Craniocerebral Trauma

Mechanism

Blunt injury is the most common mechanism; it includes both low- and high-velocity impacts. These injuries may be from a direct blow (e.g., a club) or a rapid deceleration force (e.g., falling or striking the windshield in a car crash). Motor-vehicle collisions and falls cause most of the severe TBIs.

Gunshot wounds are the most prevalent penetrating injuries ( Fig. 62.1 ), accounting for 35% of deaths from TBI under the age of 45 years in the United States. Self-inflicted injuries—for example, with nail guns—can also lead to penetrating injuries ( ; Fig. 62.2 ). Gunshot wounds are the most lethal type of brain injury, 90% resulting in death. They cause soft tissue damage, often comminuted depressed skull fractures, and direct injury to the brain tissue from the missile. Beyond the laceration along the bullet path, further damage is done by shock waves, especially with high-velocity weapons. Depending on the type of penetrating injury, contamination may be a concern. However, bullet fragments are considered sterile due to their exposure to heat from the firearm and are not routinely removed.

Vascular injury can occur with any type of TBI but is more common with penetrating trauma (25%–36% incidence) than with blunt injuries (<1%). Traumatic aneurysms, or pseudoaneurysms, can develop when all layers of the vessel wall rupture and surrounding cerebral tissue forms the aneurysmal wall. Such pseudoaneurysms can present as delayed subarachnoid hemorrhage (SAH) and can lead to death or severe disability. Therefore patients with penetrating injuries routinely undergo a cerebral angiogram to screen for traumatic pseudoaneurysm. A follow-up angiogram within the first months after a penetrating injury is recommended ( ).

Blast is a rare mechanism of injury in civilian life but is common in combat. With ongoing militarily conflicts, blast injury has become more frequent among US military personnel. American military members returned from deployment to Iraq or Afghanistan have self-reported a 12% to 20% incidence of mild TBI; explosions are recognized as a common injury mechanism ( ). Blast injuries occur as a direct result of supersonic waves of intense air (primary blast injury), from objects put in motion by the blast that hit people (secondary blast injury), and by a person being forcefully put in motion by the blast (tertiary blast injury) ( ). The brain is obviously vulnerable to secondary and tertiary blast injury, but whether primary blast forces directly injure the brain is controversial ( ). The severity of blast exposure needed to cause persistent symptoms is not clear ( ). Until research produces a definitive answer, one should consider the possibility that primary blast energy might cause an isolated mild TBI.

The severity of injury resulting from exposure to blast can range from mild to fatal. Displacement, stretching, and shearing forces of the primary blast wave can affect the brain directly and lead to such sequelae as concussion, hemorrhage, severe edema, or diffuse axonal injury (DAI). Systemic acute air embolism from pulmonary disruption is believed to occlude the blood vessels of the brain or spinal cord and lead to stroke ( ). Reports from war zones suggest that brain swelling occurs within hours after a blast injury and that the risk of mortality can be decreased by early decompressive craniectomy (DC). Others have found that cerebral vasospasm occurs more often after a blast injury than with blunt TBI and leads to a worse outcome than severe blunt TBI. Blast exposure on the mild end of the spectrum has led to somatic, behavioral, psychological, and cognitive symptoms similar to postconcussion syndrome. There is well-recognized overlap between posttraumatic stress disorder and blast injury, and misdiagnosis can occur in both directions.

Severity

There are different ways to stratify TBI by severity, and all are arbitrary. The most commonly used is the Glasgow Coma Scale (GCS), which was first published in 1974 by Graham Teasdale and Bryan K. Jennett, two neurosurgeons at the University of Glasgow ( ). The GCS assesses level of consciousness. It consists of three subscores: eye opening (maximal score 4), verbal response (maximal score 5), and motor response (maximal score 6). Despite some shortcomings, it has excellent interrater agreement (weighted kappa >0.75) for verbal and total scores and intermediate agreement (weighted kappa 0.4–0.75) for motor and eye scores ( ). Today it has been widely adopted by emergency medicine services and physicians to communicate the severity of injury in a consistent way. However, it is not designed to detect focal neurological deficits and is not a replacement for a thorough neurological examination.

A GCS score of 15 to 13 is considered to indicate mild TBI, and a score greater than or equal to 8 is a universally accepted definition of coma and severe head injury. Scores between 13 and 8 are classified as moderate. It is true that moderate and severe TBIs are rare. Mild TBI is eight times more common than moderate and severe TBIs. Moderate and severe TBIs are seen equally often. One can imagine that the GCS score shows a significant ceiling effect in patients with mild TBI; therefore more sensitive measures exist for this purpose. The two most often used are the Cantu system ( ) and the American Academy of Neurology system (1997) ( Table 62.2 )

Mild TBI is extremely common. In North America, between 1.5 and 2 million patients visit an emergency department each year for head trauma, with 70% to 90% of cases having mild TBIs. Because this number does not include the many people who choose not to seek medical attention, the true prevalence of mild TBI is difficult to ascertain.

Despite its high incidence, no objective test to diagnose mild TBI currently exists. Diagnosis is hampered by the lack of obvious injuries on computed tomography (CT) or conventional magnetic resonance imaging (MRI) and is usually based solely on clinical symptoms. Preliminary studies are investigating brain injury biomarkers to diagnose mild TBI ( ). Although initial progress has been promising, these markers are not yet used in the clinical setting ( ). Others have shown that an integrated approach with magnetoencephalography and diffusion tensor imaging (DTI) is more sensitive than conventional CT and MRI in detecting subtle neuronal injury in mild TBI and postconcussion syndrome ( ).

A concussion is defined as injury to the brain caused by a hard blow or violent shaking, producing a sudden and temporary impairment of brain function, such as a brief loss of consciousness or disturbance of vision and equilibrium. A concussion is equivalent to a mild TBI with negative CT findings. The annual incidence of such concussions in the United States is 128 per 100,000 population ( ). The characteristic loss of consciousness is believed to result from rotational forces exerted on the upper midbrain and thalamus, impairing the function of reticular neurons. Headache, nausea, dizziness, irritability, and impaired ability to concentrate can persist for days after the event. Persistence of these symptoms for weeks is called postconcussion syndrome and can last from 1 month to a year.

Patients with severe TBI (GCS score ≤8) often have injuries in at least one other organ system ( ). There is also a 5% incidence of associated spinal fractures. About one-quarter of patients with a severe TBI undergo neurosurgical intervention. Early diagnosis of TBI improves outcome by reducing secondary injury, which can develop subsequent to the impact and includes edema, hypoxia, hypertension, ischemia, and elevated intracranial pressure (ICP) ( ).

Morphology

TBI can also be classified by the underlying morphology. Thus, TBI can be subdivided between injuries to the skull itself and intracranial injuries, which can be focal or diffuse (see Table 62.1 ).