Head CT
Head CT
Head CT
of CNS Trauma
worldwide.
Gunshot wounds
Most common in adolescents and young adults
Using GCS
Mild/Minor (GCS-13-15)
Moderate (GCS 9-12)
Severe (GCS <=8)
Pathoetiologically
Primary injuries – occur at the time of initial trauma.
Secondary injuries – which occur later
Primary injuries
In head trauma, thin-sectioned NECT scans from the foramen magnum to the
vertex with both soft tissue and bone algorithm should be obtained.
Coronal and sagittal reformatted images from the axial source data are
extremely helpful.
The scout view should always be displayed and evaluated as part of study.
Who and when to image?
Major and widely used appropriateness criteria for imaging acute head
NECT in mild closed head injury with the presence of a focal neurologic deficit
All traumatized children under 2 years of age & patients over 60 years of age
Repeat CT of patients with head injury should be obtained if there is sudden clinical
Vomiting
Patient>60 yrs.
Anterograde amnesia
Seizure
The Canadian Head CT Rule in Mild Head
Trauma
Inclusion criteria
Patient has suffered minor head trauma with resultant:
loss of consciousness
GCS 13-15
confusion
amnesia after the event
Exclusion criteria
anticoagulant medication or bleeding disorder
age <16 years
seizure
High risk factors
GCS <15 two hours post injury
suspected open skull fracture
sign of base of skull fracture
vomiting more than twice
Interpretation-
age >65 years • Risk factors – YES – CT Head required
Medium risk factors
• Risk factors – NO – CT Head not required
amnesia post event >30 min
dangerous mechanism of injury
pedestrian struck by motor vehicle
occupant ejected from motor vehicle
fall from >3 feet or 5 stairs
Skull fractures
Orbit fractures
Zygomaticomaxillary fracture
Nasoorbitoethmoid fracture
Mandible fracture
Presentation
Extradural hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage
CSF rhinorrhea
Battle’s sign
Raccoon eyes
Battle’s sign
also called mastoid ecchymosis,
is an indication of fracture of middle cranial fossa of the skull
consists of bruising over the mastoid process, as a result of extravasation of blood
along the path of the posterior auricular artery.
Racoon eyes/Panda eyes sign
Periorbital ecchymosis
Sign of
Basal skull fracture
Subgaleal hematoma
Craniotomy that ruptured the meninges
Skull Base Fractures
Anterior
Frequently associated with sinonasal possibility of endangerment of
cavity &/or orbital injuries nearby structures including:
Cranial nerves
Majority have facial fractures
Internal carotid artery
Cavernous sinus
Middle
Look for the involvement of sphenoid
bone, clivus, caverernous sinuses and
carotid canal.
Posterior
May be isolated or associated with
transverse petrous fractures
May extend into the transverse or
sigmoid sinuses, jugular foramen or
hypoglossal canal.
Facial bone (Le Fort) fractures
(Midface)
involve separation of all or a portion of the midface from the skull base
the pterygoid plates of the sphenoid bone need to be involved as these
connect the midface to the sphenoid bone dorsally.
3types
Le Fort I
Horizontal fracture through the maxilla that involves the piriform aperture.
Le Fort II
Pyramidal fracture that involves the nasofrontal junction, infraorbital rims,
medial orbital walls, orbital floors and the zygomaticomaxillary suture lines.
Le Fort III
Craniofacial separation
Consists of nasofrontal junction fractures that extend laterally
through the orbital walls and zygomatic arches.
Le Fort I – Floating palate
Le Fort II – Floating maxilla
Le Fort III – Floating face
Le Fort I
Le Fort II
Skull fractures
A. Linear – sharply marginated lucent lines, low impact injury
B. Depressed – fragments imploded inwardly,
High impact injury.
Complications
facial and other cranial nerve injuries
vertigo and hearing loss
cerebrospinal fluid (CSF) leak
CSF fistula
meningitis
post-traumatic cholesteatoma
Ossicular chain dislocation.
Ossicular chain
dislocation
Pneumolabyrinth
Skull Fractures !!
When to worry ??
NECT
Best assessment of extent of soft tissue injury
Identify entry & exit wounds
Bone CT
Osseous entry and exit sites and pnemocephalus
Metallic fragments easier to evaluate
Coup-Contrecoup Injury
damage is located both at the site of impact and on the opposite side of the head
Coup-Contrecoup Injury
Subgaleal hematoma
Under aponeurosis (galea) of occipitofrontalis muscle.
External to periosteum
Not limited by sutures
Can be extensive, even life threatening
85 years old, fall from height
Epidural Hematoma (EDH)
Definition – Blood collection between inner table of skull
and outer (periosteal ) layer of dura.
Types –
Classic
Arterial
Unilateral
Supratentorial
biconvex
Variant
Unusual location, unusual etiology & unusual shape/density
EDH Classic
Best diagnostic clue
Hyperdense, biconvex, extraaxial collection on NECT
Location
Nearly all at coup site
90-95%Unilateral
Arterial
Adjacent to skull fracture
Supratentorial (65% temporoparietal, 35% frontal/parietooccipital )
5-10% posterior fossa
Size
Variable, rapid expansion
Attains maximum size at 36 hours
Morphology
Biconvex/lentiform extraaxial collection
Arterial EDH’s usually do not cross sutures except if sutural diastasis/fracture is present.
Etiology
Most often near Middle Meningeal Artery groove
Associated abnormalities
Skull fracture in 95%, may cross MMA groove
Presentation
Classic lucid interval – 50% of cases
Initial LOC – Subsequent asymptomatic time – Symptom or
coma onset
Headache, nausea, vomiting, seizures, focal neurological deficits
NECT
• Acute EDH 2/3 hyperdense,1/3 mixed
• Low density swirl sign –active bleeding with
unretracted clot
• Acute EDH with retracted clot = 60-90 HU
Unusual shape
Easily overlooked
Coronal, sagittal reformats key to diagnosis
Anterior middle cranial fossa
When fracture crosses sphenoparietal sinus
Virtually all have associated skull fractures – greater sphenoid wing/zygomaticomaxillary
Do not require surgery
1-2 cm maximum diameter
Vertex EDH
Uncommon
Linear &/or diastatic fracture
crosses superior sagittal sinus
Usually crosses midline
Clival EDH
Very rare
Linear fracture crosses basisphenoid
Lacerates clival venous plexus
Asymptomatic unless associated vascular or cranial nerve injury
Sagittal reformatted images key to diagnosis
Subdural Hematoma (SDH)
Defn – collection of blood between dura and arachnoid mater
Best diagnostic clue
CT – crescentic, extraaxial collection spread diffusely over affected hemisphere
Location
Supratentorial convexity> interhemispheric, peritentorial
Morphology
Crescent shaped, extraaxial
May cross sutures, not dural attachments
May extend along falx, tentorium, and anterior and middle fossa floors.
Chronic
Typically follows CSF density
Calcification can be seen along periphery of chronic collections, typically those
present for many years
Complications
Acute hydrocephalus – obstruction of aqueduct or 4th ventricle by clotted SAH
Delayed hydrocephalus – defective CSF resorption
vasospasm
Fisher scale
grade 1
no subarachnoid (SAH) or intraventricular haemorrhage (IVH) detected
incidence of symptomatic vasospasm: 21% 3
grade 2
diffuse thin (<1 mm) SAH
no clots
incidence of symptomatic vasospasm: 25%
grade 3
localized clots and/or layers of blood >1 mm in thickness
no IVH
incidence of symptomatic vasospasm: 37%
grade 4
diffuse or no SAH
ICH or IVH present
incidence of symptomatic vasospasm: 31%
Cerebral contusion
Brain surface injuries involving gray and continuous subcortical white matter.
Epidemiology – 2nd most common primary traumatic neuronal injury.
Presentation
Varies with severity, from mild confusion to cerebral dysfunction , seizures.
Location
Common
Anterior inferior frontal lobes
Anterior inferior temporal lobes
Less common
Parietal/occipital lobes
Posterior fossa
Location
GM-WM interface specially frontotemporal lobes.
Corpus callosum (3/4 splenium, posterior body)
Brainstem, specially dorsolateral midbrain & upper pons
Deep GM, internal/external capsule, tegmentum, fornix, corona radiata, cerebellar peduncles.
Presentation
Transient LOC, retrograde amnesia
LOC at moment of impact
Immediate coma typical
Greater impairment than with cerebral contusions, intracerebral hematoma,
extra axial hematomas
Symptoms are disproportionate to imaging findings.
Prognosis
Clinical abnormality may persist for months or longer – headache, memory and
cognitive impairment, personality change.
Severe DAI rarely causes death – 90% may remain in persistent vegetative state
Brainstem damage associated with immediate or early death
Neurocognitive deficits may persist in 100% of severe, 67% of moderate and 10 %
of mild TBI
NECT
Not very sensitive
Often normal (50-80%)
>30% with negative CT have positive MR.
Nonhemorrhagic : small , hypodense foci
Hemorrhagic : small hyperdense foci (20-50%)
Size – punctate to 15 mm
They typically become more evident over the first few days as oedema
develops around them. They may be associated with significant and
disproportionate cerebral swelling.
Diffuse axonal injury. CT scan demonstrates small hemorrhagic diffuse axonal injuries
in the deep white matter and corpus callosum.
Multiple hemorrhagic foci post MVA, involving the left thalamus and corpus callosum's splenium,
compatible with DAI.
Pneumocephalus
Presence of air within skull
Called pneumatocele if focal
Location –
Extracerebral : Epidural, subdural, subarachnoid
Intracerebral : Brain parenchyma, cerebral ventricles
Intravesicular : Arteries, veins, venous sinuses.
Etiology in head trauma
Mechanism – dural tear allows abnormal communication & introduction of
air
Blunt trauma produces skull &/or paranasal sinus fractures
Air cell involvement – Frontal> Ethmoid> Sphenoid > Mastoid.
Knife and other penetrating instruments.
When associated with a dural tear, they may be complicated by CSF
leakage, empyema, meningitis, or brain abscess. Most posttraumatic CSF
leaks cease spontaneously, and the responsible fractures may never be
visualized
Epidemiology
Present in 3% of all skull fractures
8% of paranasal sinus fractures
NECT
Very low density (-1000 HU)
Epidural
Do not move with change of head position
Subdural
Often forms air-fluid levels
Moves with change of head position.
Subarachnoid
Multifocal, non-confluent
Droplet-shaped, often within sulci
Intraventricular
Rarely in isolation
Intravascular
Most often venous, arterial rare usually fatal.
Tension Pneumocephalus
“Mount Fuji” sign
Subdural air separates/compresses frontal lobes
Causes widened interhemispheric space between frontal lobe tips, mimicking
silhouette of Mount Fuji
+- mass effect ( on frontal horns)