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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4504_Библиотеки_им_академика_М_И_Перельмана
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A. J. Tsiouris and Y. W. Lui
Fig. 7.10 Thin targeted axial bone algorithm images from a maxillofacial CT scan depict a complex comminuted fracture through the left
frontal bone and sinus (top left image, arrow). The corresponding noncontrast head CT scan demonstrates a large underlying “coup” hemorrhagic contusion (top right image, arrow) with associated SAH (top
right and bottom right images, arrowheads). Contrast is noted within
the arteries of the circle of Willis due to the concurrently performed
whole body contrast-enhanced trauma CT scan, although a small SAH
was also suspected within the suprasellar cistern (top right image). The
fracture line extended into the sphenoid bone (bottom left image, arrow)
causing a suspected CSF leak in this patient. A focus of interhemispheric air was also present, due to the fracture extending through the
air-lled sinuses (bottom right, arrow)
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Fig. 7.11 Following a fall from a ladder, a non-contrast CT scan was
performed in the emergency department that demonstrates multicompartmental post-traumatic intracranial hemorrhage including a subdural
hematoma, SAH, and a small contusion (left image, arrows) within the
gray–white matter junctions, corpus callosum, basal ganglia,
brainstem, and mesencephalon. Classication of DAI was
rst described in 1982 by Adams and colleagues based on
location of lesions. DAI grade I (mild) involves microscopic
changes in the cerebral cortex, corpus callosum, brainstem,
and cerebellum; grade II (moderate) are gross focal lesions
in the corpus callosum; and grade III (severe) are focal
lesions in the dorsolateral portions of the brainstem involving the superior cerebellar peduncle [74]. Axonal injury in
the brainstem is an important indicator for clinical degeneration to coma in DAI patients [73]. Thalamic injury may also
occur and are not included in the initial grading system but
may result in worse clinical outcomes [75].
Given the clinical importance of DAI and higher associated morbidity and mortality compared to other types of
extra-axial injuries or hemorrhagic brain contusions, imaging plays a crucial role in detection and prognosis. As always,
left lateral temporal lobe. A CT scan performed 12h later demonstrates
a marked interval increase in size of the inferolateral left temporal lobe
hemorrhagic contusion (right image, arrow)
non-contrast head CT is the modality of choice in the acute
trauma setting but often underestimates DAI extent especially for non-hemorrhagic lesions [72]. Only around 10% of
patients with DAI show hemorrhagic lesions initially
(Fig.7.13), which then can become more apparent in weeks
following injury as these areas begin to atrophy and undergo
gliosis with ex-vacuo ventricular dilatation [76]. Thus, when
patients have clinical ndings discrepant with initial CT
imaging, MRI is often used to improve sensitivity in evaluation. In the acute setting, DWI sequences can show nonhemorrhagic lesions in areas of cytotoxic or vasogenic
edema [17]. Greater degrees of signal abnormality in the corpus callosum and brainstem (grade II and III lesions) have
been shown to correlate with length of comatose state [77].
For hemorrhagic lesions, susceptibility-weighted sequences
can detect microhemorrhages with some reports showing
SWI to be six times as sensitive as T2* GRE imaging [78]
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Fig. 7.12 T2-weighted FLAIR (left image) and SWI (right image) MR
sequences demonstrate extensive chronic hemorrhagic encephalomalacia within the lateral right temporal lobe (arrows) in a patient with a
severe TBI following a high-speed motor vehicle collision. There is
Table 7.3
What
happens
Time
frame
Red blood
cells
Sequential signal intensity changes of intracranial hemorrhage on MRI (1.5T)
Hyperacute
hemorrhage Acute hemorrhage
Blood leaves the
vascular system
(extravasation)
Deoxygenation with
formation of
deoxy-Hb
<12h Hours–days (weeks in
Early subacute
hemorrhage Late subacute hemorrhage Chronic hemorrhage
Clot retraction and
deoxy-Hb is oxidized
to met-Hb
A few days 4–7days–1month Weeks–years
center of hematoma)
Intact erythrocytes Intact, but hypoxic
erythrocytes
Still intact, severely
hypoxic
associated ex-vacuo dilatation of the temporal horn of the right lateral
ventricle (left image, arrowhead). Additionally, there is evidence of
chronic hemorrhagic axonal injury involving the superior cerebellar
peduncles (right image, arrowheads)
Cell lysis (membrane disruption) Macrophages digest
the clot
Lysis (solution of lysed cells) Gone;
encephalomalacia with
proteinaceous uid
State of HbIntracellular oxy-Hb
(HbO
)
2
Intracellular
deoxy-Hb (Hb)
Intracellular met-Hb
(HbOH) (occurs
initially at periphery
Extracellular met-Hb (HbOH) Hemosiderin
(insoluble) and ferritin
(water soluble)
of clot)
Oxidation
state
Magnetic
properties
SI on
T1WI
SI on
T2WI
Ferrous (Fe
unpaired e−
2+
) no
Ferrous (Fe2+) 4
unpaired e−
Ferric (Fe3+) 5
unpaired e−
Ferric (Fe
Diamagnetic (c<0) Paramagnetic (c>0) Paramagnetic (c>0) Paramagnetic (c>0) FeOOH is
≈ or ↓ ≈ (or ↓) (no PEDD
interaction)
↑ (essentially
imaging of
high-water content
of blood, plasma)
↓ T2 PRE
(susceptibility effect
from concentration of
Hb inside RBCs)
↑↑ (PEDD
interaction)
↓↓ T2 PRE
(susceptibility effect
from concentration
of Hb inside RBCs)
↑↑ (PEDD interaction) ≈ (or ↓) (no PEDD
↑↑ No T2 PRE (more homogenous
distribution across intracellular and
extracellular compartments after
cell lysis reduces local
3+
) 5 unpaired e−
Ferric (Fe3+) 2000×5
unpaired e−
superparamagnetic
interaction)
↓↓ T2 PRE
(susceptibility effect)
susceptibility effects)
Legend: Hb hemoglobin, e electron, FeOOH ferric oxyhydroxide, ↑ increased SI relative to normal gray matter, ↓ decreased SI relative to normal
gray matter, PRE proton relaxation enhancement, PEDD proton-electron dipolar-dipolar
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Fig. 7.13 Axial non-contrast head CT images performed on a comatose patient with a severe TBI demonstrate bilateral frontal lobe acute
hemorrhagic contusions in the frontal lobes (top left and right images,
arrowheads) as well as multifocal punctate acute microhemorrhages in
a linear pattern in the left superior frontal gyrus compatible with traumatic hemorrhagic axonal shear injuries (top left image, arrow).
T2-weighted FLAIR demonstrates multifocal regions of white matter
edema within the left superior frontal gyrus (middle left image, arrow)
(Fig.7.14). Bland T2 hyperintense white matter lesions may
be present in patients with DAI but are nonspecic ndings
and can also be seen in nontraumatic causes such as ischemia, demyelination, migraines, vasculopathies, etc. A linear
pattern along the vectors of the force applied to the brain and
an association of these T2 hyperintensities with regions of
diffusion restriction and microhemorrhage are important to
distinguish DAI from other nonspecic causes [79]. More
focal regions of traumatic axonal injury (TAI) which may be
seen on MRI are also now understood to occur in less severe
clinical cases.
Diffusion tensor imaging (DTI) has emerged as an MRI
technique that can study white matter and potential white
matter injury. DTI uses orthogonal diffusion vectors and can
associated with numerous foci of microhemorrhage on SWI within the
bilateral superior frontal gyri (lower left image, arrows) conrming the
hemorrhagic axonal shear injuries. The T2-weighted FLAIR sequence
also depicts a focal region of cortical/subcortical edema (middle right
image, arrow) corresponding to cortical hemorrhage on the SWI (lower
right image, arrow) within the posterolateral left frontal lobe conrming a hemorrhagic contusion
measure directional diffusion. In group studies, DTI has
been shown to demonstrate anisotropy changes in white matter in patients with TBI compared with controls even in the
absence of T2 FLAIR and susceptibility abnormalities [80,
81]. Changes in fractional anisotropy after TBI can be
confusing (elevated vs depressed compared with normal),
and this inconsistency is now believed to relate to timing
after injury. Clinical use of DTI as a TAI biomarker remains
challenging due to heterogeneity in data acquisition and
analysis methods, variance across the normal population,
and heterogeneity of head injuries. Ongoing research is still
underway to better understand and characterize white matter
injury using multicompartment diffusion modeling and to try
to identify potential clinical uses.
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Fig. 7.13 (continued)
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Fig. 7.14 SWI demonstrates numerous punctate and linear foci of susceptibility compatible with traumatic hemorrhagic axonal shear injuries
within the subcortical white matter of the left frontal lobe and the cor-
7.8 Vascular Injury
Vascular injuries may occur with head trauma including arterial dissection, pseudoaneurysm, active extravasation, vascular occlusion, carotid cavernous stula, dural arteriovenous
stula, and venous thrombosis. Patients with severe DAI and
cerebral edema may also develop diffuse vascular injury,
which is shown when dark areas of SWI susceptibility artifact surround engorged veins indicating areas of venous stasis [82]. Several guidelines exist for imaging use when
vascular injury is suspected including the Denver and
Western Trauma Association criteria. Consensus is that any
head trauma with a skull base fracture or penetration neck
injury extending through the carotid canal, particularly zone
III (through superior angle of mandible) should be further
evaluated with angiography [83].
7.8.1 Carotid Artery-Cavernous Sinus Fistula
(CCF)
Carotid artery-cavernous sinus stula (CCF) can have different etiologies but occur in the setting of trauma when the
cavernous segment of the internal carotid artery is injured
result in a direct communication between the arterial system
and the venous system of the cavernous sinus. This stulous
connection may lead to dilation of the cavernous sinus and
secondary enlargement of the superior ophthalmic vein
(SOV) and inferior petrosal sinus [8]. Characteristic imaging
shows enlarged cavernous sinus or ipsilateral SOV with mul-
pus callosum (arrows) in a young male patient that suffered a moderate
TBI following a motorcycle accident
tiple ow voids on MRI and clinical symptoms include
injected conjunctiva, pulsatile exophthalmos, and periorbital
edema (Fig.7.15).
7.8.2 Traumatic Aneurysms
Post-traumatic intracranial aneurysms are rare, accounting
for <1% of all aneurysms and occur most commonly in children [84]. Common locations include the cavernous and
infraclinoid internal carotid artery as well as the anterior
cerebral artery. As with all intracerebral aneurysms, standard
assessments include CTA/MRA and catheter digital subtraction angiography.
7.8.3 Traumatic Vascular Dissection
Damage to the intimal layer of an artery may result in the
creation of a false lumen with blood diverting into the media
through the dissection ap. Sometimes even minor neck
injury can result in cervical vascular dissections with resultant potential vascular compromise of the brain. Intracranial
dissection is less common, and severe cases can be associated with adjacent fractures causing direct damage to the
vessels or result from rotational force in blunt head trauma
[85]. The incidence of internal carotid and vertebral artery
dissections in the setting of head trauma is 0.86% and 0.53%,
respectively [86].
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Fig. 7.15 A young male patient developed bilateral ocular proptosis
and chemosis while hospitalized for a recent severe TBI with nondisplaced skull base fracture. The axial T1-weighted MR image demonstrates enlargement of the bilateral superior ophthalmic veins, left more
than right (top left image, arrows). The coronal T2-weighted image
demonstrates small bilateral post-traumatic subdural hygromas (bottom
left image, arrowheads) and a small inferior left frontal hemorrhagic
contusion (bottom left image, arrow). The time-of-ight gradient echo
CTA and MRA are the most commonly utilized imaging
modalities and are highly accurate in the assessment of the
integrity of the cervical arteries and to assess for luminal narrowing. Anatomic black-blood MRI sequences may also
show a high intensity “crescent sign” on T1-weighted and
T2-weighted sequences indicating an intramural hematoma
at the site of the dissection with a concomitant ow void or
abnormal contour on MRA [87] (Fig.7.16). Ultrasound is
MRA demonstrates arterialized ow-related enhancement within the
bilateral cavernous sinuses and left superior ophthalmic vein (top right
image, arrows). The left ICA arterial phase digital subtraction catheter
angiogram (anteroposterior projection) conrmed the presence of a
direct carotid cavernous stula with pronounced early arterial phase
opacication of the cavernous sinuses and ophthalmic veins (bottom
right image, arrows)
also being increasingly used for detection, particularly with
B mode and color ow doppler. Conventional catheter angiography remains a useful tool for diagnosing cervical and
intracranial arterial dissections and may show features such
as the “string sign” or “ame shaped tapering,” however in
current practice is reserved primarily for endovascular
therapy.
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Fig. 7.16 CTA was performed in a young patient complaining of left
neck pain following a concussion while playing ice hockey. The CTA
demonstrates a linear intimal ap and pseudoaneurysm of the distal left
internal carotid artery located directly below the skull base compatible
with a traumatic dissection and pseudoaneurysm (left image, arrows).
7.9 Secondary Complications
7.9.1 Denition
Secondary intracranial complications are worth discussing
and can be clinically critically important. These are sequelae
that result as a series of pathophysiologic events triggered by
the initial injury that then may lead to further tissue injury
and neuron loss.
7.9.2 Intracranial Hypertension
Intracranial hypertension may result after head trauma due to
swelling, edema, or hemorrhage and can continue to increase
in the initial days after injury, leading to progressive and
sometimes precipitous decline. Suspicious imaging ndings
include diffuse sulcal effacements, compression of the ventricles, enlarging hematomas, and/or herniation. These ndings have been found to have a linear relationship with
increased intracranial pressure and can help guide manage-
Crescentic T1 and T2 hyperintensity are also present on the anatomic
T1-weighted and T2-weighted sequences performed through the upper
neck that represented the subintimal hematoma and conrmed a traumatic ICA dissection (right images, arrows)
ment including placement of ICP monitors, need for neuro
ICU care with close ICP monitoring, surgical intervention
such as CSF drainage, hematoma evacuation, or decompressive craniotomy [98].
7.9.2.1 Brain Herniation
Profound intracranial hypertension may lead to multiple secondary injuries of which brain herniation is the most dangerous. The mass effect from increased pressure can result in
obliteration of the basal cisterns, subarachnoid spaces, and
non-communicating hydrocephalus if ventricular outow is
obstructed. Compression of important vascular structures
can lead to brain infarction thus leading to a cascade of neurologic damage. Herniation patterns are described in
Table7.4.
7.9.2.2 Secondary Brainstem Hemorrhage (Duret
Hemorrhage)
Rapid downward cerebral herniation can lead to a devastating effect, hemorrhage within a compressed brainstem. CT
ndings show hyperdense blood in the brainstem typically in
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Table 7.4 Cerebral herniation types
Type of
herniation
Denition Medial cingulate
Cause Supratentorial mass
Imaging • Unilateral
Potential
vascular
structures
compromised
Other
complications
Subfalcine
(cingulate) Tonsillar
gyrus displacement
under inferior free
margin of the falx
(e.g., EDH, SDH,
mass lesion, ...)
intracranial
mass or lesion
• Falx bowing
• Compressed
ipsilateral
lateral ventricle
• Enlarged
contralateral
ventricle
(obstructed
foramen of
Monro)
ACA (pericallosal
and callosomarginal
arteries)
Intracranial
hypertension may
cause descending
transtentorial h
A. J. Tsiouris and Y. W. Lui
Descending
transtentorial
Downward
displacement of
cerebellar tonsil(s)
through foramen
magnum
Posterior fossa
mass lesion or
supratentorial mass
effect
• Inferior
displacement
of cerebellar
tonsils
• Obliterated
cisterna magna
PICA PCA SCA Contralateral PCA Venous infarction
Hydrocephalus and
syringomyelia
Downward shift of
diencephalon,
mesencephalon, and
upper brainstem
Supratentorial mass
effect
• Obliterated
perimesencephalic
cisterns with
plugging of
tentorial
incisura
• Downward shift
of pineal
calcication
• Foreshortened
and compressed
brainstem
Duret (brainstem)
hemorrhage
Ascending
transtentorial Uncal External
Superior
displacement of
the vermis through
the tentorial
incisura
Posterior fossa
mass lesion
• Obliterated
fourth
ventricle
• Effaced
superior
cerebellar and
quadrigeminal
cisterns
Hydrocephalus Progression to
Herniation of
medial temporal
lobe through
tentorial notch
Temporal mass
lesion, e.g., focal
hematoma
• Obliterated
suprasellar
cistern
• Mesencephalon
shifts to
opposite side
• Widening of
ipsilateral CPA
cistern
• Hydrocephalus
(due to
aqueductal
obstruction)
descending
transtentorial
herniation
Brain tissue
extrudes externally
through a skull
defect
Increased ICP in
association with a
traumatic or
surgical skull
defect
Occasionally can
occur with
postoperative
pressure gradient
and shifts without
frank elevation of
ICP
• Extracranial
displacement
of brain tissue
• Bone defect
(propensity to
hemorrhage)
Pressure necrosis
with swelling of
the adjacent brain
at the margins of
the defect
the lower midbrain/ventral pons. A recent large meta- analysis
implicated damage to anteromedial basilar artery perforators
after sudden descending herniation [88] as the main cause.
Outcome in the setting of Duret hemorrhage is poor and
often fatal.
7.9.3 Ischemia andInfarction
Post-traumatic ischemia is another secondary effect of
trauma that leads to poorer clinical outcomes. MRI is most
sensitive to detect secondary ischemic injury as areas of
increased signal intensity on T2-weighted images with corresponding restricted diffusion [89]. The most common post-
traumatic ischemic injury is inicted on the ipsilateral
posterior cerebral artery territory due to supratentorial mass
effect. Causes can be extra-axial or intracranial hemorrhage
resulting in mass effect and downward transtentorial herniation. Buildup of supratentorial pressure and mass effect may
ultimately lead to impingement of the posterior cerebral
artery between the free edge of the tentorium and the herniating brain. Anterior cerebral artery impingement can occur
along the free edge of the falx in the setting of subfalcine
herniation. Frank compression of the middle cerebral artery
is less common [89, 90]. More distal vessel compromise can
also occur relating to vasospasm in the setting of acute subarachnoid hemorrhage.
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7.9.4 Infections
Penetrating head trauma (Figs.7.17 and 7.18) involving contaminated foreign objects or the introduction of non-sterile
portions of the patient’s own anatomy (paranasal sinuses,
skin, etc.), which then penetrate the intracranial compartment can introduce bacteria and other infectious agents. The
spectrum of post-traumatic infection ranges from local
wound/scalp infection and cellulitis to more hazardous intracranial infections such as meningitis, ventriculitis, cerebritis,
Fig. 7.17 Gunshot wound to the left parietal lobe by a stray bullet in a
young child, initial non-contrast CT scan. The 3D volume rendered
reconstructed CT scan through the skull and the sagittal CT scan reconstructed images demonstrate a complex elevated comminuted fracture
through the bilateral parietal bones (top left and right images, arrows).
Axial non-contrast CT scan images demonstrate the bullet fragments
lodged within the left parietal lobe associated with multiple foci of
intracranial air and microhemorrhage (bottom left and right images,
arrows). The non-contrast CT scan also shows diffuse sulcal effacement
and ventricular compression compatible with diffuse cerebral edema
and raised ICP
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