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  Traumatic brain injury can be classified by severity into mild (Glasgow Coma Scale [GCS] ≥14), moderate (GCS 9–13), and severe (GCS ≤ 8) categories.

  
  
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  An emergent noninfused head computed tomography is the imaging modality of choice in patients with cranial trauma.

  
  
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  Patients with intracranial hemorrhage can quickly deteriorate and require frequent neurological re-evaluations.

  
  
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  Limit secondary brain injury by identifying and addressing concurrent hypoxemia, hypotension, and increased intracranial pressure.

Between 1.2 and 2 million patients sustain some form of traumatic brain injury (TBI) in the United States every year. Fortunately the majority of cases (~80%) are mild, as moderate and severe TBI is associated with significant long-term disability and death. In fact, head injuries are the leading cause of traumatic death in all patients younger than 25 years. Currently more than 50,000 deaths and 370,000 hospitalizations are attributable to TBI on an annual basis. The associated costs of caring for patients with acute and chronic TBI are astronomical, exceeding $4 billion per year. TBI occurs as the normal physiologic function of the brain is disrupted by either direct (object striking the cranium) or indirect (acceleration/deceleration) forces. Patterns of injury can be classified as either primary (occur at the time of impact) or secondary (develop over time owing to neurochemical and inflammatory responses). Patients with TBI can be further stratified by their Glasgow Coma Scores (GCS) into mild (GCS ≥14), moderate (GCS 9–13), and severe (GCS ≤8) categories (Table 85-1)

Cerebral circulation is dictated by the cerebral perfusion pressure (CPP), and ensuring adequate blood flow is of the utmost importance in patients with TBI. The CPP is proportional to the difference between the mean arterial pressure (MAP and the intracranial pressure (ICP) (CPP ∝ MAP – ICP). The intracranial space is a fixed volume, and the ICP is determined by the amount of brain tissue, blood, and cerebrospinal fluid (CSF) within it. Increases in either of these variables will cause secondary elevations in the ICP. The brain can autoregulate cerebral perfusion under normal physiologic conditions, but cannot do so at the extremes of either MAP or ICP. Therefore, processes that significantly decrease the MAP (eg, traumatic shock) or increase the ICP (eg, intracranial hemorrhage) may impair cerebral perfusion and exacerbate secondary brain injury.

The following is a list of specific injury patterns seen in patients with TBI:

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  Concussions represent a traumatic alteration in neurologic function in the absence of abnormalities on computed tomography (CT) imaging. Symptoms including recurring headaches, sleep disturbances, and difficulties with concentration that can persist for months (postconcussive syndrome).

  
  
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  Skull fractures can be categorized by location (basilar vs calvarium), pattern (linear, depressed, or comminuted), and by whether they are open or closed injuries.

  
  
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  Cerebral contusions represent punctate intraparenchymal hemorrhages with surrounding edema and occur most commonly in the frontal, temporal, and occipital lobes. Contusions that occur both at the direct site of injury and the opposing side of the brain secondary to indirect deceleration forces are known as coup and contrecoup injuries, respectively.

  
  
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  Traumatic subarachnoid hemorrhage (SAH) is the most common abnormality recognized on posttraumatic CT imaging. Traumatic SAH occurs when injury to the small subarachnoid vessels leads to secondary hemorrhage within the subarachnoid space.

  
  
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  Subdural hematoma (SDH) is most commonly encountered in patients with significant cerebral atrophy (elderly, alcoholics). They occur when excessive shearing forces injure the small bridging veins in the subdural space. SDHs classically appear on CT imaging as crescent-shaped hematomas that freely cross suture lines. As a distinct history of trauma may not be present, always maintain a high index of suspicion in elderly patients with nonspecific mental status changes.

  
  
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  Epidural hematoma (EDH) is most commonly seen in patients with temporoparietal skull fractures and secondary injury to the middle meningeal artery. They occur when high-pressure arterial bleeding separates the dura from the inner table of the skull to form a hematoma. EDHs are classically lentiform or bean-shaped in appearance on CT imaging and do not cross the cranial suture lines (Figure 85-1). The classic presentation is a patient with blunt head trauma who initially appears well after the injury (the so-called lucid interval) only to rapidly decompensate several hours later.

  
  
  
  

  
  

  Figure 85-1.

  
  

  CT scan of the head showing an epidural (patient’s left) and a subdural (patient’s right) hematoma.

  
  

  
  
  
  
  
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  Diffuse axonal injury (DAI) occurs when sudden deceleration mechanisms transmit shearing forces diffusely across the axonal fibers of the brain. CT imaging is nonspecific, and patients tend to have poor outcomes.

  
  
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  Penetrating brain injury is usually catastrophic because of the immense amount of kinetic energy transmitted to very sensitive brain tissues. Mortality rates from gunshot wounds to the head approach 90%.

In addition to the specific injury patterns listed previously, TBI can lead to drastic increases in ICP, resulting in herniation. Transtentorial herniation of the temporal lobe uncus is the most common form and typically presents with altered mental status and a dilated or blown pupil secondary to compression of the oculomotor nerve (cranial nerve [CN] III). Transforaminal herniation of the cerebellar tonsils through the foramen magnum can occur with significant increases in the ICP, especially with posterior fossa hemorrhages, and is rapidly fatal due to compression and consequent dysfunction of the brainstem.