TRAUMA IN THE ELDERLY

Published on 10/03/2015 by admin

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CHAPTER 78 TRAUMA IN THE ELDERLY

Benjamin Braslow, Donald R. Kauder, C. William Schwab

The age at which a person becomes elderly has not been resolved by a clear consensus in the literature, but most agree that it falls in the span between ages 55 and 75. According to the 2000 census, 35 million (12.4%) Americans were over age 65, and by 2050, this age cohort is projected to reach 86 million (20.7%). The elderly constitute the most rapidly growing segment of the U.S. population. Today’s elderly enjoy a level of physical freedom unmatched by prior generations. Improved access to health care and assisted living communities allow many older Americans to function relatively independently well into their ninth decade. Traumatic injuries very often compromise this autonomy, creating dependence on relatives or caregivers for assistance with activities of daily living. Unfortunately, a number of physical factors predispose the elderly to injury, including diminished postural stability, motor strength, coordination, visual acuity, and hearing. These common changes often lead to an inability to recognize and avoid many environmental hazards, thus converting normal daily activities into treacherous and frequently lethal events. In direct correlation with this rapid expansion of this sector of the population, hospitals are treating increased numbers of geriatric trauma patients. In 2001, over 3.2 million elderly patients who sustained unintentional injuries were evaluated in U.S. emergency departments; 2.2 million (68.7%) were admitted. These patients have been shown to have more adverse outcomes, including case fatality rates and complications. In 2002, unintentional injury was the fifth leading cause of death in the United States overall and the ninth leading cause of death in those aged 65 and older, accounting for over 33,000 victims. Survivors exhibit a higher prevalence of functional impairment, often requiring longer hospital stays and complex discharge arrangements. Not surprisingly, the elderly, comprising just over one-tenth of the population, account for nearly one-third of health care resources expended on trauma.

PHYSIOLOGY

There are numerous physiologic changes that influence the treatment of injury in elderly patients. With advancing age there is a normal, unavoidable, progressive loss of functional reserve in each organ system. The degree of loss is subject to individual variations and is distinct from the pathologic loss of function associated with comorbid diseases prevalent in senescence. Such conditions include but are not limited to hypertension, pulmonary disease, cardiovascular disease, diabetes, and renal failure. This combination of diminished reserve and concomitant disease significantly limits the ability of the elderly trauma patient to absorb physical insult and subsequently recover. It also impacts the care rendered to such patients at every level of intervention, from prehospital provider to trauma surgeon to surgical intensivist to physical therapist.

Most significantly, the cardiovascular system demonstrates age-related changes that affect the elderly patient’s response to severe trauma. With age there is a progressive loss of myocytes and a compensatory increase in myocyte volume in both ventricles along with fat cell infiltration in the interstitial space of the ventricular walls and septum. The myocardium progressively stiffens, resulting in decreased diastolic relaxation and slowed ventricular filling. The heart becomes less efficient, with a progressive decrease in its ejection fraction. Stroke volume is diminished, leading to an increased reliance on the atrial contribution to increase end-diastolic volume in order to maintain cardiac output. The heart can be extremely sensitive to both hypovolemia and hypervolemia, resulting in a very narrow therapeutic window. Further, there is a decreased inotropic and chronotropic response to both endogenous and exogenous betaadrenergic stimulation and progressive deterioration of the conducting system by cell atrophy, fibrosis, and calcification. This ultimately leads to a lowering of the maximal achievable heart rate and of the ability to adequately increase cardiac output during stress. Structural changes in the arterial tree also affect cardiac function in the elderly. Arterial intimal hyperplasia with concomitant atherosclerosis produces stiffness of the arterial walls, resulting in a reduction of diastolic pressure despite systolic hypertension and limiting coronary blood flow. This becomes most clinically important during stress, when myocardial oxygen demand increases but coronary blood flow is restricted. Prescription antihypertensive medications such as beta-blockers, calcium channel blockers, and diuretics—all very commonly prescribed for the elderly population—can also play a major role in the impairment of the cardiovascular response to stress and injury. The multifaceted age-related decline in cardiovascular function makes it incumbent upon the treating trauma physician to carefully plan treatment regimens and closely monitor this patient population during resuscitation.

The aging process significantly affects pulmonary physiology as well. With age, costal cartilage becomes calcified and the chest wall becomes more rigid, decreasing lung compliance. Respiratory muscles atrophy, and an increased reliance on diaphragm function and abdominal musculature for breathing develops. Forced vital capacity is decreased, as is forced expiratory volume in one second (FEV1). Lung parenchymal changes are noted with aging as well. Fusion of adjacent alveoli occurs, which decreases surface tension forces and reduces pulmonary elastic recoil. Thickening of the alveolar basement membrane decreases gas-diffusing capability, resulting in V/Q mismatch and higher alveolar-arterial oxygen gradients. There is also decreased airway sensitivity and efficiency of the mucociliary clearance mechanism. A history of smoking compounds the deleterious affects of aging on pulmonary anatomy and function. Clinically, these changes manifest as decreased cough effectiveness, predisposition to aspiration and pneumonia, and decreased compensatory responses to hypoxia and hypercarbia. Aggressive pulmonary toilet, adequate pain control, judicious use of mechanical ventilation, and careful monitoring of fluid status become imperative in preventing pulmonary complications in the elderly trauma population.

Anatomic changes evident in the elderly kidney include cortical mass loss secondary to glomerulosclerosis (acellular obliteration of glomerular capillary architecture) and tubular senescence. Hypertension, diabetes mellitus, and atherosclerosis accelerate these processes. Physiologically, these changes manifest as a reduced glomerular filtration rate (GFR). After the age of 40 years, the GFR decreases 1 ml/min/year. Tubular senescence blunts the reabsorption and secretion of solutes. Most significant is the decreased capacity to reabsorb sodium and to secrete potassium and hydrogen ions. The juxtaglomerular apparatus in elderly patients produces less renin and limits the response to aldosterone. The response to antidiuretic hormone is also attenuated. All of these changes mandate hypervigilant monitoring of fluid, electrolyte, and acid base balance in the injured elderly patient, especially those requiring surgery, during which massive fluid shifts are expected. Yet another factor leading to hypovolemia is a decreased thirst response, which often predisposes them to hypovolemia. Predicting decreased renal function in the acute setting can be difficult. A reduction in muscle mass with age often results in a normal serum creatinine despite a reduced creatinine clearance. Age-adjusted formulas for creatinine clearance are much better estimates of renal function in the elderly patient than serum creatinine levels. Potentially nephrotoxic agents, such as intravenous radiographic contrast, should be used with extreme caution even if serum creatinine levels appear within normal limits.

Significant age-related changes also occur in the central nervous system. Cortical atrophy progresses with age, resulting in an increased volume of the subdural space. This allows for greater movement of the brain during traumatic impact, which can result in serious parenchymal damage. Relatively minor mechanisms of injury may result in more frequent subdural and subarachnoid hemorrhage secondary to greater shearing forces on parasagittal bridging veins. Large volumes of blood may accumulate intracranially before symptoms of intracranial hypertension develop. This process is compounded by the frequent use of anticoagulant and/or antiplatelet medications in this population for a variety of prophylactic and therapeutic indications. Likewise, a greater degree of brain swelling may occur before symptoms appear. Vision, auditory function, vibrotactile sensation, reflex timing, and pain perception are all blunted with age. These changes, in combination with age-related deterioration in cognitive ability, memory, and information processing, not only contribute to an increased predisposition to injury in the elderly, but also may obscure their post-traumatic evaluation.

Changes in the musculoskeletal system have significant impact on the elderly patient’s predisposition to injury. There is a progressive loss of muscle mass and strength with age. Loss of motor neurons, collagen and adipocyte infiltration, and diminished myosin-ATP activity are also contributing factors. Progressive erosion of cartilage and ligamentous stiffening, especially in weight-bearing joints, affects mobility and can be a source of chronic pain. Attempts at postural compensation can alter weight-bearing mechanics and cause injury to other musculoskeletal structures. Age-related bone loss secondary to osteoporosis causes further loss of strength and greater susceptibility to fracture, most commonly seen in the hip, pelvis, wrist, and ribs. Vertebral collapse is associated with progressive kyphosis, which alters the center of gravity and contributes to balance disturbances. This process is more pronounced in women but is relevant to both sexes. Women lose up to 35% of cortical bone mass and 50% of trabecular bone mass over their lifetime; men lose about one-third less. These changes in strength and flexibility contribute to progressive limitation of movement, making the elderly patient more vulnerable to injury and complicating the recovery process.

Neurohumoral senescence is also quite common. There is a global decreased sympathetic response to stress in the elderly. This is multifactorial, related to neurologic, musculoskeletal, and endocrine alterations associated with age. Thermoregulation is impaired secondary to a decreased cutaneous vasoconstriction response to cold environments, which renders the elderly trauma patient more susceptible to hypothermia. Immune function also shows an age-related decline, specifically related toT-lymphocyte-mediated immunity. The response of T lymphocytes to interleukin 2 is impaired, as is the stress-related increase in natural killer-cell activity. These changes increase the elderly trauma patient’s susceptibility to infection. Furthermore, markers of the systemic response to surgical stress (tumor necrosis factor α, interleukin 6, and CD11b/CD18 expression) have been shown to be more elevated after surgical stress in older (compared with younger) patients. This increase in cytokine response to surgical stress has been postulated to increase the incidence of systemic inflammatory response syndrome in the elderly and may explain an increased incidence of postoperative morbidity.

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