Diabetes-Associated Bladder Dysfunction in the Older Adult

Abstract

Diabetic cystopathy is a chronic complication of diabetes with a classic triad of symptoms: decreased bladder sensation, increased bladder capacity, and impaired detrusor contractility.

This article discusses age- and diabetes-related changes that affect lower urinary tract function. The article also reviews bladder function in the older adult diabetic, explores bladder dysfunction prevention, and suggests management strategies for diabetic cystopathy.

Introduction

The effects of aging on renal function and the lower urinary tract can be exacerbated by superimposed chronic disease, particularly diabetes mellitus.

Diabetic nephropathy, a life-threatening condition, has received considerable attention. Diabetic cystopathy (DC) has received less, although it is a chronic complication that affects day-to-day life, predisposes individuals to urinary tract infections (UTIs), potentiates renal complications, and poses obstacles to optimum health.

It is insidious in onset, characterized by increased length of time between voiding. Prevalence is estimated to be between 32% to 45%.

Cerebral control and central coordination of micturition is complex and not entirely understood. Voiding is mediated by various structures, including the pontine micturition center, periaquaductal gray matter, and frontal lobe.

Lesions in the cortex, such as those caused by stroke, transient ischemia, or a dementing illness, affect voluntary control as a result of damage to the centers for cerebral control and voiding coordination.

Recent changes to standardized terminology of lower urinary tract function relating to detrusor overactivity recognize the frequent relation to neurologic conditions, such as stroke, referring to this as neurogenic detrusor overactivity.

Urge incontinence in older women has been associated with increased risk of falls and nontraumatic fractures.

Age-related changes in the urinary tract are difficult to differentiate from those of disease pathophysiology.

Current thought suggests that cellular- and tissue-level aging includes smooth muscle degeneration and deposition of increased connective tissue, in addition to axonal degeneration and possible alterations to cholinergic (decreased muscarinic receptors) and adrenergic responses. These anatomical and neurologic alterations result in functional changes in the lower urinary tract, as shown in Table 1, but do not themselves cause urinary incontinence.

The age-related changes do not cause urinary incontinence, but they may predispose the elderly patient to:

• Urge urinary incontinence: the involuntary leakage of urine associated with a strong urge to void

• Stress urinary incontinence: leakage with increased abdominal pressure

• Overflow incontinence: leakage associated with urinary retention

Nocturnal urinary output also appears to change with age, with higher rates of urine excretion at night in older subjects.

Much of the research examining this phenomenon has involved frail hospital patients and nursing home residents, so whether variation in AVP level is a norm of aging or potentially a result of other disease processes is subject to debate.

Finally, functional limitations may contribute to incontinence in at-risk patients. For example, mobility changes or pain from musculoskeletal disease, such as arthritis or osteoporotic spinal compression fractures, can make toileting and continence difficult.

Agnosia and apraxia may develop in people with an Alzheimer dementia, leading to difficulties carrying out activities of daily living. These limitations, produced as effects of comorbid diseases, need to be considered in the assessment of the diabetic person with bladder dysfunction.

The most likely cause of incontinence in the patient with DC is overflow incontinence, although the presenting symptoms might suggest stress or urge urinary incontinence.

Patients with DC also are at increased risk of detrusor overactivity, but whether this results from DC alone or cerebral perfusion issues associated with hypercholesteremia, transient ischemic attacks, or stroke is not clear.

The classic triad of bladder symptoms associated with DC includes decreased bladder sensation, increased bladder capacity, and impaired detrusor contractility with resultant increased postvoid residual (PVR) urine.

Increased PVR leaves the individual prone to UTIs, a common cause of acute confusion and functional decline in older adults. A possible link between deterioration of renal function and chronic asymptomatic bacteriuria in individuals with diabetes has been postulated.

Neuropathies in diabetics have been extensively studied in recent years, but none of these large trials included outcome measures relating to bladder dysfunction.

Increasingly, DC is described as a manifestation of autonomic neuropathy, although some believe it also represents peripheral somatic neuropathy.

Several classification systems for diabetic neuropathy have been suggested, but none has included specific lower urinary tract function. Greene, Stevens, and Feldman proposed that genitourinary neuropathy fits within the autonomic neuropathy category, along with sudomotor, cardiovascular, and gastrointestinal neuropathies (Table 2). Autonomic neuropathies are thought to be serious and irreversible complications of diabetes.

Autonomic neuropathies in diabetes result in axonal degeneration, demyelination, and fiber loss. Hyperglycemia has been implicated as a primary contributor to development of neuropathic complications.

Tight control of blood glucose decreases long-term neurologic and microvascular complications of diabetes, but the precise relationship of glycemic control and duration of diabetes to DC is not known. One possible mechanism of glucotoxicity in nervous tissue is increased polyol pathway activity in which accumulations of sorbitol and fructose induce damage. The exact mechanism of damage has not yet been elucidated.

Other possible contributors to diabetic nerve damage include immune mechanisms, microvascular insufficiency, deficiency of growth factor, and decreased expression of laminin, a glycoprotein important in nerve regeneration.  It even has been suggested that blood glucose concentration affects the rate at which aging occurs and that diabetes may be a syndrome of premature aging.

Diabetic autonomic neuropathy also may underlie the blunting of the usual nocturnal fall in blood pressure, a cardiovascular dysautonomia in which the normal circadian rhythm of sympathovagal function declines.

Assessment of the older diabetic individual with symptoms of bladder dysfunction includes identification of age-related changes and risk factors arising from physiologic, psychosocial, and environmental influences.

History and Symptom Assessment

A description of the symptoms as experienced by the older adult or perceived by the caregiver is an important first step. Because DC is often insidious, the onset may be difficult to describe precisely.

The classic symptoms of overflow incontinence or reduced contractility bladder are weak stream, hesitancy in starting urination, dribbling (if high residual and resultant overflow incontinence are present), a sensation of incomplete emptying, leaking with increased abdominal pressure, and infrequent voiding.

Some elders present with only urgency and frequency, others with recurrent UTIs.

Physical Examination

Physical examination includes complete neurologic evaluation with assessment of anal sphincter tone and saddle anesthesia.

Examination of the rectum assesses stool presence and consistency and, in men, prostatic size and shape. In women, a gynecologic examination assesses pelvic organ prolapse and pelvic floor muscle tone, estrogenization of the vaginal tissue, and the presence of Candida albicans, to which diabetic women are prone.

Because DC is a manifestation of autonomic neuropathy, screening for other signs of autonomic dysfunction may be included, particularly heart rate and orthostatic hypotension assessment measured by blood pressure while the patient is lying and standing.

It is not clear whether cardiovascular autonomic neuropathy occurs with or progresses at the same rate as DC, but the presence of cardiovascular dysautonomia may identify other problems that need to be addressed.

Laboratory and Other Investigations

Microscopic urinalysis (and urine culture, if indicated), creatinine, blood urea nitrogen, and periodic urine microalbumin to assess renal function are part of initial assessment. Serum glucose and glycosylated hemoglobin, which reflects 2 to 3 months of glycemic control, also should be obtained.

Because one of the hallmarks of DC is an increase in residual urine, the PVR should be measured either by portable ultrasound or in-and-out catheterization.

Ideally, PVR should be measured within minutes of voiding. Norms for acceptable levels of PVR have not been established. A suggested normal range in the older adult is between 50 mL and 150 mL.

A bladder diary, as shown in Table 3, is also part of the initial investigation and helps evaluate the amount and type of fluid ingested and voiding patterns. Most older patients have no difficulty completing a bladder diary.

Detailed assessment of bladder function with urodynamic studies is indicated if initial management is not successful or for patients whose symptoms are mixed, such as urgency or stress incontinence (Table 4).

Urodynamic findings common to DC include impaired sensation, increased bladder capacity, reduced or absent detrusor contractility, inability to initiate voiding, and an increased PVR.  Detrusor overactivity with reduced contractility, linked to cerebral lesions for which diabetics are at increased risk, also may be diagnosed. Because client-reported symptoms do not always match actual quantified function, information from urodynamics can help develop an appropriate plan of management, including medications (Table 5).

Psychosocial and Cognitive Assessment

Because older diabetics are at risk for stroke and impaired cognition, the assessment should include baseline mental status, for example, completion of a standardized screening tool such as the Mini-Mental State Examination.

Obtaining a cognitive history from a family member or caregiver helps determine whether impaired cognition is an issue. Functional and cognitive information should include activities of daily living and inquiries about difficulties with memory, language, agnosia, apraxia, and behavioral changes.

Little research has been published to guide practice in DC management. Evidence is modest at best for all interventions except glycemic control. Preventing further diabetes-associated neuropathy is an important goal in modifying or eliminating risk factors. Other management goals include symptom relief, infection prevention, renal function maintenance, continence, and adequate bladder emptying. Table 6 summarizes strategies for DC management.

Glycemic Control

Hyperglycemia has been linked to neuropathy and other complications of diabetes. Strategies to achieve optimal glycemic control include diet (including increased fiber), exercise, and weight loss. Individuals with diabetes should be referred to a self-management teaching program for education on glycemic control. Age should not be a barrier to making an education referral. If cognitive impairment is an issue, the caregiver also must participate.

Glycemic targets for preprandial self-monitored blood glucose levels are 80 to 120 mg/dL (4.4 to 6.7 mmol/L). The target for glycated hemoglobin level is less than 7 and should be monitored routinely as part of follow-up. These targets may be modified upward for some older individuals, especially if they are prone to hypoglycemic episodes.

Individuals who are not able to attain this target by diet and exercise alone will require oral glucose lowering agents, insulin, or both.

Other preventive measures include hypertension and hyperlipidemia control and smoking cessation. Angiotension converting enzyme (ACE) inhibitors frequently are used in diabetes for both blood pressure control and treatment of atherosclerotic renal vascular disease.

The target blood pressure for individuals with diabetes is less than 130/85.

Scheduled Toileting and Double Voiding

Advising patients to void every two to four hours during the day and to use a double voiding technique may improve bladder emptying, improve continence, and minimize risk of infection. Because DC is gradual in onset, it may be useful to encourage the diabetic client to begin this habit even if the PVR is below 150 mL.

Double voiding involves attempting to empty the bladder by staying on the toilet and trying to void more than once with each trip to the toilet. Elders with cognitive impairment might need supportive cuing from caregivers to carry out the strategy. These noninvasive strategies are worth trying, although their effectiveness has not been studied. Teaching these strategies should be followed with periodic measurement of PVR in patients with elevated residual urine to ensure that adequate bladder emptying is achieved.

Bladder Expression

Bladder expression, either by abdominal straining (Valsalva maneuver) or manual compression of the lower abdomen (Credé's maneuver), has been studied in the spinal cord population but not in the diabetic population.

Manual compression is contraindicated in the presence of increased intravesical (bladder) pressure, vasal reflux, or vesico-uretero-renal reflux.  The effectiveness has not been systematically studied. Wein cautiously suggests this technique might be successful in those with an areflexic (hypotonic or atonic) bladder with some outlet denervation, presenting as stress incontinence.

Intermittent Catheterization

Intermittent catheterization (IC) is one approach to achieve bladder emptying in DC when voiding strategies alone are ineffective.

Most of the research on IC has involved patients with spinal cord injury and children with myelomeningocele.

No evidence supports the choice of either sterile or clean technique in the diabetic population, and most individuals reuse catheters washed with soap and water and air-dried.

If urethral irritation occurs, a single-use hydrophilic catheter is available that provides an evenly lubricated mucoid surface and can be more comfortable than a standard plastic catheter inserted with a water-soluble lubricant.

Only one study of IC in older people was identified. Bennett and Diokno demonstrated that older adults were able to learn IC with careful education and support.

However, many individuals may be uncomfortable with touching the urethra, and older women may be less likely to understand the anatomy of the female genitalia.

Case reports demonstrate that older women with diabetes have been taught IC; however, reluctance to accept the strategy should be recognized.

The most appropriate frequency of performing IC is not known. The important concept is to maintain a low vesicle pressure so that there is no reflux to the kidneys or risk to renal function.

Recommendations for catheterization vary from once, twice, or four times daily to developing an individual routine by use of a bladder diary, noting the combined volume of voided and catheterized urine with a total of 400 to 500 mL.

Strategies to Manage Nocturnal Polyuria

Nocturnal polyuria arises from possible age-related changes and from autonomic neuropathy in diabetes. Eliminating nocturnal polyuria may not be realistic, but the impact may be minimized by taking most of the fluid for the day in the morning or early afternoon, avoiding caffeinated beverages in the evening, and ensuring the bladder is empty before going to bed. Placing a commode by the bedside at night may reduce risk of falls and fractures.

Pharmacologic Strategies

No effective medications currently are available to assist with bladder emptying in DC.

Bethanechol, a parasympathomimetic agent, has been used with inconsistent results. Research on agents such as aldose reductase inhibitors, which inhibit the accumulation of sorbitol and fructose to potentially improve neuropathy, advanced glycosylation end product, and neurotrophic factors may lead to future treatment options.

Intranasal 1-deamino-8-D-arginine vasopressin has been used to reduce nocturnal polyuria, but the safety of this option in elders is not clear. Alpha blockers may be helpful in outlet obstruction from prostatic enlargement.