Aging and Rehabilitation

Gary S. Clark

Patrick Kortebein

Hilary C. Siebens

Aging, an integral part of living, is typically accompanied by gradual but progressive physiologic changes and an increased prevalence of acute and chronic illnesses. Although neither a disease nor a disability per se, aging nonetheless is associated with a higher incidence of physical impairment and functional disability. Many of these functional difficulties occur from the interactions of decreased physiologic reserve with chronic illness. Ongoing research suggests effective interventions to prevent, delay, minimize, or reverse such physiologic declines (1,2). Appropriate roles for geriatric rehabilitation accordingly include not only intervening to reverse disability caused by specific disease or injury (e.g., stroke, hip fracture) but also contributing to preventive gerontology by virtue of promoting structured physical fitness (i.e., wellness) programs and early rehabilitation for common musculoskeletal disorders to avoid progression to disability (1, 2, 3, 4).

Significant contributions of rehabilitation to care of older adults include functional assessment (including evaluation of underlying impairments contributing to functional loss and disability) with realistic goal setting, interdisciplinary team care, and efficacious adjustment of therapy interventions (e.g., timing, setting, intensity) to prevent, reverse, or minimize disability (2,5,6). Given the burgeoning number of older persons living longer, Rusk’s observation, as modified by Kottke, becomes ever more relevant: “As modern medicine adds years to life, rehabilitation becomes increasingly necessary to add life to these years” (7). The goals of this chapter are to:

Discuss relevant aspects of epidemiology and physiology of aging
Examine the impact of the environment on function in older adults
Review data on patterns of functional decline in older adults, with particular attention to the effects of hospitalization
Identify general principles of assessing functional loss as a basis for formulation of rehabilitation plans of care
Detail appropriate rehabilitation interventions for a number of disabling clinical syndromes and conditions that occur frequently in older adults.

AGING—EPIDEMIOLOGY AND PHYSIOLOGY

Demography and Epidemiology of Aging

Demographic Imperative

The context for the increasing interest, and concern, about health care needs of older adults is found in demographic projections of an expanding elderly population in the United States and other developed countries. At the turn of the 20th century, one of every 25 Americans (4%) was 65 years of age or older. By 1994, this population had increased to one of every eight Americans (12.6%), or 33.2 million (8,9). While the elderly population grew 11-fold during this interval, the under-65 population only increased by a factor of three. Current projections indicate that 86.7 million, or one of every five Americans (20.7%), will be 65 years of age or older by the year 2050 (10). By 2029, all “baby boomers” (Americans born post-WW II, between 1946 and 1964) will be 65 years or over (10). Between now and 2030, the fastest growing segment of the population will be the 65 to 74 year olds, increasing from the current 6.3% to 10.4%. Between 2030 and 2050, however, the 75+ population will outpace the 65 to 74 cohort, reaching 11.6% of the population (every ninth American), while the 65 to 74 year olds will account for 9.0% (10).

Distribution of the elderly is uneven across the United States, with 50% living in just nine states. While California has the greatest number of citizens over the age of 65, Florida has the highest proportion of elderly (18.6%) (8). There are also ethnic aging trends, with projections that by 2050 the proportion of older white individuals will have decreased to 67% (from 87% in 1990), with corresponding increases of older Hispanic and black American citizens of 16% and 10%, respectively.

This demographic phenomenon is not limited to the United States, as a number of developed countries (including Italy, Japan, Germany, Sweden, and Great Britain) show 20% or more of their populations over age 65 (8). As of 1994, there were 357 million older people worldwide, representing 6% of the total population.

There is increasing recognition of differences in health care needs and issues among subgroups of older people. Of particular significance from a health care standpoint is the rapidly expanding relative proportions of the population age 65 years and older who are 75 to 85 years of age (old old) and 85 years of age or older (oldest old). These groups include many of the so-called “frail elderly,” with a disproportionately high prevalence of disabilities and consumption of health services (11). Another related dynamic is recognition of increasing racial and ethnic health disparities among older Americans, as the relative proportions of racial and ethnic minorities increase: from 2003 to 2050 the proportion of Non-Hispanic whites will decrease from 83% to 61%, while Hispanics will increase from 6% to 18%, blacks from 8% to 12%, and Asians from 3% to 8% (12).

Compression of Morbidity

Older people also are living longer: 1990 statistics estimated a longevity at 65 years of age of 15.0 years for men and 19.5 years for women; this is projected to increase further to 17.1 and 22.6 years, respectively, by the year 2040 (13). Contributing factors to these increases in longevity include improved access to health care, advances in medical care, overall healthier life-styles, as well as better health prior to age 65 (14). The increasingly delayed occurrence of death at all ages appears in part to be due to reduced lethality of such diseases as stroke, cancer, and myocardial infarction, resulting from risk factor reduction as well as improved health care interventions (9). Increasingly, people are surviving their initial encounter with these previously fatal diseases, resulting instead in chronic illness. This trend has been termed the fourth stage of epidemiologic transition (i.e., the postponement of death from degenerative diseases) (15). These significant reductions in mortality are associated with an increasing risk for development of various chronic diseases. Certainly, the incidence and prevalence of many potentially disabling chronic illnesses increase substantially among older adults, including arthritis, osteoporosis with associated fractures, stroke, amputation, and various neurodegenerative disorders (e.g., Alzheimer’s disease, Parkinsons disease) (2,10,11,13).

This demographic imperative has far-reaching implications for increasingly limited U.S. health care resources and dollars: current national direct cost of medical services for older individuals with chronic conditions is in excess of $470 billion (in 1990 dollars), with a projected near doubling by the year 2050 (13). In 2004, the average annual health care expenses were $8,900 for the 65+ population, compared to $3,028 for the under 65 population (10). The old-old and oldest-old groups consume the greatest proportion of resources, and a disproportionate amount of these health care costs represent nursing home and other institutional care (11). While the overall proportion of elderly individuals residing in nursing homes decreased from 6.8% in 1982 to 4.2% in 1999, these rates vary dramatically by age (16). Only 1% of young old (65 to 74 year olds) reside in nursing homes, contrasted with 20% of the oldest old (85 years of age or older) (9). In fact, the latter group comprises 45% of all elderly nursing home residents.

From another perspective, however, the vast majority of the 85-or-older population is not in nursing homes, and half of those in nursing homes do not necessarily need to be there because they have potentially preventable (or reversible) disabilities related to their chronic disorders (17). In fact, it appears that much of the increased health care cost associated with aging (across all health care settings) is significantly related to activity limitation, rather than chronic disease (18). Fortunately, there is increasing evidence that disability among older individuals may be decreasing (16,19). Reports of limitation of activity due to a chronic condition in the 65+ population have continued to decrease, from 38.7% in 1997 to 32.6% in 2006 (12).

These findings continue to lend credence to the concept advanced by Fries in 1980 of “compression of morbidity,” in which he predicted that if the age of onset of disability could be significantly delayed (e.g., with regular exercise, healthier diets, elimination of smoking, improved health care interventions) in the context of a relatively “fixed” life span, then terminal predeath disability could be compressed into a shorter interval (20). He postulated that health care needs for older people would decrease because they would be relatively healthy and functional until shortly before their death. A related prediction was that this anticipated short duration of predeath morbidity, and accompanying disability, would be expected and accepted with acknowledged futility of medical intervention. There is consistent evidence of increased health care costs associated with aging, with one study documenting nearly one half of life-time health care costs occurring after age 65 (21). Interestingly, although a number of reports have documented dramatically increasing health care costs near the end of life, it should be noted that these are costs of dying, not of aging per se (22). Further, there is evidence suggesting that the incremental costs associated with extending life may actually plateau or even decrease (23, 24, 25). These findings are of critical significance in the context of increasing focus on cost containment and debate over the feasibility and appropriateness of rationing of health care (26). Twenty years after his initial predictions, Fries (and others) cites increasing evidence in support of the trend of compression of morbidity, even though the mechanisms are not clear (27,28). He reiterates the importance of a research agenda focused on delineation of the epidemiology of disability, determination of the fundamental basis of age-associated chronic conditions, and identification of effective interventions for preventing or delaying resulting disability (27). This call to action has been echoed by others as well (1,2,21). On the other hand, Kane raises disturbing questions regarding potentially adverse economic, cultural, and individual consequences of successfully overcoming the aging (and dying) process and urges ongoing dialogue to further explore these ethical questions (29).

Active Life Expectancy

A derivative of research into longevity and epidemiology of aging relates to issues of quality of life, given the increased incidence of frequently disabling chronic disorders such as degenerative neurologic diseases (e.g., Alzheimer’s disease, Parkinson’s disease), degenerative musculoskeletal conditions (e.g., osteoporosis, osteoarthritis), and multisensory losses (e.g., cataracts, presbycusis). One concept that attempts to delineate quality of life for older individuals has been termed “active life expectancy,” referring to the proportion of remaining life span characterized by functional independence (30). This concept, also referred to as “disability-free life expectancy,” has been expanded to consider both physical and cognitive impairments, as well as their interrelationships (28,31). A significant gender difference in active life expectancy with aging has been identified. As can be seen in Table 59-1, older men have a greater proportionate active life expectancy at all ages. However, due to greater longevity, older women enjoy longer actual durations of active life expectancy than older men, until age 85 (31,32). A recent longitudinal British study confirmed a gender difference, with men aged 65 showing 79% active life expectancy (12.1 of 15.3 years) and women aged 65 showing 57% active life expectancy (11.0 of 19.4 years) (28). Further investigation into
dynamics impacting active life expectancy reveals the deleterious effects of diabetes (decreased total life expectancy and active life expectancy at all ages, with a 25% reduction in active life expectancy in 85 year olds) and depression (reduction of active life expectancy by 6.5 years in 70-year-old males and by 4.2 years in 70-year-old women) (33,34).

TABLE 59.1 Active Life Expectancy (Remaining Years of Functional Independence, Compared to Projected Longevity) by Gender and Age Cohort

Age	Males	Females
65	82% (11.9 of 14.4 y)	73% (13.6 of 18.6 y)
85	50% (2.6 of 5.2 y)	35% (2.3 of 6.4 y)
95	20% (0.6 of 3.2 y)	10% (0.4 of 3.7 y)
Adapted from Manton KG, Stallard E. Cross-sectional estimates of active life expectancy for the U.S. elderly and oldest-old populations. J Gerontol. 1991; 46(suppl):170-182.

Comorbidity, Frailty, and Disability

Although the increasing incidence and prevalence of (often multiple) chronic diseases with aging is well documented, there is no one-to-one correlation between either disease and illness (35) or disease and disability (19). A significant proportion of older people are limited in the amount or kind of their usual activity or mobility secondary to chronic impairments: over 60% of adults with functional impairments due to chronic health problems are 65 years of age or older (13). However, disability in this older population can also be very dynamic, with frequent transitions between periods of independence and disability and levels of disability (36,37). Also, the overall health of progressive cohorts of older persons has been changing. Although there have been predictions that future generations may well be healthier than current generations, due in part to higher levels of education and health awareness (36), there are disturbing trends of increasing obesity and diabetes in older adults, with significant associated morbidity and mortality (10).

FIGURE 59-1. Definitions of frailty, comorbidity, disability. (From Fried LP, Ferrucci L, Darer J, et al. Untangling the concepts of disability, frailty, and comborbidity: implications for improved targeting and care. J Gerontol Med Sci. 2004;59(3):255-263.)

Fried et al. have helped to clarify the dynamics of interrelationships among comorbidity, frailty, and disability—terms frequently used interchangeably—by providing discrete definitions of each entity and describing the synergistic impact of each on the other(s) (38). As seen in Figure 59-1, Disability accordingly is defined as “difficulty or dependency in carrying out activities essential to independent living” (such as activities of daily living [ADLs], mobility, instrumental activities of daily living [IADLs]), while Frailty is “a physiologic state of increased vulnerability to stressors that results from decreased physiologic reserves, and even dysregulation, of multiple physiologic systems.” Frailty appears to represent an aggregate expression of risk resulting from age- or disease-associated physiologic accumulation of subthreshold decrements affecting multiple physiologic systems (38). Fried cites evidence in support of a phenotype of the clinically frail older adult, characterized by the presence of a critical mass of three or more “core elements” of frailty (weakness, poor endurance, weight loss, low physical activity, and slow gait speed) (39). Comorbidity is commonly defined as the concurrent presence of two or more disease processes in the same individual. Fried suggests that comorbidity is the aggregation of clinically manifested diseases present in an individual, while frailty is the aggregate of subclinical losses of reserve across multiple physiologic systems (38).

FIGURE 59-2. Overlap of frailty, comorbidity, disability. (From Fried LP, Ferrucci L, Darer J, et al. Untangling the concepts of disability, frailty, and comborbidity: implications for improved targeting and care. J Gerontol Med Sci. 2004;59(3):255-263.)

Fried further documents the interrelationships between frailty, comorbidity, and disability (Fig. 59-2), noting that frailty and comorbidity each predict disability, while disability appears to exacerbate frailty and comorbidity (38). While medical care for each of these entities is typically complex, particularly when they coexist, Fried specifically notes that rehabilitation interventions for disabled older adults to regain function and/or prevent further functional decline need to factor in recognition and treatment of frailty and comorbidity to maximize likelihood of success. She cites growing evidence to suggest that frailty, comorbidity, and disability may be preventable, but with different intervention strategies (38). The importance of prevention is reinforced by the clear association of each entity, especially when concurrent, with higher health care costs and poorer survival (38,40). Recent research is further differentiating between various subtypes of disability in older individuals (transient, short-term, long-term, recurrent, and unstable) and their relative clinical significance (41).

In summary, an increasing proportion of older people are living longer and are at increased risk of developing varying (and changing) degrees of comorbidity, frailty, and functional losses with disability. The challenge for health care providers, accordingly, is to try to prevent the onset/progression of these entities with early and effective medical and rehabilitation interventions, to reverse or at least minimize their deleterious effects on health and function.

Successful Aging

Distinctions have been made between aging processes representing “primary aging” (i.e., apparently universal changes that occur with aging, independent of disease and environmental effects) and “secondary aging,” which includes lifestyle and environmental consequences and disease associated with the aging (42,43). A number of tenets associated with aging research are being reexamined, particularly with the observation that a pathologic process may exaggerate an aging process believed to be normal, even before the disease is detected clinically (42). There is increasing evidence that the nonpathologic processes of aging are distinct from, but not necessarily independent of, the pathologic processes of disease (38,44).

Most studies of normal aging have focused on the physiological and biochemical changes occurring with aging, with explicit exclusion of disease. However, it is increasingly apparent that such factors as personal habits (e.g., diet, exercise, nutrition), environmental exposures, and body composition may have significant impact on observed aging changes (43). Rowe has proposed a conceptual distinction between “successful aging” and “usual aging” (45). He suggests that “successful aging” could be characterized by minimal or no physiologic losses in a particular organ system and would comprise a relatively small subset of the total “normal” (i.e., nonpathologic) aging population. The remaining majority of “normal” older adults demonstrate “usual aging,” with gradually progressive but significant declines in various physiologic functions.

The significance of this concept lies in the implications for modifiability of usual aging by virtue of addressing such variables as level of physical activity, diet and nutrition, and environmental exposures (27,43,44). This principle is demonstrated in studies documenting the effects of exercise, diet, and drugs on the usual aging observations of carbohydrate intolerance. Rowe proposes that geriatric research into health promotion initiatives concentrates on increasing the proportion of older adults who “successfully age” by identifying and modifying extrinsic risk factors contributing to “usual aging” and decreasing the manifestations of “pathologic aging” by preventing or minimizing adverse effects of acquired disease processes (45). This would reinforce the previously described concept of compression of morbidity, with greater active life expectancy. Indeed, studies are helping to determine which factors distinguish high-functioning older adults from other populations of older adults (28,33,43,46).

Theories of Aging

With continuing research, it appears likely that there is no single cause of aging (44,47). The current concepts of aging characterize the process as extremely complex and multifactorial and suggest that various theories of aging should be viewed not as mutually exclusive, but rather complementary (47). From this perspective, hypotheses based on passive (i.e., random) and/or active processes of genetic programming could be considered in conjunction with superimposed nongenetic
mechanisms (e.g., environment, lifestyle), producing varying individual vulnerability (42,44,45,48). Certainly this would help explain the well-documented phenomenon of differential aging, whereby individuals of the same species appear to age at different rates (44,46). Multiple levels of research suggest that rates of aging are affected to varying extents by heredity, lifestyle, environment, occurrence of disease, and psychological coping abilities (17,32,42,46).

Active investigation continues in the areas of neuroendocrine pacemakers, telomere shortening, and attenuation of inducible stress responses (48, 49, 50, 51). A number of studies have also focused on the phenomena of apoptosis and autophagy, related to cell death of proliferating and postmitotic cells respectively, as well as mitochondrial degradation in long-living cells (52,53). There is some evidence suggesting that pathologic stimulation of apoptosis may result in a number of degenerative disorders commonly associated with aging, whereas inhibition appears to be associated with a variety of forms of cancer (52).

Physiology of Normal Aging

The normal aging process involves gradual decreases in organ system capabilities and homeostatic controls that are relatively benign (i.e., asymptomatic or subclinical) in the absence of disease or stress (35). Although the older person progressively adapts to these changes without need (or desire) for outside intervention, the steady decreases of physiologic reserves make older adults potentially vulnerable to functional decline as a result of acute and/or chronic illnesses (42,54). Characteristics of aging include:

Decreased reserve capacity of organ systems, which is typically apparent only during periods of exertion or stress
Decreased internal homeostatic control (e.g., blunting of the thermoregulatory system, decline in baroreceptor sensitivity)
Decreased ability to adapt in response to different environments (e.g., vulnerability to hypothermia and hyperthermia with changing temperatures, orthostatic hypotension with change in position)
Decreased capacity to respond to stress (e.g., exertion, fever, anemia) (35)
The end result of these age-related declines is an increased vulnerability to disease and injury, or frailty (38).

Problems in Study Design

Inherent with studying physiologic changes in aging adults are several potentially confounding variables, which are unique to this population. Awareness of these dynamics will facilitate more accurate interpretations of clinical studies of older adults, with particular reference to generalizability.

Definition of Normal

A significant concern, in view of the heterogeneity of the aging population, is what is truly normal. As noted, there is great variability in rates of aging among healthy elderly and wide variations in individual performance. Further complicating any analysis is a superimposed dispersion of skills due to frequency of significantly impaired function from disease, environment, and lifestyle (32,35). More than 80% of the population over 65 years has at least one chronic disease and 50% two or more disorders (31). Of concern is whether the relative minority of older people who have escaped serious illness should be considered “normal” for the purpose of studies of aging and whether the results of such studies can be generalized to the rest (majority) of the older population.

On the other hand, it is important clinically to be able to differentiate the physiologic consequences of aging (i.e., normal aging) from those of accompanying disease (i.e., pathologic aging) (3). Because detection of disease depends on determination that a patient is other than normal, it is critical to define appropriate age-adjusted criteria for clinically relevant variables in the elderly (55). Although many laboratory values do change gradually with aging, abnormalities should not be a priori attributed to old age. In fact, a number of age-related changes may resemble the changes associated with a specific disease (44). For example, an age-related decline in glucose tolerance is well documented. So dramatic is this change that most people over 60 years of age would be diagnosed as diabetic if traditional criteria, based on studies of primarily younger patients, were applied (56).

Methodology Limitations

A number of methodological problems are associated with the study of aging. Well recognized are frequent discrepancies in age reporting, with a tendency to distort upwardly (57). This is coupled with difficulties in verifying reported ages, due in part to lost or nonexistent birth records.

Another major problem in the design and evaluation of aging studies is the relative validity of both cross-sectional and longitudinal studies. Cross-sectional studies, although easier and less costly (in time and money) to perform, often overemphasize (but may also underestimate) age-related changes (58,59). This can result from a cohort bias, due to significant differences in educational, nutritional, health, and social experiences of people born in different decades. Contributing further to this distortion is the high proportion of elderly in the United States who were foreign born, with relatively less schooling. This has implications in particular for studies of psychological and cognitive changes with aging (19).

On the other hand, longitudinal studies tend to underestimate changes due to aging, primarily as a result of withdrawal and survivor biases with high drop-out rates (46,54,58). Some studies have experienced as much as a 50% drop-out rate over just a 10-year period, leading to questions of self-selection for relative preservation of function (and again, the issue of “supernormals”). Subtle changes in methodology over time may introduce laboratory drifts that are difficult to differentiate from true age-related changes (8). A further concern with serial measurements is the potential for distortion due to learning effects.

Mean Versus Maximal Performance

Another issue in the characterization of aging is that a focus on “average” or “mean” changes in various parameters can
hide remarkable individual variation, particularly regarding peak performance (20). Consider marathon running, which tends to attract a very select (“supernormal”) population, and, thus, individuals with a higher maximal aerobic capacity. For example, a 50-year-old male with a marathon time of 3.5 hours is in the 99th percentile for his age group, yet this same time would not be an age group record until over 80 years of age. Although there also is a slow linear decline in maximal aerobic performance with aging based on world age-group records, this is only on the order of about 1% per year between the ages of 30 and 70 years (20).

Effects of Age on Organ System Performance

There are several general principles regarding aging effects on the performance of various organ systems (60).

Wide Individual Differences in Rate of Aging

Variation between healthy people of the same age is far greater than the variation due to aging alone, and the range of variability increases with aging (20). Linear regressions show average changes with aging, but variation between subjects is so great that it is not always possible to determine accurately if age decrements are linear over the entire age span or whether the rate of decline accelerates in later years (61). However, Fleg et al. recently reported that VO_2max declines more precipitously after the age of 70, especially in men, irrespective of habitual physical activity (62).

Different Organ Systems Age at Different Rates

There is great individual variation in the rate of decline for various organ system functions (35). For instance, there is up to a 60% decline in maximal breathing capacity with aging but only a 15% decline in nerve conduction velocity and basal metabolic rate during the same time interval. Another demonstration of this principle is the localized cellular growth, aging, and death that occur continuously in some tissues and organs (e.g., hematopoietic system, skin, mucosa). Furthermore, a significant decline in function of one organ system (e.g., kidney) does not necessarily entail a similar decline in other organ systems (60).

Age Changes with Complex Performances

Complex performances (e.g., running) will show greater changes with aging because of the need to coordinate and integrate multiple organ system functions (e.g., rate, degree and sequence of muscle contraction, balance, proprioception, vision, cardiovascular response), as opposed to simple performances involving a single system (e.g., renal glomerular filtration) (60).

Age Changes in Adaptive Responses

Adaptive responses (e.g., to temperature change or change in position) are most affected by aging due to a decline in the effectiveness of physiologic control mechanisms (e.g., sensory feedback), which is magnified during stressful situations (e.g., disease, sudden changes in environment) (35,60).

Prevention and Reversibility of Physiologic Decline

There is little question that biologic systems, regardless of the direct effects of aging, can be profoundly influenced by environment and lifestyle (32,35,43). Obvious examples include the deleterious effects of smoking and a sedentary versus active lifestyle (63,64).

The modifiability or plasticity of aging is demonstrated by studies in which performance can be improved despite age, within relatively broad ranges (20,65). Physical training can improve or even reverse age-related declines in aerobic power and muscle strength (66, 67, 68). These gains have been demonstrated to translate to improvements in functional skills (69,70).

Functional Implications of Organ System Aging

The clinician must be aware of specific age-related physiologic changes to properly understand disease in the elderly because these changes significantly influence not only the presentation of disease but also the response to treatment and potential complications that may ensue. Similarly, such knowledge is essential to understand the underlying mechanisms of functional deterioration secondary to disease and to formulate effective rehabilitation approaches (3). The following is a summary of clinically significant physiologic changes that occur with aging.

Hematologic System

Although anemia (i.e., hemoglobin <13 g/dL in men and <12 g/dL in women) (71) occurs with increasing prevalence with aging, there is convincing evidence that it is not a normal consequence of aging and should be investigated, especially if hemoglobin is less than 10.5 g/dL (72, 73, 74). Anemia in older people appears to be due most commonly to iron deficiency (typically from GI blood loss) or chronic disease (such as infection, polymyalgia rheumatica, or cancer) (73). Other potential causes include hemolysis (e.g., secondary to lymphoma, leukemia, or medication effect), B₁₂ deficiency (pernicious anemia, diet), or folate deficiency (diet). Of note, d-dimer levels have been shown to double with aging, with even more dramatic increases among blacks and functionally impaired older individuals (75). Increases in the erythrocyte sedimentation rate and C-reactive protein levels also have been noted with aging (76,77).

The functional consequences of anemia can be significant because of further reduction of reserve capacity, such that previously subclinical disease states may become symptomatic (e.g., orthostatic blood pressure changes, change in anginal pattern with lower exercise tolerance) (74,78). This has obvious implications with regard to tolerance of relatively intensive and sustained rehabilitation exercise programs. There is also evidence of correlation of even relatively mild anemia with impaired mobility (79,80). A very anemic older patient may present with nonspecific fatigue and confusion, with the potential for misdiagnosis and mistreatment (72).

There are several related hematologic changes with aging that can affect pharmacokinetics, particularly drug distribution. Decreased drug binding for highly protein-bound drugs (e.g., warfarin, meperidine, tolbutamide) may result in a higher
unbound, or free, drug concentration with correspondingly magnified actions (81). This effect is even more significant for patients taking multiple drugs because of competition for fewer binding sites.

The volume of distribution is also altered in older adults due to a reduction in total body water and lean body mass, with a relative increase in body fat (82). As a result, water-soluble drugs (e.g., digoxin, cimetidine) tend to have a smaller volume of distribution, with higher plasma concentrations and greater pharmacological effect (83). Conversely, fat-soluble drugs (e.g., diazepam, phenobarbital) usually have a larger volume of distribution because of relatively greater storage in fatty tissue. This may result in delayed therapeutic effects, with the potential for unexpected late toxicity. By the same token, prolonged drug effects are seen after dosage change or discontinuation because of the amount of drug stored in adipose tissue (81).

Gastrointestinal System

The term “presbyesophagus” has been used to describe multiple changes in the esophageal function commonly observed with aging, such as delayed esophageal emptying, incomplete sphincter relaxation, and decreased amplitude of peristaltic contractions. Only the latter appears to be a direct result of aging, but it is not clinically significant; the other changes are related to associated disease processes and may have significant clinical ramifications (84). Most importantly, there is an increased risk of aspiration with aging due to less coordinated swallowing.

Age-related changes occur throughout the gastrointestinal (GI) system although the more distal portion is most affected (85). Alterations in colon function include slightly decreased force and coordination of smooth muscle contraction resulting in slower transit time, as well as impaired rectal perception of feces (86). The high incidence of constipation in older people accordingly is thought to be related to multiple additional factors, such as low dietary fiber and fluid intake, sedentary habits, and various associated diseases interfering with intrinsic bowel function (e.g., parkinsonism, stroke) (87). A variety of medications are potentially constipating as well, including minerals (e.g., aluminum antacids, iron, calcium), opiates, nonsteroidal anti-inflammatory drugs (NSAIDs), antihypertensives (e.g., calcium channel blockers, clonidine), anticholinergics (e.g., tricyclic antidepressants, neuroleptics, antispasmodics), and sympathomimetics (e.g., pseudoephedrine, isoproterenol, terbutaline) (88). Prolonged use of stimulant laxatives or enemas can also impair bowel contractility and result in constipation or obstipation (87). Older adults often report straining and hard bowel movements along with their constipation (89). Straining may indicate rectal dyschezia (i.e., impaired rectal sensation and contractility).

Fecal incontinence in older people is due most commonly to overflow incontinence secondary to fecal impaction but can also occur as a result of decreased sphincter tone, cognitive impairment (e.g., from drugs, dementia), diarrhea, or dyschezia (87,89). Diarrhea among elderly patients is most frequently caused by fecal impaction, intestinal infection, or drugs (e.g., broad-spectrum antibiotics, digoxin toxicity) but also can be due to chronic laxative abuse (90). More appropriate interventions for bowel regulation include increasing diet fiber, using bulk agents or stool softeners, and avoiding frequent use of enemas or laxatives.

Despite these physiologic changes with aging, little effect is seen on absorption of most orally administered drugs (83). Drug absorption in general is more significantly affected by concomitant administration of multiple drugs; in particular, antacids and laxatives bind to or reduce dissolution of other medications (81).

Hepatic System

The primary changes in the hepatic system with aging involve a gradual progressive decline in liver size (5% to 15%) and hepatic blood flow, as well as slowing of hepatic biotransformation, specifically and most consistently microsomal oxidation and hydrolysis (83,86). This can have major implications on the circulating concentration of certain drugs and their metabolites, depending on the mode of metabolism and clearance. Drugs with high first-pass clearance (e.g., propranolol, propoxyphene, major tranquilizers, tricyclic antidepressants, antiarrhythmic drugs) are cleared less effectively owing to reduced hepatic blood flow, resulting in greater bioavailability (81). Comorbid processes such as congestive heart failure can exacerbate these effects.

Drugs metabolized by means of phase I biotransformation (i.e., oxidation, reduction, hydrolysis) tend to have prolonged elimination in older people (e.g., diazepam, chlordiazepoxide, prazepam), whereas those undergoing phase II metabolism (i.e., glucuronidation, acetylation, sulfation) generally are not affected by aging changes (e.g., oxazepam, lorazepam, triazolam) (81,88).

It is important to note that studies of drug elimination with aging demonstrate significant interindividual variability that is likely due to genetic variation as well as the effects of such factors as smoking, alcohol, caffeine intake, diet, and concurrent use of other medications (83). As a result, caution should be exercised when using age-based guidelines for dosage determination (61).

Renal System

There are a number of age-related anatomic and physiologic changes in the kidney, including decreases in renal mass, number and functioning of glomeruli and tubules, renal blood flow, and glomerular filtration rate (91, 92, 93). These reductions in renal function have major implications for drug excretion, with prolonged half-lives for those drugs cleared primarily by glomerular filtration (e.g., cimetidine, aminoglycosides, digoxin, lithium, procainamide, penicillin, chlorpropamide) (81).

Studies show a mean age-related decrease in renal function of about 1% per year, with a decrease in creatinine clearance of 7.5 to 10 mL per decade; however, there is wide variability, with up to a third of older individuals showing no significant decline (92). Because of a corresponding decline in daily urinary creatinine excretion (reflecting decreases in muscle mass), there is no significant change in serum creatinine level with
aging. As a result, neither serum blood urea nitrogen (BUN) (which is dependent on dietary intake and metabolic function) nor creatinine is valid for accurately gauging renal function in older people (81).

Other common physiologic changes with aging include impaired ability to concentrate and dilute urine, impaired sodium conservation, reduction of urine acidification, and decreased ability to excrete an acid load (91). This erosion of reserve capacity allows maintenance of fluid and electrolyte homeostasis under normal conditions, but not with sudden changes in volume, acid load, or electrolyte balance. As a result, older people are more vulnerable to hyponatremia, hyperkalemia, dehydration, and perhaps most seriously, water intoxication (56,94).

Because of difficulty in concentrating urine in conjunction with a blunted thirst mechanism, a hypernatremic state with attendant mental confusion can result if an elderly person is stressed by higher than usual insensible losses (e.g., high or prolonged fever, heat exposure, exercise) with poor fluid intake (94). This is pertinent in a rehabilitation setting because patients are often engaged in vigorous activities and may become dehydrated relatively easily.

Just as older patients are prone to volume depletion when deprived of salt, acute volume expansion from an elevated sodium load caused by inappropriate intravenous fluids, dietary indiscretion, or intravenous radiographic contrast dye can result in congestive heart failure, even in elderly patients without preexisting myocardial disease (81,95). A further potential complication of the use of radiocontrast materials in the elderly is the risk of acute renal failure, which is exacerbated by the presence of preprocedure dehydration (91). Because renin and aldosterone plasma concentrations are decreased by 30% to 50% in the elderly, with increased susceptibility to hyperkalemia, potassium-sparing diuretics (e.g., spironolactone, triamterene) should be used with great caution (88).

Hyponatremia due to water intoxication may be the most serious electrolyte disorder of older adults (56,94). Most frequently complicating an acute illness, the clinical picture includes nonspecific signs of depression, confusion, lethargy, anorexia, and weakness. Serum sodium concentrations below 110 mEq/L may result in seizures and stupor. The syndrome of inappropriate antidiuretic hormone secretion (SIADH), with water retention and hyponatremia, can occur with infections (e.g., pneumonia, meningitis), strokes, various drugs (e.g., diuretics), or the stress of anesthesia and surgery (92).

Pulmonary System

Although progressive declines in pulmonary function are observed with aging, in the absence of significant pulmonary, cardiovascular, or neuromuscular disease, these declines are reflected primarily as a loss of reserve capacity without major functional limitations at rest (96). However, impaired pulmonary function on spirometric testing does indicate increased risk for subsequent disability and several common causes of death in older people, including cardiovascular disease and chronic obstructive pulmonary disease (COPD) (97,98). Changes in pulmonary function observed with aging reflect effects of aging per se (in the pulmonary as well as cardiovascular and neuromuscular systems) together with the cumulative effects of inhaled noxious agents (especially cigarette smoke and air pollutants) and infectious processes (96). The latter typically have a far greater impact on pulmonary function.

Progressive decline in a number of pulmonary function tests has been documented with aging, including vital capacity, maximum voluntary ventilation, expiratory flow rate, and forced expiratory ventilation (96). These declines reflect aging changes in the pulmonary system combined with those in related organ systems, which are collectively stressed by the maximum volitional inspiration and expiration required to complete the tests. Examples include stiffening of the rib cage from degenerative calcification of costochondral cartilage (i.e., decreased compliance), weakening of intercostal and abdominal muscles, and increased airflow resistance from small airway narrowing due to decreased elasticity (97). Residual volume and functional residual capacity increase, related to the loss of elastic recoil (increased compliance), although total lung capacity remains unchanged.

Normal gas exchange requires both uniform ventilation of alveoli and adequate blood flow through the pulmonary capillary bed. With increasing age, there is a progressive ventilation-perfusion imbalance due to collapse of small peripheral airways with decreased ventilation of alveoli, resulting in a linear decline in pO₂ with aging (pO₂ = 110 – [0.4 × age]) (96). Due to altered thoracic mechanics, pO₂ in older individuals is lower in the supine position than with sitting or standing. No changes occur in pCO₂ or pH, and oxygen saturation is typically normal or only slightly reduced.

This reduction in arterial oxygen tension is clinically relevant because it represents an additional loss of reserve. Elderly patients are more vulnerable to significant hypoxia from a relatively minor insult (e.g., anemia, congestive heart failure, respiratory infection) or the stress of physical inactivity because they are closer to the steep slope of the oxygen-hemoglobin dissociation curve (96). Blunting of central and peripheral chemoreceptor responsiveness exacerbates this vulnerability further: both hypercapneic and hypoxic ventilatory responses markedly diminish with aging, independent of lung mechanics. There is a significant increase in sleep-related breathing disorders with aging, and this appears to be related to this phenomenon (56).

Maximal oxygen consumption (VO_2max), an overall measure of exercise capacity and cardiopulmonary fitness, depends on pulmonary ventilation, cardiac output, peripheral circulatory control (i.e., ability to shunt blood to exercising muscles), and muscle oxidative capacity (i.e., oxygen extraction from the blood). Although a progressive decline in VO_2max is observed with aging, this does not appear to be on a pulmonary basis (97,99). In fact, it appears that decreases in VO_2max in older adults with mild to moderate COPD are due primarily to cardiac and peripheral muscle deconditioning resulting from limited activity levels (97). Regular exercise to maintain or improve fitness is critical with aging because it is possible to
improve fitness with training at any age, and this is associated with a reduced vulnerability to stress or disease (and thereby increased active life expectancy) (65,69,100, 101, 102). The tendency of physicians and society to tolerate (or even encourage) decreased activity among older people, in conjunction with trends toward obesity and increased recumbency, probably contributes more to poor pulmonary function than aging alone (97,103).

Although most attention regarding the high incidence of pneumonia in the elderly is focused on immunologic declines, there appear to be contributing factors, direct or indirect, relating to the pulmonary system itself. Because many pneumonias result from aspiration of the infecting organism, impaired mucociliary function and decreased chest wall compliance with weaker cough (resulting in impaired ability to clear aspirated material or secretions) likely play a role (96,97). Other nonimmunologic contributing factors may include dysphagia, disruption of lower esophageal sphincter integrity, various esophageal disorders, and reduced levels of consciousness.

Cardiovascular System

A number of established tenets about the aging cardiovascular system have been revised, based on continuing research using more rigorous methodologies to exclude occult disease and controlling for degree of habitual physical activity. As a result, it now appears that cardiac output at rest and during graded exercise is relatively unaffected by age directly (56,99,104). Although resting heart rate does not change with aging, maximal heart rate with exercise does decrease progressively, related to decreased chronotropic responsiveness to adrenergic stimuli. The clinical formula reflecting this decline in maximal heart rate involves subtracting the age from 220 for men and (0.8 × age) from 190 for women (100,104). Decreased inotropic responsiveness to adrenergic stimulus results in decreased myocardial contractility, with decreased ejection fraction and increased risk of congestive heart failure (105). Maintenance of cardiac output at rest and with modest exercise is accomplished by early involvement of the Frank-Starling mechanism, with increased stroke volume via higher left ventricular end-diastolic volumes (56,104).

TABLE 59.2 Office Management of Orthostatic Hypotension

Orthostatic hypotension is defined as a reduction in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10mm Hg within 3 minutes of assuming an erect posture. However, the significance of any decrease in blood pressure upon standing should be evaluated in context with associated symptoms.
Regardless of whether orthostatic hypotension is symptomatic or asymptomatic, the elderly patient remains at significant risk for future falls, fractures, transient ischemic attacks, and myocardial infarction.
Orthostatic hypotension can be acute or chronic. Acute causes include hypotensive medications, dehydration, and adrenal insufficiency. Chronic causes can be further sub-divided into those related to aging or age-related blood pressure elevation (physiologic causes) and those due to central or peripheral autonomic nervous system diseases (pathologic causes).
The diagnostic evaluation of orthostatic hypotension should include a comprehensive history and physical examination, careful blood pressure measurements, and laboratory studies.
Goals of treatment in the elderly patient include ameliorating symptoms, correcting any underlying cause, improving the patient’s functional status, and reducing the risk of complications, rather than trying to attain an arbitrary blood pressure goal.
In the most cases, treatment of orthostatic hypotension begins with nonpharmacological interventions, including withdrawal of offending medications (when feasible), physical maneuvers, compression stockings, increased intake of salt and water, and regular exercise.
If nonpharmacological measures of fail to improve symptoms, pharmacologic agents should be initiated. Fludrocortisone, midodrine, nonsteroidal anti-inflammatory drugs, caffeine, and erythropoietin have all been used to treat orthostatic hypotension due to autonomic failure.

From Gupta V, Lipsitz L. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med. 2007;120:841-847.

Another age-associated change is a decrease in the rate of early diastolic filling, with a much greater dependency on late filling through atrial contraction (104). As a result, older people are more vulnerable to deleterious effects of atrial tachycardia or fibrillation, including congestive heart failure (99,105).

Both cross-sectional and longitudinal studies demonstrate decreases in maximal oxygen consumption with aging, regardless of habitual activity levels (63,99,106). However, physically active people retain significantly greater maximal aerobic capacity with aging compared to their sedentary counterparts (65). In fact, trained elderly subjects may have greater maximal oxygen consumption than sedentary subjects who are much younger (66). Furthermore, endurance training, even when begun in old age, can significantly improve exercise capacity (65,100). Of clinical relevance is that the energy of walking represents an increasing percentage of the total aerobic capacity with advancing age, such that walking becomes a very effective physical conditioning activity (107).

A final age-related physiologic change in the cardiovascular system with important clinical applications is decreased baroreceptor sensitivity (107,108). This results in a diminished reflex tachycardia on rising from a recumbent position and accounts in part (possibly along with blunted plasma renin activity and reduced angiotensin II and vasopressin levels) for the increased incidence of symptomatic orthostatic hypotension in the elderly (Table 59-2), as well as cough and micturition syncope syndromes (104,109).

Immunologic System

Significant alterations in immunocompetence occur with aging, involving both cellular and humoral immune functions (110,111). Although the total number of lymphocytes decreases by about 15% in older adults, this does not appear to contribute significantly to the marked decline in immunocompetence (112). There is a decline in lymphocyte proliferation in response to antigen stimulation in older adults, as well as a higher incidence of anergy (110). Age-related shifts have been observed in the regulatory activities of T cells (i.e., fewer T cells with suppressor or helper activity) and monocytes or macrophages.

Changes in humoral immunity with aging include increases in circulating autoantibodies and immune complexes, with decreased antibody production (110). The latter is characterized by an attenuated response to immunization, with difficulty maintaining specific serum antibody levels.

The increased susceptibility of the elderly to infection is a function of both these age-related changes in immune function and the frequency of concomitant factors that further impair host defenses (e.g., diabetes, malignancy, vascular disease, malnutrition, and stress) (110). Altered local barriers to infection, such as skin breakdown or an indwelling urinary catheter, often compromise resistance to infection further. Common infectious processes in the elderly include influenza, pneumonia, urinary tract infection, sepsis, herpes zoster, and postoperative wound infections.

Of particular clinical relevance is the fact that older people react differently to infections than do their younger counterparts. There is a less active leukocytosis in response to inflammation, and the total white blood cell count often is not increased (although usually there is still a shift of the differential count to the left) (113). The older patient may have less pain or other symptomatology, and frequently absent, or only low-grade, fever.

Endocrine System

The endocrine system also undergoes significant changes as we grow older. There is a gradual decrease in glucose tolerance with aging, although the fasting blood sugar level remains relatively unchanged (56). Accordingly, age-adjusted criteria for diabetes mellitus have been developed. This age-related decline in glucose tolerance is due to reduced sensitivity of tissues to the metabolic effects of insulin or insulin resistance (114,115). Compounding these aging changes are secondary conditions that further reduce tissue sensitivity to insulin, including lifestyle changes (e.g., obesity, diet changes, stress, sedentary lifestyle), other diseases (e.g., chronic infections, prolonged immobilization), and effects of medications (45,116). Older adults with diabetes are also at increased risk for common geriatric syndromes (e.g., depression, falls) (117).

Of clinical importance is the risk for untreated hyperglycemia, osmotic diuresis, and dehydration, potentially leading to hyperosmolar nonketotic coma or ketoacidosis (116). Certain drugs can cause or potentiate hyperglycemia (e.g., thiazide diuretics, glucocorticoids, tricyclic antidepressants, phenothiazines, phenytoin) (118). Control of serum glucose in older diabetics with oral sulfonylureas or insulin can be fragile, with significant risk for hypoglycemia. However, even borderline hyperglycemia appears to result in accelerated atherosclerosis and multiple end-organ involvement (56). On the other hand, recent data indicate that extremely tight glycemic control in type 2 diabetics may also be harmful (119). Of interest are the contributions of obesity and physical inactivity to the increased incidence of diabetes in older adults and the benefits of weight loss and regular exercise in improving control (45).

There are multiple other endocrine changes associated with aging. The primary clinical impact of altered thyroid physiology with aging is the need to maintain a high index of suspicion for the unusual presentation of thyroid disease (120). Presenting signs and symptoms of the older thyrotoxic patient may include palpitations, congestive heart failure, angina, atrial fibrillation, major weight loss associated with anorexia, and either diarrhea or constipation (121). Goiter and serious ophthalmopathy frequently are absent. Apathetic hyperthyroidism may not be recognized until late in the course of illness: patients appear depressed and withdrawn, with clinical clues of muscle weakness, dramatic weight loss, and cardiac dysfunction (116). Signs and symptoms of hypothyroidism essentially are unchanged with aging, but the diagnosis still may be delayed because of the many similarities between the stereotype of senescence and the hypothyroid state (e.g., psychomotor retardation, depression, constipation, cold intolerance). In view of the higher incidence of hypothyroidism in older adults, routine periodic screening of thyroid function is warranted (121).

The relationships among the hypothalamus, pituitary, and adrenal cortex remain unchanged with age, with preserved diurnal rhythm and stress response (116). However, in older women, serum cortisol concentrations vary more over the course of a day, and mean daily cortisol and ACTH (adrenocorticotrophic hormone)-stimulated serum cortisol levels are higher (122,123). Primary adrenocortical disease is uncommon in the elderly. Significant hyponatremia or hyperkalemia, suggestive of adrenocortical insufficiency, is not uncommon in the elderly but more often is secondary to drugs (e.g., thiazide diuretics, chlorpropamide, carbamazepine) (88).

Age-related changes in gonadal function are well documented. There are variable and gradual declines in serum testosterone levels in healthy men with aging, likely due to partial testicular failure; however, there is no indication for routine androgen replacement (56,124). Postmenopausal declines in estrogen levels are well documented, with clinical expression variably including vasomotor instability syndrome (i.e., hot flashes), atrophic vaginitis, and osteoporosis (43,125). Controversy continues over prophylaxis and treatment of the latter, particularly with regard to potential benefits of dietary supplements and exercise (43,45,126). The reader is referred to Chapter 39 for further details.

Thermoregulatory System

Older people have only a mildly impaired temperature regulation system due to a combination of diminished sensitivity to temperature change and abnormal autonomic vasomotor
control (127). As a result, they have a reduced ability to maintain body temperature with changes in environmental temperature and are vulnerable to both hypothermia and hyperthermia (56,94). The risk of hypothermia is compounded further by impaired thermogenesis (i.e., inefficient shivering), with potential aggravation by a variety of conditions (e.g., hypothyroidism, hypoglycemia, malnutrition) or medications (e.g., ethanol, barbiturates, phenothiazines, benzodiazepines, narcotics) (94). Conversely, diminished sweating (due to higher body temperature to initiate sweating and decreased sweat production) is a major contributing factor in heat exhaustion and heat stroke in hot conditions (Fig. 59-3). Hypohidrosis is aggravated by anticholinergics, phenothiazines, and antidepressants (88). Two thirds of deaths from heat stroke occur in people over 60 years of age, reflecting this impairment in regulatory systems. This has major implications for rehabilitation exercise programs, particularly when combined with a tendency for dehydration (65).

FIGURE 59-3. Thermoregulatory changes with aging.

Sensory System

Deterioration of vision is one of the most recognized sensory changes occurring with aging. The most common visual change with increasing age is a gradual loss of the ability to increase thickness and curvature of the lens to focus on near objects (i.e., presbyopia) and physiologic miosis (56). Cataract formation, with opacification of the lens, occurs to some degree in 95% of the 65-or-older population. The elderly are also at significantly higher risk for further disease-related visual decrements (e.g., glaucoma, macular degeneration, diabetic retinopathy) (128). The result of these various changes is a loss of visual acuity, decrease in lateral fields of vision, decline in both dark adaptation ability and speed of adaptation, and higher minimal threshold for light perception. These changes have obvious implications in relation to the higher incidence of falls in the elderly, particularly at night (129,130).

Gradual decline in hearing acuity (i.e., presbycusis) also is characteristic of aging, although again a number of treatable disorders can cause superimposed hearing loss (e.g., wax occluding the outer canal, cholesteatomas, acoustic neuromas). Older people most commonly manifest a conductive hearing loss, possibly due to increased stiffness of the basilar membrane or distortion of perceived sound with increase in threshold sensitivity, narrower range of audibility, abnormal loudness, and difficulty discriminating complex sounds (131). Continuing advances in hearing aid technology make remediation of such hearing deficits increasingly feasible (132). Early recognition and treatment of hearing impairments are particularly critical in the presence of cognitive deficits to avoid adverse sequelae of social isolation and development of paranoid ideations or frank psychiatric reactions (129).

Neurologic System

Numerous changes in the functioning of the neurologic system have been noted with aging (133). Three important areas of dysfunction accompanying normal aging include declines in short-term memory, loss of speed of motor activities (with slowing in the rate of central information processing), and changes in posture, proprioception, and gait (56).

The major controversy over neurologic changes with aging concerns cognitive functioning. A significant proportion of the observed decline in fluid intelligence with aging appears to be related to a decrease in the rate of central information processing (134, 135, 136). There is progressive deterioration in performance after age 20 on timed motor or cognitive tasks, including abstraction tests (e.g., digit symbol substitution test), reaction time tasks, and other tests requiring speed in processing of new information. Although there are declines with aging in motor and sensory nerve conduction velocities and rate of muscle contraction, they account for only a fraction of these slowed responses (135).

Many aspects of learning and memory remain relatively intact during normal aging, including immediate or primary memory as measured by digit span recall, retrieval from long-term storage, storage and retrieval of overlearned material, and semantic memory (137). However, age-related impairments have been documented consistently in tasks involving episodic short-term memory and incidental learning (138). Examples include difficulties with free recall of long (i.e., supraspan) lists of digits or words and paired-associate and serial rate learning, for both visually and verbally presented material. What these investigations indicate is that older adults are capable of new learning, but at a slower rate (137).

Because much of rehabilitation involves learning, these findings have major implications for rehabilitation programming for elderly people with disabilities. This is particularly true in the context of superimposed cognitive deficits, given that intellectual ability is an important determinant of the effectiveness of a standard geriatric rehabilitation program (4).

A final area of neurological age-related physiologic changes involves posture, proprioception, and gait (139). Older people in general are noted to demonstrate progressive declines in coordination and balance, related in part to impaired proprioception (140). This may have significant implications for degree of mobility and stability, although there are a number of common, potentially concomitant, pathologic changes that may contribute further to gait problems in the elderly (e.g., vertebral compression fractures with kyphosis, arthritis, degenerative cerebral changes, cerebral infarcts) (130,141).

Musculoskeletal System

There is a well-documented progressive loss of muscle strength with aging, on the order of 14% to 16% per decade (men and women) for lower-extremity muscles and 2% (women) to 12% (men) per decade for upper-extremity muscles (59). A major contributing factor to this observed decline in strength appears to be an overall decrease in muscle cross-sectional area and mass with age (142). However, there may be significant contributions of cellular, neural, or metabolic factors to changes in strength, as loss of strength was observed even without loss of muscle mass (59). Further, significant gains in muscle strength, as well as functional mobility, have been demonstrated in older individuals with a structured, high-intensity resistance exercise program, even in frail nursing home residents up to 96 years of age (143).

The high prevalence of both osteoporosis and degenerative joint disease (i.e., osteoarthritis) in the elderly again raises the question about normal physiologic changes versus ubiquitous pathologic processes (45,144). The physiologic changes and sequelae associated with osteoporosis are discussed further in Chapter 39.

Distinction of the “disease” of osteoarthritis from the normal or usual aging changes that occur in weight-bearing joints can be made on a biochemical basis: with osteoarthritis, there are increases in the water content of cartilage and the ratio of chondroitin-4-sulfate to chondroitin-6-sulfate, with decreases in keratin sulfate and hyaluronic acid content (the opposite of what occurs in aging) (144). There is a strong relationship between aging and osteoarthritis: Degenerative joint changes in weight-bearing joints are essentially a universal occurrence in both genders by 60 years of age (145). These changes include biochemical alteration of cartilage, especially the proteoglycan component, with reduced ability to bear weight without fissuring; focal fibrillation and ulceration of cartilage, and eventual exposure of the subchondral bone (144). The wear and tear hypothesis of osteoarthritis suggests that this process is the result of the cumulative stresses of a lifetime of joint use. Accordingly, “primary” osteoarthritis results from the stress of repetitive weight loading (e.g., spine, knees) or strain (e.g., distal interphalangeal joints), whereas “secondary” osteoarthritis may be related to occupational factors or congenital factors with unusual patterns of stress (e.g., congenital hip dysphasia). There appear to be other factors operating, however, because there are specific differences in distribution and prevalence between genders and races, and other explanatory models have been proposed (145, 146, 147). Obesity appears to be a risk factor for knee osteoarthritis in particular, although it is not clear whether this is due to a mechanical or a metabolic etiology. Further details regarding arthritis can be found in Chapter 31.

Genitourinary System

Benign prostatic hyperplasia is an almost universal occurrence in men older than 60 years of age and develops under hormonal rather than neoplastic influence (148). Of note is that the median lobe of the prostate, which is not palpable rectally, can cause a ball-valve obstruction during micturition. Accordingly, after ruling out other etiologies (e.g., anticholinergic or diuretic medication side effects), cystoscopy should be considered in patients with persisting obstructive symptomatology but minimal prostatic tissue on rectal examination to detect median lobe hypertrophy (149). Usual indications for surgical intervention (e.g., prostatectomy) include increasing obstructive symptoms, recurrent/persistent gross hematuria, bladder calculi, recurrent infections, and postvoid residual volumes greater than 100 mL (148,150).

Incontinence in the elderly, although increasingly prevalent with advancing age, should be regarded as a symptom of underlying disease; it does not result from the natural aging process (151). Normal aging typically results in decreases in bladder capacity, ability to postpone voiding, detrusor contractility, and urinary flow rate (152). Postvoid residual volumes are typically increased, with a tendency for increased urine output later in the day, as well as propensity for uninhibited detrusor contractions. Each of these changes predisposes older adults to incontinence, but none alone precipitates it. Common medical conditions associated with incontinence are listed in Table 59-3, while precipitating (and reversible) causes of transient incontinence are detailed in Table 59-4.

The primary clinical significance of these aging changes is that the new onset, or exacerbation, of incontinence in an older person is likely due to a precipitating factor outside the urinary tract (151). Usually, remedial intervention can restore continence.

TABLE 59.3 Common Medical Conditions Associated with Incontinence in the Elderly

Condition		Effect on Continence
Neurologic disease
	Cerebrovascular disease; stroke	DO from damage to upper motor neurons; impaired sensation to void from interruption of subcortical pathways; impaired function and cognition
	Delirium	Impaired function and cognition
	Dementia	DO from damage to upper motor neurons; impaired function and cognition
	Multiple sclerosis	DO, areflexia, or sphincter dyssynergia (dependent on level of synergy)
	Multisystem atrophy	Detrusor and sphincter areflexia from damage to spinal intermediolateral tracts
	Normal-pressure hydrocephalus	DO from compression of frontal inhibitory centers; impaired function and cognition
	Parkinson’s disease	DO from loss of inhibitory centers; impaired function and cognition; retention and overflow from constipation
	Spinal cord injury	DO, areflexia, or sphincter dyssynergia (dependent on level of injury)
	Spinal stenosis	DO from damage to detrusor upper motor neurons (cervical stenosis); DO or areflexia (lumbar stenosis)
Metabolic disease
	Diabetes mellitus	Detrusor underactivity due to neuropathy, DO, osmotic diuresis; altered mental status from hyper- or hypoglycemia; retention and overflow from constipation
	Hypercalcemia	Diuresis; altered mental status
	Vitamin B₁₂ deficiency	Impaired bladder sensation and detrusor underactivity from peripheral neuropathy
Infectious disease
	Herpes zoster	Urinary retention if sacral dermatomes involved; outlet obstruction from viral prostatitis in men; retention and overflow UI from constipation
	Human immunodeficiency virus	DO, areflexia, or sphincter dyssynergia
	Neurosyphilis	DO, areflexia, or sphincter dyssynergia
	Tuberculosis	Inanition and functional impairments (sterile pyuria found in ≤50% of genitourinary TB cases)
Psychiatric disease
	Affective and anxiety disorders	Decreased motivation
	Alcoholism	Functional and cognitive impairments; rapid diuresis and retention in acute intoxication
	Psychosis	Functional and cognitive impairments; decreased motivation
Cardiovascular disease
	Arteriovascular disease	Detrusor underactivity or areflexia from ischemic myopathy or neuropathy
	Congestive heart failure	Nocturnal diuresis
Other organ system diseases
	GI disease	Retention and overflow UI from constipation
	Musculoskeletal disease	Mobility impairment; DO from cervical myelopathy in rheumatoid arthritis and osteoarthritis
	Peripheral venous insufficiency	Nocturnal diuresis
	Pulmonary disease	Exacerbation of stress UI by chronic cough
DO, detrusor overactivity; TB, tuberculosis; UI, urinary incontinence.
Adapted from DuBeau CE. Interpreting the effect of common medical conditions on voiding dysfunction in the elderly. Urol Clin North Am. 1996;23(1):11-18, with permission.

Contrary to stereotypes, although there is a decrease in sexual functioning with aging, most older people retain sexual interest and desire and to a variable extent, capability (153, 154, 155). Older men experience a decrease in ability to have psychogenic erections and require more intense physical stimulation for erection; erections may be partial, and orgasm with ejaculation may occur without full engorgement (156). The force of ejaculation is less, along with a less intense sensation of orgasm. Impotence may be caused by a variety of diseases (e.g., atherosclerosis, diabetes, hypothyroidism) and medications (e.g., antihypertensives, phenytoin, cimetidine). Treatment of erectile dysfunction in older men has been revolutionized with development of the vacuum tumescent device, advances in penile prostheses, and availability of such medications as sildenafil and alprostadil (157,158).

Older women experience postmenopausal changes, including increased fragility of the vaginal wall and attenuation of the excitement phase (e.g., decreased vaginal lubrication) (153). Common sexual difficulties identified included partner’s impotence, anorgasmia, decreased libido, and insufficient opportunities for sexual encounters. Despite these changes, most women maintain the ability to engage in sexual intercourse throughout the life cycle (159).

TABLE 59.4 Precipitating Causes of Transient Incontinence in the Elderly

Cause	Comment
Delirium, confusion state	UI resolves once underlying cause(s) treated
Urinary infection	UI may be only symptom of infection; antibiotic trial warranted in asymptomatic persons only on initial evaluation and with new onset/exacerbation of UI
Atrophic urethritis, vaginitis	Aggravates stress or urge UI; agitation can be presenting symptom in demented patients
Medications	Any agent that impairs cognition, mobility, fluid balance, bladder contractility, or sphincter function; many agents impair several functions
Psychiatric disorders	Severe depression or psychosis
Increased urine output	Frequency or nocturia; causes: excessive fluid intake, diuretics, hyperglycemia, hypercalcemia, volume overload (congestive heart failure, venous insufficiency, hypothyroidism, hypoalbuminemia, and drug-induced peripheral edema)
Restricted mobility	Treat underlying cause; provide a urinal or bedside commode
Stool impaction	Urge or overflow UI; fecal incontinence common
UI, urinary incontinence.
Adapted from Resnick NM. Urinary incontinence in the elderly. Med Grand Rounds. 1984;3:281-290.

IMPACT OF THE ENVIRONMENT ON THE HEALTH OF OLDER ADULTS

Psychological and Social Issues in Aging

Ageism and Myths of Aging

Butler coined the term “ageism” (or agism) to describe negatively biased perceptions of older people by the younger population in today’s youth-oriented culture, as well as perceptions of old age by elderly individuals themselves (160). There are many adverse sequelae of ageism, including devaluation of older people (by themselves, as well as others both younger and older), diversion of health care professional focus from the real health problems of older patients, the dearth of physicians interested and trained in geriatric medicine, and lack of curriculum time in medical schools regarding geriatrics (161, 162, 163). There is even new evidence of a negative impact of perceived discrimination on mortality in older adults (164). According to Rowe, it is time to “discard the many derogatory myths about older people, who are often seen as sick, senile, silly, sexless, and sedentary, as well as inflexible, irritable, noncontributing, and too old for preventive interventions” (165). Many of today’s older adults are survivors of the Depression and the World Wars—they built much of the life and standard of living we now enjoy. The evidence is clear: the majority of elderly are cognitively intact, live independently in the community, and are fully independent in ADL (17,19).

Cumulative Changes

There is increasing awareness of the critical interrelationships, particularly for older people, of physical health, mental health, and life circumstances. The emotional and life stress associated with major losses are well documented, and older people may be exposed progressively to multiple significant losses: job, income, health, functional ability and independence, parents, spouse, siblings, children, friends, social roles and status, and self-esteem (166). There are in fact few norms or defined role expectations regarding appropriate behavior or activities in old age (167,168). Bereavement, isolation, poverty, illness, and physical disability all are associated with a higher incidence of depression in older adults (169), which in turn is associated with decreased physical and cognitive functioning, disability, and increased mortality (34,170, 171, 172).

Social Support Networks

Social support networks include a wide variety of sources that can be categorized as informal (family), semiformal (church, clubs, family doctor, local pharmacist), and formal (health care system, social service agencies, insurance companies, etc.) (173,174). Older persons often use supports from a combination of these networks (13). There is mounting evidence of the positive impact of social support networks on the cognitive, health, and functional statuses of older individuals (174, 175, 176).

Elderly people with children usually live near them and visit frequently or at least maintain regular telephone contact (177). Older people without children tend to maintain closer ties with young relatives or with siblings (178). It is important to consider the extended family, including cousins, in-laws, and others, with regard to support networks, rather than just immediate household members (167,174,179).

Institutionalization of an impaired older person usually is the last resort for families, used only when all other efforts fail; in fact, 64% of individuals over the age of 85 who are dependent in self-care or homemaking still live in the community (180). Families, rather than the formal system of government and agencies, provide the bulk (up to 90%) of personalized long-term care for their disabled older relatives (13). This includes home health and nursing care, personal care, household maintenance, transportation, cooking, and shopping. In 1990, 73% of elderly disabled individuals relied exclusively on such informal support and care networks (13).

With advancing age, however, older adults tend to have increasingly limited and relatively fragile support systems. Dependency in aging parents can result in significant physical, emotional, and financial stresses on their family network (177). An alternative support system may evolve gradually over a period of time as the older person loses family support (e.g., death of spouse and siblings, children moving away and unable to actively assist). Such a system might include friends and neighbors in an extended network to assist with shopping, cooking, cleaning, and self-care (174

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