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Essentials of Head Trauma Imaging

Courtney Frey, J. Michael Hazenfield

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Cite this article as: Courtney Frey and J. Michael Hazenfield, Essentials of
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 Essentials of Head Trauma Imaging

Authors: Courtney Frey, M.D. and J. Michael Hazenfield, M.D.

Courtney Frey, M.D.

Neuroradiology Fellow

Division of Neuroradiology

University of Cincinnati Medical Center

Cincinnati, Ohio

J. Michael Hazenfield, M.D.

Assistant Professor of Radiology

Division of Neuroradiology

University of Cincinnati Medical Center

Cincinnati, Ohio

Please direct queries to:

Courtney Frey, M.D.

Neuroradiology Fellow

Division of Neuroradiology

University of Cincinnati Medical Center

234 Goodman Street

Cincinnati, OH 45267

513-584- 1584

freyct@ucmail.uc.edu
Abstract:

Head trauma is a common indication for neuroimaging in the emergency room. CT is the

modality of first choice, as it is quick, safe, and effective in evaluating for life threatening intracranial

hemorrhage and mass effect. CT is also best for evaluating for skull fractures which may alter

management and lead to further imaging studies. MRI is reserved for selected patients, particularly when

the clinical exam does not match the CT imaging findings, such as is diffuse axonal injury. Emergency

room physicians and radiologists, particularly those in-training, would benefit from a consistent approach

and search pattern for evaluating head trauma. We offer a comprehensive “outside to inside” approach to

head trauma imaging, discussing not only common but subtle “should not miss” findings and their clinical

correlation.

Introduction

Head injury is a very common occurrence, with 600,000 new traumatic brain injuries per

year in the United States alone1. Non-contrast CT has become the modality of choice in the

initial evaluation of patients with acute head trauma. This is mainly due to widespread CT

availability, fast imaging acquisition times, and also due to its sensitivity for the evaluation of

hemorrhage, mass effect, herniation, and fractures. MR is usually reserved for select patients and

has a larger role in subacute to chronic traumatic brain injury. Imaging is not indicated for every

patient that has head trauma. Multiple clinical guidelines are available to help clinicians decide

when imaging is indicated, such as the Canadian CT Head Rule2, and the New Orleans Criteria3.

They are all slightly different, but generally speaking a persistent headache, vomiting, acute
neurological deficit, or secondary physical exam signs of high impact head trauma will prompt

imaging4.

When interpreting a head CT after trauma, a systematic approach should be followed.

With the junior radiologist or Emergency Room physician in mind, we suggest here an “outside-

to- inside” search pattern. This includes evaluation of the scalp and soft tissues, skull and facial

fractures, intracranial extra axial hemorrhages, mass effect, herniation, and intraparenchymal

injuries, with particular attention to “danger zones” where important findings should not be

overlooked.

Extra-cranial Contents

Scalp

A quick look at the scalp and overlying subcutaneous tissues about the head and face can

provide an early clue as to where the patient was hit. The analysis of the scalp can provide clues

as to the severity of the trauma, and which areas to look for coup and countercoup injuries.

Here, it is important to notice that the countercoup injury (opposite to the impact site), is usually

more severe5. Sometimes the primary finding in an imaging study is outside the expected area of

interest. An example of this is shown in Figure 1, which shows a “scalping” injury in which the

majority of the patient’s scalp was avulsed off after her long hair became caught in a circular

saw6,7. This is an extreme example, but it shows that sometimes a major finding may not be

readily apparent to the radiologist unless a strict search pattern is followed.

Calvarium

Evaluation of the bony skull is best done using thin collimation (i.e. 1-2 mm) CT slices,

as well as a bone reconstruction algorithm to enhance the edges of the bony cortex. In the skull,

sutures should be directly opposed to each other without significant space in between. Normal

sutures appear irregular, while often the lucent line created by a skull fracture is very straight.

The symmetry of normal sutures can also be used if a fracture or sutural diastasis is suspected. If

a fracture plane is identified, it is useful to follow the fracture line to its extreme edges, as the

forces that generated the fracture may cause fracture planes in adjacent bones that are less

obvious. Normal vascular or peripheral nerve grooves created by neuro-vascular structures

traversing the bone may be asymmetric, but are differentiated from non-displaced fractures by

their well-corticated margins and overall decreased sharpness8.

In the young pediatric patient population, where many sutures are unfused, 3D shaded

reconstructions of the skull can be helpful to increase the conspicuity of fractures and increase

the reader’s confidence in interpretation.

Fractures can be linear or depressed. Linear fractures consist of a single fracture that

extends through the thickness of the skull and are generally non-displaced. There may be

associated with extra-axial hemorrhage if they cross vascular structures, such as the dural venous

sinuses or the middle meningeal groove. They may also cause diastasis of the skull sutures.

Non-displaced linear skull fractures are usually managed non-operatively9.

Depressed fractures occur after higher impact trauma, and describe a situation in which

one fracture fragment is depressed deeper than the uninvolved skull. These more often require

surgical intervention, as 90% are open, so called “compound fractures,” meaning they are
associated with an overlying scalp laceration and predisposed to infection. Patients suffering

from compound fractures are predisposed to infection, post-traumatic epilepsy, or persistent

neurological defect. If surgery is delayed the infection rate goes up dramatically. Recent

neurosurgical literature recommends operative management of compound fractures depressed

greater than the thickness of the skull, or closed depressed fractures with fragment depression

greater than 1 centimeter, frontal sinus involvement, or pneumocephalus among other clinical

criteria10.

Although this article is not able to cover all types of fractures comprehensively, all

clinicians should be aware that if a fracture runs through the expected course of a major vascular

channel such as the bony carotid canal or a major venous sinus, further workup should be done

by contrast enhanced vascular imaging. CT-angiogram or CT-venogram should be pursued

depending on the structure suspected to be injured. If the clinician is unsure if a CTA or CTV

should be obtained, at our institution a “midphase” CT vascular study is available where the

contrast bolus timing is delayed between 5-8 seconds longer than for a dedicated CT Angiogram.

When present, these central skull base fractures typically present with a fluid level in the

sphenoid sinus (Figure 2), which can be a subtle but helpful sign.

Fractures of the temporal bone require special attention as the temporal bone houses

essential structures of the middle and inner ear, the petrous portion of the internal carotid artery,

and multiple cranial nerves. A temporal bone fracture should be suspected in a trauma patient

with opacified mastoid air cells. Temporal bone fractures may be classified as “otic capsule

sparing” or “otic capsule violating” based on if the fracture plane traverses the bony labyrinth of

the inner ear (Figure 3). This consists of the cochlea, semicircular canals, and vestibule. Otic

capsule violating fractures more often cause sensorineural hearing loss, CSF otorrhea, and facial
nerve injuries. Otic capsule sparing fractures are more likely to cause intracranial complications

such as hemorrhage11.

Facial Structures

A discussion of imaging head trauma would not be complete without discussion of facial

trauma, as they often present together. There are a broad range of facial fractures ranging from

clinically insignificant to unstable fractures requiring prompt intervention. A comprehensive

review of all fractures is not possible, but several of the more common locations and patterns

will be reviewed here.

As the nose is the most anterior portion of the face and among the weaker facial bones12,

it is frequently fractured. In frontal motor vehicle collisions, the nasal bone is the most common

bone fractured, and in assault it is the most common isolated fracture12,13. Isolated nasal bone

fractures generally do not require urgent intervention, but are important to recognize as they will

be frequently encountered.

Fractures involving the orbit can be more serious and require prompt diagnosis. One of

the most common fractures seen are orbital “blow out” fractures, in which a direct blow to the

eye causes increased pressure and leads to fracture through one or more orbital walls. Medial

orbital blowout fractures displace the lamina papyracea, the medial wall of the orbit, and

intraorbital fat medially. Inferior blow out fractures involve the inferior orbital wall, and may

cause orbital contents to herniate into the maxillary sinus. As demonstrated on Figure 4, the

rectus muscles of the eye can become displaced or entrapped with these types of fractures. If

there is bony impingement or significant displacement of the intraocular muscles, the possibility
of muscle entrapment should be raised. Although reportedly the sensitivity of CT for detecting

extra-ocular muscle entrapment is greater than 70%14, muscle entrapment is a clinical diagnosis

based on the patient's ability to move the globe through its full range of motion. There are also

other types of muscle injuries (lacerations, intramuscular injuries) in which CT is less sensitive14.

Fractures involving the orbital roof can cause a communication between the orbit and the

intracranial vault, and can violate the dura. If the dura is violated, an intracranial approach

would be necessary15. Other complications of orbital trauma include globe rupture, lens

dislocation, retained foreign body, retinal and choroidal hemorrhages, or intraocular

compartment syndrome16. One useful finding for globe injury is recognizing decreased

dimension of the anterior chamber, which can represent an open globe injury (Figure 5). The

imaging findings need be put together with the patient’s symptoms and ophthalmologic exam for

accurate diagnosis in many instances.

A more complex but relatively common fracture pattern is the zygomaticomaxillary

complex (ZMC) fracture. The zygoma forms the malar eminence of the cheek and also

contributes to the lateral orbital wall and orbital floor. ZMC fractures are also called “tripod” or

more properly, “tetrapod” fractures because the zygoma has four different attachments to the

face and skull. It articulates with the frontal bone, the sphenoid, the maxilla and with the

temporal bone via the zygomatic arch 15. ZMC fractures can be variable but usually involve the

zygomatic arch, the inferior and lateral orbital rims, and the anterior and posterior walls of the

maxillary sinus (Figure 6). These fractures often require fixation as they disrupt bony buttresses

that are essential for structural integrity to the face. Complications of ZMC fractures include

enophthalmos or other globe displacement, visual compromise, extraocular muscle dysfunction,

trismus, or substantial cosmetic deformity17. An understanding of the ZMC fracture pattern can

help to quickly recognize and categorize complex facial fractures.

In high impact crush-type facial trauma, another type of injury that may appear are Le

Fort type fractures, in which portions of the midface are separated from the skull base. The key

to recognizing these transfacial fractures is involvement of the pterygoid plates of the sphenoid

bone which connect the midface to the sphenoid15. In type 1, a horizontal fracture plane

separates the alveolar ridge containing the roots of the teeth from the upper face, so called

“floating palate”. In type 2, a pyramidal shaped fracture plane from the posterior alveolar ridges

with apex at the nasofrontal suture separates the entire maxilla from the upper face (Figure

7). Type 3 is a complete craniofacial dissociation in which the zygomatic arch and nasofrontal

suture are separated15. The Le Fort classification may be different on one side than the other.

Intracranial Contents

A search pattern of the intracranial contents with variable windowing on CT is desired.

Extra-axial spaces might be carefully examined first, the brain parenchyma could follow and

lastly the ventricular system. The most common findings after significant trauma are

hemorrhagic changes or mass effect.

As optimal visualization of acute findings is not possible using only one CT window

setting, it is important to understand windowing in CT. “Window width” includes the range of

Hounsfield units (the CT measure of density) which is included in the grey display of the CT

image. “Window level” is the midpoint of the window width, also in Hounsfield units. Any

pixel with a density higher than the upper end of the window width will be white, and any pixel
with a density lower than the lowest end of the window width will be black, and those in

between will be shades of grey. A “narrow” window will look very grainy, but is useful for

picking out subtle density differences within a tissue of interest, for example when evaluating the

grey-white matter differentiation for signs of ischemia. A “wide” window would be more useful

to evaluate the bones, sinuses, or very dense acute subdural hematomas adjacent to the skull,

although visualization of the brain parenchyma will be limited. Various other window settings in

the middle of these extremes could be used as a primary working window in which the brain

parenchyma, cerebral sulci, and other CSF spaces are easily evaluated. For example, in Figure

8, two different window settings emphasize the epidural hematoma on one case, and the

associated bone fracture on the other. It would be difficult to see both of these findings only

using one window setting.

Intracranial hemorrhage includes both extra-axial and intra-axial hemorrhage. Extra-

axial blood may be epidural, subdural, subarachnoid blood, or intraventricular. Intra-axial

hemorrhage is within the parenchyma itself and includes contusions or larger space-occupying

hematomas.

Extra-axial Spaces

Epidural hematomas occur in the potential space between the dura and the calvarium.

They are usually called by traumatic laceration of an artery. Epidural hematomas can invoke

fear in physicians because of their potential for rapid expansion; which can lead to sudden

increases in mass effect, intracranial pressure, and resultant herniation. As the epidural blood is

separated from the brain by the dura, patients can sometimes have a “lucid interval” in which the
patient is relatively asymptomatic after their initial injury followed by rapid decompensation.

Most (90-95%) epidural hematomas in adulthood are associated with a skull fracture (Figure 8)

and are biconvex (“lens-shaped”). Most epidural hematomas are arterial in origin, although

venous epidural hematomas may be seen when the fracture is adjacent to a dural sinus, such as at

the vertex (Figure 9). Epidural hematomas tend to not cross suture lines as the dura is most

adherent to the periosteum at the sutures. A few caveats are that if a fracture plane crosses the

suture, if the suture is diastatic, or if the epidural is venous in origin, the epidural hemorrhage

may cross a suture18.

Epidural hematomas are usually uniformly bright on non-contrast CT as they present

acutely. Two reliable signs which can suggest impeding enlargement are the “swirl sign”19 of

mixed un-clotted and clotted blood (Figure 10) and the “spot sign” of active extravasation on

CTA (Figure 11). Although the “spot sign” has been originally described in the setting of a

spontaneous intraparenchymal hemorrhage, in our experience seeing active arterial extravasation

in an extra-axial hematoma is a very similar phenomenon. In spontaneous intraparenchymal

hematomas, the spot sign predicted hematoma expansion with a sensitivity of 91% and a

sensitivity of 89%20. These patients should be monitored closely and may require surgical

decompression.

In subdural hematomas, blood accumulates beneath the dura but above the arachnoid

membrane. They are thought to be caused by tearing of bridging cortical veins, which drain into

the dural sinuses. Subdural hematomas are crescentic in shape and have more broad mass effect

on the cerebral hemispheres rather than the focal mass effect of epidural hematomas (Figure 12).

As subdural hematomas may present acutely or may follow a more chronic course, they vary in

density and conspicuity on CT (Figure 13). Therefore, the extra-axial spaces around the brain
must also be viewed in multiple different window settings as explained above. Extremely bright,

acute subdural hematomas may blend in with the hyperdense calvarium. Similarly, subdural

hematomas can be isodense to the brain, therefore changing the display window and level can be

helpful.

CSF density subdural collections may be acute or chronic. If they are acute, they are

more accurately referred to as a “subdural hygroma,” thought to be secondary to a laceration of

the subarachnoid membrane. They generally have less mass effect and cause less problems than

hematomas, but it is important to know that even CSF density collections can represent sequelae

of acute trauma (Figure 14).

Subarachnoid hemorrhage (SAH) is blood between the pia and arachnoid membranes.

Trauma is the most common cause of subarachnoid hemorrhage, and postulated mechanisms

include bleeding into the subarachnoid space from adjacent parenchymal contusion or tearing of

ependymal tissue in the interventricular region21. Subarachnoid hemorrhage is seen as linear

hyperdensity in the cerebral sulci, or diffuse hyperdensity when it is located within the basilar

cisterns (Figure 15). In traumatic subarachnoid hemorrhage, the cerebral sulci of the convexities

are a more common location than the basal cisterns. It is typically not a large amount of

subarachnoid hemorrhage. A large amount of subarachnoid hemorrhage, especially if it is within

the basilar cisterns, should prompt workup for an underlying ruptured aneurysm. Small amounts

of subarachnoid blood can concentrate within certain locations, including the interpeduncular

cistern, Sylvain fissures, occipital horns, and the foramen magnum. Traumatic subarachnoid

hemorrhage alone tends to have a better prognosis than other forms of hemorrhage, but when

present with other types of hemorrhage confers a worse prognosis22,23. A large amount of SAH

may cause vasospasm or communicating hydrocephalus.

 Intraventricular blood may be seen as a primary phenomenon, or may be secondary to a

large amount of blood in the subarachnoid space or adjacent parenchyma. Intraventricular blood

can be easy to overlook when it is layered dependently in the occipital horns of the lateral

ventricles. Sometimes this finding may be the only clue that the patient has suffered significant

head trauma. Intraventricular hemorrhage is also important to recognize, as it may clog the

ventricles and cause an obstructive hydrocephalus if present in a large amount.

Intra-axial Spaces – Brain Parenchyma

Cerebral contusions are impact injuries to the brain parenchyma. They can be either

hemorrhagic or non-hemorrhagic. Contusions can occur anywhere, but most commonly occur

along the surface of the brain which is in contact with irregular bone, such as the inferior frontal

lobes and anterior inferior temporal lobes (Figure 16). During an acceleration/deceleration

injury, the skull base stops and the brain may be injured along the irregular surface. As

parenchyma along the skull base can be difficult to evaluate due to beam hardening artefact from

the adjacent bone, special attention should be taken to assess these areas for subtle injury.

Half of all patients with cerebral contusions show increase in contusion size on follow-up

CT scan, most commonly within the first 12 hours. Additionally, larger contusions seem to

progress more rapidly24. Any cerebral contusion should have a short-interval follow-up head CT

as substantial increases in size or coalescence into a larger hematoma are not rare. In our

institution, a 6 hour follow-up head CT is the agreed upon algorithm.

The main complication of all these various forms of hemorrhage is mass effect upon the

brain with resultant increased intracranial pressure, and, if not treated in a timely fashion,
herniation of the brain causing ischemia or respiratory arrest. The degree of mass effect can be

quantified and compared between studies by measuring midline shift at a pre-determined

structure, such as the septum pellucidum anteriorly or the pineal gland posteriorly. Too much

lateral midline shift on the supratentorial brain will cause subfalcine herniation, in which the

cingulate gyrus herniates under the falx25.

If the mass effect progresses, or if there is diffusely increased intracranial pressure, uncal

herniation may develop, in which the medial pole of the temporal lobe effaces the ipsilateral

portion of the suprasellar cistern. If the mass effect becomes even more severe, the entire

suprasellar cistern and quadrageminal cisterns may become effaced, called “central” herniation

which causes mass effect on the brainstem. If the cerebellar tonsils herniate through the foramen

magnum, this is called tonsillar herniation. Any form of herniation can be life threatening;

however the mass effect on the brainstem is especially worrying due to the potential for

respiratory arrest. One unique form of hemorrhage related to herniation and brainstem

compression is a Duret Hemorrhage (Figure 17)26. This hemorrhage develops within the

midbrain or upper pons from the traumatic downward displacement of the brainstem. The

treatment is surgical decompression in combination with medical management to help control

intracranial pressure.

Additionally, if there is a large displacement of brain tissue, the cerebral arteries and

cranial nerves may be compressed. For example, with severe subfalcine herniation, one or both

of the anterior cerebral arteries may be compressed against the falx and occluded, with resulting

infarct25. Ischemia and/or infarct is confirmed on CT by loss of grey-white matter differentiation

(Figure 18). As an example of cranial nerve involvement, a common sign of increased

intracranial pressure is a “blown pupil” (a non-reactive, dilated pupil), which is due to

entrapment of the ipsilateral third cranial nerve on the tentorium due to mass effect from the

uncus.

Danger Zones

After primary survey of the intracranial contends is done, it may be beneficial to look at

certain areas of the brain and CSF spaces that are known to hide hemorrhage or subtle fractures.

Table 1 shows five of these “danger zones,” which include dependent CSF and intraventricular

spaces where hemorrhagic byproducts tend to accumulate, as well as fluid levels in normally

aerated structures that can suggest skull base or temporal bone fractures. These areas should

always be scrutinized as significant findings can be overlooked in these locations.

Role of MRI in Head Trauma

Previously, the imaging discussion has been limited to CT. MRI has limited use in the

initial evaluation of acute head trauma for several reasons. Limited availability of the MRI

magnet in most hospitals often means patients may need to wait for hours or sometimes days,

whereas CT can be obtained in minutes. Before undergoing MRI, patients must be screened for

metal in their bodies which requires either an alert, cooperative patient, or time consuming

radiographs of the entire body. Additionally, patients who have been shot or may have other

metallic foreign bodies related to trauma could prevent them from being a candidate for

MRI. Of note, although many bullets are not ferromagnetic, some bullet casings and

ammunition are actually ferromagnetic. Thus, a safer assumption when evaluating for a potential

MR study is that bullet fragments could contain ferromagnetic material 27.

 Despite these limitations, MRI does have a role in the workup of head trauma after the

patient has been stabilized. It is used to evaluate for diffuse axonal injury (DAI), a shearing type

of axonal injury related to rapid acceleration/deceleration of the brain typically seen in high

speed velocity motor vehicle collisions, which can also present with hemorrhagic and non-

hemorrhagic forms. Typical findings include micro bleeds at the cortical-subcortical junction,

and linear micro-hemorrhages in the deep white matter tracts including the corpus callosum.

These are better visualized on gradient-echo (GRE) or susceptibility weighted imaging (SWI)

(Figure 19). The non-hemorrhagic forms are less common and present as T2 signal hyper-

intensities in a similar distribution (Figure 20).

In patients who have sustained a deceleration injury and are not regaining consciousness,

DAI should be suspected. DAI requires MRI to confirm the diagnosis and evaluate the severity

of injury. In some cases, small hemorrhages in typical locations can also be seen on

CT. Although imaging do not always correlate with clinical status, it generally confers a poor

prognosis and affected patients often require prolonged rehabilitation. In severe DAI, a high

percentage of patients are left in a persistent vegetative state.

MRI can also be used to diagnose hypoxic ischemic injury, which may be difficult to

appreciate on an early head CT. Although this injury is not directly related to trauma, patients

can sometimes present similarly (i.e. an unresponsive patient rushed to the emergency room). It

may also be encountered if the patient stops breathing secondary to a traumatic brain injury.

Other common presentations are drug overdose, “found down,” or patient requiring intubation in

the field. MRI findings include restricted diffusion in the cortex, thalami, basal ganglia,

hippocampi, or cerebellum.
Conclusion / Summary

The use of a consistent search pattern and approach to head trauma imaging can help the

junior radiologist or emergency medicine physician to accurately diagnose and triage patients

with life-threatening injuries. We have discussed our experience and routine approach, and the

importance of a thorough evaluation starting from the scalp (coup and countercoup injury

concepts), skull and facial fractures (key types and complications such as intracranial

hemorrhage / vascular injury, infection, CSF leakage), diverse types of extra-axial and

parenchymal hemorrhagic changes as well as secondary trauma complications such as hypoxic

ischemic injuries and brain mass effect.

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Figure Legends

Figure 1: Scalp Injury. (A,B) Axial and Coronal CT Images showing extensive scalp avulsion injury. Circle
indicating lack of scalp soft tissues. Scalping injuries are rare in the developed world, but they are more
common in third world countries, where machinery with rotary mechanisms is not designed with
important safeguards in mind6,7

Figure 2: Central Skull base Fracture. Axial CT shows linear lucency through the sphenoid with the
presence of sphenoid sinus fluid.

Figure 3: Temporal Bone Fracture. Axial CT images showing, (A) Otic capsule sparing temporal bone
fracture which does course through the middle ear ossicular chain. (B) Otic capsule violating temporal
bone fracture, seen extending through the cochlea and vestibule.

Figure 4: Orbital Fracture. (A,B) Coronal and Axial CT images showing medial orbital wall fracture with
medial rectus muscle entrapment. Arrows depicting muscle herniation through fracture.
Figure 5: Globe rupture. Axial CT through the orbits showing decreased anterior-posterior dimension of
the anterior chamber of the left globe.

Figure 6: Zygomaticomaxillary Complex (ZMC) Fractrure. Axial (A) and coronal (B) CT images show
fractures involving the zygomatic arch (circle), the lateral orbital rims (arrow), and the anterior and
posterior walls of the maxillary sinus (circle).

Figure 7: LeFort 2 Fracture. (A) CT images showing pyramidal shaped fracture plane from the posterior
alveolar ridges with apex at the nasofrontal suture, separates the entire maxilla from the upper face. (B)
Volume rendered reconstruction. In the same patient.

Figure 8: Epidural Hematoma. 34 year old male who fell from 25 feet. Axial CT images with “extra-axial
spaces” windowing (A) and bone windowing (B) showing lentiform shaped mixed density epidural
hematoma (A) associated with complex fracture (B) involving the left frontal and left parietal bones.

Figure 9: Venous Epidural Hematoma. Axial (A,B) and coronal CT images (C) showing extra-axial
hematoma spanning the dural reflection and adjacent to the superior sagittal sinus (A,C) and frontal
skull fracture (B).

Figure 10: Swirl sign. Axial CT image shows mixing of clotted and un-clotted blood (arrow) consistent
with active bleeding in extra-axial hematoma.

Figure 11: Active contrast extravasation. (A) The "spot sign" on CTA shows arterial contrast (arrow)
within the hematoma, not in a blood vessel. This represents actively extravasating blood. (B) Repeat
Head CT 3.5 hours later shows marked enlargement of the epidural hematoma, which also is seen to
cross midline. The patient went on to require craniotomy for evacuation and decompression.

Figure 12: Acute Subdural Hemorrhage. (A,B) Axial CT images showing acute subdural hemorrhage
represented by a crescent hyperdensity following the shape of the calvarium with extension along the
tentorium leaflet (arrow on A) and falx cerebri (arrow on B).

Figure 13: Subacute Subdural Hemorrhage. Axial CT image shows hemorrhage with density similar to
brain. Clue to diagnosis is the cerebral sulci that do not extend to the inner margin of the calvarium, as
depicted by dotted line.
Figure 14: Subdural Hygroma. A 78 year old female suffered a fall in the nursing home. Coronal (A)
and axial (B) noncontrast CT images show a right CSF density subdural collection exerting mild mass
effect on the right convexity. (C) An axial CT from one month earlier before the patients fall shows no
collection was present, confirming that this was a result of acute trauma. Images courtesy of Dr.
Humberto Morales.

Figure 15: Subarachnoid and Intraventricular Hemorrhage. 59 year old suffered MVC. (A) Axial CT
image show intraventricular blood layering in the occipital horns (white arrow) and scattered
subarachnoid hemorrhage within the cerebral sulci (black arrow). (B) Dependent layering blood in the
interpeduncular cistern, this can be a very subtle but important finding in the presence of subarachnoid
hemorrhage.

Figure 16: Intraparenchymal hemorrhage. Axial CT image shows hemorrhagic contusion occurring in a
typical temporal lobe location, overlying the hard petrous ridge of the temporal bone.

Figure 17: Duret Hemorrhage. Axial CT shows hyperdensity within the midbrain / upper pons,
secondary to traumatic downward displacement of the brainstem.

Figure 18: Diffuse Cerebral Edema. (A,B) Axial CT images showing blurring of the grey-white matter
differentiation with complete sulcal effacement in a patient with a traumatic brain injury. Note cortical
contusion in the left temporal lobe (arrow on A)

Figure 19: Hemorrhagic shear injury. (A) CT and (B) Axial Gradient-Echo MR images showing multiple
traumatic hemorrhagic changes in the grey-white matter junction.

Figure 20: Diffuse Axonal Injury. (A) Subtle hypodensity in the genu of the internal capsules on CT (black
arrows) as well as genu of the corpus callosum (grey arrow). (B,C,D) MRI nicely depicts the T2 signal
alternation without susceptibility to suggest hemorrhage. (D) Diffusion restriction also confirms diffuse
axonal injury.
Table 1: Five head CT findings which are easy to overlook but can indicate significant injuries.