review of traumatic brain injery

1. DR: MUNIR SUWALEM

2. TBI is caused by a bump, blow or jolt to the
head or a penetrating head injury that
disrupts the normal function of the brain.

3.  There are approximately 1.5 million people in
the U.S. who suffer from a traumatic brain
injury each year. 50,000 people die from TBI
each year and 85,000 people suffer long
term disabilities.

4. The top causes of TBI are:
 MVA
 Firearms or explosions
 falls
 fighting

6. Mechanisms of Injury
 . Open Head Injury
Results from bullet wounds, etc.
Largely focal damage
Penetration of the skull
Effects can be just as serious as closed brain injury
 . Closed Head Injury
Resulting from a slip and fall, motor vehicle crashes,
etc.
Focal damage and diffuse damage to axons
Effects tend to be broad (diffuse)
No penetration to the skull
 . Deceleration Injuries (Diffuse Axonal Injury)

7. EEppiidduurraall hhaaeemmaattoommaa
 EDH occurs in the potential
space between the dura and
the cranium
 EDH results from interruption
of dural vessels, including
branches of the middle
meningeal arteries(most
common), veins, dural venous
sinuses, and skull vessels..

8.  As many as 10-20% of all patients with
head injuries are estimated to have
EDH.
 Approximately 17% of previously
conscious patients and have EDH,
deteriorate into coma .

9. The most commonly region involved with
EDH is the temporal region (70-80%)
because the temporal bone is relatively thin
and the middle meningeal artery is close to
the inner table of the skull.
The incidence of EDH in the temporal region
is lower in pediatric patients because the
middle meningeal artery has not yet formed

10.  Commonly unilateral and associated with
skull fracture .
 CT sign include a biconvex hyperdense
elliptical collection with sharply defined edge
( mixed density suggests active bleeding )
 The haematoma dose not cross suture lines
except at falx which may separate it.

13. SSuubbdduurraall hhaaeemmaattoommaa
 Occurs in the subdural space
(potential space b/w dura and
arachnoid membranes)
 85% is unilateral
 Caused mainly by traumatic
tearing of bridging veins in the
subdural space
 The skull fracture +/-

14.  Acute SDH present within 24 hours of injury
with decreased level of consciousness or
decline mental status
 On CT a crescent fluid collection b/w the brain
and inner skull
 Crosses the suture lines but not dural
reflections

15.  The appearance of SDHs on CT varies with
clot age and organization.
 Hyper-acute(first hour): appear relatively iso-dense
to the adjacent cortex.
 Acute: appear as homogenous hyper-dense
(HU more 50-60 ).
 Sub-acute (3-21 days) the density droping to
(30 HU) ; iso-dense.
 Chronic ( more than 4 wks ): becomes hypo-dense
and reach to (0 HU)

17. SSuubbaarraacchhnnooiidd
hheemmoorrrrhhaaggee
 SAH refers to extravasation of blood into
the space b/w the pia and arachniod
membranes.
 Rapidly progresses to coma.
 Its complications include
hydrocephalus,cerbral vasospasm
leading to infarction and transtentorial
herniation secondary to raised ICP.

18.  Non cotrast CT is
sensitive within 4-5
hrs , appears as high
density haemorrhage
in the corticlal
sulci ,basal cisterns,
sylvian fissures
,superior cerebrallar
cisterns and in the
vintricles.

20. BBrraaiinn ccoonnttuussiioonn
 Brain Contusions are formed in 2
ways :
Direct trauma and
acceleration/deceleration injury.
 Occur often at the inferior and
polar surface of the frontal and
temporal lobes .
 Contusions develop in surface of
grey matter tapering into white
matter.

21.  Non-contrast CT usefull in the early post
traumatic period , but the MR is best
modality for demonstrating of edema and
contusion distribution

23. Diffuse aaxxoonnaall iinnjjuurryy
 High speed injury with streching or shearing
of brain tissue.
 Associated with LOC 50%, and persistent
vegetative state.
 Mortatility 30-40% , good outcome 20-30%

25.  DAI typically consists of several
focal white-grey matter interface
lesions measuring 1-15mm ,as
well as in the corpus callosum
and brainstem is characteristic
finding in the acute setting.

26.  50-80% demonstrate a normal CT scan upon
presentation, and delayed CT may be helpful
in demonstrating edema or spots of
hemorrhages.
 MRI is better to demonstrating the small
petechial haemorrhage where not observed
through CT scan, but the because the MR is
often out of order so the CT is best.