Traumatic brain injury (TBI) is the impairment in brain function after direct or indirect forces to the brain. The force of an object striking the head or a penetrating injury causes direct injury. Indirect injuries occur from acceleration/deceleration forces that result in the movement of the brain within the skull.
TBI can be classified as mild, moderate, and severe. Mild TBI includes patients with a Glasgow Coma Scale (GCS, see Table 160-1) score ≥14. Patients may be asymptomatic with only a history of head trauma, or may be confused and amnestic of the event. They may have experienced a brief loss of consciousness and complain of a diffuse headache, nausea, and vomiting. Patients at high risk in this subgroup include those with a skull fracture, large subgaleal swelling, focal neurologic findings, coagulopathy, age >60 years, or drug/alcohol intoxication.
Moderate TBI include patients with a GCS score of 9 to 13. Overall, 40% of these patients have a positive CT scan and 8% require neurosurgical intervention.
The mortality of severe TBI (GCS score <9) approaches 40%. The immediate clinical priority in these patients is to prevent secondary brain injury, identify other life-threatening injuries, and identify treatable neurosurgical conditions.
Prehospital medical personnel often may provide critical parts of the history, including mechanism and time of injury, presence and length of unconsciousness, initial mental status, seizure activity, vomiting, verbalization, and movement of extremities. For an unresponsive patient, contact family and friends to gather key information including past medical history; medications (especially anticoagulants); and recent use of alcohol or drugs.
Clinically important features of the neurologic examination that should be addressed include assessing the mental status and GCS; pupils for size, reactivity, and anisocoria; cranial nerve function; motor, sensory, and brainstem function; and noting any development of decorticate or decerebrate posturing.
Infants with TBI demonstrate a global diminished level of responsiveness. Pupillary or facial asymmetry, extremity motor function abnormality, or a decreased sucking reflex may be found. Signs of increased intracranial pressure in infants include decreased arousal, lethargy, seizure, vomiting, apnea, and bradycardia. Signs or symptoms of TBI in the older child include headache, nausea, vomiting, diminished level of consciousness, motor weakness, visual changes, hypertension, bradycardia, and respiratory arrest.
Skull Fractures. Depressed skull fractures are classified as open or closed, depending on the integrity of the overlying scalp. Although basilar skull fractures can occur at any point in the base of the skull, the typical location is in the petrous portion of the temporal bone. Findings associated with a basilar skull fracture include hemotympanum, cerebrospinal fluid (CSF) otorrhea or rhinorrhea, periorbital ecchymosis (“raccoon eyes”), and retroauricular ecchymosis (Battle sign). In children, linear skull fractures that result from a fall from a small height (<4 ft) generally are not associated with the development of clinically significant intracranial lesions. Significant intracranial injuries in children often occur after falls from more extreme heights or higher impact collisions.
Cerebral Contusion and Intracerebral Hemorrhage. Common locations for contusions are the frontal poles, the subfrontal cortex, and the temporal lobes. Contusions may occur directly under the site of impact or on the contralateral side (contrecoup lesion). The contused area is usually hemorrhagic with surrounding edema, and occasionally associated with subarachnoid hemorrhage. Neurologic dysfunction may be profound and prolonged, with patients demonstrating mental confusion, obtundation, or coma. Focal neurologic deficits are usually present.
Traumatic Subarachnoid Hemorrhage. This condition results from the disruption of subarachnoid vessels and presents with blood in the CSF. Patients may complain of diffuse headache, nausea, or photophobia. Traumatic subarachnoid hemorrhage may be the most common CT abnormality in patients with moderate or severe TBI. Some cases may be missed if the CT scan is obtained less than 6 hours after injury.
Epidural Hematoma. An epidural hematoma results from an acute collection of blood between the inner table of the skull and the dura mater. It is typically associated with a skull fracture that lacerates a meningeal artery, most commonly the middle meningeal artery. Underlying injury to the brain may not necessarily be severe. In the classic scenario, the patient experiences loss of consciousness after a head injury. The patient may present to the ED with clear mentation, signifying the “lucid interval,” and then begin to develop mental status deterioration in the ED. A fixed and dilated pupil on the side of the lesion with contralateral hemiparesis is a classic late finding. The high pressure arterial bleeding of an epidural hematoma can lead to herniation within hours of injury. An epidural hematoma appears biconvex on CT scan.
Subdural Hematoma. A subdural hematoma (SDH), which is a collection of venous blood between the dura matter and the arachnoid, results from tears of the bridging veins that extend from the subarachnoid space to the dural venous sinuses. A common mechanism is sudden acceleration-deceleration. Patients with brain atrophy, such as in alcoholics or the elderly, are more susceptible to a SDH. In infants, SDH is strongly associated with nonaccidental trauma. In acute SDH, patients present within 14 days of the injury, and most become symptomatic within 24 hours of injury. After 2 weeks, patients are defined as having a chronic SDH. Symptoms may range from a headache to lethargy or coma. It is important to distinguish between acute and chronic subdural hematomas by history, physical examination, and CT scan. An acute subdural hematoma appears as a hyperdense, crescent-shaped lesion that crosses suture lines.
Herniation. Diffusely or focally increased intracranial pressure (ICP) can result in herniation of the brain at several locations. Transtentorial (uncal) herniation occurs when a subdural hematoma or temporal lobe mass forces the ipsilateral uncus of the temporal lobe through the tentorial hiatus into the space between the cerebral peduncle and the tentorium. This results in compression of the oculomotor nerve and parasympathetic paralysis of the ipsilateral pupil, causing it to become fixed and dilated. When the cerebral peduncle is further compressed, it results in contralateral motor paralysis. The increased ICP and brainstem compression result in progressive deterioration in the level of consciousness. Occasionally, the contralateral cerebral peduncle is forced against the free edge of the tentorium on the opposite side, resulting in paralysis ipsilateral to the lesion—a false localizing sign. Central transtentorial herniation occurs with midline lesions in the frontal or occipital lobes, or in the vertex. Bilateral pinpoint pupils, bilateral Babinski signs, and increased muscle tone are found initially, which eventually develop into fixed midpoint pupils, prolonged hyperventilation, and decorticate posturing. Cerebellotonsillar herniation through the foramen magnum occurs much less frequently. Medullary compression causes flaccid paralysis, bradycardia, respiratory arrest, and sudden death.
Penetrating Injuries. Gunshot wounds and penetrating sharp objects can result in penetrating injury to the brain. The degree of neurologic injury will depend on the energy of the missile, whether the trajectory involves a single or multiple lobes or hemispheres of the brain, the amount of scatter of bone and metallic fragments, and whether a mass lesion is present.
Shaken Baby Syndrome. This potential life-threatening head injury in children <2 years is caused by rapid acceleration and rotation of the head. Shearing injuries of the brain or intracranial vessels and cervical spine injuries may result. Almost half of children found with this syndrome exhibit no external signs of trauma, so clinical vigilance must remain high.