INTRODUCTION AND EPIDEMIOLOGY
The elderly have worse outcomes following trauma because of physiologic changes that occur with aging. They are more susceptible to serious injury from low-energy mechanisms, less able to compensate from the stress of injury, and more likely to suffer complications during treatment and recovery. Emergency physicians should have a higher suspicion for injury and lower threshold for diagnostic testing and admission than in younger patients.
While studies most commonly define geriatric trauma by an age of 65 or older, some have shown mortality to increase by as young as 45 years of age.1 The U.S. Census Bureau projects that those ≥65 years old will increase from 15% of the population in 2014 to 21% by 2030.2 These older patients consume trauma resources at a greater rate than younger patients.3
The difficulty in describing the elderly population derives from the discrepancy between chronologic and physiologic age. Chronologic age is the actual number of years the individual has lived, whereas physiologic age describes the functional capacity of the patient’s organ systems. Studies have shown a clear association between age and mortality. Comorbid diseases have been shown to be associated with increased mortality after minor and moderate injuries in all age groups.4
The physiologic changes of aging complicate recovery from injury and make assessment of injury more difficult. With age, myocytes are lost and replaced by collagen. Contractility and compliance decrease for any given preload.5 An 80-year-old person will have approximately 50% of the cardiac output of a 20-year-old, even without significant coronary artery disease. Maximal heart rate and cardiac output decrease with age. Aging myocardium has a decreased chronotropic response to catecholamines and is dependent on preload (intravascular volume). Hypovolemia can easily result in shock. Deterioration of the cardiac conduction system leads to atrial fibrillation and bundle branch blocks. Medications, especially digoxin, β-blockers, and calcium channel blockers, impair the tachycardic response to catecholamines, both impairing the body’s inability to compensate for hemorrhage and making heart rate an unreliable predictor of hypovolemia.
Chest wall compliance, respiratory muscle strength, and the capacity for oxygen exchange all decrease with age. The response to hypoxia may decline by 50% and that to hypercarbia by 40%, such that the patient may not appear to be in respiratory distress despite impending respiratory failure.6 Because of weakened respiratory muscles and degenerative changes in the chest wall, maximum inspiratory and expiratory force may be decreased by up to 50% compared with younger patients. Age-related reductions in vital capacity, functional residual capacity, and forced expiratory volume can limit older patients’ ability to compensate for chest injuries.
Renal function declines with age and predisposes patients to dehydration, requiring medication dose adjustments and making them susceptible to acute kidney injury.
This state of decreased physiologic reserve and resistance to stressors, now formally referred to ...