Geriatric Anesthesia - Are You Ready?

Increased life expectancy and reduced mortality from chronic age-related disease continue to enlarge that fraction of the surgical patient population considered elderly. These apparently beneficial demographic changes have further amplified the societal impact of the increasing per capita health care costs that already represent a formidable fiscal burden for modern societies. As they age, adult patients also exhibit an increasingly complex array of unique physical responses to environmental and socioeconomic conditions and to concurrent disease states. Survival to adulthood and beyond permits the full expression of even the most subtle genetic differences between individuals, differences that might not be fully apparent over shorter life span intervals. People are never more alike than they are at birth, nor more different or unique than when they enter the geriatric era. Precise assessment and appropriate perioperative management of the elderly surgical patient represents a great challenge to all medical health care providers.

Surgical procedures in the elderly will continue to require a disproportionately large share of societal and institutional health care resources. Routine postoperative hospitalization and intensive care, especially after major trauma, are frequently protracted and may be further complicated by infection, poor wound healing and by multiple organ system failure for critically ill elderly patients. Of equal concern are recent findings that postoperative cognitive dysfunction may persist at least three months after otherwise uncomplicated surgery.

Although they represent only 12 percent of the United States population, individuals 65 years of age or older undergo almost one-third of the 25 million surgical procedures performed annually, and they consume about one-third of all health expenditures and fully one-half of the $140 billion annual U.S. federal health care budget. Therefore, every anesthesiologist in contemporary practice eventually becomes a subspecialist in geriatric medicine, with a special responsibility for delivering cost-effective health care to older adults.

In its broadest sense, gerontology refers to the study of aging.¹ Biogerontologists usually limit their scope to the physiological and biochemical, rather than the socioeconomic, aspects of aging. Although many gerontologists study human aging exclusively, others have extended their interests to a cellular or subcellular level and therefore this discipline may encompass the study of nonhuman organisms. In contrast, geriatrics, a term with origins early in this century, is more specific because it describes the medical subspecialty that focuses upon care of the elderly patient.² Geriatricians are physicians who specialize in the care of the elderly patient.

Studies of human aging have been further complicated by difficulties in discriminating clearly between aging itself and the consequences of age-related disease and cohort-specific effects that make data from cross-sectional studies ambiguous. Cross-sectional studies measure physiologic parameters simultaneously in young and in elderly subjects. Therefore, changes due to undiagnosed age-related disease may be erroneously attributed to age itself. Similarly, this experimental design cannot be controlled for cohort-specific factors such as nutritional and environmental history, genetic background or prior exposure to infectious agents. Consequently, data from cross-sectional studies rarely permit unambiguous conclusions regarding the effect of age itself on any one measured physiologic parameter. Many of the "classic" cross-sectional studies of aging in the gerontologic literature must be reconsidered.

Some biogerontologists feel that processes of aging can be unequivocally identified only when a longitudinal study is used to supplement carefully performed cross-sectional studies. For some measurements such as glomerular filtration, data from longitudinal studies have validated the results of earlier cross-sectional investigations.³ However, longitudinal studies of human aging require an arbitrary chronological "starting point" for the geriatric era that may change significantly during the duration of the study itself because of increases in life expectancy.⁴ They also have intrinsic sources of error.⁵ In addition, the validity and utility of the data they generate are subject to the evolution or revision of physiologic concepts and measurement techniques over the long time period required to study human aging.

Processes of aging are usually distinguishable from age-related disease by the fact that they are universally present in all members of an elderly population and, in longitudinal studies of aging subjects, become progressively more apparent with increasing chronological age. Aging is a universal and progressive physiologic phenomenon characterized by degenerative changes in both the structure and the functional reserve of organs and tissues. It produces many physical manifestations due to reduced connective tissue flexibility and elasticity or the degeneration of highly structured molecular arrangements within specialized tissues. At the tissue level, cross-linking, glycosylation, or similar dysfunctional interactions occur.⁶ The difference between maximum capacity and basal levels of function is organ system functional reserve, a "safety margin" available to meet the additional demands imposed by trauma or disease, or by surgery, healing and convalescence. Cardiopulmonary functional reserve, for example, can be quantified and assessed clinically using various exercise or maximal stress tests. However, there is at present no comparable approach to assessment of renal, hepatic, immune, or nervous system functional reserve. It is simply assumed that the functional reserve of these organ systems is reduced in elderly patients and that this is the mechanism by which the obvious susceptibility of elderly patients to stress- and disease-induced organ system decompensation occurs.

CONCEPTS OF AGING

Life span is an idealized, species-specific biologic parameter that quantifies maximum attainable age under optimal environmental conditions. Historical anecdote suggests that human life span has remained constant at 110 to 115 years for at least the past 20 centuries.⁷ In contrast, life expectancy describes an empirical estimate of typical longevity under prevailing or predicted circumstances. Advances in medical science and health care have improved life expectancy dramatically in industrialized societies and increased their relative "agedness" but do not appear to have altered human life span. The mechanisms that control the aging process and determine life span remain unknown. Perhaps because gerontology is a relatively new discipline, theories of aging have been presented from various individual perspectives, many without any logical interconnection or relationship.

In general, however, theories of aging fall into two major categories. One group can be described as stochastic because it is essentially time- and probability-dependent. The nonstochastic group includes those theories proposing that there are programmed or predetermined mechanisms that explain aging. Nonstochastic theories of aging share a common theme of a "biological clock" or "life pacemaker" for each species.⁸ In order to effect processes of aging throughout the organism, the pacemaker tissue or organ must itself have widespread interaction with all other organ systems. Therefore, this type of theory usually involves a neuroendocrine or immune mechanism.

The "error-catastrophe" theory of aging is a stochastic concept. It postulates that random errors of protein synthesis due to faulty nucleic acid transcription or translation eventually accumulate to compromise cellular function and produce the physical signs of aging. However, there is little evidence that the individual cells of older subjects contain more defective protein than do young cells. This theory also fails to explain the dramatically different patterns of aging that are seen in various animal species that share a common ecosystem and are exposed to similar catabolic environmental forces such as ionizing radiation. Similarly, a "genetic wear and tear" theory of aging proposes that recurrent damage to nuclear deoxyribonucleic acid (nDNA) eventually exhausts intrinsic intracellular capacity for nuclear chromosomal repair, leading to a critical loss of functioning cellular and tissue elements. Although there is a general correlation between species longevity and DNA repair capacity, there is no firm evidence that the ability to recover from random nDNA damage is, in fact, progressively or universally compromised in older human subjects.⁹

However, investigations of oxidative phosphorylation in aging mitochondria suggest that progressive increases in the incidence of defects within mitochondrial DNA (mDNA) may lead to a decline in bioenergetic capacity and a progressive reduction in the efficiency with which free radical species such as superoxide, routinely produced in the mitochondria during aerobic metabolism, are scavenged from the cytosol of aging cells.¹⁰ Free radicals damage the unsaturated fatty acid and nucleic acid components of cells and cross-link protein molecules, eventually damaging cellular microarchitecture.¹¹ Superoxide dismutase appears to be the most important endogenous enzymatic scavenger of free radical species and, in fact, it is present in higher concentrations within human cells than in the cells of species with a shorter life span. A relatively recent proposal suggests that cellular aging is due to a "vicious cycle" of diffuse bioenergetic failure in the mitochondria of metabolically-active tissues.¹² This mechanism, which may be thought of as progressive failure of a genetically-determined capacity to clear random damage to mDNA by free-radicals, is compatible with both stochastic and nonstochastic theories and falls within the larger evolving concept that aging is a consequence of a lifetime of "oxidative stress." ^13,14

References:

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• Gerontology
  
  
• Cardiovascular and Autonomic Nervous System Aging
  
  
• Physiology of the Cardiovascular Effects of General Anesthesia in the Elderly
  
  
• Cardiovascular Response to Spinal Anesthesia in the Elderly
  
  
• Hemodilution Tolerance in Elderly Patients
  
  
• Aging and the Respiratory System
  
  
• Aging and the Urinary System
  
  
• Perioperative Renal Insufficiency and Failure in Elderly Patients
  
  
• Thermoregulation in the Elderly
  
  
• Pharmacokinetic and Pharmacodynamic Differences in the Elderly
  
  
• Induction Agents
  
  
• Opioids
  
  
• Muscle Relaxant Selection and Administration
  
  
• Aging and the Central Nervous System
  
  
• Postoperative Delirium in the Elderly
  
  
• Safe Sedation of the Elderly Outside the Operating Room
  
  
• Age-Related Disease
  
  
• Anesthetic Risk and the Elderly
  
  
• Perioperative Complications in Elderly Patients
  
  
• Preanesthetic Evaluation for the Elderly Patient
  
  
• Managing Medical Illness in the Elderly Surgical Patient
  
  
• Ethical Challenges in the Anesthetic Care of the Geriatric Patient
  
  
• Critical Care of the Elderly Patient
  
  
• The Elderly Trauma Patient
  
  
• Postoperative Pain Control in the Elderly Patient
  
  
• Chronic Pain in Older Individuals: Consequences and Management
  
  
• Palliative Care in Geriatric Anesthesia
  

The views expressed herein are those of the authors and do not necessarily represent or reflect the views, policies or actions of the American Society of Anesthesiologists.

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