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1122 PART 10: The Surgical Patient
• Antiseizure prophylaxis with phenytoin is recommended for the
prevention of early posttraumatic seizures, that is, within 7 days
of the TBI. Routine prophylaxis later than 1 week following TBI is
not recommended
• Recent studies have not demonstrated an overall beneficial effect
of steroids on outcome and there is level I evidence that high-dose
methylprednisolone increases mortality after moderate to severe TBI.
• After TBI, persistent ICP >20 is associated with poor outcome
and there are limited data—class III and II level evidence—that
patients responding to ICP lowering treatments have a lower FIGURE 118-2. Head CT in bone window. There is a linear skull fracture in the left
mortality and better outcome. occipital region (arrow). There is also an underlying epidural hematoma which is not
adequately visualized in this bone window.
INTRODUCTION tissues and indirect injuries. Indirect injuries result from the sudden accel-
eration and deceleration of the brain floating within the surrounding cere-
Traumatic brain injury (TBI) is a major cause of morbidity and mortal- brospinal fluid (CSF), encased by the dura and rigid cranial vault, leading
ity worldwide and in the United States. TBI is caused by a blunt force to rotational and shearing forces that impact neurovascular tissue against
or penetrating injury to the head that causes brain dysfunction. The bone. TBI from blast injury may be related to indirect injury generated by
severity of TBI may be evident immediately or may initially appear to be pressure or shock waves and other less understood factors.
mild, only to deteriorate later and often rapidly. Symptoms of traumatic Contre-coup brain injury refers to contusions or other lesions that
brain dysfunction include unconsciousness, amnesia, focal deficits, and occur on the side contralateral or 180° from the force of impact; coup
cardiorespiratory instability due to brain stem dysfunction. TBI may be injury refers to ipsilateral injury directly below the impact. Contusions
isolated but is often accompanied by additional injuries. are localized injuries to the cerebral parenchyma that occur when the
Of an estimated 1.7 million people in the United States that sustain brain is pushed or jarred against the bony components of the skull
TBI each year, about 52,000 die before reaching the hospital and 275,000 resulting in hemorrhage, edema, or necrosis. Contusions are typically
are hospitalized. TBI accounts for one-third of trauma-related mortality. observed at the frontal poles, orbital frontal lobes, temporal poles, and
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Children less than 5 years of age, teenagers aged 15 to 19, and adults over cortex above the Sylvian fissure (Fig. 118-1).
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65 are the most likely to sustain TBI. Patients over the age of 75 have the Skull fractures may be single or multiple, linear, or depressed
highest rates of TBI-related hospitalization and mortality. Males, in any age (Fig. 118-2). Basilar fractures are associated with cerebrospinal fluid
group, are more likely than females to suffer TBI. Including all age groups, (CSF) leak and meningitis as well as a greater risk of cranial nerve and
falls are the leading cause of TBI (35.2%), but motor vehicle crashes (MVC), vascular injury. Scalp lacerations above fractures are termed open frac-
the second leading cause of TBI (17.3%), are the leading cause of TBI-related tures and have a greater risk of infection.
death (31.8%). The elderly are more likely to present with fall-related TBI Temporal bone fractures can injure the middle meningeal artery
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and young adults aged 20 to 24 years are more likely to die of MVC-related or a branch thereof resulting in hemorrhage into the epidural space,
TBI. In military combat, blast injuries (61.9%) and gunshot wounds (19.5%) between the inner table of the skull and above the dura termed epidural
account for the majority of TBI. The rising incidence of TBI may be related hematoma. Epidural hematomas may also result from meningeal vein
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to both an aging population as well as overall population expansion. 1 or dural sinus damage. Epidural hematomas are more common in chil-
dren and young adults since the dura is not as adherent to the skull as
HEAD TRAUMA: MECHANISMS OF INJURY in the elderly (Fig. 118-3). The classic clinical presentation of epidural
Head injuries can result from direct blunt or penetrating trauma to the hematoma is a brief loss of consciousness followed by a neurologically
head and from indirect processes including acceleration-deceleration intact interval, followed by sudden deterioration, coma, and death from
and blast forces. herniation within hours. The treatment is immediate neurosurgical
Direct trauma leads to scalp and skull injury and both direct and indi- evacuation or, if not available in time, a burr hole can be lifesaving.
rect injury can damage the dura, blood vessels, and brain. Penetrating Subdural hematomas collect beneath the dura and result from lac-
trauma may result from relatively slow moving objects such as knives or eration of the bridging cortical veins. The venous bleeding that results
projectiles such as bullets, or blast-generated fragments moving at super- in subdural hematomas usually is slower, resulting in a more gradual
sonic speeds that damage the scalp, skull, and neurovascular tissue by lac-
eration, thermal, and pressure-generated forces. Blunt or nonpenetrating
injuries result in skull fracture, direct trauma to underlying neurovascular
FIGURE 118-3. Head CT revealing a large, fatal, epidural hematoma (EH) in a patient
who fell while intoxicated. Note the lenticular shape which is characteristic of EH. EHs are
usually limited by sutures where the dura is most adherent. The anterior portion is limited by
FIGURE 118-1. Head CT demonstrating bifrontal contusions after a fall. The inferior the coronal suture, while the posterior portion is limited by the lambdoid suture. EHs are easily
orbital region is a common location for contusions because of bony ridging in the orbital roof. treated with surgery and are usually associated with an excellent prognosis if recognized early.
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