Imaging modalities in trauma
Radiography
Radiography is not adequately sensitive in the detection of intracranial pathology and doesn’t have a role in traumatic brain injury (TBI) ( Fig. 15.1 ). ,
Computed tomography
Computed tomography (CT) is the imaging modality of choice in acute head trauma for several reasons :
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CT is quick and widely available. It can typically be completed in 15 minutes or less.
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CT is highly sensitive for the detection of intra- and extraaxial hemorrhage.
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CT is also superior in the detection of bony details, including fractures of the skull and/or face. , ,
Magnetic resonance imaging
Magnetic resonance imaging (MRI) is inferior to CT in the acute setting for these reasons , :
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It takes much longer to complete an examination.
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It provides less detailed evaluation of bony structures.
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It’s more sensitive to motion artifact.
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It is much more difficult managing sick and potentially crashing patients in an MRI machine compared with a CT scanner.
Primary effects of neurotrauma
Extraaxial hemorrhages
Epidural hematoma
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On head CT, an epidural hematoma is classically seen as a hyperdense extraaxial collection of blood external to the dura with a biconvex or lentiform shape that does not cross cranial sutures ( Fig. 15.2 ).
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It is typically arterial in origin, and usually the middle meningeal artery is the culprit. , ,
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It is often associated with skull fracture (90%–95% of the time). When this holds true, the temporal bone is most commonly involved bone ( Fig. 15.3 ). , ,
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Typically, 30% to 50% have a secondary associated pathology (i.e., mass effect, secondary herniation, contrecoup subdural hematoma, or cerebral contusions).
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Most patients require emergent surgical evacuation. If the size is less than 1 cm with no cerebral edema, some can be managed nonoperatively.
Subdural hematoma
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Noncontrast CT is the best initial study, but MRI is better able to depict extent and age in the nonacute setting.
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On a head CT, a subdural hematoma is seen as an extraaxial collection of blood located between the dura and arachnoid with a crescentic shape that spreads diffusely across cranial convexities, as it can extend across cranial sutures but not dural attachments ( Figs. 15.4 and 15.5 ).
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Findings on brain MRI are variable in appearance secondary to the different appearance of blood on MRI depending on its age ( Figs. 15.6 and 15.7 ).
Please see Table 15.1 for summary of the appearance of blood products on CT and MRI depending on stage of injury.
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Typically, subdural hemorrhage is secondary to traumatic tearing of bridging cerebral veins. The trauma may be very minor, especially in elderly patients as they are predisposed to tearing secondary to cerebral atrophy.
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Patients with ventricular shunts are at a higher risk because the shunted system does not act as a natural tamponade. ,
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The hematoma can grow slowly with increasing risk for mass effect and herniation if not identified and treated early.
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According to the Brain Trauma Foundation guidelines, patients symptomatic subdural hematomas (SDH) greater than 1 cm in thickness and/or an associated midline shift greater than 5 mm, with decreasing Glasgow Coma Score (GCS) score or showing signs of herniation are treated surgically. Otherwise, patients with av small and/or asymptomatic SDH can be managed nonoperatively.
Stage | Content | Computed Tomography | T1WI | T2WI | Mass Effect | Time Course |
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Hyperacute | Oxy-hemoglobin | High density | Mild hyperintensity | High intensity with peripheral low intensity | +++ | <6 h |
Acute | Deoxy-hemoglobin | High density | Isointense to low intensity | Low intensity | +++ | 6–72 h |
Early Subacute | Intracellular methemoglobin | High density | High intensity | Low intensity | +++/++ | <3 days–1 week |
Late Subacute | Extracellular methemoglobin | Isodense | High intensity | High intensity with rim of low intensity | ± | 1–2 weeks to months |
Chronic | Hemosiderin | Low density | Low intensity | Low intensity | − | 2 weeks–years |
Subarachnoid hemorrhage (SAH)
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Trauma is the most common cause. A ruptured aneurysm is the most common nontraumatic cause. ,
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It is thought to be secondary to disruption of small subarachnoid vessels or direct extension into the subarachnoid space.
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Collections of blood can be seen on CT as linear areas within the perisylvian regions, the anteroinferior frontal and temporal sulci, and over the hemispheric convexities.
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Traumatic subarachnoid hemorrhages are commonly seen adjacent to cortical contusions and under acute epidural and subdural hematomas ( Fig. 15.8 ).
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On MRI, the affected cerebrospinal fluid (CSF) spaces with acute subarachnoid hemorrhage will show hyperintense signal on T1 and fluid-attenuated inversion recovery (FLAIR) and hypointense signal on gradient echo (GRE) sequences.
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Clinical presentation of SAH is most often in the form of headache, classically defined as maximal onset and the worst headache of my life. Delayed vasospasm can occur approximately 7 days after onset of SAH and can lead to ischemic symptoms. , ,
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Supportive therapy is the primary treatment. Oral or intraarterial calcium channel blocker can be given to prevent secondary vasospasm. , ,
Parenchymal injuries
Cerebral contusions
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Cerebral contusion is the medical term for a brain bruise , which can be hemorrhagic or nonhemorrhagic. It typically involves the gray matter and underlying subcortical white matter.
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The majority of cerebral contusions are secondary to blunt head trauma caused by forceful impact of the cerebrum against the skull surface. ,
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Cerebral contusions are commonly associated with traumatic subarachnoid hemorrhage in the adjacent sulci.
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The most common areas affected are temporal lobes and inferior surfaces of the frontal lobes. , They are usually multiple, variable in size, and bilateral.
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Contusions 180 degrees opposite the site of a direct impact (coup) are common and called contrecoup lesions ( Fig. 15.9 ).
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Petechial hemorrhages with associated surrounding hypodense areas of edema are most common finding on head CT. However, head CT scan of patients with cerebral contusion can commonly appear normal.
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Brain MRI is much more sensitive than CT for detecting cerebral contusions. ,
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FLAIR sequence is most sensitive for detecting cortical edema and associated subarachnoid hemorrhage, which appears as hyperintense foci.
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GRE sequence is the most sensitive sequence to detect parenchymal hemorrhages ( Fig. 15.10 ).
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