Traumatic Intracerebral Hemorrhage

Traumatic intracerebral hemorrhages are defined as hematomas 2 cm or larger that are not in contact
with the surface of the brain and are present in 15% of autopsy cases of severe head injury. Lobar
intracerebral hemorrhages are those that involve a lobe of the brain and occur usually in the temporal
or frontal lobes (Fig. 338-17). The pathogenesis of intracranial hemorrhage (ICH) is likely due to
deformation and rupture of the intrinsic blood vessels (single or multiple) at the time of injury. Damage
to multiple small blood vessels can result in the coalescence of many smaller hemorrhages (Fig. 338-
18). Traumatic ICHs are often multiple, and 28% are associated with subdural and 10% with epidural
hematoma, and they can arise in areas that appear normal on CT scans obtained soon after injury. One
third to half of individuals with traumatic ICH are unconscious on admission, but up to 20%
demonstrate a classic lucid interval before the onset of coma. Patients who are deeply comatose with
large hematomas have a high mortality rate. Large hematomas act as space-occupying lesions and
result in intracranial hypertension and then transtentorial herniation. PET studies have shown marked
hypoperfusion and hypometabolism around hematomas and in the ipsilateral hemisphere.
Traumatic intracerebral hemorrhages can evolve with time, and the rate and extent of increase in
volume are related to factors such as the type and size of injured vessel, blood pressure, and any
underlying bleeding tendency. Individuals receiving antiplatelet or anticoagulant therapy, such as
warfarin or direct thrombin inhibitors, are at increased risk for intracerebral hemorrhagic complications
in TBI.72,73
Neuroimaging has shown that many traumatic hematomas develop hours to days after the injury and might not be visible on
scanning soon after the traumatic event. Delayed traumatic intracerebral hematoma (DTICH) is a common cause of secondary
neurological deterioration after head injury, and progressive increase in size of the ICH has been reported in up 51% of patients
on repeated CT scans in the first 24 hours. Delayed traumatic intracerebral hematoma can occur in severely brain-injured
patients, but it may also be seen in patients sustaining relatively mild injuries.

Figure 338-17. Acute traumatic lobar hemorrhage in the left temporal lobe.
PRIMARY AND SECONDARY BRAIN INJURY
Traditionally, CNS injury has been divided into primary and secondary phases. Primary injury refers to
the damage stemming from mechanical forces occurring at the time of the traumatic insult. 1
Secondary injury is a complex series of interrelated molecular processes initiated by the primary injury
that causes progressive loss of CNS cells for weeks and months after the primary injury has ceased.
Remarkably, this loss can be seen a long distance away from the site of a focal primary injury. These
secondary injury processes are discussed in detail and include potentially avoidable entities such as
hypoxic-ischemic injury, edema and intracranial hypertension, ionic dysregulation and excitotoxicity,
metabolic dysfunction, inflammation, and axonal degeneration (Fig. 341-1).
Both primary and secondary brain injury can be further classified as focal or diffuse. The distinction
between focal and diffuse injuries is historically derived from the presence or absence of radiographic
mass lesions on computed tomography scan. 2,3 This distinction has now evolved to also consider the
distinct pathobiologic processes that occur in regions local to and remote from the point of impact.
Although these terms are conceptually helpful, it must be remembered that all TBIs involve focal and
diffuse damage to some degree.

RELATIONSHIP BETWEEN MECHANICAL FORCES AND BRAIN INJURY

The brain can be subject to tremendous injury as a result of rapid deceleration and rotational forces
even if the cranium never contacts a solid object (e.g., pure inertial injuries). Such injury forces are
often seen in motor vehicle accidents (although an additional impact component usually occurs as
well). The brain moves substantially within the cranial cavity in response to these forces 4,5 because it is
anchored within the cranial cavity by only the parasagittal bridging veins, perisinusoidal granulations,
cranial nerves, and tentorium. Movement of the brain forward toward the anterior cranial-basal
structures, particularly the sphenoid ridges, concentrates force at the bases of the frontal lobes and
the tips of the temporal lobes. 5 Surface contusions are thus much more frequent at these sites than
elsewhere. There is evidence in the human brain that shearing force also concentrates in the deep
white matter structures such as the corona radiata, explaining the frequent finding of parasagittal
gliding contusions.6 Lastly, it is generally believed that shearing forces transmitted through the
brainstem and the reticular activating system are responsible for immediate loss of consciousness
(LOC).
Studies completed in the last century substantially informed the complex relationship between applied
forces and the resulting brain injury. Thibault and Gennarelli used a primate impact acceleration injury
model to characterize the relationship between the magnitude of acceleration/deceleration force, the
time duration over which it is applied, and the consequences for the intracranial contents.7 Brief, high-
intensity deceleration forces are prone to tearing parasagittal bridging veins, causing an acute
subdural hematoma. When the deceleration forces are of higher magnitude and longer durationas is
commonly seen in motor vehicle accidentsdiffuse axonal injury (DAI) is more likely. When both the
magnitude and the duration of the deceleration force are less, concussion can result and few structural
effects are seen when the brain is examined either ultrastructurally or by light microscopy. At the
opposite extreme are impact injuries in which the stationary head is subjected to crushing forces (e.g.,
slow-moving machinery). Such injuries classically produce massive fractures, extra-axial hematomas,
and contusions, yet these patients usually do not lose consciousness because axonal injury is absent
and the reticular activating system/projection fibers are not disturbed.

IMAGING FINDINGS IN ACUTE TRAUMATIC BRAIN INJURY

Skull Fractures
When evaluating the cross-sectional CT and MRI, begin by examining the extracranial structures for
evidence of scalp trauma, such as a laceration, subgaleal hematoma, or radiopaque foreign body. 50 The
subgaleal hematoma is located beneath the subcutaneous fibrofatty tissue and superficial to the
temporalis muscle.50
Skull fractures can be classified as linear, depressed, comminuted, compound (open), or diastatic. The
linear fracture is the most common type of skull fracture. 50 As mentioned earlier, the nondisplaced
linear skull fractures may be difficult to detect, even on CT, if the fracture plane is parallel to the plane
of section. Fortunately, isolated linear fractures without associated intracranial pathology are usually
clinically insignificant. Depressed and comminuted (i.e., multiple bone fragments) skull fractures are easily detectable
on CT. Depressed fractures are often (but not invariably) associated with an underlying cortical contusion. A skull fracture that
communicates with an open wound in the overlying scalp, resulting in communication between the intracranial space and the
outside world, is a compound fracture. In a compound depressed fracture, the underlying dura is exposed and may be disrupted
under the fracture site, and there is an increased risk of infectious complications. This is usually a neurosurgical emergency
warranting removal of the contaminated bone fragments and dural repair in order to prevent infection.50 Diastatic fractures
occur from separation of the cranial sutures and are more frequent in children than in adults. 50