Scheetz, Linda J. EdD, RN, FAEN
Unintentional injuries have ranked among the top 10 leading causes of death and disability among adults aged 65 years and older for several decades.1 According to the National Center for Injury Prevention and Control,1 slip-and-fall injuries are the leading cause of death in this population, accounting for nearly half of all 2007 injury fatalities, followed by motor vehicle crashes, which accounted for an additional 17.4% of the fatalities. Motor vehicle crash injuries include those in which the older person was a driver or occupant in a vehicle involved in a crash or was a pedestrian, motorcyclist, or bicyclist struck by a vehicle. In the decade from 1997 through 2007, the number of licensed drivers aged 65 years and older increased 19% to 31 million.2 Of these drivers, 183 000 were injured in motor vehicle crashes during 2008. Although older adults account for approximately 12% of the US population, in 2008, they accounted for 15% of all traffic fatalities, 14% of all vehicle occupant fatalities, and 18% of all pedestrian fatalities.2 In 2008, there were 5569 drivers involved in fatal crashes and 803 pedestrian fatalities among adults aged 65 years and older.2 Most motor vehicle crash injuries involving older drivers occurred during the daytime and on weekdays and involved other vehicles.2 Compared with younger drivers, older drivers were twice as likely to be driving the vehicle that was struck, and in 22% of the crashes, the older driver was turning left.2
Older adults have higher mortality rates at each point of the trimodal death curve: immediate (at the scene), early (within 24–48 hours of injury), and delayed (after 48–72 hours).3 Little is known about the long-term survival trajectory of severely injured older adults, but evidence suggests that their injuries contribute to a shortened life span. Research supports the notion of a quadramodal curve for older trauma patients, as the effects of trauma linger for years following the injury and may result in premature death.4,5
Many older adults survive their injuries only to die later from complications, such as multiple organ failure or sepsis, whereas others experience considerable functional or cognitive disabilities that diminish their quality of life and leave them dependent on the care of others. Previous research suggests that data-driven, goal-directed resuscitation produces favorable responses in critically injured older adults.6
The purpose of this article is to describe the impact of life-threatening injuries in an older adult population, specifically those sustained in motor vehicle crashes, as they relate to anatomic and physiologic changes that occur with aging, the metabolic response to injury, the role of preexisting diseases and medications taken to treat these diseases, and postinjury complications.
Anatomic and Physiologic Changes That Occur With Aging and How They Relate to Injury
Anatomic changes that occur with aging increase the vulnerability to injury, whereas physiologic changes decrease the body's ability to respond to the physical insult of injury and may mask the physiologic expression of the injury. Perhaps the most notable effect is seen in a decrease in physiologic reserve, which may be the most significant factor related to postinjury mortality in an older population.7 Table 1 describes some of the age-related changes and their effects related to injury risk, detection of injuries, and injury outcomes.
Table 1-a: Selected ...Image Tools
Table 1-b: Selected ...Image Tools
The aging cardiovascular system undergoes degenerative anatomic, physiologic, histologic, and electrophysiologic changes that compromise function, increasing the risk of ischemia, rhythm disturbances, and heart failure.10 Cardiac conduction defects and a decrease in the sensitivity to intrinsic catecholamines limit the older person's ability to mount a tachycardic response in the presence of occult hemorrhage, thereby masking the severity of the injury at the injury scene.3 Several studies have pointed to the unreliability of systolic blood pressure (SBP) as an indicator of hemorrhagic shock in older persons.16,17 During the period of compensated hemorrhagic shock, heart rate typically increases to maintain circulation. As this compensatory mechanism fails, SBP falls. However, in older persons, the drop in SBP is not as dramatic as that seen in younger persons. In fact, older hypertensive persons may experience a drop in blood pressure indicative of significant bleeding, although their blood pressure still falls within normal triage parameters.3 Recent studies suggest that the SBP cut point for predicted mortality in injured older adults is approximately 110 mm Hg,16,17 compared with a lower cut point of 95 mm Hg for younger adults.16
Respiratory muscles weaken with age, and degenerative changes occur, decreasing chest wall compliance and maximum inspiratory and expiratory force.3 Other respiratory changes, including decreased elastic recoil, weakness of respiratory muscles, decreased reserve volume, decreased lung expansion, loss of alveolar surface area with diminished gas exchange, and ineffective cough reflex, predispose the older injured adult to postinjury pneumonia, acute respiratory distress syndrome (ARDS), and respiratory failure.10
Musculoskeletal changes lead to considerable functional impairment and balance and gait instability. A loss of muscle strength and bone density decreases the stability of the musculoskeletal system and increases the risk of falls. Also, the loss of bone density increases the susceptibility to fractures. Older persons sustain rib and sternum fractures from the loading effects (transfer of crash energy) when the shoulder seatbelt locks during sudden deceleration in a motor vehicle crash.9,11 As sudden deceleration occurs in frontal impact crashes, the individual continues moving forward at the precrash vehicular speed until he or she encounters the locked shoulder seatbelt, at which point energy transfer occurs and the bone fractures, regardless of air bag deployment.11 In one study, the proportion of fatalities among older persons who were wearing lap-shoulder seatbelts increased to 40.4% in individuals aged 65 to 79 years and 44.6% in persons aged 80 years and older, compared with 30.5% in the 40- to 49-year-old reference group.18 Other skeletal changes, such as changes in the cervical vertebrae, limit hyperextension of the neck, increasing the difficulty of endotracheal intubation following injury.3 Similarly, skeletal stiffening makes it difficult to position older injured patients for radiological studies.
Endocrine System Changes
Cortisol production remains steady with aging; however, levels of dehydroepiandrosterone and dehydroepiandrosterone sulfate decrease, resulting in glucocorticoid excess.12 Concomitantly, an aging endocrine system increases insulin resistance leading to hyperglycemia. Early hyperglycemia in critically injured older adults has been associated with a 2-fold increase in mortality and a 30% increase in multiple organ failure.13 Aging produces fibrotic changes in the thyroid gland, decreased triiodothyronine (T3) secretion and a lower metabolic rate. Thermoregulation is less effective, increasing susceptibility to hypothermia in older trauma patients.
Immune System Changes
Studies of the aging immune system suggest that changes occur in both innate and adaptive immune processes and affect the individual's ability to respond to immune system challenges, potentially increasing morbidity and mortality.8 Cell-mediated immunity diminishes, and there is a corresponding decrease in T-cell count and function.12 A depressed antibody response places the older individual at risk for infection.12
Brain atrophy that occurs with aging predisposes older adults to intracranial bleeding, as there is more intracranial space allowing for movement of the brain and tearing of the vasculature during sudden impact. In one study, significant intracranial injuries, including subdural and epidural hematomas, contusions, and depressed skull fractures, occurred in 9.2% of patients aged 65 years and older.19 Of these patients, only 55.8% presented with focal neurologic deficits, increasing the likelihood that these injuries would go unrecognized by emergency medical services providers. In another study of older adults with moderate to severe traumatic brain injuries, the mean initial Glasgow Coma Scale score for survivors was 14.2 (±1.9), indicating near-normal Glasgow Coma Scale scores that might easily mask significant neurologic injury.20
Neurosensory impairments that increase the risk for injury or make evaluation of the injury more difficult include hearing loss, diminished vision, diminished lower limb proprioception, and cognitive decline.14 Older adults across all age groups experience high-frequency hearing loss, whereas adults older than 70 years also experience mid- and low-frequency hearing loss.21 This poses an increased risk of injury among older pedestrians and drivers because of a diminished ability to hear vehicular horns, sirens, or other warnings of impending danger.
Approximately 90% of adults aged 65 years and older have diminished vision requiring refractive lenses.22 Optical changes are the major reason for decline in visual acuity and include yellowing of the lens that distorts colors in the blue spectrum, a slower speed at which light enters the eye, and less light entering the eye because of shrinkage of the pupil and opacity of the lens.23 These changes are problematic for older drivers who experience limited light and dark adaptation and are nearly blinded when moving from light to dark or dark to light environments, such as entering or exiting roadway tunnels. Additional problems include glare, motion perception, restricted field of view, distorted colors, and loss of peripheral vision.23
Cognitive decline increases the risk for injuries and makes injuries more difficult to evaluate. Research suggests that some degree of cognitive impairment occurs nearly universally with aging and increases as age increases.24 Cognitive decline is a risk factor for falls, pedestrian injuries, and motor vehicle crashes.25,26 Older drivers are at risk for motor vehicle crashes because of declines in attention, processing speeds, and executive function. Finally, older persons who experience cognitive decline and confusion may be difficult to evaluate after injury.
Other neurologic changes, such as diminished lower-limb proprioception, strength, and control, are factors in unintended acceleration (when the driver steps on the gas instead of the brake and causes a crash14) and might pose a risk factor for pedestrian injury, especially on uneven surfaces or when stepping off curbs into roadways.
Renal system changes, including interstitial fibrosis, decreased renal tubule length, basement membrane thickening, nephron sclerosis and hypertrophy, and arteriole atrophy, result in diminished blood flow, secretion, and absorption.10 Decline in glomerular filtration rate can precipitate acid-base disturbances, fluid and electrolyte imbalance, and renal failure following injury.10,15
Metabolic Response to Injury
Traumatic injury initiates a complex interaction of inflammatory, vascular, metabolic, and endocrine events that occur in 2 phases: catabolic and anabolic.27 This process is mediated by 4 interactive physiologic mechanisms having local and systemic effects: sympathoadrenal axis, hypothalamic-pituitary-adrenal (HPA) axis, acute-phase response, and vascular endothelium (Table 2).27 The catabolic phase, often lasting several weeks, mobilizes the body's fuel stores, which are transported to vital organs, immunologically active tissue, and wounds to optimize function and support healing. The anabolic phase follows and may last for several months. During this time, the body works to restore function by accelerating protein synthesis to build new muscle and replenish depleted stores of protein, carbohydrates, and fat. The anabolic phase ends when metabolic processes return to normal and nitrogen balance is restored. This response is blunted in older persons who are severely injured. The decrease in physiologic reserve further hampers the body's ability to recover.27 The following discussion describes events that occur in the catabolic and anabolic phases of the metabolic response.
Table 2: Physiologic...Image Tools
The goal of the early catabolic phase is to restore hemostasis and preserve circulatory volume. Four major events occur in the early phase: (1) the sympathoadrenal axis stimulates the sympathetic nervous system, increasing metabolism; (2) a vascular endothelial response alters vascular permeability; (3) an acute inflammatory response neutralizes bacteria, cleans up cellular debris, and promotes hemostasis; and (4) stimulation of HPA axis activity mobilizes substrates for energy and maintains fluid balance. Glycolysis, glycogenolysis, gluconeogenesis, and lipolysis mobilize stored energy to meet increased metabolic demands. Intrinsic catecholamine release decreases insulin secretion, whereas insulin resistance increases, ensuring the availability of glucose to vital organs.27,28
Injury activates the acute inflammatory response and the extrinsic coagulation cascade. Severely injured older patients develop systemic effects rapidly. Local activation of macrophages, polymorphoneutrophil granulocytes, and cytokines mediates the acute inflammatory response.28 Macrophages secrete cytokines, proinflammatory factors (tumor necrosis factor α, interleukin 1, interleukin 6, interleukin 8), and an anti-inflammatory factor, interleukin 10, producing local and systemic effects from the injury.28 Additional proinflammatory factors, including prostaglandins, thromboplastin, kinins, complement, histamine, proteases, and free radicals, are also released.28 Proinflammatory factors activate inflammatory cells, allowing them to clear dead tissue and kill bacteria.28 Tumor necrosis factor α, interleukin 1, and interleukin 6 exhibit tissue factor on their cellular surface. Tissue factor induces the activation of factor VII, which initiates the extrinsic coagulation cascade, promoting clot formation and hemostasis.29
Vasodilation increases blood flow, which carries inflammatory cells, oxygen, and nutrients to the injured area. Within a few hours of the injury, large numbers of cytokines are mobilized to the injured area, controlling and mediating the inflammatory response.28 Locally, as capillary permeability increases, fluid and protein leak from the vessels into the interstitial compartment, resulting in tissue edema. Recent studies in older adults described changes in cytokine production and a suppressed anti-inflammatory response to an external stimulus as well as chronic low-grade inflammation related to zinc deficiency.30,31
In response to injury, the HPA axis stimulates the release of anterior and posterior pituitary hormones, which mobilize substrates for energy, promote retention of salt and water to maintain fluid balance, and control the effects of cytokines to minimize the inflammatory response.27 Adrenocorticotropic hormone, released by the anterior pituitary gland, stimulates the release of cortisol and aldosterone. Cortisol increases gluconeogenesis, proteolysis, and lipolysis, while decreasing nonessential glucose use and the accumulation of inflammatory cells. Aldosterone release stimulates sodium reabsorption. Antidiuretic hormone, released by the posterior pituitary gland, promotes water reabsorption. In addition, secretion of adrenaline, glucagon, renin, and angiotensin increases, whereas insulin secretion decreases.28 The increased sympathetic nervous system activity and renin-angiotensin secretion increase heart rate, blood pressure, and cardiac output. Decreased insulin secretion in conjunction with increased cortisol production and decreased dehydroepiandrosterone and dehydroepiandrosterone sulfate promote hyperglycemia. The HPA axis also induces the anterior pituitary gland to release endorphins, which promote analgesia.28
The response to injury in older patients is influenced by changes that occur with aging. A diminished sensitivity to intrinsic catecholamine release blunts the sympathetic nervous system stimulation of the cardiovascular system. Cardiac conduction defects limit the older person's ability to mount a tachycardic response to sympathetic nervous system stimulation. Oxygen delivery is reduced and consumption is decreased to suboptimal levels, less than the proposed resuscitation endpoint of 170 mL/min/m2.3
Later in the catabolic phase, large protein and fat stores are used in an attempt to meet the accelerated energy requirements imposed by the healing process. The magnitude of this response is proportionate to the severity of the injury and injury mediation by resuscitation, surgery, and other clinical interventions.28 These activities further stress older patients who may have been malnourished before their injury.
The transition from catabolism to anabolism is marked by progressive wound healing and improvement in nitrogen balance. As nitrogen loss decreases, retained water is excreted, and the individual begins to improve, the transition from a catabolic state to an anabolic state occurs.27 This phase can take several months. Unfortunately, in some patients, a sustained hypercatabolic response leads to hypermetabolism, hyperdynamic circulation, and subsequent multiple organ failure.27 Survival in severely injured older patients is dependent, in part, on the restoration of depleted nutrients, rebuilding of skeletal muscle, and restoration of nitrogen balance.
Effects of Preexisting Disease on Injured Older Adults
Preexisting disease in older trauma patients is a significant factor in mortality. The risk of death associated with preexisting disease increases in both middle-aged and older patients who have moderate and severe injuries.32,33 A landmark study by Morris et al34 described the effects of preexisting disease on mortality and revealed that cirrhosis, congenital coagulopathy, ischemic heart disease, chronic obstructive pulmonary disease, and diabetes significantly increased mortality odds. Compared to adults with no preexisting disease, those with 1 or more of these 5 preexisting diseases were twice as likely to die, and those with 2 or more preexisting disease were nearly 3 times as likely to die. Morris et al34 reported that among persons with congenital coagulopathy, ischemic heart disease, chronic obstructive pulmonary disease, and diabetes, the odds of dying were greater for persons whose injuries were mild to moderate. Surprisingly, the odds of dying related to the presence of preexisting disease decreased after the age of 65 years and in the presence of severe and very severe injuries. However, even among adults aged 65 to 74 years, the mortality odds associated with preexisting disease were 25% greater for those whose injuries were severe and 34% for those whose injuries were very severe compared with the mortality odds among less severely injured persons in the same age group. Among adults older than 74 years, the mortality odds were 8% to 16% greater in the presence of severe and very severe injuries compared with the odds among persons of the same age whose injuries were less severe.
Morris et al34 concluded that for adults aged 65 years and older whose injuries were severe, the risk of mortality from injury alone was sufficiently high so that the effect of preexisting disease was negligible. Subsequent studies suggested that renal disease, congestive heart failure, cancer, and rib fractures also contributed to an increased risk of mortality.35–38
Further complicating the issue of preexisting diseases are the drugs prescribed to treat them. Older trauma patients with underlying cardiovascular disease who take warfarin, clopidogrel, and β-blockers have an increased mortality risk that is many times higher than that in patients without such risk factors.20,38
Triage and Resuscitation
Accurate triage at the injury scene is the first line of defense in maximizing survival and limiting damage. Unfortunately, published triage data indicate that older adults are likely to be undertriaged, a situation in which life-threatening injuries are present, but the patient is transported to a nontrauma center hospital.39 One factor that may contribute to undertriage is the therapeutic preinjury use of β-blockers and calcium channel blockers, which blunt the tachycardic response in the presence of occult hemorrhage.3 Other factors contributing to undertriage are not clearly understood, but may be related to emergency medical services provider training, limited resources, adverse weather conditions, and geographic distance to the nearest trauma center. Seriously injured patients should be transported to the nearest trauma center. When this is not feasible, the patient should be transported to the nearest hospital and arrangements made for timely interfacility transfer to a higher level of care.
Failure to recognize life-threatening injuries at the scene of the crash deprives patients of the opportunity for aggressive resuscitation and definitive care that are necessary to prevent mortality and limit disability. A recent study of a random national sample of adults aged 55 years and older injured in motor vehicle crashes revealed that 21.7% were undertriaged.39
Other recent studies of triage in older injured adults in Maryland and Washington state revealed an undertriage rate of 49.9% in Maryland and a trauma team activation rate of only 14% in Washington.40,41 Numerous earlier studies provided similar evidence, leading to a presumption that current triage criteria do not facilitate detection of severe injuries in this population.
The problem of undertriage is of special concern in older adults because injury mortality increases with age, beginning at the age of 40 years, and is independently influenced by sex, the presence of preexisting conditions, and the body region injured.32,33,36,37 Injury patterns of undertriaged older adults involved in motor vehicle crashes revealed that most sustained multiple injuries, including a preponderance of brain injuries, chest injuries, extremity fractures, and cervical spine fractures, all of which were severe or very severe.42 Brain injuries were second in frequency only to extremity fractures. Most undertriaged patients who sustained critical brain injuries presented in the emergency department with Glasgow Coma Scale scores that were normal or near normal, underscoring the difficulty of evaluating injury severity in an older population. Chest injuries included pulmonary contusions, vascular lacerations, and rib and sternum fractures, indicators of the fragility of the skeletal system in older persons and the vulnerability to contact injuries from seatbelts and vehicular structures.
Emergency Department Triage and Resuscitation
Little has been written about the accuracy of triage of older injured persons in the emergency department. When older injured persons arrive in the emergency department by personal vehicle or basic life support ambulance, potentially life-threatening injuries might be missed, especially if the patient is a poor historian or downplays the injury, or if the injury mechanism is perceived to be minor. A recent study of the sensitivity of the Emergency Severity Index algorithm for identifying Emergency Severity Index level I geriatric patients (those who require immediate resuscitation) revealed that only 46% were accurately identified.43
The goal of initial trauma resuscitation is to reverse shock by restoring circulatory blood volume and oxygen delivery to the vital organs. If resuscitation fails, the person dies within a brief period of time. Severely injured older persons who survive initial resuscitation often develop an overwhelming inflammatory response that becomes systemic, leading to hypoperfusion and further injury to vital organs.
A decade ago, the Eastern Association for the Surgery of Trauma published practice guidelines for geriatric trauma, which included resuscitation.44 The Eastern Association for the Surgery of Trauma recommended an aggressive approach to resuscitation for most older patients, including judicious fluid resuscitation, vasoactive drugs as needed, and hemodynamic monitoring. However, association researchers noted the lack of randomized clinical trials and even prospective observational studies, thus precluding strong evidenced-based practice recommendations. In addition, the Eastern Association for the Surgery of Trauma group noted the lack of resuscitation endpoint studies for older trauma patients. More recently, Callaway and Wolfe3 advocated for aggressive resuscitation of unstable older trauma patients and expedient goal-directed evaluation and treatment of all older trauma patients. Moreover, they noted the importance of observing vital-sign trending in this population and cautioned clinicians to avoid complacency in the presence of normal vital signs. Diagnostic markers of occult hypoperfusion should be monitored and early treatment implemented.
Callaway and Wolfe3 recommended the following measures for older trauma patients: (1) pulmonary artery catheters for any patient who presents with physiologic compromise, significant injury (trauma score <14), high-risk mechanism of injury or preexisting disease with altered cardiovascular function, and (2) aggressive intravenous fluid, blood, and inotropes to maximize cardiac index. Callaway and Wolfe3 suggested that base deficit and lactate clearance should guide hemodynamic resuscitation and that reasonable resuscitation endpoints include a cardiac index of 4 L/min/m2 or an oxygen consumption index of 170 mL/min/m2. Newer technology to evaluate hypoperfusion, such as the use of near-infrared spectroscopy, is undergoing evaluation and may offer an effective noninvasive strategy for monitoring tissue perfusion.
Complications From Injury
The risk of complications in older adults is related to the direct effects of their injuries, changes that occur with the aging process, preexisting diseases, accurate triage, resuscitation efforts, and subsequent management. Approximately 32% of the deaths among older trauma patients are associated with preventable complications, and 62% are caused by multiple organ failure or sepsis.45 Common complications include coagulopathies, infection, systemic inflammatory response syndrome (SIRS), ARDS, and multiple organ dysfunction syndrome (MODS). A discussion of managing complications is beyond the scope of this article; however, prevention, early recognition, and goal-directed therapy are essential in reducing mortality.
Coagulopathies ensue from hypothermia and preinjury treatment with anticoagulants and antiplatelet agents. Motor vehicle crashes often leave patients exposed at the crash scene, while emergency medical services providers attend to their injuries. Even with moderate environmental temperatures, older injured patients lose body heat rapidly. Hypothermia alters the dynamics of the coagulation cascade and can lead to disseminated intravascular coagulation. Therapeutic anticoagulation to treat preexisting cardiovascular disease also poses a threat to older injured patients, especially in those with brain injuries. Those with brain injuries who have therapeutic levels of anticoagulation appear to have an increased risk of bleeding; however, the literature presents conflicting evidence. Fortuna et al46 reported no increased risk, whereas Ivascu et al,20 Wong et al,47 Franco et al,48 and Williams et al49 reported significant increases in mortality.
Because of diminished immune system effectiveness, injured older patients have nearly double the risk of infection compared with younger patients.50 Sources of infection include wound contamination and nosocomial infections related to poor hand hygiene among caregivers, intravascular catheters, indwelling urinary catheters, and mechanical ventilation. Older patients who have underlying pulmonary disease or chest and lung injuries are at an increased risk for ventilator-associated pneumonia. Etiology of ventilator-associated pneumonia is probably multifactorial, including depletion of plasma protein C levels,51 transfusion of blood products,52 emergent intubation and emergency department length of stay,53 aspiration of colonized gastric and oropharyngeal secretions that enter the lower airway during endotracheal cuff manipulation, suction equipment and methods, the use of heated humidifiers, frequency of ventilator circuit changes, and kinetic versus traditional bed.54 Because of the older patient's inefficient immune system, ventilator-associated pneumonia and other infections may progress to sepsis, SIRS, and eventual organ failure.
A systemic inflammatory response occurs in the presence of moderate to severe injury, often progressing to a hyperinflammatory response and SIRS, with or without infection. In one recent study, investigators reported that 61% of patients sustaining life-threatening injuries developed SIRS.55 Another study of patients with severe sepsis and severe noninfectious SIRS revealed that trauma was the attributable etiology of severe noninfectious SIRS in 17.2% of intensive care unit patients, and multiple organ failure was the leading cause of death.56
Changes in vascular permeability that are characteristic of the metabolic response to injury lead to edema in the lung, resulting in ARDS.27 Recent evidence suggests that the intestinal lymphatics serve as the primary transport conduit for nonbacterial gut-derived factors implicated in the development of ARDS and MODS.57 Because these lymphatics empty first into the lungs and heart via the thoracic duct, the lungs are often the first organ to fail. Results from a study of ARDS outcomes in older surgical intensive care unit patients revealed a mortality rate of 51.9%, which was not significantly different from that of younger patients, although the authors acknowledged this mortality rate was lower than the rate of 69% to 80% reported in previous studies.58
Multiple organ dysfunction syndrome is a leading cause of late-injury deaths in adults with multiple trauma.59 Age alone is an independent predictor of MODS as evidenced by the presence of early indicators of shock.6 Ischemic-reperfusion injury and sepsis precipitate a series of events leading to SIRS and, later, MODS.59 Animal studies revealed that toxins produced in the mesenteric lymphatics move through the lymphatic system, causing cellular injury and inflammation.60 Cytokine and complement responses to injury are important mediators of MODS pathogenesis.61 However, little research investigating MODS in an older population exists. The animal studies that have been conducted point to the significance of an aging immune system; however, the clinical relevance to the development of SIRS and MODS in older adults is unclear.7 Other evidence suggests that early hypothermia, ARDS, and isolated cervical spinal cord injury are risk factors among severely injured patients.31,62–64
Results from a study of older patients with more than 40% total body surface area burns revealed that MODS developed in 52% of patients older than 40 years and in 60% of those with inhalation injuries.65 Overall mortality rate was 86.8% among persons whose Sequential Organ Failure Assessment score was 6 or more. Mortality increased with the number of organs that failed: 1 organ, 22.2%; 2 organs, 40%; 3 organs, 93.3%; and 4 organs, 100%.
Compared with younger adults, older adult patients face greater challenges in the presence of injury. Their body systems are less capable of responding to the insult of injuries because of anatomic and physiologic changes that occur with aging, including decreased physiologic reserve. They are more likely to have multiple preexisting diseases and take medications to treat these diseases, which may further compromise their injured state. Postinjury complications produce additional challenges that compromise older patients' recovery and may lead to premature mortality. Although older trauma patients have higher mortality rates than younger patients, the majority survive,30 and many eventually return to independent or preinjury functional status.3 Prompt identification of injuries, aggressive resuscitation, and timely goal-directed therapy are keys to their survival and return to an optimal functional status.
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complications; critical care; elderly; metabolic response; physiologic changes; severe injury