According to census projections, the elderly population in the United States, defined as age more than 65 years, is experiencing the largest growth in history. Members of the post-World War II “baby boom” (75 million people born from 1946 to 1964) were 46–64 years old in 2010. By the year 2030, the elderly population will number 38 million and, by 2050, 1 in 5 Americans will be elderly.1
The ever-increasing mobility and active lifestyles of today’s elderly places them at increased risk for serious injury. In fact, data from the National Trauma Data Bank (NTDB) for the year 2014 revealed that 39% of all patients in the registry were 55 years old or older and the mortality for this group was 54% of all deaths reported to the NTDB.2 Injury is now the fifth leading cause of death in the elderly population.3
The elderly have a higher morbidity and mortality, have more preexisting medical problems, and demonstrate a senescent physiologic response to injury when compared to younger individuals. The reasons for the differing response are unknown, the literature is contradictory in places, and there are few prospective randomized trials that focus specifically on the elderly. This is best demonstrated by a lack of consensus on the definition of what age constitutes elderly. Historically, geriatric patients were considered to be patients over the age of 65 years as noted above; however, there are a variety of organ specific injuries that demonstrate rising morbidity and mortality at chronological ages less than 65 years. As such, elderly patients should be assessed by the degree of frailty and viewed from the vantage of the physiologic response to an injury or injury complex rather than a specific age. Despite these limitations, this chapter focuses on an overview of care for the injured geriatric patient.
Declining cellular function is part of the aging process. Eventually, this will lead to organ failure. The aging process is characterized by impaired adaptive and homeostatic mechanisms, resulting in an increased susceptibility to the stress of injury. This is commonly perceived as decreased physiologic reserve. Insults commonly tolerated by younger patients can lead to devastating results in the elderly patient. Differences in the metabolic response to injury were studied by Frankenfield et al.4 In their study, they compared injured patients by dividing them into those older than 60 years and those who were younger. These investigators concluded that the metabolic response to injury is significantly attenuated in the elderly population. This was demonstrated by the older group having less fever, less oxygen consumption, more hyperglycemia, and more azotemia.4 This may be driven by the fact that there is evidence that immune function is significantly attenuated during the aging process and that cytokine response is impaired, as well. This immune senescence is, in part, is characterized by reduced neutrophil function. Butcher et al5 investigated a group of patients who sustained mild trauma (hip fracture) and were older than 65 years of age. Neutrophil phagocytic function was assessed immediately after injury, and patients were then followed for 5 weeks for clinical infection. When compared to a younger cohort, the older patients had a significant reduction in neutrophil phagocytic function as measured by significantly depressed superoxide production.5 Additionally, nearly half of the elderly population suffered bacterial or fungal infection within the study period, compared to no infection in the younger patients. These authors suggested that the defect in the aging immune system may be a result of falling dehydroepiandrosterone (DHEA); that is, in the presence of the physiologic stress of injury, patients have an obligatory rise in corticosterone levels, which is immune suppressive.
Cardiovascular comorbidities are most frequently seen in the elderly patient. Cardiac function declines by 50% between the ages of 20 and 80 years. The declining function is combined with a decreased sensitivity to catecholamines, so the expected cardiovascular response to hypovolemia may not be apparent.6 This may be further complicated by a variety of medications, including β-blockers.7 The cellular elements of the conductive system and the myocytes themselves are gradually replaced by fat and fibrous tissue. The resultant stiffer heart is more prone to dysfunction and to dysrhythmias. Atherosclerotic changes in the arteries are common, and valvular anatomy is changed by tissue thickening. In addition, the increased afterload causes an increase in systolic blood pressure and enlargement of the heart. The system is generally well-compensated while at rest; however, in the event of hypovolemia, elderly patients generally are unable to compensate with tachycardia and an increase in cardiac output. There is a blunted response to adrenergic stimulation, as well, as there are decreased baroreceptor reflexes in response to hypovolemia. As such, the response by the aged heart is generally characterized by an increase in systemic vascular resistance. Despite “normal” blood pressure, many of these patients have evidence of tissue hypoperfusion.8
There are significant anatomic and physiologic changes associated with aging that occur in the respiratory system. With age related loss in bone density, there is development of thoracic kyphosis, and rib calcification is associated with a decrease in transverse thoracic diameter. In addition, muscle mass is reduced and the elastic recoil of the lung decreases with age. These anatomical changes result in decreased compliance of the chest. This results in a reduction in functional residual capacity and gas exchange.9 The elderly also have a decreased cough reflex, decreased function of the mucociliary epithelium, decreased response to foreign antigens and an increase in oropharyngeal colonization with microorganisms. These changes place the elderly patient at risk for hospital acquired pneumonia.10
The alveolar surface area decreases after the age of 30 years. This results in decreased alveolar surface tension which ultimately interferes with alveolar gas exchange. The alveoli are also noted to flatten and become shallow, thereby decreasing the effective surface area for gas exchange. Diffusion capacity is decreased because of the decrease in effective surface area and an increase in alveolar-capillary membrane thickness.11
Above the age of 50 years, renal mass is lost as progressive sclerosis of the glomeruli occurs. Between the ages of 50 and 80 years, there is a decrease in glomerular filtration rate (GFR) by about 45%.6 Generally, this is not detected by routine renal function testing, as it is accompanied by a decrease in total muscle mass and production of creatinine. The Cockroft-Gault formula should be used with caution to estimate the degree of dysfunction in the basal state and should not be used in the acutely stressed patient. Furthermore, the endocrine response of the kidney to antidiuretic hormone (ADH) and aldosterone is abnormal. This results in a decrease in the ability of the kidney to concentrate urine. Elderly patients may be able to maintain a deceptively adequate urine flow despite hypovolemia. As such, urine output should be used cautiously as a surrogate for renal perfusion.12,13
Many elderly patients are azotemic at baseline. The normal thirst response to dehydration may be impaired, and this is especially true in patients with underlying neurologic disease. These age related changes in renal function put the older patient at significant risk for acute kidney injury following trauma and the confounding nephrotoxic insults following injury. Likewise, the elderly are at risk for developing untoward effects of aggressive volume resuscitation such as hyperchloremic metabolic acidosis and volume overload. Care must be maintained when dosing renally excreted drugs to these patients.
Older people undergo an obligatory loss of lean body mass. This loss is estimated to be about 4% every 10 years after the age of 25. This loss then increases to approximately 10% after the age of 50. The loss of muscle is accompanied by a proportional increase in adipose tissue. From a skeletal aspect, osteoporosis is a common feature of aging. That results in a loss of 60% of trabecular bone and 35% of cortical bone.14 This makes the elderly individual at risk for fractures, especially those involving the vertebrae, hip, and distal forearm. There are age associated changes of the joints and cartilages resulting in osteoarthritis and other degenerative features affecting nearly all joints, as well. Degenerative changes in the cervical spine are particularly worrisome in the older population, and mobility is greatly affected putting this area at risk for injury—particularly during oral intubation.15
Skin changes with aging are well-documented. As the epidermis becomes thinner, changes in the epidermal-dermal rete pegs places patients at risk for a shear injury. There is a decrease in the skin adnexa resulting in increased skin dryness and slower healing, as well. Overall, there is decreased sensation, decreased vascularity, and impaired lymph flow, all impacting normal wound healing. Skin changes and depressed wound healing may complicate underlying fractures, specifically pelvic fractures and open fractures.16
There are age related changes that affect endocrine function. The tissue responsiveness to thyroxin and its production is reduced.6 Secretion of cortisol does not seem to change with aging, but given decreases in DHEA production, this may predispose the physiologically stressed elderly patient to a hypercortisone state (Table 44-1).
Organ system | Functional changes | Implications for care |
---|---|---|
Cardiac | Declining function Decreased sensitivity to catecholamines Decreased myocyte mass Atherosclerosis of coronary vessels Increased afterload Fixed cardiac output Fixed heart rate (β-blockers) | Lack of “classic” response to hypovolemia Risk for cardiac ischemia Dysrhythmias Elevated baseline blood pressure |
Pulmonary | Thoracic kyphoscoliosis Decreased transverse thoracic diameter Decreased elastic recoil Reduced FRC Decreased gas exchange Decreased cough reflex Decreased mucociliary function Increased oropharyngeal colonization | Increased risk for respiratory failure Increased risk for pneumonia Poor tolerance to rib fractures |
Renal | Loss of renal mass Decreased GFR Decreased sensitivity to ADH and aldosterone | Routine renal labs will be normal (not reflective of dysfunction) Drug dosing for renal insufficiency Decreased ability to concentrate urine Urine flow may be normal with hypovolemia Increased risk for acute kidney injury |
Skin/soft tissue/musculoskeletal | Loss of lean body mass Osteoporosis Changes in joints and cartilages Degenerative changes (including c-spine) Loss of skin elastin and subcutaneous fat | Increase in body fat Increased risk for fractures Decreased mobility Difficulty for oral intubation Risk of skin injury due to immobility Increased risk for hypothermia Challenges in rehabilitation |
Endocrine | Decreased production and response to thyroxine Decreased DHEA | Occult hypothyroidism Relative hypercortisone state Increased risk of infection |
Maintaining homeostasis in the face of physiologic stress is a demonstration of good functional reserve. Declining functional reserve in the elderly may precipitate a decline in performance when the patient is exposed to chronic or acute illness. When faced with a physical insult homeostasis may be poorly maintained (Fig. 44-1). The decline in functional reserve is heterogeneous, and a variety of factors will impact the magnitude of the loss of functional reserve. These include age-related disease and their treatments, genetics, lifestyle choices, and environmental factors. It is clear that older patients do not tolerate injury as well as younger patients. What is not clear is the reason for this discrepancy as previously noted. The impact of preexisting medical problems,17,18,19 in combination with a declining functional reserve, often results in a poor outcome after trauma. This impact on outcome can be reduced by an aggressive management approach to the patient.
FIGURE 44-1
The functional reserve is the difference between basal function (red line) and maximal function (blue line). Even in healthy individuals, this functional reserve is reduced. (From Muravchick S. Geroanesthesia: Principles for Management of the Elderly Patient. St. Louis, MO: Mosby; 1997, with permission. Copyright © Elsevier.)
Surgeons have intuitively recognized the impact of aging on the patient’s ability to tolerate operations and trauma. Recently, there has been a growing body of literature to objectively evaluate the aged patient for risk stratification purposes.20,21,22 Although we would like to be able to use functional reserve clinically, there is no standardized method for measuring and quantifying this heterogeneous parameter. Conceptually, the closer a patient is able to approach maximal organ function in the face of stress, the better the likelihood for recovery and a favorable outcome. Since functional reserve cannot be quantified, frailty is now recognized as a surrogate that can be used clinically. Frailty is recognized as a unique aspect of health status that can be a marker of decreased reserves and increased vulnerability in elderly patients. In other words, frailty is a phenotypic expression of physiologic reserve and resistance to stressors. Recently, the American College of Surgeons National Surgical Quality Improvement Project developed guidelines on preoperative assessment of the geriatric patient.23 Included among a variety of evaluations and assessments is frailty scoring. Fried et al proposed a widely accepted operational definition that is composed of five parts (Fig. 44-2).24
FIGURE 44-2
Frailty score: operational definition.24 (Reproduced with permission from Chow WB, Rosenthal RA, Merkow RP, et al. Optimal preoperative assessment of the geriatric surgical patient: a best practices guideline from the American College of Surgeons National Surgical Quality Improvement Program and the American Geriatrics Society. J Am Coll Surg. 2012;215:453-466. Copyright © American College of Surgeons. Published by Elsevier, Inc. All rights reserved.)
Understanding the impact of frailty on an older trauma patient is important. It can predict discharge disposition and may have a role in goals-of-care discussions with patients and families. Investigators from the University of Arizona have developed and validated a trauma-specific frailty index (TSFI). Over a 2-year period, 200 patients were evaluated using their 15-variable TSFI, and patients were assessed for favorable or unfavorable discharge dispositions. The investigators were able to demonstrate that the TSFI reliably predicted a patient’s discharge disposition, whereas age itself was not predictive.25 Assessment of frailty in the elderly trauma patient will have an increasing role for patient care, resource utilization, and research.
Improper triage seems to contribute to the poor outcomes experienced by some elderly trauma patients. The effectiveness of triage can be evaluated by looking at the interaction between injury severity and complication rate, mortality, or requirement for intervention.26 Although there are data suggesting that undertriage of elderly patients increases mortality rates, a recent population based study disputes this notion.27 These investigators evaluated data from 6015 patients in three counties in California and four from Utah. There was no difference in mortality in patients taken to trauma centers when compared to those taken to nontrauma centers. It should be noted that only 244 patients had an ISS greater than 15. Caution must be exercised in interpreting the conclusions of this study, but it certainly suggests that more work is needed to evaluate the impact triage has on elderly trauma patients. Elderly patients with severe injuries who are not treated with full trauma-team activation are considered undertriaged. Multiple studies have shown a large incidence of undertriage as compared to younger patients, so undertriage can be viewed as a modifiable risk factor for poor outcome in the older patient.26,27,28,29,30,50 Lehmann et al demonstrated that the classic physiologic criteria for trauma team activation, that is, blood pressure and heart rate, both failed to independently predict hospital mortality or the need for urgent interventions.28 These authors attributed the older patient’s “pseudostability” to declining functional reserve and the interaction of premorbid medications. Use of initial vital signs in the elderly population can be misleading. In a study from Los Angeles, patients 70 years of age and older who were admitted to the trauma center were reviewed. The hypotension or tachycardia criteria for trauma team activation (TTA) were not met in 63% of patients with an ISS greater than 15% and 25% of patients with an ISS greater than 30. In this study the overall mortality in “stable” patients not meeting any of the standard TTA criteria was 16%.26 The National Trauma Triage Protocol now suggests that a systolic blood pressure (SBP) of 110 mm Hg be used as a criterion for transport to a trauma center for patients above the age of 65 years. Brown et al from Pittsburgh recently evaluated data from the NTDB and were able to show that the new criterion of a SBP of 110 mm Hg in patients older than 65 increased the sensitivity in predicting mortality in geriatric trauma patients.31 In a similar approach, the group at the University of Arizona has suggested that the Shock Index (SI = HR/SBP) can be used as a field triage tool for elderly patients. Using data from the NTDB, these investigators were able to demonstrate that an SI greater than 1 reliably predicted mortality with statistically better fidelity than the individual components of the index.32
Interestingly, an apparently “minor” injury can have major impact on the older patient. Rib fractures and pulmonary contusions can lead to an abrupt decompensation, and injuries such as intracranial hemorrhage are commonly underappreciated. It has been suggested that a patient age of 70 or older be used as a criterion for trauma team activation.26 The age at which triage and management issues become problematic is controversial, also. The current recommendation of the ATLS program is 55 years of age.33 This is based on data from the Major Trauma Outcome Study (MTOS) which noted a significant increase in mortality between the ages of 45 and 54 years.34 TRISS uses a similar age cutoff, although a recent work examining TRISS methodology seems to indicate an older age is more accurate. Using the Ohio trauma registry, Caterino et al examined mortality trends. Regression analysis identified 70 years of age to be the most promising cutoff for predicting increased odds of mortality.29
The airway of the elderly patient poses specific challenges for providers as these individuals have a significant loss of protective airway reflexes. Patients may have dentures or be edentulous with the former making bag-mask ventilation easier, while arthritic changes may make mouth opening difficult. Finally, when performing rapid sequence intubation, the doses of barbiturates, benzodiazepines, and etomidate should be reduced between 20 and 40% to minimize the risk of cardiovascular depression.35
The anatomical and physiologic changes in the respiratory system associated with aging are reviewed above. Changes in the compliance of both the lungs and the chest wall result in an increased work of breathing with aging. These changes associated with the possibility of nutritional deficits and the supine position place the elderly trauma patient at high risk for respiratory failure. Given a suppressed heart rate response to aging, respiratory failure may present in a more insidious fashion. Diagnosis can sometimes be difficult in interpreting clinical and laboratory information in the face of preexisting respiratory disease or nonpathologic changes in ventilation associated with age. Frequently, decisions to secure a patient’s airway and provide mechanical ventilation may be made prior to fully appreciating underlying premorbid respiratory conditions. As noted above, the risk of ventilator associated pneumonia and the possibility of prolonged ventilation are significant.35 The role for noninvasive mechanical ventilation in the acute resuscitative phases of trauma care seems to be very limited and is likely associated with significant risk to the patient.
Age-related changes in the cardiovascular system place the elderly trauma patient at significant risk for being mislabeled as being “hemodynamically normal.” Since the elderly patient may have a fixed heart rate and cardiac output, the response to hypovolemia will occur by increasing systemic vascular resistance. To further demonstrate the lack of classic symptoms as they relate to cardiovascular pathology, Chong et al evaluated troponin I levels following emergency orthopaedic surgery in 102 patients over the age of 60, and 52.9% had elevated levels. The majority of patients with elevated troponin levels had no cardiac symptoms, but had an increased mortality within 1 year of the event. Furthermore, since many elderly patients have preexisting hypertension, the seemingly “acceptable” blood pressure may truly reflect a relative hypotensive state. As such, identifying the patient who has significant tissue hypoperfusion is mandatory. Several measurements continue to be used to make this diagnosis. These include base deficit, serum lactate, age-adjusted Shock Index, and tissue-specific end-points.8,36,37,38 Resuscitation of the geriatric hypoperfused patient is the same as all other patients and based upon appropriate fluid and blood administration. The elderly trauma patient with evidence of circulatory failure should be assumed to be bleeding. Given the incidence of elderly people with preexisting disease states, however, one should keep in mind that some physiologic event may have triggered the incident leading to injury. Ultimately an aggressive approach to resuscitation of the elderly patient with overt shock or tissue hypoperfusion should result in acceptable outcomes. Less aggressive measures based upon the patient’s age are not acceptable.
Traumatic brain injury (TBI) is a problem of epidemic proportion in the elderly population, and older age is a known variable for a poor outcome following brain injury.39 Aging will cause the dura to become more adherent to the skull. Additionally, older patients are more commonly prescribed anticoagulant and antiplatelet medications for preexisting medical conditions. These two factors place the elderly individual at high risk for intracranial hemorrhage. Atherosclerotic disease is common with aging and may contribute to a primary or secondary brain injury. Moderate cerebral atrophy will permit intracranial pathology to initially present with a normal neurologic examination. Early identification and timely appropriate support including correction of therapeutic anticoagulation can improve outcomes.40
Musculoskeletal changes associated with the aging process pose special concerns during the initial assessment of the elderly trauma patient. Loss of subcutaneous fat, nutritional deficiencies, chronic medical conditions, and associated medical therapies will place the elderly patient at risk for hypothermia and the risks associated with immobility (pressure ulcers, delirium). Rapid evaluation and early mobilization will prove to minimize morbidity.
In the elderly age group, traumatic brain injury (TBI) accounts for more than 80,000 emergency department visits each year of which a majority result in hospitalization. Falls are the leading cause of TBI for people over the age of 65 years (51%), followed by motor vehicle collisions (9%).39 Health care costs associated with the treatment of TBI in the elderly exceeded $2.2 billion in 2003.41
The current evidence-based approach to treating severe TBI in the adult is a “one size fits all” approach that neglects specific issues of the older adult. An investigation using the New York State Trauma Registry compared mortality and functional outcome in elderly versus younger patients.42 In this study, Susman et al demonstrated increased mortality in patients older than 65 years, but also showed that mortality increased as patients aged. These investigators also showed that a majority of elderly patients sustain TBI from falls and appear to have only a mild traumatic brain injury at admission, but still have a much higher mortality as compared to younger patients. This same group then looked at the total effect of age on mortality after TBI.43 They concluded that mortality from TBI increases after 30 years of age, but has a sharp rise after the age of 70. Given the anatomic changes associated with aging on the brain and the fact that a majority of elderly patients present with a Glasgow Coma Scale (GCS) consistent with a mild brain injury, a high index of suspicion must be maintained with the elderly patient presenting with any mechanism of head trauma. To address this, Mack et al investigated the use of computed tomography (CT) of the brain in elderly patients.44 This study specifically looked at mild brain injury (GCS 13–15). In their study of 133 elderly patients, 14.3% had radiographic evidence of acute intracranial pathology. The authors noted that there were no useful clinical predictors of intracranial injury and recommended liberal use of CT of the brain, also. In addition to a higher mortality in general, patients surviving hospitalization will require aggressive rehabilitation. In a multi-institutional trial, a group of elderly patients surviving their initial moderate to severe brain injury (Head AIS = 3) were evaluated following discharge from acute care. In this cohort there were few patients with a low GCS who survived, and this left patients with a GCS of 13–15 to be evaluated. Functional outcome for these patients, as measured by the Glasgow Outcome Scale (GOS) and modified Functional Independence Measure (FIM), was good to excellent. Older patients, however, required more inpatient rehabilitation and took longer to recover when compared to younger patients.45 Aggressive initial management and long-term rehabilitation in the elderly patient with TBI is required for acceptable outcomes.