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Ct head
1. CT Head in Primary Effects
of CNS Trauma
Dr. Manmohan Shrestha
2. Head Injury
Neurotrauma is the common cause of death and disability
worldwide.
Of all head injured patient-
10% sustain fatal brain injury.
5-10% neurotrauma survivors have permanent serious neurologic deficits
20-40% have moderate disability.
A number have minimal brain trauma
3. Etiology
Falls
Common in children and elderly
Gunshot wounds
Most common in adolescents and young adults
Motor vehicle and auto-pedestrian collisions
All ages
4. Classification of Head Trauma
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
6. MDCT
Workhorse of brain trauma imaging
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.
7. Who and when to image?
Major and widely used appropriateness criteria for imaging acute head
trauma have been published:
I. The American College of Radiology appropriateness criteria
II. New Orleans Criteria
III. The Canadian Head CT Rule
8. The American College of Radiology
appropriateness criteria
NECT in mild closed head injury with the presence of a focal neurologic deficit
and/or other risk factors
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
deterioration, regardless of initial imaging findings.
9. New Orleans Criteria in Minor Head Injury
CT indicated if GCS =15 Plus any of the following-
Headache
Vomiting
Patient>60 yrs.
Intoxication (drugs, alcohol)
Anterograde amnesia
Seizure
10. 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
11. High risk factors
GCS <15 two hours post injury
suspected open skull fracture
sign of base of skull fracture
vomiting more than twice
age >65 years
Medium risk factors
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
Interpretation-
• Risk factors – YES – CT Head required
• Risk factors – NO – CT Head not required
12. Skull fractures
Usually occur following significant head injury and may herald
underlying neurological pathology.
Objective – to depict the location & extent of fractures and
identify associated injuries to vital structures.
Aids in surgical planning and in the prevention of
complication such as CSF leak.
14. Presentation
head injury following impact trauma, e.g. fall, RTC
symptoms associated with underlying injury
Extradural hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage
there may be an associated base of skull injury
CSF rhinorrhea
Battle’s sign
Raccoon eyes
15. 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.
16. Racoon eyes/Panda eyes sign
Periorbital ecchymosis
Sign of
Basal skull fracture
Subgaleal hematoma
Craniotomy that ruptured the meninges
17. Skull Base Fractures
Anterior
Frequently associated with sinonasal
cavity &/or orbital injuries
Majority have facial fractures
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.
possibility of endangerment of
nearby structures including:
Cranial nerves
Internal carotid artery
Cavernous sinus
18.
19. 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.
20. Le Fort I – Floating palate
Le Fort II – Floating maxilla
Le Fort III – Floating face
23. Skull fractures
A. Linear – sharply marginated lucent lines, low impact injury
B. Depressed – fragments imploded inwardly,
High impact injury.
C. Elevated – elevated rotated skull segment
D. Basilar
E. Diastatic
Usually affect children <3 yrs. old
Follows a cranial suture and causes it to separate
Usually accompanied by linear skull fracture
F. “Growing skull fracture”
Difficult in acute stage
Progressively widening
Lucent lesion with rounded, scalloped margins
CSF and soft tissue trapped within expanding fracture.
26. Ping pong/ Pond skull fracture
called a 'ping pong' fracture because it resembles a ping
pong ball that has been indented inwards with a finger.
Depressed skull fracture of the infant skull caused by inner
buckling of the calvarium.
Fracture line is not visualized radiologically.
It is seen in newborns because of the soft and resilient nature
of their bones (like greenstick fracture of long bones)
Periosteum and dura are intact
Pathology – birth trauma or postnatal blunt traumas
29. Growing skull fracture/Leptomeningeal cyst
Trauma 1 month ago. Recent right parietal progressive
scalp swelling
Difficult in acute stage
Progressively widening
Lucent lesion with rounded,
scalloped margins
CSF and soft tissue trapped within
expanding fracture.
occur secondary to skull fractures
causing dural tears, allowing
the leptomeninges and/or cerebral
parenchyma to herniate into it.
• Rt. parietal widened linear fracture.
• Area of encephalomalacia under the fracture
• Rt. parietal small subgaleal small cyst of CSF density.
30. Temporal bone fractures
Types (acc. to long. axis of petrous temporal bone)
Longitudinal
Transverse
Mixed
Complications
facial and other cranial nerve injuries
vertigo and hearing loss
cerebrospinal fluid (CSF) leak
CSF fistula
meningitis
post-traumatic cholesteatoma
Ossicular chain dislocation.
32. Skull Fractures !!
When to worry ??
Overlies a dural venous sinus
Overlies the middle meningeal artery
Overlies “eloquent cortex” ( Sensory-Motor cortex)
Depressed > “table-width”
Open/compound
Traverses Internal carotid artery canal
Temporal bone fractures.
33. Missile and penetrating injury
Cranial trauma from high-velocity projectile (typically gunshot wound) or with
sharp object.
34. General features
Best diagnostic clue
Single or multiple intracranial foreign
bodies, missile tract
Pneumocephalus, entry +- exit wound.
Size
Small linear tract if small caliber and low
velocity
Large linear tract if large caliber and
high velocity
Skull fractures
Intracranial hemorrhage
EDH, SDH,SAH
Haemorrhagic tract
Intracerebral or intraventricular
hemorrhage
Vascular injury
Pseudoaneurysm, dissection, AV fistula
CSF leak
Secondary effects
Ischaemia and infarction
Brain herniation
35. CT findings
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
39. Subgaleal hematoma
Under aponeurosis (galea) of occipitofrontalis muscle.
External to periosteum
Not limited by sutures
Can be extensive, even life threatening
42. 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.
43. 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
44. Homogenous hyperdense biconvex epidural
Hematoma in in right temporal convexity.
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
46. Figure - Delayed epidural hematoma. A, Acute subdural hematoma over the
left parietal convexity. Note the small hemorrhagic contusion in the left parietal
lobe. B, The patient has undergone craniectomy and drainage of the subdural
hematoma. Note the new posterior parieto-occipital epidural hematoma.
Posterior fossa EDH – delayed
symptom onset, slow expansion,
increased mortality
47. Q) Why EDH do not cross the sagittal suture lines ?
Because the right halve is separated from the left halve by a deep fold in the outermost
membrane enveloping the brain, the Dura mater, called the Falx Cerebri which runs
along the Sagittal suture which at the base is affixed to the skull so can't be crossed
from right to left or the other way around:
49. 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
50. Vertex EDH
Uncommon
Linear &/or diastatic fracture
crosses superior sagittal sinus
Usually crosses midline
51. 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
52. 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.
Etiology
Tearing of bridging cortical veins
Age of SDH
Hyperacute – upto 12 hours
Acute – 12-48 hours
Subacute – 3 days to 3 weeks
Chronic – 3 weeks to months
Poor prognosis
Surgery required if thickness>10mm, midline shift
53. CT Findings
Hyperacute
Heterogenous or hypodense
Acute
60% homogenously hyperdense
40% mixed hyper-, hypodense with active bleeding (Swirl sign)
Subacute
Iso to hypodense
GM-WM junction displaced medially
Progression from hyper to iso to hypodense over nearly 3 weeks.
Recurrent hemorrhage results in mixed density.
Chronic
Typically follows CSF density
Calcification can be seen along periphery of chronic collections, typically those
present for many years
** If no new hemorrhage, density decreases by +- 1.5 HU
56. Unilateral isodense SDH & Importance of window width
If isodense SDH suspected, use wide window.
If unilateral isodense, look for –
unexplained mass effect
Ventricular or pineal displacement
Absence of visible sulci on the affected side
57. Bilateral isodense SDH
Squeezing together of the frontal horns to give a “rabbit’s ears” appearance &
effacement of the basal cisterns.
Appears as pseudosubarachnoid hemorrhage
Apparent increased attenuation (though HU remains 30-40), within the basal cisterns which
simulates SAH.
58. CT Comma Sign
characteristic sign seen in head trauma.
It is the presence of concurrent epidural and subdural hematomas, which gives the
characteristic appearance of this sign as a "comma" shape.
60. Traumatic SAH (tSAH)
Blood contained between pia & arachnoid membranes
Epidemiology – 33% with moderate TBI, 60% with severe TBI.
Best diagnostic clue – High density on NECT
Location
Focal –adjacent to contusion, EDH, SDH, fracture, laceration
Sylvian fissure, inferior frontal subarachnoid spaces most common
Diffuse – in subarachnoid space &/or basal cisterns
Pathology – bleeding from cortical arteries/veins.
Associated abnormalities
Contusions
EDH
SDH
Diffuse axonal injury
61. Poor prognosis
Amount of tSAH on initial CT correlates with delayed ischemia
Associated with moderate to severe TBI results in increased morbidity & mortality.
Complications
Acute hydrocephalus – obstruction of aqueduct or 4th ventricle by clotted SAH
Delayed hydrocephalus – defective CSF resorption
vasospasm
62. 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%
63.
64.
65. 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.
66. Location
Common
Anterior inferior frontal lobes
Anterior inferior temporal lobes
Less common
Parietal/occipital lobes
Posterior fossa
Injury at contrecoup site is
usually more severe
67. Morphology
Early
Patchy ill-defined superficial foci of punctate or linear
hemorrhage along gyral crests.
24-48 hours
Existing lesions enlarge & become more hemorrhagic,
new lesions may appear.
Chronic
Encephalomalacia with volume loss
Multiple, bilateral lesions in 90% of cases.
68. CT findings
Early
Patchy, ill-defined, low-density edema with small foci of
hyperdense hemorrhage
24-48 hours
Edema, hemorrhage and mass effect often increase
New foci of edema and hemorrhage may occur.
Chronic
Become isodense (at 2 weeks ) then hypodense
Encephalomalacia with volume loss (at 1 month)
Repeat CT recommended if initial exam negative but symptoms persist for
24-48 hours.
Enhancement occurs at acute & subacute stage in areas of
blood-brain-barrier breakdown
74. Diffuse Axonal Injury (DAI)
Traumatic axonal stretch injury.
Most common primary traumatic neuronal injury
Etiology
caused by rotational forces that produce shear strain, resulting in tissue damage. Shear strain is
maximum at the junction of tissues with different densities, such as the gray–white junction
Best diagnostic clue
Microbleeds
Punctate lesions at corticomedullary junction, corpus callosum, deep gray matter, brainstem.
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.
75. 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
76. 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.
77. Diffuse axonal injury. CT scan demonstrates small hemorrhagic diffuse axonal injuries
in the deep white matter and corpus callosum.
78. Multiple hemorrhagic foci post MVA, involving the left thalamus and corpus callosum's splenium,
compatible with DAI.
79. 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.
80. 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
81. 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.
82.
83. 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)