Assessment and Management of Traumatic Injuries in Older Adults

Etiology

Falls are the most common mechanism of injury in older adults, followed by motor vehicle accidents and burns. According to the United States Centers for Disease Control and Prevention (CDC), in 2014 alone, older Americans experienced 29 million falls, causing 7 million injuries, costing an estimated $31 billion in annual Medicare costsDetermining the cause of the fall is an important element of the care plan for each patient, as the fall may result from an isolated mechanical process or a systemic condition that puts the patient at risk for additional falls. When assessing these patients, the patient’s functional status before the fall, along with the location and circumstances of the fall, should be considered.[2][3] Even if a reliable mechanical cause of the fall can be established, a complete medical evaluation should be considered to evaluate for a pathological condition that caused the fall. Occult anemia, electrolyte abnormalities, and disorders of glucose metabolism should be considered.[4]

Attention should also be paid to the possibility of cardiovascular causes of the fall, including orthostatic hypotension, dysrhythmia, and myocardial infarction. Other pathological states that can lead to falls include infection from urinary, pulmonary, or soft tissue sources. Neurologic disorders, including primary or secondary seizures, should be on the differential diagnosis. The role of polypharmacy and potential disruptions to normal physiologic function cannot be understated.

Epidemiology

Trauma is the fifth leading cause of death in older adults and accounts for up to 25% of all trauma admissions nationally. Those aged 65 and older are more prone to traumatic injuries due to factors such as decreased bone density, slower reflexes, and a higher prevalence of comorbidities. Special considerations include polypharmacy, decreased functional reserve, and increased morbidity and mortality compared to younger adults.[5][6] Mortality from traumatic injuries increases after age 70 when adjusting for injury severity score. Prehospital trauma triage criteria specific to older adults improve the identification of those needing trauma center care.

Pathophysiology

Aging brings about a host of fascinating physiological changes that reflect the resilience and adaptability of the human body. While certain functions may slow down, the body often compensates remarkably by developing greater efficiency in some processes and prioritizing essential functions. The many anatomic and physiologic changes in multisystem organ function associated with normal aging must be considered when caring for an older patient with a traumatic injury.

Nutritional

Older patients may present with various degrees of malnutrition. Malnutrition may be due to a lack of protein or total caloric intake. Various mineral and supplement deficiencies should also be considered. These nutritional shortcomings may be multifactorial, such as living on a fixed income, inability to obtain healthy food from stores, reduced appetite, poor taste, and inability to prepare meals or feed oneself. Nutritional deficiencies have significant effects, including decreased healing capability and reduced immune responses. Malnourished older patients with traumatic injuries are at a higher risk for morbidity and mortality.

Integument/Musculoskeletal

Older individuals have decreased lean body mass, loss of tissue elastance, thinning of the skin, and an overall increase in total body fat. Skin thinning makes thermoregulation more difficult, and older individuals are much more susceptible to hypothermia, even in warm weather conditions. Skin becomes much less resistant to shearing forces as the overall elastic content decreases, increasing susceptibility to skin tears and avulsions even with minor energy transfers. An increase in total body fat results in a larger distribution volume; this needs to be considered when administering medication.

Bone density is often decreased via demineralization processes, such as osteopenia and osteoporosis. Loss of bone density coupled with loss of lean muscle mass leads to loss of strength and locomotion, balance issues, and decreased ability to produce heat through shivering. Furthermore, loss of bone density leads to a higher risk of fracture with lower energy injury mechanisms.

Neurologic

Neurohumoral responses in older patients are often blunted, which leads to a slower and less vigorous response to stimuli. Older patients frequently have neurocognitive decline and may present with reduced sensation to nervous stimuli. Comorbidities, such as diabetes, can lead to peripheral neuropathy, a loss of sensation and proprioception, and increased susceptibility to pressure wounds and injuries from falls.

The brain parenchyma also atrophies and loses volume with age, leading to stretching of the bridging dural veins. When an older individual has a sudden inertial change, such as a fall with a head strike, these veins are at high risk for rupture, leading to subdural hemorrhage. Compounded with the fact that the brain shrinks in size, but the calvarium maintains a fixed volume, clinical changes associated with intracranial hypertension often present in a delayed fashion as it takes more blood volume to lead to brain compression and shift. This process is somewhat protective because older patients may not immediately have significant clinical deterioration or need emergent surgical intervention to evacuate the hemorrhage.

Because normal parenchymal atrophy occurs with aging, there may also be systemic changes, such as a decreased ability to autoregulate blood flow. Older patients are more likely to take multiple medications, and adverse effects of these medications could lead to drowsiness, loss of energy, oversedation, and loss of balance and memory. Prescribed medications can increase the risk of falls, motor vehicle accidents, and other mechanisms of injury.

Cardiovascular

Connective tissue stiffening comes with age, and this change notably affects arteries, veins, and the myocardium. The aging heart becomes stiffer and less compliant, losing the ability to increase contraction and cardiac output when experiencing a more significant preload. With time, the cardiac conduction system becomes more fibrotic, and the myocardium becomes less responsive to neurohumoral effects; this all leads to a decreased ability to preserve cardiac output, defined as the product of heart rate and stroke volume.

For relatively mild hypovolemia, whether due to poor intake with associated dehydration or volume contraction or related to injury with hemorrhage, the resultant drop in preload significantly affects the overall cardiac output in older adults. When the vascular system is desensitized to neurohumoral effects, there is less ability for the systemic vascular resistance to increase the peripheral blood pressure or for the venous system to contract, leading to a decreased ability to increase preload.[7]

Polypharmacy can have several effects on the cardiovascular system in this demographic. Beta-blockers, calcium channel blockers, and cardiac glycosides may lead to negative inotropic, dromotropic, and chronotropic effects. Under normal circumstances, this is the desired effect of the medication; with an acute insult, these medications prevent the injured host from mounting a normal physiologic response to compensate and maintain homeostasis.

Shock, defined as global tissue hypoperfusion, is often clinically defined as a systolic blood pressure less than 90 mm Hg. This definition is often incomplete for many patients, especially those older than 65. Current literature supports a systolic blood pressure of 110 mm Hg as a better benchmark for identifying occult shock. Furthermore, multiple indices have been utilized to better detect occult shock instead of using one discrete variable, such as heart rate, blood pressure, or urine output, as all are insensitive. The shock index is a more sensitive indicator and is calculated as the quotient of the systolic blood pressure and the heart rate (shock index= heart rate/systolic blood pressure). A shock index of 0.5 to 0.7 is considered normal. However, when it is greater than 0.7, the patient is deemed to be in shock.[8] Further iterations of this index have also been proposed, which are felt to be more sensitive, such as the respiratory-adjusted shock index (RASI). RASI is calculated by multiplying the shock index by (respiratory rate/10). When the RASI is greater than 1.3, it suggests that the patient is in occult shock.[9]

Pulmonary

Overall, pulmonary function deteriorates in older adults. With age, the elastic recoil of lung parenchyma decreases as the number of crosslinking elastic fibers decreases. Older adults typically have less functional residual and vital lung capacities, with the total lung capacity either staying the same or mildly decreasing.[10] Formal pulmonary function testing often reveals that this population has lower forced expiratory volumes over 1 second and forced vital capacity. Therefore, the respiratory reserve is limited, and the ability to adapt compensatory physiologic processes to hypoxia, hypercarbia, and metabolic abnormalities, such as acidosis, is blunted. Clinically, even small perturbations to the older patient may manifest in respiratory failure, and often, the clinical signs or symptoms may be subtle.

Additionally, as older adults lose lean muscle mass, their ability to recruit secondary respiratory muscles is decreased. Along with loss of tissue elastance and greater total body fat deposition, there is a decrease in chest wall compliance. Age-related osteoporosis may also alter thoracic geometry, reducing diaphragmatic curvature and decreasing maximal transdiaphragmatic pressure.[11]

Suboptimal nutritional intake also contributes as older individuals often have inanition contributing to respiratory failure as they tire from attempting to compensate for metabolic disturbances. Atelectasis is very common in this demographic, and atelectasis can lead to underlying ventilation-to-perfusion mismatch with a resultant increase in pulmonary shunting. 

The ability to maintain proper pulmonary hygiene also decreases with age, and there is often chronic airway colonization with microbes. The normal pseudostratified ciliated epithelium and goblet cells, which are responsible for the mucociliary escalator, fail to remove microbes and particulate matter from the lower airways, and the older adult’s cough is often weak due to loss of muscle mass, which prevents effective pulmonary hygiene.

Chronic aspiration due to dysphagia is often seen in this patient population, which significantly affects the underlying pulmonary function. Chronic aspiration should be considered in all older adults with a history of obesity, sedating medications, gastroparesis associated with diabetes, or gastroesophageal reflux to prevent worsening aspiration and respiratory failure if laid supine. Strict aspiration precautions and, if indicated, gastric tube decompression should be considered to prevent this possibly catastrophic event. 

Gastrointestinal

Poor dentition leads older patients to become edentulous, necessitating prosthetic dentures. Loss of the ability to chew foods can lead to poor nutritional intake. Salivary glands also atrophy, leading to decreased saliva production, which impairs the lubrication of the food bolus, making the process of deglutition more challenging. Transfer of the food bolus from the oropharynx to the esophagus is also impaired and can lead to aspiration as prior protective aerodigestive reflexes are often blunted or absent.

Multiple medications affect the gastric lining and acidic milieu. These alterations can worsen the protective mechanisms of the gastric wall and lead to gastritis and other forms of peptic ulcer disease. The pharmaceutical alkalization of gastric acid can lead to microbial overgrowth. In this case, if aspiration does occur, it can lead to a higher rate of pulmonary infection.

Gastric and intestinal wall integrity is also affected by age, leading to poor absorption of both micro- and macronutrients and malnutrition. Additionally, overall motility is slowed as the tissues become less responsive to neurohumoral and endocrine stimuli. Older adults have been shown to have an increased number of uncoordinated esophageal contractions and decreased gastric emptying.[10] This can lead to a higher risk of reflux in this age group. 

Over time, the liver loses its overall parenchymal mass, and blood flow to the liver decreases, resulting in a worsening ability to filter the bloodstream. The liver’s intrinsic ability to make proteins, such as albumin, is also diminished, which can lead to a decrease in oncotic pressure and worsening of the third-spacing of fluids. Also, free drug concentrations can increase in the face of hypoalbuminemia, leading to unwanted toxicities and adverse effects.[10]

Decreased hepatic production of thrombopoietin can lead to thrombocytopenia due to decreased stimulation of the megakaryocytes in the bone marrow. Vitamin K-dependent clotting factors are also diminished due to poor oral vitamin K intake and loss of hepatic synthetic function. Both factors can lead to a higher risk of coagulopathy in the geriatric trauma population. 

Genitourinary

Urinary incontinence exists at a higher rate in older persons. This condition is partially due to neurohumoral desensitization of the bladder detrusor muscle. When the detrusor fails to contract, postvoid residual volumes can increase, leading to higher rates of bacterial overgrowth with infection and postobstructive renal failure. Prostatism in men is another common cause of the inability to micturate completely. Medications common to the older adult population may lead to acute urinary retention as well. Urinary tract infection is another common occult cause of altered mental status and should be sought early and appropriately treated if found.

Like other organs, the kidneys also are subject to parenchymal tissue loss with age. The nephron load in the renal cortex is most affected. The glomerular filtration rate is decreased, leading to problems with the clearance of solutes and water reabsorption, which in turn leads to disturbances in fluid and electrolyte homeostasis. Seeing a decrease in creatinine as lean muscle mass decreases with age is not uncommon, but there can also be an associated increase in the tubular secretion of creatinine. As a result, serum creatinine levels can be within the normal range but may be misleading as renal function may still be grossly impaired.

Creatinine clearance, CCR (mL/minute)= {[(140 - age) x mass (kg)] /(serum creatinine x 72)}, is often a better way to measure and determine renal function, especially in the older population. Creatinine clearance is known to decrease with age variably and may be due to vascular changes in the kidney leading to glomerulosclerosis, tubular atrophy, and interstitial fibrosis.[12] Many medications may need to be renally-adjusted to prevent nephrotoxicity.

Neurohumoral stimulation of the kidneys also declines with age. The renin-angiotensin-aldosterone system is downregulated, making the host less responsive to hypovolemia and salt retention. As renal function declines, the kidney becomes less responsive to hypoxia, leading to decreased erythropoietin production and anemia. The ability of vitamin D to undergo hydroxylation also decreases, putting older patients at higher risk for osteomalacia and osteoporotic fractures.

Hematologic

Bone marrow mass may also decrease with age. Fat replaces marrow, and hematopoietic reserves decline. The marrow itself also becomes less sensitive to stimulatory hormones. The functionality of the red cells, platelets, and leukocytes all develop qualitative defects even though, quantitatively, they may be normal.

Anemia is prevalent in older adults, and a differential should be obtained. The mean corpuscular volume helps delineate the cause of the anemia further. Macrocytic anemia is usually caused by folate or B12 deficiencies, most commonly caused by poor nutritional intake or absorption issues, both seen in older adults. Microcytic anemia is often due to iron deficiency or other dietary inadequacies, but it can be secondary to other causes, such as occult blood loss. Anemias should be evaluated and corrected to help preserve or increase oxygen-carrying capacity.

Immune

Decrements in immune function are commonly seen in older individuals. Loss of immune function has been found to contribute to increased infection risk, autoimmune disorders, and malignancies. Generalized malnutrition with vitamin and mineral deficiencies is often seen and is a significant cause of immune dysfunction.

Endocrine

Older adults are at higher risk for impaired glucose tolerance or diabetes due to a relative decrease in insulin secretion by β-cells and peripheral insulin resistance.[13] Many older patients are on systemic steroids, which may lead to hyperglycemia, immunosuppression, and decreased wound healing rates. Furthermore, chronic glucocorticoid therapy is associated with hypothalamic-pituitary-adrenal axis suppression, which puts patients at risk for adrenal suppression, requiring stress dosing at times of surgery, traumatic injury, or during critical illness. Also, many older adults are on thyroid hormone replacement therapy, and critically ill patients may become hypothyroid or euthyroid-sick. The astute clinician should keep these common endocrinopathies in mind when caring for an older adult with traumatic injuries.

History and Physical

The history and physical examination of an older adult with a traumatic injury require a comprehensive and meticulous approach, recognizing the complexities of aging. The history should include details of the trauma event, preexisting medical conditions, medications, and baseline functional status, including cognitive and sensory abilities. Particular attention should be paid to medications that affect coagulation, cardiovascular stability, and cognitive function, as these can significantly impact the patient’s response to trauma. All resources available for collateral information should be utilized.

During the physical examination, clinicians must carefully assess for subtle signs of injury, which may be masked by age-related changes such as reduced pain sensation and altered mental status. A thorough physical examination entails vital signs, neurological status, and a head-to-toe assessment to identify potential injuries. Often, vital signs appear normal until the patient deteriorates rapidly, as physiologic reserve is poor in this population. Blood pressure and pulse may mislead and be altered by polypharmacy. Bruising, skin tears, and hematomas should be evaluated for underlying injury. Comorbid conditions must be taken into consideration. Given the higher risk of complications, even seemingly minor trauma in older adults warrants a detailed and cautious evaluation to ensure optimal care and outcomes.

Evaluation

Advanced trauma life support protocols should be followed during the initial evaluation of an older patient with a traumatic injury. A complete assessment, including medical, cognitive, functional, and social assessments, should be performed. Due to the possibility of subtle pathological disease states or occult injury, a thorough evaluation should be considered even if a reliable history of a mechanical fall can be established.[14][15]

Older adults with traumatic injuries should be evaluated for frailty upon admission. Frailty is considered a syndrome of physiologic deterioration that may occur with aging and is often characterized as an inability to adapt to acute illness or stress, which leads to a more significant number of complications, including the need for long-term care, disability, and even death.[16]

Frailty is not solely defined by age. Many patients younger than 65 have chronically poor health and meet the definition of frailty. Frailty has traditionally been thought of as a physical deterioration in which patients exhibit weight loss, loss of lean muscle mass with associated weakness, and decrease in walking speed, all secondary to biological deterioration. However, newer views of frailty incorporate this concept with the idea that there is also a concurrent deficit accumulation, such as social impairment and cognitive decline. 

No gold standard test is currently available to detect frailty; many tools have been developed to help determine who is most at risk for an adverse outcome or prognosis. One of these easily applied screening tools is the FRAIL scale. The FRAIL score looks at fatigue, resistance (ability to climb 1 flight of stairs, ambulation (ability to walk 1 block), illnesses (>5), and loss of weight (>5%). A score of 0 is best, and 5 is worst, where scores of 3 to 5 are considered frail, 1 to 2 pre-frail, and 0 good health.[17][18] One trauma-specific frailty index for older adults has been developed, which utilizes 15 variables that can be abstracted from a patient’s chart to help clinicians plan discharge disposition.[19]

Other tools have been developed to aid in the prognostication for in-hospital mortality in older adults with traumatic injuries. One of these is the geriatric trauma outcome score (GTOS); (age) + (2.5 × injury severity score) + 22 (if packed red blood cell transfused within ≤24 hours of admission). This tool has been validated as a prognostic indicator for in-hospital mortality.[20] Newer predictors of mortality after trauma in this population have recently been published. The quick elderly mortality after trauma is scored on the initial patient presentation, and the full elderly mortality after trauma is calculated after radiologic evaluation. Both scores were found to estimate the probability of in-hospital mortality accurately.[21]

Treatment / Management

Based on the history and physical examination coupled with risk factor assessment, general screening laboratory tests such as complete blood count, comprehensive metabolic panel, electrocardiogram, urinalysis, and radiographic studies should be considered. Central nervous system imaging should be considered in patients taking antiplatelet or anticoagulant medications if the mechanism of injury raises suspicion for injury.[22][23][24] Patients taking anticoagulants found to have a significant intracranial hemorrhage require aggressive treatment. Reversal of the anticoagulant should be considered in the appropriate clinical context and should be based on institution-specific guidelines.(B2)

Oral anticoagulants, such as dabigatran, apixaban, and rivaroxaban, are indicated for various clinical conditions that affect older adults. These include treatment of venous thromboembolism, stroke prophylaxis in nonvalvular atrial fibrillation, and acute coronary syndrome. The novel direct oral anticoagulants have a different mechanism of action than warfarin, which acts to inhibit Xa and thrombin IIa in the coagulation cascade. Reversal of the anticoagulation caused by newer oral anticoagulants requires specific agents. Dabigatrin has a monoclonal antibody reversal agent, idarucizumab.[25]Andexanet alfa can be used to reverse anticoagulation in patients taking factor Xa inhibitors, such as apixaban and rivaroxaban.[26]

Reversal of anticoagulation caused by warfarin historically relied on using vitamin K and fresh frozen plasma (FFP). Recent literature suggests that relying on vitamin K and FFP might be less effective than using vitamin K and prothrombin complex concentrates.[27] Vitamin K and FFP therapy often require 30 to 60 min to thaw the FFP. Further, large volumes of FFP in the range of 30 mL/kg (4 to 12 units) are often required for adequate reversal. The time to infuse the necessary volume of FFP can complicate and delay care. Treatment with vitamin K and prothrombin complex concentrates avoids these limitations. Prothrombin complex concentrates do not require blood group system compatibility testing, and infusion volumes are less than 100 mL.

Differential Diagnosis

When evaluating older patients with traumatic injuries, it is crucial to consider a broad range of differential diagnoses due to the complexity and variability of age-related physiological changes. The differential diagnoses should encompass both common and less obvious conditions that may mimic or complicate traumatic injuries. Accurate diagnosis requires careful consideration of the patient's history, physical examination findings, and any underlying health issues that could influence the presentation and management of trauma. In the context of geriatric trauma, important considerations include the following:

• Altered mental status
• Focal neurological deficits
• Headache
• Ischemic stroke
• Intraparenchymal hemorrhage
• Nontraumatic intracranial bleed
• Subdural hematoma
• Subarachnoid injuries
• Traumatic brain injury

Prognosis

Patients who are older with trauma have a higher mortality rate than younger patients. The prognosis of patients who are older with trauma often hinges on several critical factors, including the severity of the injury, the presence of comorbid conditions, and the patient’s overall functional status. Older adults typically face a more challenging recovery compared to younger individuals due to diminished physiological reserves and the increased likelihood of complications such as infections, cardiovascular events, and delayed wound healing. For example, patients who are older with 3 to 4 rib fractures have a 19% increased mortality risk and 31% risk of pneumonia, and these risks increase with each additional rib fracture.[28] 

As evidence-based medicine and informed care have evolved, the prognoses for patients who are older and severely injured have steadily improved.[29] With prompt, specialized care and a multidisciplinary approach, many patients can achieve meaningful recovery and improved quality of life. Early intervention, tailored treatment plans, and effective rehabilitation are key to enhancing outcomes and minimizing long-term impacts. Overall, while the prognosis for patients who are older with trauma can be guarded, a well-coordinated care strategy can significantly improve the likelihood of a favorable outcome.

Complications

Complications in patients who are older with a traumatic injury are often more frequent and severe due to the physiological changes associated with aging. These complications may include infections, such as pneumonia or urinary tract infections, which can exacerbate the patient's condition and complicate recovery. Cardiovascular complications, such as myocardial infarction or arrhythmias, are also a significant risk due to the stress of trauma on an aging heart.

Additionally, patients who are older are more prone to prolonged immobilization, which can lead to deep vein thrombosis, pulmonary embolism, and muscle atrophy. Delayed wound healing and the potential for delirium or cognitive decline further complicate the clinical picture. Addressing these risks requires vigilant monitoring, proactive management strategies, and a multidisciplinary approach to ensure optimal outcomes and mitigate the impact of these complications.