CT EVALUATION OF
Consultant ,Radiology & Imaging
leading cause of death in children and
Peak age – 15 -24 yrs
Secondary peak > 50 years of age.
Twice as often among males compared to
Generaly caused by motor vehicle
accidents, fall, assaults, violence and
sports & recreation
HEAD TRAUMAHEAD TRAUMA
C.T is the most important step in evaluation for head
and contiguous spine injuries.
In a typical head injury windows and window level are
1) Brain window
2) Intermediate window : to assess the subdural
or epidural hematoma.
3) Bone window : to determine the presence or
absence of a bony fracture.
HEAD TRAUMAHEAD TRAUMA
sometimes valuable for following reasons:-
Show small extra-axial blood collection in sub-dural and
Show non-haemorrhagic paranchymal lesions diffuse axonal
Higher sensitivity in the sub-acute and chronic stages of head
MR is useful to show long term effects of head injury.
( MR sometimes fail to demonstrate the sub-arachnoid
haemorrhage, better seen in C.T )
MRI is generally following C.T, when C.T does not resolve the
nature of brain injury.
HEAD TRAUMAHEAD TRAUMA
Scalp hematoma / subgaleal soft tissue swelling
Subgaleal extrusion of macerated brain through comminuted
skull fracture .
Atreiovenous fistula or pseudo-aneurysm; usually involve
superficial temporal or occipital arteries.
could be linear,depressed or diastatic and may involve cranial
vault or skull base.
Skull radiographs and C.T are effective to demonstrate
SUTURAL DIASTASIS/ DIASTATIC FRACTURE:
Width of the suture more than 3 mm is recognized as sutural
diastasis. (normally sutures are no wider than 2 mm.)
In adult diastasis of lambdoid suture is most common,could be
FRACTURE OF SKULL BASE:
• Basilar skull fracture should be sought when blood behind
tympanic membrane, otorrhoea, rinorrhoea, echymosis
surrounds the orbits without direct orbital trauma,intracranial
air,air fluid level in PNS or mastoid air cells.
• High- resolution cranial C.T with thin section is best
modalities to detect basilar fracture.
• Basilar fracture cause compression or entrapment of cranial
• petrous bone fracture causes- ossicular chain dislocation.
• fracture of optic canal cause loss of vision.
• Sphenoidal fractures can also be associated with disruption
of intra- cavernous internal carotid artery, leading to pseudo-
aneurysm or a carotid cavernous fistula.
• Usually occurs within first 24 or 48 hours, delayed
development or enlargement seen
In 10 to 30%.
• Etiology - due to damage of middle meningeal artery.
- laceration of diploic veins.
- dural sinus
• located between the skull and dura with a focal
biconvex configuration. EDH may cross dural
attachments but not sutures.
• Most common site temporo-parietal area. Posterior
fossa EDH are relatively uncommon.
• On C.T scan, uncommonly EDH may be bilentricular
crescentic or irregular.
• Brain adjacent to most EDHS is severely flattened or
displaced. Secondary herniation are very common.
* C.T findings Acute, Sub-acute and Chronic.
Acute epidural haematoma- 2/3 uniformly high density 1/3
homogenous in attenuation
Isodene area due to serum
Hypodense area within indicate active bleeding
Sub-acute EDH- Homogenously hyperdense – consists of
solid blood clot.
Chronic EDH – Hetrogenous or decreased attenuation as
well as enhancing membrane peripheral enhancecment
represent dura or membrane formation.
* Imaging criteria whether a epidural haematoma may be
treated conservatively are-
(1) Diameter less than 1.5 cm
(2) A minimal mid line shift of less than 2 mm
(3) The patient must be intact neurologically without focal
• SDHS are interposed between the dura and
arachnoid. . Post traumatic subdural collection
may be filled with CSF when there is tear in the
arachnoid then called CSF hygroma.
• Tpypically cresent shaped with concave medial
and convex lateral border, which may
• May cross suture lines but not dural
• COMMON SITES:
- over the fronto-parital convexities.
- middle cranial fossa
- para- falcial area.
- inter- hemispheric fissure
Adjacent to the tentorium – may simulate intra- axial lesion.
• Supra tentorial SDHS located adjacent to the tentorium
shows well-defined medial margin corresponding to the
edge of tentorium and sheet like area of increased density
that slopes laterally
• Infra tentorial SDHS located below the tentorium shows a
sharp lateral margin corresponding to the edge of tentorium
and increased density that slopes later
• Posterior fossa SDHS are rare.
• C.T Shows as crescent shaped extra- axial
collection with a convex lateral and concave
medial border. Occasionally may be biconcave
• ACUTE SDHS- Homogenously hyperdense
- Up to 40%- mixed hyper/ hypodense
- due to unclotted blood
- serum extruded
during clot retraction
- Rarely isodense- in patients with – coagulopathies
& severe anemia
• Isodense within a few day to a few weeks.Difficult to
diagnosis clues -
Effacement of cortical sulci over cerebral convexity
Mid line shift
Delayed enhancement C.T scan performed after 4 to
CHRONIC SDHS :- Typically low attenuation in
Mixed density in 5% cases- due to recurrent haemorrage
Enhancement following contrast
Shows calcification in 0.3 to 2.7% cases
Hypodense collection equal to CSF density.
More crescentic & bilateral
At surgery show clear fluid and lack of a membrane.
• Due to damage to blood vessels on the pia-
• Intra- parenchymal haematoma rupture into the
ventricular system may gain ascess to
Subarachnoid space via the foramina of magendie
• Complication show communicating hydrocephalus
due to fibroblasti
• C.T is the modality of choice in the evaluation of
SAH. SAH typically appear as an area of
hypendensity in the basal cisterns, the sulci
overlying cerebral convexities,the sylvian fissure
and inter- hemispheric fissure.
• Normal calcified or ossified flex may be
mistaken for parafalcine in older adolescents.
• “ Pseudo sub- arachnoid haemorrhage” is
seen incase of sever diffuse cerebral oedema
• Posterior parafalcine or inter-hemispheric SAH
can mimic the “Empty delta sign’’ of superior
sagittal Sinus thrombosis.
• SAH is rapidly cleared from the subarachnoid
space. The majority of C.T scans performed
within 1Week will appear normal.
INTRA - VENTRICULAR HAEMORRHAGEINTRA - VENTRICULAR HAEMORRHAGE
IVH are associated with other manifestations ofIVH are associated with other manifestations of
primary intra-axial brain trauma . Such as DAIprimary intra-axial brain trauma . Such as DAI
,deep cerebral gray matter and brain stem,deep cerebral gray matter and brain stem
lesions .lesions .
C.T shows high density intraventricular bloodC.T shows high density intraventricular blood
with or without a fluid level.with or without a fluid level.
Occasionally focal choroid plexux haematomaOccasionally focal choroid plexux haematoma
Bilateral or multiple.
Frequently associated with SAH & SDHS
Most frequently noted at the time of injury .
may be delayed with 48 hours. .
Differentiated from hemorrhagic contusion
by sharply marginated margin, perifocal
hypodensity and mass effect.
ACUTE HEMATOMA - < 3 DAYS
Homogenous high density lesion (50 -70 HU) with
irregular well - efined margins.
Usually surrounded by low attenuation (oedema,
contusion ) with mass effect.
SUBCUTE HEMATOMA ( 3 – 14 DAYS )
NCCT : Gradual decrease in density from
periphery inward and becomes isodeme
to brain Parenchya (1-2 HU per day during 2nd
CECT : Peripheral rim enhancement at inner border
of perilesional lucency.
CHRONIC HEMATOMA : > 14 DAYS
Gradual Decreased / hypodensity .
Later show lucent hematoma (cephalomalacia due
to proteolysis and phagocytosis +surrounding
atrophy) with adjacent sulcal enlargement and
ventricular dilation with ring blush ( DDX : tumor )
DIFFUSE AXONAL INJURY:-
Most common type of primary traumatic injury .
PATHOGENESIS Cortex and deep structures
move all different speed resulting in shearing
strain along the course of white matter tracts
especially all gray- white matter junction with
axonal tears followed by Wallerion degeneration .
Disruption of accompanying blood vessels show
numerous small hemorrhage foci .
Diffuse & Bilateral
DIFFUSE AXONAL INJURY:-
Locations ( according to severity of trauma )
a) lobar white matter at cortico-medullary junction
more common para sagital region of frontal lobe
+ periventricular region of temporal lobe,
occasionally in parietal and occipital lobes.
b) Internal + external capsule, corona radiate,
cerebral peduncles .
c) Corpus callosum
d) Brain stem – postero lateral quadrants of mid
brain + upper pons.
DIFFUSE AXONAL INJURY:-
C.T – Findings
- Early imaging may be subtle or normal .
- Foci of decreased density.
- May show some degrees of cerebral
- May show small focal hemorrhage or small
petechial haemorrhage particularly at
gray-white junction and corpus callosum.
- May show extensive injury.
Common type of primary intra-axial lesion .
In 21% of head trauma patients.
PATH :- Tissue necrosis, capillary disruption,
petechial hemorrhage followed by
liquefaction + oedema after 4 to 7 days
.contusion may be hemorrhagic or non-
MECHANISM :- Linear acceleration –
deceleration forces / penetrating trauma /
1. COUP :- Direct impact to stationary brain. Injury at
the site of impaction.
2. COUNTER COUP :- Impact of moving brain on
stationary clavarium opposite to the site of the coup
and produced injury.
Contusions are typically superficial foci of punctate
or linear hemorrhages that occur
along gyral crests.
Location - Multiple bilateral lesion , temporal lobes
most frequently involved.
- Bneath an acute subdural hematoma.
- Initial findings may be subtle or absent.
- Early findings focal / multiple poorly defined
areas of low attenuation with irregular contour
intermixed with a few tiny areas of increased
density ( petechial hemorrhage)
- Diffuse oedema and mass effect in immediate
post-traumatic period,then gradually diminish
- Some degree of contrast enhancement.
- Isodense to brain after 2 – 3 weeks.
DEEP CEREBRAL AND BRAIN STEM INJURY
Less common than DAI and cortical contusions.
Represent 5% to 10% of primary traumatic brain
Most are induced by shearing forces,
Most patients have profound neurologic deficits
and a poor prognosis..
C.T. Scan - often normal initially.
- Petechial hemorrhages can sometimes be seen
in lateral brain stem, periaquedctal region region
and deep gray matter nuclei.
M.R shows brain stem lesions nicely.
SECONDARY TRAUMATIC LESION
Infraction - ipsilateral ACA
compressed against flax.
Extra cranial herniation
SEQUELAE OF TRAUMA
1) Encephlomalacia and atrophy.
2) Pneumocephalus, Pneumatocele formation.
3) CSF Leaks and Fistulae.
4) Acquired Encephalocele or leptomeningeal cyst.
5) Cranial nerve injuries.
6) Diabetes incipidus.
9) Subdural Hygroma.
10) Post traumatic abscess.
• C.T is important modality for evaluation of
an emergency patient with cranio-cerebral
• Early & accurate ct evaluation cause
better patients outcomes with a decrease
morbidity & mortality statics.
& Decrease in trauma related medical