restricted mobility Arthritis Pain Foot problem Orthostatic hypotension Fear of falling Stool impaction 10% of older adults admitted to hospital or referred to incontinence clinics Urge or overflow incontinence Disimpaction resolves incontinence Established Incontinence Detrusor overactivity (DO) is the most common type (OAB: overactive bladder) Has 2 physiologic subsets: Contractile function is preserved Contractile function is impaired (DHIC) 4

5 Established Incontinence Stress incontinence Established Incontinence Causes unrelated to lower urinary tract: Outlet obstruction Detrusor underactivity Functional incontinence: deficits in cognition and mobility Diagnostic Approach: History Transient causes Functional impairment: basic activities of daily living ADLs i.e. transferring from bed, walking, bathing, toileting, eating, and dressing Advanced instrumental: activities of daily living i.e. shopping, cooking, driving, managing finances, using telephone Diagnostic Approach: History Precipitancy: abrupt sensation that urination is imminent Precipitant leakage: with no warning of imminent urination, the abrupt gush of urine in absence of stress maneuver Diagnostic Approach: History Frequency: get the context Increased frequency may be due to voiding habit, preemptive urination, stable but poorly compliant bladder, excess urine production, depression, anxiety Normal frequency in those with DO due to restricted fluid intake 5

6 Diagnostic Approach: History Diagnostic Approach: Voiding Diary Nocturia Assess sleep Assess time in bed Medications at bedtime BLADDER DIARY Name: Date / / Time (Please specify AM or PM) Dry=0 Wet: Mild =1 Moderate = 2 Severe = 3 Volume Urinated Circumstances of void or leakage Fluids at bedtime Diagnostic Approach: Voiding Diary Voided volumes Functional bladder capacity Pattern of voiding and leakage Cause of leakage Guide therapy Diagnostic Approach: Physical Examination Signs or neurologic diseases: delirium, dementia, stroke, Parkinson s, neuropathy Atrophic vaginitis Heart failure Peripheral edema Rectal exam: impaction, prostatic nodularity, volitional contraction of rectal sphincter Stress testing and PVR measurement Diagnostic Approach: Laboratory Investigation BUN/ creatinine Urinalysis Serum sodium, calcium, glucose 6

7 Behavioral: Adjusting the timing of fluid excretion Scheduled/ prompted voiding for cognitively impaired Providing bedside commode Pelvic floor muscle exercise (Kegel): practice several times a day e.g. three sets of contractions building up from 3 seconds to 10 seconds in duration Biofeedback Anticholinergics are mainstay of pharmacologic treatment Human bladder has five cholinergic muscarinic receptor subtypes M2 and M3 types are found on detrusor muscle Most smooth muscle contractions are mediated via the M3 type M2 type contributes to bladder contraction in certain disease states e.g. outflow obstruction and denervation Antimuscarinics Oxybutynin Tolterodine Fesoterodine Trospium Darifenacin (selective M3) Solifenacin (selective M3) β-3 agonist Mirabegron Class adverse events Antimuscarinics (attributed to M2 blockade) Dry mouth Blurry vision/dry eyes Constipation Confusion/delirium β-3 agonist HTN Tachycardia Headache/ dizziness nausea Important considerations for treatment with antimuscarinics: Bladder botox injections Sacral nerve stimulation Monitor PVR Xerostomia 7

8 Nocturia: desmopressin To be used with extreme caution in older adults Vasopressin analogue Fluid retention Hyponatremia- even up to 6 months Increases Ca excretion Decreases K excretion Therapy- Stress Incontinence Mostly behavioral Weight loss Therapy of precipitating conditions- cough/ vaginitis Pelvic muscle exercises No effective pharmacotherpay Surgical management Suburethral sling Periurethral bulking injections Insertion of artificial sphincter Therapy- Outlet Obstruction Conservative measures Modification of fluid intake Modification of voiding habits Pharmacotherapy α-adrenergic antagonist relax the smooth muscle tone at the bladder neck and prostate Therapy- Outlet Obstruction α-adrenergic antagonist Non-selective: terazosin, doxazosin Orthostasis, hypotension Selective: tamsulosin, alfuzosin more specifically target the bladder neck and prostate and have fewer adverse cardiovascular side effects Therapy- Outlet Obstruction 5-α reductase inhibitors: Finasteride, dutasteride inhibit the conversion of testosterone to dihydrotestosterone Therapy- Outlet Obstruction Combination therapy with both α-blocker and 5-α reductase inhibitor drugs is more efficacious Reduces risk of urinary retention epithelial atrophy and reduction of prostate volume up to 25 percent over time 8

9 Therapy: Summary No obstruction and low PVR: anticholinergics mirabegron No obstruction and high PVR cautious trial of anticholinergic with close attention to the PVR mirabegron Therapy: Summary BOO with low PVR α-blockers/ 5-α reductase inhibitor/ combination anticholinergics can be added if OAB symptoms persist BOO with high PVR α-blockers/ 5-α reductase inhibitor/ combination anticholinergics can precipitate retention Refractory OAB Therapy: Summary Sacral neuromodulation Botulinum toxin Questions! 9