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Traumatic brain injury is the leading cause of injury-related death in the United States and the predominant cause of death in young people under the age of 44 years.1–3 Although the exact magnitude of the problem of brain injury in the United States is unknown, data compiled by Rosenwasser et al³ suggest that ~500,000 new cases of brain injury are seen in our nation’s emergency departments (EDs) annually. Of these, 30 to 40% are moderate to severe, with a mortality and serious morbidity rate of nearly 10% each.³

Resuscitation of mild [Glasgow Coma Scale (GCS) score 13–15), moderate (GCS 9–12), and severe brain injuries (GCS ≤ 8) differs both in intensity and timing. During the last two decades, most research has focused on the pathophysiology and treatment of severe cerebral injury. Unfortunately, there is little consensus regarding the resuscitation of those patients sustaining a mild head injury. Certainly this subset of patients has a much lower risk of death or disability; however, as many as 1.4% of patients who are admitted awake and alert following a mild brain injury will deteriorate, and some will die.⁴ Stein et al⁴ retrospectively reviewed 1538 mild head injury patients and found that those presenting to the ED with an initial GCS score of 15 have a 13% risk of having positive computed tomography (CT) findings. This proportion increases to nearly 40% in those presenting with an initial GCS of 13 (class III data).⁴ Shackford et al⁵ demonstrated similar results (class III data). This is a compelling argument for expedient CT evaluation of these patients.⁶

Those who present with moderate to severe head injury are a much different subset of patients. Although there is some controversy surrounding the ideal resuscitation of patients with an initial GCS ≤ 12, it is well documented that any treatment modality employed in the care of these patients, beginning in the prehospital setting, must be aimed at preventing secondary brain injury.^1,7–10

Brain injury can be categorized as either primary or secondary in nature. Primary injury is a direct result of the initial trauma. Impact to the skull results in displacement of the brain within its confines, often resulting in axonal shearing, contusion, or vascular disruption. Other than continued prevention campaigns, little can be done to ameliorate the effects of primary injury. Secondary insults are generally due to the evolution of the brain injury or to subsequent complications. Common causes of secondary brain injury include hypoxia, hypotension, cerebral ischemia, cerebral edema, alterations in cerebral blood flow, and intracranial hypertension. Aggressive resuscitation of head-injured patients can prevent secondary brain injury and improve morbidity and mortality.1

Literature Review

Emergency Medical Systems

Effective resuscitation of head-injured patients must begin upon activation of the Emergency Medical Services (EMS) system. It is imperative that providers of advanced life support are dispatched to the accident scene and that the patient is transported expeditiously to a hospital that can provide the requisite level of care. In 1990, Smith et al¹¹ demonstrated that patients treated in trauma centers had a significantly lower mortality rate than those treated in nontrauma settings (class III data). Meredith et al¹² suggested the use of the straightforward motor component of the GCS (GMR) as an accurate means for EMS dispatchers to immediately identify patients in need of high-level prehospital care and mobilization of trauma center resources (class III data). Presumably the GMR is simple enough for a witness at the scene to assess. A citizen activating the EMS system could provide the dispatcher with the information that the patient is able or unable to accomplish simple tasks. This knowledge may alter triage decisions.

Airway

In the past 20 years, the importance of early recognition of brain injury and the effects that the prevention of secondary injury have on outcome have been elucidated.¹⁰ As in the resuscitation of any trauma patient, securing a patent airway is primary. Most patients with severe brain injuries are unable to protect their airways and require intubation. Hypoxia is among the most common and lethal of all secondary insults.⁹ Chesnut et al¹⁰ furnished evidence that prehospital hypoxia is highly predictive of increased morbidity and mortality in these patients (class II data).

The role of EMS providers in airway control is controversial. The time required to accomplish field intubation may result in a delay in transport. In the particular subset of severely head-injured patients with a subdural hematoma, it has been “strongly contended” that the single controllable factor most affecting morbidity and mortality is the timing of surgical intervention (class III data).¹³ In fact, Haselsberger et al¹⁴ demonstrated that when the time from injury to definitive care exceeds 2 hours, the mortality rate nearly doubles (class III data). However, there is also strong evidence that prehospital endotracheal intubation is associated with significantly improved survival (class III data).¹⁵ It seems reasonable that if intubation will not significantly delay transport or if transport time to definitive care is expected to be prolonged (as in many rural areas), airway control should be accomplished. In urban settings with short transport times, it may not be necessary, particularly with the realization that field intubation may compromise spinal immobilization. Certainly, any patient who is unresponsive, apneic, or at risk for aspiration must have some attempt at airway control.

Breathing

In the past, severely head-injured patients were thought to benefit from routine and aggressive hyperventilation. While hyperventilation does initially decrease intracranial pressure (ICP) by causing cerebral vasoconstriction, this vasoconstriction increases cerebral vascular resistance and reduces cerebral blood flow (CBF).² Marion et al¹⁶ demonstrated that CBF often drops significantly in the 24 hours following head trauma. This is most pronounced in the first few hours (class II data). The additional decrease in CBF provided by hyperventilation places the patient at greater risk for cerebral ischemia.² Although there have not been any studies investigating the outcome of brain-injured patients following prehospital hyperventilation, the Brain Trauma Foundation’s Guidelines for Prehospital Management of Traumatic Brain Injury17 suggest (at the level of an option) that ventilatory rates greater than 10 breaths per minute (for an adult) during patient transport should be used only as a temporizing measure for profoundly injured patients exhibiting signs of herniation (e.g., posturing, pupillary asymmetry, or fixed and dilated pupils). In the hospital setting, hyperventilation should be utilized only if increased ICP is refractory to other forms of treatment. If this intervention becomes necessary, ventilation should be guided by serial blood gases, with a target PaCO₂ between 30 and 35 mmHg.¹⁸