Introduction

An estimated 1.7 million people sustain traumatic brain injuries (TBI) annually in the United States, with total costs estimated at $60 billion per year [1,2]. Overall, TBI-related deaths account for one-third of all trauma-related deaths, or 53,000 deaths annually in the United States [2]. Traumatic brain injuries result primarily from falls (35%), motor vehicle collisions (17%), and direct blows to the head (16%) [2]. Men are more likely to sustain TBI than women for virtually all age groups. Children aged 0–14 account for approximately one-third of the cases of TBI [3]. Children (up to age 18) and adults over 75 years old are more likely to present to the ED, and are more likely to die from head injuries [2].

The initial brain insult occurs from direct impact, acceleration/deceleration injury, or penetrating wound resulting in bleeding, contusion, and ultimately cell death. Prevention measures include use of helmets, seat belts, car seats for children, and efforts to reduce falls in the elderly [4]. Once the primary brain injury has occurred, reversal of the insult is impossible. Prevention of secondary brain injury is the goal of therapeutic intervention. Treatment must start with initial management on scene, and continue until the eventual resolution of the patient’s injuries. Aggressive treatment of severe head injury patients has been shown to be cost-effective, with an increase in quality-adjusted life-years when all costs are considered [5].

A review of a few physiological concepts is necessary for health care providers to understand how to prevent secondary brain injury. Cerebral perfusion pressure (CPP) is equal to the mean arterial pressure (MAP) minus the intracranial pressure (ICP). Measuring an accurate MAP in the prehospital setting may be difficult, making the systolic blood pressure (SBP) a surrogate that has been used in published guidelines and research. Rapid rises in ICP cause compression of the brain within an enclosed space (skull). As the pressure increases, the brain can be pushed downward, herniating in several possible directions. This herniation can cause compression of cranial nerves, posturing, changes in respiration, paralysis, and sudden death.

Management of severe traumatic brain injury is focused on transport to a trauma center while preventing secondary brain injury. Secondary brain injury occurs through a complex biological cascade, which can continue for hours to days. Both hypotension and hypoxia are independently associated with increased mortality and poorer neurological outcomes [6]. When hypotension and hypoxia occur together, a 75% mortality rate has been reported [7].

Primary assessment

The initial management of all injured patients should begin with airway, breathing, and circulation. Adequate oxygenation must be considered a critical priority in brain-injured patients. Hypoxemia occurs more frequently in brain-injured patients than is clinically suspected or recognized. Even a single episode of hypoxemia (SaO₂ <90%) can add to the overall morbidity, and has been associated with a 150% increase in mortality [8,9]. Supplemental oxygen should be administered to all potential TBI patients with continuous monitoring of the oxygen saturation using pulse oximetry. Adequate circulation is also important in the head-injured patient. Just a single episode of hypotension, defined as a systolic blood pressure less than 90 mmHg, is associated with increased morbidity, and with a 150% increase in mortality [9]. Intravenous fluids should be administered to maintain a systolic blood pressure of at least 90 mmHg [10]. The optimal fluid choice for volume restoration and maintenance of blood pressure has been intensely debated [11,12]. Isotonic crystalloid is recommended in both adults and children. Alterations in mental status due to hypoglycemia can easily be mistaken for those related to a traumatic brain injury. Patients with altered mental status should have a fingerstick glucose checked in the prehospital setting.