Radiology Presentation

1. CT EVALUATION OF
HEAD TRAUMA
Dr.A.K.M.Salauddin
Consultant ,Radiology & Imaging
Bangladesh

2.  leading cause of death in children and
young adults.
 Peak age – 15 -24 yrs
 Secondary peak > 50 years of age.
 Twice as often among males compared to
females.
 Generaly caused by motor vehicle
accidents, fall, assaults, violence and
sports & recreation
HEAD TRAUMAHEAD TRAUMA

3.  COMPUTED TOMOGRAPHY:-
 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
used:-
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

4. MRI
 sometimes valuable for following reasons:-
 Show small extra-axial blood collection in sub-dural and
epidural spaces.
 Show non-haemorrhagic paranchymal lesions diffuse axonal
injury,contusion.
 Higher sensitivity in the sub-acute and chronic stages of head
trauma.
 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

5. (A) PRIMARY TRAUMATIC LESION.
(a) skull fracture, scalp hematoma/ laceration
(b)primary neuronal injury –
1.diffuse axonal injury.
2.contusions-
 cortical contusions
 subcortical gray matter/deep cerebral injury
 primary brain stem injury.
(c)primary hemorrhages-
1.Extra-axial haemorrhage
 Epidural hematoma
 Subdural hematoma
 Subarachnoid haemorrhage.
2.Intracerebral haemorrhage
 Intracerebral hemorage
 Intraventri cular haemorrhage
HEAD TRAUMAHEAD TRAUMA

6. (A) PRIMARY TRAUMATIC LESION
(d) Primary vascular injuries-
Traumatic arterio – venous fistulae-common carotid Cavernous fistula.
Arterial pseudo-aneurysm – Location: branches of ACA+MCA Cavernous
portion of ICA.
Arterial dissection/laceration/transaction/occlusion.
Dural sinus laceration/thrombosis/.occlusion.
Cortical vein rupture/thrombosis.
(e) Traumatic pia – arachnoid injury -
post traumatic arachnoid cyst
Subdural hygroma
(f) other --- cranial nerve injury.
HEAD TRAUMAHEAD TRAUMA

7. (B) SECONDARY TRAUMATIC LESION
1) Cerrebral herniation
2) Traumatic ischemia , infartion
3) Diffuse cerebral oedema
4) Diffuse hypoxic injury
5) Secondary “delayed’’ hemorrhage
6) Secondary brain stem injury or
haemorrhage .
7) Others --e.g. fatty embolism , infection
HEAD TRAUMA

8.  SCALP LESION
 Scalp laceration
 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.
 SKULL FRACTURES:
 could be linear,depressed or diastatic and may involve cranial
vault or skull base.
 Skull radiographs and C.T are effective to demonstrate
fractures..
 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
bilateral.
HEAD TRAUMA

9.  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
nertves.
• 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.
HEAD TRAUMA

10. FRACTURE OF SKULL

11. FRACTURE OF SKULL

12.  EPIDURAL HEAMATOMA:
• 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.
HEAD TRAUMA

13.  EPIDURAL HEAMATOMA:.
* 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
deficit.
HEAD TRAUMA

14. EPIDURAL HEAMATOMA

15. SUBDURAL HEMATOMA:
• 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
extends diffusely.
• May cross suture lines but not dural
attachments.
HEAD TRAUMA

16.  SUBDURAL HEMATOMA:
• 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
laterally
• Posterior fossa SDHS are rare.
HEAD TRAUMA

17.  SUBDURAL HEMATOMA:
• C.T Shows as crescent shaped extra- axial
collection with a convex lateral and concave
medial border. Occasionally may be biconcave
shape.
• ACUTE SDHS- Homogenously hyperdense
- Up to 40%- mixed hyper/ hypodense
- due to unclotted blood
- serum extruded
during clot retraction
- C.S.F
- Rarely isodense- in patients with – coagulopathies
& severe anemia
HEAD TRAUMA

18.  SUBACUTE SDHS:-
• 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
6 hours.
 CHRONIC SDHS :- Typically low attenuation in
uncomplicated SDHS.
 Mixed density in 5% cases- due to recurrent haemorrage
 Enhancement following contrast
 Shows calcification in 0.3 to 2.7% cases
 SUBDURAL HYGROMA:-
 Hypodense collection equal to CSF density.
 More crescentic & bilateral
 At surgery show clear fluid and lack of a membrane.
HEAD TRAUMA

19. SUBDURAL HEMATOMA

20. SUBDURAL HEMATOMA

21. SUBARACHNOID HAEMORRAGE:-
• Due to damage to blood vessels on the pia-
arachnoid.
• Intra- parenchymal haematoma rupture into the
ventricular system may gain ascess to
Subarachnoid space via the foramina of magendie
and luschka.
• 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.
HEAD TRAUMA

22.  SUBARACHNOID HAEMORRAGE:
• 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.
HEAD TRAUMA

23. SUBARACHNOID HAEMORRAGE

24. 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
noted.noted.
HEAD TRAUMA

25. INTRAVENTRICULAR HAEMORRHAGE

26. INTRACEREBRAl HEMATOMA:
 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.
HEAD TRAUMA

27. INTRACEREBRAl HEMATOMA:
ACUTE HEMATOMA - < 3 DAYS
 C.T :-
 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
&
3rd
week).
 CECT : Peripheral rim enhancement at inner border
of perilesional lucency.
HEAD TRAUMA

28. INTRACEREBRA HEMATOMA:
 CHRONIC HEMATOMA : > 14 DAYS
C.T findings
 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 )
HEAD TRAUMA

29. INTRACEREBRAl HEMATOMA

30. 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
HEAD TRAUMA

31. 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.
HEAD TRAUMA

32. DIFFUSE AXONAL INJURY:-
 C.T – Findings
- Early imaging may be subtle or normal .
- Foci of decreased density.
- May show some degrees of cerebral
swelling.
- May show small focal hemorrhage or small
petechial haemorrhage particularly at
gray-white junction and corpus callosum.
- May show extensive injury.
HEAD TRAUMA

33. DIFFUSE AXONAL INJURY

34. CONTUSION:-
 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-
hemorrhagic.
 MECHANISM :- Linear acceleration –
deceleration forces / penetrating trauma /
direct impaction.
HEAD TRAUMA

35. CONTUSION:-
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.
HEAD TRAUMA

36. CONTUSION:-
 C.T
- 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
over time.
- Some degree of contrast enhancement.
- Isodense to brain after 2 – 3 weeks.
HEAD TRAUMA

37. CONTUSION

38. DEEP CEREBRAL AND BRAIN STEM INJURY
 Less common than DAI and cortical contusions.
 Represent 5% to 10% of primary traumatic brain
injuries.
 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.
HEAD TRAUMA

39. DEEP CEREBRAl & BRAIN STEM INJURY

40. PRIMARY VASCULAR INJURIES
1.Traumatic arterio – venous fistulae-common
carotid Cavernous fistula.
2. Arterial pseudo-aneurysm – Location: branches of
ACA+MCA
Cavernous portion of ICA.
3. Arterial dissection/laceration/
transaction/occlusion.
4. Dural sinus laceration/ thrombosis / occlusion.
5. Cortical vein rupture / thrombosis.
HEAD TRAUMA

41. SECONDARY TRAUMATIC LESION
1) Cerrebral herniation
2) Traumatic ischemia , infartion
3) Diffuse cerebral oedema
4) Diffuse hypoxic injury
5) Secondary “delayed’’ hemorrhage
6) Secondary brain stem injury or
haemorrhage .
7) Others --e.g. fatty embolism , infection
HEAD TRAUMA

42. CEREBRAL HERNIATIONS
 subfalcine
 transtentorial – desending
ascending
 translar ( trans sphenoidal ) - desending
ascending
 tonsilar
 miscellaneous - ( e.g – trans dural / trans cranial )
( Most common subfalcine & transtentorial
herniation)
HEAD TRAUMA

43. CEREBRAL HERNIATIONS

44. SECONDARY TRAUMATIC LESION
 Infraction - ipsilateral ACA
compressed against flax.
 Extra cranial herniation

45. HEAD TRAUMA
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.
7) Hydrocephalus.
8) Atrophy.
9) Subdural Hygroma.
10) Post traumatic abscess.

46. CONCLUSION :-
• C.T is important modality for evaluation of
an emergency patient with cranio-cerebral
trauma.
• Early & accurate ct evaluation cause
better patients outcomes with a decrease
morbidity & mortality statics.
& Decrease in trauma related medical
costs.
HEAD TRAUMA

47. THANK YOU