Clinical Geriatrics

This article is the fourth in a continuing series on trauma care and the older adult. The series discusses the growing problem of trauma in the elderly, including its causes and possible ways to prevent it, care in the acute stages, and manifestations and treatment strategies when trauma involves the torso, spine, brain, and hip. Authors include skilled experts in the trauma field representing various specialties at the R Adams Cowley Shock Trauma Center at the University of Maryland Medical Center and the University of Maryland School of Medicine.

Introduction
Traumatic brain injury (TBI) is a leading cause of mortality and disability in the United States. In the elderly, defined as persons age 65 years and older, trauma is the seventh leading cause of death, and TBI is responsible for over 80,000 Emergency Department (ED) visits annually.¹ As the baby boom generation ages, the number of people over the age of 65 will reach 71 million by 2030 and represent 20% of the U.S. population. Between 2005 and 2050, the elderly population is projected to more than double. The population of those over the age of 85 years is expected to increase in a similar fashion to greater than 20 million in the same time period.² As a result of this increase in the number of elderly persons, age-related TBI is expected to increase as well. In 2006, over $2.8 billion was spent on treating TBI in those older than age 65 years.³ Older age has been well recognized as an independent predictor of worse outcome after TBI, even with relatively minor head injuries.^4,5

Epidemiology
Unintentional death was the ninth leading cause of death among those over age 65 years in 2006.⁶ A significant number of those deaths were from TBI. The leading causes of TBI in the elderly are falls (28%), motor vehicle crashes (20%), and struck by/against events, including pedestrians struck (19%).¹ Most falls are from ground level and occur in or around the home.⁷ The rate of falls requiring hospitalization increases from 339 per 100,000 in people age 65-69 years old to 3637 per 100,000 in those age 85 years and older.⁸

Physiology of Traumatic Brain Injury
Trauma to the head results in mechanical damage to the parenchyma of the brain. Concussions, even without radiographic evidence of parenchymal damage, can lead to cerebral edema, increased intracranial pressure (ICP), and secondary ischemia.⁹ The initial insult occurs when force is transmitted to the brain tissue, which leads to cellular damage. The ensuing cascade of cellular changes leads to the cerebral edema and the secondary injury, which occurs over hours to days after the traumatic event. In addition to the direct parenchymal damage, the mechanical forces can lead to hemorrhage.

The intracranial space is a fixed volume. Once there is no more space to accommodate the extra volume of the mass, blood, or fluid, increased ICP will ensue. Various intrinsic mechanisms exist to prevent increases in ICP after trauma. These include shunting of the cerebrospinal fluid (CSF) to the spinal subarachnoid space, increasing CSF absorption, and shunting venous blood out of the skull.¹⁰ If this compensation fails, the ICP rises. Elevated ICPs are a marker for poor outcome. A mean ICP greater than 20 mm Hg has been shown to increase mortality.^11,12

Cerebral blood flow is difficult to measure directly. Therefore, clinically, we follow the cerebral perfusion pressure (CPP). This is calculated as the difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP-ICP). Normally, ICP ranges from 0 to 10 mm Hg. In people without TBI, autoregulation keeps cerebral blood flow constant, provided the person has a MAP between 50 and 150 mm Hg. Patients with TBI lose that mechanism of autoregulation, and thus the CPP is approximated by the MAP.