A. Traumatic brain injury (TBI) is a leading cause of death and long-term disability and results in an enormous economic cost to society. More than 1.7 million head injuries occur each year, accounting for 275,000 hospitalizations and 53,000 deaths. At least 5.3 million or 2% of the U.S. population live with disabilities resulting from TBI. Outcomes from TBI have improved with improved critical care and multidisciplinary management teams made up of trauma surgeons, intensivists, neurosurgeons, and others. The use of advanced monitoring techniques and evidence-based approaches to TBI management have also contributed to these improved outcomes.

A. Head trauma can be categorized as closed or penetrating. The most frequent causes for closed TBI are motor vehicle accidents, falls, and assaults. Frequent causes of penetrating TBI are gunshot wounds or fragmentation injuries in the military population.

A. Primary brain injury—occurs at time of injury as a result of direct trauma to brain tissue.

B. Secondary brain injury—occurs after initial injury, causing additional insults to the brain. This is usually secondary to hypoxia, hypotension, intracranial hypertension, and/or complex inflammatory cascade.

C. Increased intracranial pressure (ICP) may be a result of mass effect imparted during the primary injury, such as a hematoma, or as a result of edema from secondary processes. Much of the management of TBI is aimed at preventing or treating elevated ICPs.

1. Monro-Kellie doctrine → The skull is a rigid compartment containing brain tissue, cerebrospinal fluid (CSF), and intravascular blood. Because this space is unable to expand, any change in its contents (intracranial mass lesion or diffuse edema) must be followed by a subsequent reduction in other components in order to compensate. This eventually leads to a decrease in cerebral blood flow and brain perfusion.

2. Herniation occurs when ICP rises to the point where brain contents herniate through a skull compartment opening (either through the tentorial incisura, below the falx cerebri, or through the foramen magnum), occluding blood flow to the brain.

3. Brain death occurs when cerebral edema and herniation eliminate adequate blood flow to the brain, resulting in widespread infarction. Brain death is defined as the irreversible cessation of all brain cortical and brainstem functions.

A. History of traumatic event and neurologic status at the scene.

B. Neurologic examination.

1. Examination for scalp lesions, skull fractures (open or closed), and CSF leak.

2. Pupil size and reactivity.

3. Motor and sensory examination.

a. Uncal herniation syndrome includes ipsilateral fixed, nonreactive pupil, and contralateral hemiparesis (rarely ipsilateral-“Kernohan notch phenomenon”).

b. Peripheral and central reflex examination.

c. Glasgow coma scale (GCS) (Table 111-1).

C. Radiographic studies.

1. Noncontrast computed tomography (CT) scan of the head is often used as a primary radiographic study for evaluation of a patient with a head injury. It is an adequate modality for evaluating most skull fractures, mass lesions including hematomas and contusions, and other processes including hydrocephalus or cerebral edema. May also be used serially for patients whose neurologic exams are not obtainable or unreliable.

2. CT angiography is the screening test of choice to rule out blunt vascular injury (BVI) in the trauma patient. Injury patterns which are associated with BVI are c-spine fractures, midface fractures, and lateralizing
neurologic signs not explained on brain CT. CT angiography, magnetic resonance (MR) angiography, or conventional cerebral angiography may also be used to characterize any lesion found.