Virtual Editions: LUTS in the elderly series.  The objective of this review is to critically examine the causal relationship between medication use and lower urinary tract symptoms (LUTS) in the elderly.

Keywords: medication, LUTS, elderly
Authors: A part of the series LUTS in the elderly, compiled by Cara Tannenbaum
Corresponding Author: Cara Tannenbaum, MD, MSc, Université de Montréal, Montréal, Quebec, Canada,Faculties of Medicine and Pharmacy, The Michel Saucier Endowed, Chair in Pharmacology, Health and Aging Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, 4545 Queen Mary Road, Suite 7824, Montreal, QC H3W 1W5.    E-mail:  cara.tannenbaum@umontreal.ca

Abstract

The objective of this review is to critically examine the causal relationship between medication use and lower urinary tract symptoms (LUTS) in the elderly. Studies were identified in PubMed from 1980 to 2010 using the search terms; urinary frequency, urinary urgency, nocturia, incontinence or voiding disorders AND medications or drugs. The bibliographies of abstracted articles were used to locate other relevant studies. The findings confirmed that medications causing polyuria, such as loop diuretics (Level 3 evidence) and lithium (Level 4 evidence) are associated with urinary frequency. Symptoms of urinary urgency can also be precipitated by loop, but not non-loop diuretics (Level 3 evidence). Treatment-emergent peripheral edema from NSAIDs, calcium channel blockers, thiazolidinediones and some GABAergic analgesic agents can result in night-time dependent fluid redistribution and cause nocturnal diuresis, nocturia and nocturnal polyuria (Level 4 evidence). Randomized controlled trials and large epidemiologic studies consistently implicate estrogen use in precipitating or exacerbating incontinence. The use of alpha-blocking agents is also associated with incontinence (Level 2 evidence), although loop diuretics are not (Level 2 evidence). Benzodiazepines, ACE  inhibitors, cholinesterase inhibitors and other centrally-active agents have only variably been linked to the onset of incontinence (Level 3-4 evidence). More rigorous studies are also needed to unravel the relationship between anticholinergic agents, alpha-adrenergic agonists, calcium channel blockers and NSAIDS with voiding dysfunction and urinary retention (Level 3-4 evidence).   

Introduction

Many commonly used medications have been proposed to inadvertently interfere with bladder and/or sphincter function, or indirectly impair the ability to toilet.[1] Urinary frequency, urgency and nocturia may plausibly be caused or exacerbated by a variety of prescription drugs acting via different mechanisms. Polypharmacy occurs frequently in the elderly, and as such, the older patient is at increased risk for lower urinary tract symptoms (LUTS) that are precipitated or exacerbated by physiologic changes induced by these medications. Instead of adding to this medication cascade with yet another pharmaceutical to treat drug-induced LUTS, the clinician should identify the original culprit medication and consider discontinuing or replacing it with an alternate therapy whenever possible. 
Although several medication classes have theoretical deleterious effects on the lower urinary tract, strong evidence for causality is lacking. There exist several reasons for this gap in the literature. The first explanation is bias by indication: it is often difficult to tease out whether urinary symptoms result from the treatment itself, or from the underlying disease for which the treatment was prescribed. One example of this conundrum is the association between urinary incontinence and the acetylcholinesterase inhibitors, prescribed for Alzheimer’s disease. By increasing cholinergic activity, acetylcholinesterase inhibitors improve cognition, but may also provoke detrusor contractions. A 7% incidence of incontinence has been reported with new consumption of cholinesterase inhibitors.[2, 3] A competing hypothesis holds that the patient’s worsening dementia, which led to the prescription of these drugs, independently contributes to functional impairment and the onset of incontinence.    
A second reason why a direct cause-effect relationship between certain medications and LUTS is challenging to prove relates to the difficulty designing and implementing prospective studies that test for treatment-emergent harmful effects. Beyond the prohibitive ethical considerations involved in mounting such studies, LUTS in the elderly areis often multifactorial in nature, and the logistics of recruiting a homogeneous group of LUTS-free elderly and administering targeted medications with the aim of observing LUTS-related side effects is a complex undertaking. This review therefore focuses on the evidence provided by existing clinical trials or case series, as well as large observational studies derived from population datasets. For the most part, these studies were neither designed nor powered to detect a primary outcome of LUTS in the elderly.  

Methods

The review is organized by LUTS and has been divided into 5 sections: urinary frequency, urinary urgency, nocturia, incontinence and voiding disorders. A search of the literature was conducted in PubMed from 1980 to 2010 using the search terms “medication” or “drug” and one of each of the section titles.  The search was restricted to human studies published in the English language. The bibliographies of abstracted articles were used to locate other relevant studies. Each medication class that was identified was also searched against the LUTS terms independently, for example, “diuretics” and “urinary frequency”.  On rare occasions, aAdditional search terms were sometimes added, such as “polyuria” and “nephrogenic diabetes insipidus” for lithium. Whenever possible, recent reviews are cited that summarize the data on a particular drug class. 

Results

1. Urinary frequency
Two medication classes have been associated with urinary frequency: the use of diuretics and chronic lithium therapy. Our search revealed only 2/12 relevant publications when the term “diuretics” was crossed with “urinary frequency” and none with lithium. However, 5/16 relevant articles were found when lithium was searched with the terms polyuria and nephrogenic diabetes insipidus. The strongest evidence associating diuretic use with urinary frequency comes from a clinical series of 172 hypertensive and heart failure patients, mean age 80. [4] The use of loop diuretics was significantly associated with increased urinary frequency (odds ratio=OR=6.62; 95% confidence interval=CI=2.58-16.94), a relationship that persisted in multivariate analyses accounting for age, sex, and cardiovascular diseases and other drugs. Non-loop diuretics were not associated with symptoms of urinary frequency. A theoretical mechanism explaining the difference between loop and non-loop diuretics on urinary frequency is that responsiveness to antidiuretic hormone is generally reduced with the use of loop diuretics compared to non-loop diuretics, and therefore more urine is produced.  Lithium, on the other hand, has been shown to impair renal concentrating ability in at least 54% of patients on chronic lithium therapy.[5] However, this defect translates into overt polyuria in only 19-33% of cases and no data is available to support or refute its association with urinary frequency.[5, 6] 
2. Urinary urgency
Only the use of loop diuretics has been associated with urinary urgency in case series analysis (OR=4.09; 95% CI=1.75-9.59).[4]  In multivariate analyses adjusting for age, sex, comorbidities and polypharmacy, the association remains only borderline significant (OR 2.50; 95% CI=1.00-6.27) (Level 3 evidence). Use of non-loop diuretics is not associated with overactive bladder symptoms (urinary frequency or urgency).
3. Nocturia
Nocturia can occur with or without nocturnal polyuria, defined as night-time excretion of greater than one third of the total daily urine production.  Nocturnal polyuria has been associated with the presence of increased edema in the legs, and presumed redistribution of this fluid at night in the supine position leading to nocturnal diuresis.[7]  Fluid retention and accumulation in the lower extremities can occur as a side effect of several different medication classes, however our search yielded no studies that provided direct evidence linking consumption of pharmaceutical agents with nocturnal polyuria.  The recommendation to avoid medication-associated edema for the treatment of nocturia is therefore based on expert opinion and clinical experience only.[1] Peripheral edema has been reported most frequently with non-steroidal anti-inflammatory agents (NSAIDS), certain calcium-channel blockers, the thiazolidinedione glucose-lowering drugs, and the GABAergic analgesics (gabapentin and pregabalin).  Both the non-selective NSAIDS and newer COX-2 inhibitors have been associated with decreased glomerular filtration and sodium excretion leading to a higher risk of fluid retention.[8]   Ankle edema occurs with all types of calcium channel blockers, presumably due to vasodilation, with the highest prevalence of 30% in patients taking the dihydropyridine agent, nifedipine.[9, 10] In a randomized controlled trial comparing nifedipine to a beta-blocking agent, bisoprolol in older adults with diastolic hypertension, patients on nifedipine reported a higher incidence of pedal edema and nocturia.[11]  Unfortunately, no placebo group was available for comparison, and many patients were concomitantly taking non-loop diuretics. Pedal edema has also been reported by up to 25% of patients on 2-year therapy with the oral hypoglycemic agent pioglitazone.[12-14]   Postulated mechanisms of action of the thiazolidinedione oral hypoglycemic agents include increased sodium reabsorption, increased plasma volume and peripheral vasodilatation. Lastly, GABAergic analgesics such as pregabalin have also been shown to induce peripheral edema in a dose-dependent fashion, with an incidence ranging from 8% to as high as 17% in diabetic patients treated concomitantly with pregabalin and oral thiazolinediones.[15, 16]
4. Incontinence
Few rigorously designed studies have examined the effect of medication exposure on incident urinary incontinence.[17]  Only post-menopausal hormone therapy has been examined in the context of a large randomized placebo controlled trial, with findings indicating a positive and significant effect on the risk of de novo incontinence in women.[18] In the Women’s Health Initiative study, the risk for new hormone replacement users aged 50 to 79 years was highest for stress incontinence (estrogen and progesterone: relative risk 1.87, 95% CI 1.61-2.18; estrogen alone: relative risk 2.15, 95% CI 1.77-2.62), followed by mixed incontinence (estrogen and progesterone: relative risk 1.49, 95% CI 1.10-2.01; estrogen alone: relative risk 1.79, 95% CI 1.26-2.53). The combination of estrogen and progesterone had no significant effect on developing urge incontinence (relative risk 1.15, 95% CI 0.99-1.34), but estrogen alone increased the risk by 30% (relative risk 1.32, 95% CI 1.10-1.58). The Health, Aging and Body Composition longitudinal cohort study confirmed this hormone-associated increased risk of incident incontinence in women aged 65 years and older, even when accounting for other health and functional status factors (odds ratio 1.60, 95% CI 1.08-2.36).[19] Among women experiencing incontinence at baseline in the Women’s Health Initiative Study, the frequency and amount of incontinence significantly worsened at 1-year follow-up with both estrogen and combination therapy.  [18]   This deleterious effect of combined therapy for exacerbating existing stress and urge incontinence was replicated in the Heart and Estrogen/Progesterone Replacement Trial, where the number of incontinent episodes per week increased an average of 0.7 in the hormone group and decreased by 0.1 in the placebo group (p <.001).[20]  A number of mechanisms from animal studies have been proposed to explain estrogen’s effect on the lower urinary tract, such as increased bladder contractility or decreased urethral collagen cross-linking, but these remain theoretical.[21] 
Alpha-blockers are the only other medication class found to be associated with incident incontinence.[19] Current consumption of antihypertensive alpha-blocking agents (prazosin, doxazosin and terazosin) incurred a 5-fold greater risk of incident incontinence among older women participating in the Health, Aging and Body Composition longitudinal cohort study. [19] In a separate case control study, 20/49 women taking alpha-blocking antihypertensives experienced incontinence compared to 8/49 controls (40.8 vs. 16.3%, p<0.0; odds ratio 2.5, 95% CI 1.22-5.13), a relationship that no longer persisted when patients on loop diuretics were excluded from the analysis.[22]  Upon discontinuation of the alpha-blocking agents, 13/18 of the women with incontinence reported total or almost complete resolution of their urinary symptoms.[22]  Alpha-blocking agents plausibly precipitate incontinence by reducing urethral pressure, however the type of urinary incontinence was not specified in either study. 
Data on benzodiazepines are conflicting. In cross-sectional analyses, benzodiazepine use has been associated with a 33-72% increased risk of  incontinence in both women and men,[23, 24] but this relationship has not been replicated in a large longitudinal study examining incident incontinence.[19] The latter study examined the effect of benzodiazepines as part of a group of all centrally acting medications, and this may have attenuated a class-specific effect. [19] Benzodiazepines bind to GABAA receptors in the central nervous system and could potentially have an effect on the lower urinary tract system either directly, by causing relaxation of striated pelvic floor muscles, or by interfering with afferent sensory messages from the bladder;, or indirectly through their effect on mobility and toileting ability. Further research is needed to dissociate the potential effect of benzodiazepine dose and drug (long vs. short-acting) on these various intermediate outcomes. 
Although earlier cross-sectional analyses suggested that diuretics may be implicated in causing incontinence,[24, 25] existing evidence now suggests that this may not be the case.  The Health, Aging and Body Composition longitudinal cohort study found no relationship between the current use of  loop, thiazide or potassium sparing diuretics and the onset of incontinence over a three-year period. [19] Another large epidemiologic study also found no link between incontinence and the use of diuretics in both sexes.[26]  Only in a small subset of men with proven detrusor overactivity who underwent urodynamic studies, was diuretic use associated with incontinence.[26]  The use of loop diuretics was clearly not associated with incontinence after adjustment for age, sex, comorbidities and polypharmacy in the clinical case series that we reported earlier. [4] As such, there is currently no good evidence linking incontinence with the use of diuretics. 
Two clinical case studies provide evidence that cholinesterase inhibitors can precipitate incontinence in older adults with dementia.[2, 3] In the first series of 94 patients started on a cholinesterase inhibitor, 7 developed incontinence (7.4%).[2] Incontinence proved transient in the majority of patients, but persisted in one, and led to discontinuation of the cholinesterase inhibitor in another.  In the second series of 216 patients attending a memory clinic, the use of cholinesterase inhibitors again precipitated or worsened incontinence in 7%.[3]   The proposed mechanism is increased cholinergic transmission at muscarinic receptor synapses in the bladder wall leading to enhanced detrusor contractility. 
Cough occurs in up to 50% of patients taking angiotensin-converting enzyme (ACE)  inhibitors,[27] and can produce or exacerbate stress incontinence by increasing urethral pressure. A number of case reports were found that describe cough-induced stress incontinence upon initiation of an ACE inhibitor, which remits upon discontinuation [28, 29]. One case series reported a 10% incidence of severe drug-induced stress incontinence in diabetic post-menopausal women initiating ACE inhibitors.[30] 
Other central-nervous system drugs, such as the selective serotonin reuptake inhibitor (SSRI) antidepressants, narcotics and antipsychotics present conflicting evidence with regards to incontinence. One compelling retrospective cohort study found that exposure to SSRIs significantly increased the risk of incident incontinence by 75%, or an extra 14 cases of incontinence per year.[31] However, urinary retention has also been reported with some SSRIs, and studies with the mixed mechanism antidepressant duloxetine (a dual norepinephrine and serotonin re-uptake inhibitor) suggest that these agents may have a continence-promoting effect, so the data remain inconclusive.[32]  Whereas cross-sectional surveys have reported significant associations between incontinence and exposure to antidepressants and narcotics,[25]  longitudinal analysis have not.[19] Similar to the benzodiazepines, further research is needed to tease out whether there are class or dose effects, and whether the conditions for which these drugs are prescribed are causative factors in and of themselves.  

Voiding disorders

Because of the complex mechanism of micturition, many drugs can potentially interact with the voiding process via different modes of action.[33] Impaired emptying and full-blown urinary retention are more likely to occur in susceptible older individuals who already have diminished detrusor function.[34]  In one large longitudinal cohort study of middle-aged and older men, calcium channel blockers, beta-blockers and other non-diuretic antihypertensive and antiarrythmic agents (e.g. disopyramide) were found to increase the risk of urinary retention 2-to-3-fold, whereas diuretics, tranquilizers and antidepressants did not.[35]  A case series of 100 patients with urinary retention revealed that drugs with anticholinergic properties such as oxybutynin, amitriptyline, and medications used for the common cold were responsible for 12% of cases.[36]  Although many case reports implicate agents with anticholinergic activity, such as risperidone and the bladder antimuscarinics, the incidence of urinary retention from clinical trials of these drugs is low.[33]  And wWhile post-operative pain control with opioid analgesics has been associated with incident urinary retention, it is unclear whether it is the pain, the fluid management or the drugs that triggers voiding dysfunction.[37]   NSAIDs, because of their inhibition of  prostaglandin synthesis, were found to double the risk of urinary retention in a dose dependent fashion in a single large population-based case-control study, however this data needs to be reproduced in a prospective fashion.[38]  In conclusion, more research is needed to determine the level of evidence implicating each drug class in voiding disorders. Until then, it would be prudent to discontinue all potential drugs with anticholinergic or opioid receptor binding affinities in the event of voiding symptoms. 

Table 1: Commonly used medications that may cause or exacerbate LUTS in the elderly

Associated symptom

Medication

Proposed mechanism

Level of evidence

 

Urinary frequency

Loop diuretics

 

Lithium

 

Polyuria

 

Polyuria

Level 3

 

Level 3/Level 4

Urinary urgency

 

Loop diuretics

 

Polyuria

Level 3

Nocturia

NSAIDs

Calcium channel blockers

Thiazolinedione oral hypoglycemics

GABAergic analgesics

 

Fluid retention with peripheral edema which redistributes at night causing nocturnal diuresis

Level 4

Incontinence

 

Estrogen alone*

Estrogen + progesterone*  

 

Alpha-blocking* antihypertensives 

 

Benzodiazepines

 

 

 

Diuretics

 

Cholinesterase inhibitors

 

Angiotensin converting enzyme inhibitors

 

Other centrally active agents (narcotics, antipsychotics, antidepressants)

                   

Unknown

Unknown

 

Reduced urethral tone

 

Relaxation of urethral sphincter, interference with afferent sensory messages or mobility impairment which could interfere with toileting

 

NO ASSOCIATION

 

Increased detrusor contractility

 

Cough-induced stress incontinence

 

 

Sedation, mobility impairment, constipation, unknown

Level 1

Level 1

 

Level 2/Level 3

 

 

Level 4

 

 

Level 2/Level 3

 

Level 3

 

Level 3/Level 4

 

 

Level 3/Level 4

Voiding disorders

 

Alpha-adrenergic agonists

 

Anticholinergic medication

 

NSAIDs

 

Increased urethral tone

 

Impaired detrusor contractility

 

Relaxation of the detrusor muscle via inhibition of prostaglandin activity

Level 4

 

Level 4

 

Level 3


*evidence available for women only

Levels of evidence:  
Level 1 = systematic reviews, meta-analyses, good quality RCTs
Level 2 = RCTs, good quality prospective cohort studies
Level 3 = case-control studies, case series
Level 4 = expert opinion

References 

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2. Hashimoto M, Imamura T, Tanimukai S et al. Urinary incontinence: an unrecognised adverse effect with donepezil. Lancet 2000; 356: 568.
3. Starr JM. Cholinesterase inhibitor treatment and urinary incontinence in Alzheimer's disease. J Am Geriatr Soc 2007; 55: 800-1
4. Ekundayo OJ, Markland A, Lefante C et al. Association of diuretic use and overactive bladder syndrome in older adults: a propensity score analysis. Arch Gerontol Geriatr 2009; 49: 64-8.
5. Boton R, Gaviria M, Batlle DC. Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy. Am J Kidney Dis 1987; 10: 329-45.
6. van Melick EJ, Meinders AE, Hoffman TO, Egberts TC. Renal effects of long-term lithium therapy in the elderly: a cross-sectional study. Int J Geriatr Psychiatry 2008; 23: 685-92.
7. Torimoto K, Hirayama A, Samma S et al. The relationship between nocturnal polyuria and the distribution of body fluid: assessment by bioelectric impedance analysis. J Urol 2009; 181: 219-24; discussion 24.
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Date added to bjui.org: 21/03/2011 (publication information)
This content is exclusive to bjui.org website.
DOI: 10.1002/BJUIw-2011-011-web

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VIRTUAL EDITIONS: Medications that contribute to LUTS in the elderly: A Review

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