TRAUMATIC BRAIN INJURY

Indarwati Setyaningsih

Neurology Dept, Faculty of Medicine

Gadjah Mada university
RS Dr Sardjito

Yogyakarta
 TRAUMATIC BRAIN INJURY

a mechanical trauma to the head , directly or indirectly

that causes neurological dysfunction  a physical
impairment , cognitive impairment, or psychosocial
dysfunction  temporary or permanent.
 CLASSIFICATION

The classification consists of :

1. Pathologic
• Cerebral comotion
• Cerebral contusion
• Cerebral laceration
2. Location
• Diffus lesion
• Brain Vasculer damages
• Focal lesion
Cont ...
CLASSIFICATION

• Focal lesion
o Cerebral contusion and laceration
o Intracranial hematoma
• Extradural hematoma (epidural
hematoma)
• Subdural hematoma
• Intraparenchym hematoma
o Subarachnoid hematoma
o Intracerebral hematoma
o Intracerebellar hematoma
 Concussion Cerebral
State of ↓ consciousness that occurred right after
the injury occurs , temporarily (up to within a few
hours)

Commoio Cerebral
↓ consciousness < 10 minutes due to head injury, no
neurological abnormalities.

Concussion & comosio  mild head injury clinically,

because of GCS score 13-15, loss of consciousness
< 10 minutes, and no neurological abnormalities.
 Cerebral Contusion

Injury the brain tissue that is heavier than concussion,

with characteristics of nerve cells and axonal damage,
with capillary bleeding & edema of brain tissue.
Piameter still intact
 Diffuse Axonal Injury

• Totally brain damage, coma since the

injury occurred, but insisted there is no
lesions on the cranial CT.
• Damage to blood vessels &
parenchyma diffuse in anatomic pathology.
• Edema (+) CT with subtle signs of diffuse
•  diffuse axonal injury & diffuse axonal injury, including
haemorrhage in the corpus
vascular injury callosum and at the interface
• Prognosis is generally poor of grey white matter.
 Acute Extradural Haematoma
(Epidural hematoma)

- Incidence  2 - 40 years old  prone to extradural

haematoma because of the less adhesive nature of the
dura to the skull  1.5% of all head injuries, a male
predominance.
- Most often related to a fractured skull with associated
bleeding from the middle meningeal artery.
- 80 %  a lucid interval followed by rapid deterioration
of consciousness.
Cont ...
Acute Extradural Haematoma
(Epidural hematoma)

Clinical manifestation :
• Lucid interval
• Decrease of consciousness
• Late hemiparese kontralateral lesion
• Pupil anisokor
• Babinsky reflek kontralateral lesion
• Temporal fracture
 Cont ...
Acute Extradural Haematoma
(Epidural hematoma)

- 60 %  a dilated pupil, ipsilateral to

the haematoma in 89% of cases.
- Appearances on CT  bikonveks.
- Vol > 150 ml  a poor prognosis.
- Vol estimation  0.5 X height X
length X depth was moderately
reliable.

Right Frontal Acute

Extradural Haematoma
Cont ...
Acute Extradural Haematoma
(Epidural hematoma)

- Decompressive surgery < 4 h of the injury, although this

target was achieved in only 32% of cases in a recent
series.
- Pupillary size and reaction is a well-established
prognostic indicator, although patients with fixed dilated
pupils of short duration can make a satisfactory recovery.
 Subdural Haematoma

• cause by the tearing of bridging vein in durameter –

arachnoid space (subdural space)
• Classification based on interval lucid :
• Acute  0- 5 days
• Subakut  5 days – weeks
• Kronik  > 3 months
 Acute Subdural Haematoma

• >> male , > 80%  coma (GCS less than 8).

• CT  Crescent-shaped appearance
• Poor prognostic > 60 yo, radiological signs  haematoma
> 10 mm, & midline shift > 20 mm.
• Operation management within 3–4
h of injury significantly ↓ mortality.
Multivariate analysis  a delay in
time is directly related to outcome,so
early operation should be initiated
when appropriate.

A Fatal Right-sided Acute

Subdural Haematoma
 Chronic Subdural Haematoma

• Incidence of 5/100 000/year (up to 58/100 000/year in

> 70 yo, chronic subdural  haematoma is common.
• Risk factors include anticoagulation treatment, alcohol
abuse, seizures, and CSF shunts.
• A traumatic history  half the cases.
• Presentation is usually insidious and comprises any of
the following: headache, confusion, slurred speech, or
stroke-like symptoms.
 Chronic Subdural Haematoma

• CTshows an isodense or hypodense

subdural collection
• Although treatment is simple,morbidity
& mortality are serious and a recent study
 reduced survival for at least one year
after treatment
chronic subdural
haematoma in an
elderly patient,
increasingly confused
over several weeks
 Intracerebral Haematoma (ICH)

• Mortality for traumatic

intracranial haematoma is
high; 75% & up to 47% in
> 65 yo
• Temporal or bilateral
haematomas, associated
with an acute subdural
haematoma  worse Computed tomogram
CT  presence of a left- outcome. showing bifrontal
sided ICH & parietal contusions in a patient
fracture following an who was assaulted.
assault
 Traumatic Subarachnoid
Hemorrhage

• Most common CT finding in

moderate to severe TBI
• If isolated head injury, may present
with headache, photophobia and
meningismus
• Nimodipine reduces death and
disability by 55%
 Head Injury-Normal Physiology

• ↑ in the volume of any of those intracranial

contents  ↑ intracranial pressure.
1. The brain can swell (edema)
2. Excess blood can accumulate due to
hemorrhage
3. Cerebrospinal fluid can accumulate due to
blockage of outflow
 Head Injury-Pathophysiology

 Primary injury
• Irreversible cellular injury as a direct result of
the injury
• Prevent the event
 Secondary injury
• Damage to cells that are not initially injured
• Occurs hours to weeks after injury
• Prevent hypoxia and ischemia
Cont...
Head Injury-Pathophysiology

 TBI is a process, not an event!

Secondary injury can be more damaging than primary
injury

 4 Main Mechanisms of Brain Injury :

1. Brain Contusion
2. Increased intracranial pressure ( ICP)
3. Diffuse Axonal Injury
4. Ischemic and/or hemorrhagic
 Mechanism 1: Brain Contusion

• A brain contusion is defined by cell death

accompanied by hemorrhage (leakage of
blood)
• The soft brain tissue is vulnerable to
contusion in head trauma
• Often occurs at a site distant from the point of
impact.
 Mechanism 2 : ↑ ICP

• The intracranial vault is a fixed volume  Bone

does not expand!
• There is only one way out of the intracranial
vault --> the foramen magnum
• When the brain is squeezed through the FOM
(herniation)  brainstem is compressed,  †
 Mechanism 3: Diffuse Axonal Injury

• Occurs in up to 1/2 of traumatic brain injuries

• Is a diffuse form of injury, meaning that damage
occurs over a more widespread area than in
focal brain injury
• Involves the shearing of axons in the white
matter tracts
 Severe TBI - Prognosis

• The Impact of ICP: ICP > 20 mmHg during

hospitalization  47% mortality vs. patients with
mean ICP < 20 mmHg  17% mortality (p < 0.001)
• 17%  seizures during the 2-year post-trauma period
• The length of time in a coma correlates  post-
traumatic amnesia & recovery times
 Head Injury-Initial Evaluation
and Management

 Prevent Secondary Brain Injury

• Hypoxemia
• Hypotension
• Anemia
• Hyperglycemia
• Evacuation of mass
 Spectrum of Traumatic Brain Injury

Mild TBI
GCS 14-15
80% of all TBI
• Low Risk
GCS 15 and no LOC, amnesia, vomiting
Less than 0.1% risk of hematoma requiring evacuation
• Medium Risk
GCS 15 and LOC, amnesia, vomiting
1-3% risk of hematoma requiring evacuation
CT should be done in medium risk mild TBI
 Spectrum of Traumatic Brain Injury

Mild TBI
• High Risk
GCS 14-15
Neurologic deficits
Up to 10% risk of hematoma requiring evacuation
Anyone with coagulopathy, drug/alcohol consumption,
epilepsy, age >60 and previous neurosurgery
• Disposition
No CT indicated or negative CT with GCS 15-Home
GCS 14 and negative CT-Observation admit
 Spectrum of Traumatic Brain Injury

Moderate TBI
• GCS 9-13 • 50% morbidity
• 10% of all TBI • 40% positive CT
• <20% mortality • 8% NS intervention

Severe TBI
• <10 make moderate
• GCS <9
recovery
• 10% of all TBI
• 40% mortality
 Intracerebral Pressure

Mannitol
• Osmotic agent
• Effects ICP, CBF, CPP and brain metabolism
• Free radical scavenger
• Reduces ICP within 30 minutes, last 6-8
hours
• Volume expansion, reduces hypotension
• Dosage :0.25-1 gm/kg bolus
 Specific Head Injuries

Skull Fractures
• Basilar Fracture
Most common-petrous portion of temporal bone, the EAC & TM
Dural tear
• CSF otorrhea • Hemotympanum
• CSF rhinorrhea • Vertigo
• Battle Sign • Hearing loss
• Raccoon Sign • Seventh nerve palsy
CSF testing
• Ring sign, glucose or CSF transferrin
Should be started on prophylactic antibiotics
• Ceftriaxone 1-2 gm
 Complications-Long Term
Sequela

• Seizure Disorder
2% Early post-traumatic incidence
Increased to 30% in children, alcoholics & with ICH
Prophylactic antiepileptics reduce early occurrence
 Use not supported by the literature
• Concussion
- Vertigo - Nausea
- Dizziness - Headache -
Vomiting - Photophobia
- Cognitive/Memory dysfunction
 Complications-Long Term
Sequela

• Concussion
Up to 80% may have symptoms at 3 months
15% may have symptoms at 1 year
Persistence of these symptoms is termed Postconcussive
Syndrome
85-90% recover after 1 year
Risk factors:
-Female
- Litigation
- Low socioeconomic status
 Level of Consciousnes Based on GCS

Category GCS Clinical Manifestation CCT

Minimal 15 Unconscious (-), Normal
neurological deficit (-)
Mild 13-15 Unconscious <10 ‘, Normal
Neurological deficit (-)
Moderate 9-12 Unconscious >10 ‘ - 6 h, Abnormal
neurological deficit (+)
Severe 3-8 Unconscious > 6 h, Abnormal
neurological deficit (+)

Note : 1. classification for triage

2. if abnormalitas CCT was intracranial hematoma 
severe brain trauma
 Surgical Indication

1. Epidural hematome
a. >40cc + midline shift , brainstem normal
b. >30cc fossa posterior + pressure sign to brainstem (+)
or hydrocepalus, brainstem normal
c. EDH progresive
d. EDH minimal with LOC not indication

Perdossi, 2006
2. Subdural hematome
a. SDH >40cc/5mm , GCS>6, brainstem normal
b. SDH minimal and LOC not indication
c. SDH + edema cerebral/contusion with midline shift
, brainstem normal

Perdossi, 2006
3. Intracerebral hematoma post trauma
a. Progresive of LOC
b. cushing refleks (+)
c. Deterioration of focal deficit
4. Impresi fracture > 1 diploe
5. Fracture of basis cranium & cerebral laseration
6. Open frakture of basis cranium
7. Edema cerebral massive with ↑ ICP
Perdossi, 2006
 Outcome and prognosis

• Minor injuries (GCS 13–15), 47% have moderate to severe

disabilities at 12 months and a third do not return to work.

• Moderate injuries (GCS 9–12), 45% have moderate to severe

disabilities, &

• 48% of those severely injured have moderate to severe

disabilities, only 14% have a good outcome at 12 months.
 POST
CONCUSSIONAL SYNDROME

CONFIDENTIAL 38
CONFIDENTIAL 39
SPINAL CORD iNJURY
 • extreme vibration of the cord
Transient concussion • temporary loss of function 24-48 hrs
• No neuropathologic changes

 a bruising  bleeding, edema, and

possible necrosis from the edematous
compression
Contusion
 The neurological involvement  severity
of contusion and necrosis

Type Of Laceration
SCI

Compression of cord substance

Complete transection of the cord

 (Young, 2002)
Location and Severity of Lesion

Complete and Incomplete Lesion

Characteristics Complete Lesion Incomplete Lesion

Motoric (-) below the lesion often (+)

Protopatic (pain, temperature) (-) below the lesion often (+)

Propioseptic (joint position, vibration) (-) below the lesion often (+)

Sacral sparing Negative Positive

Spine X-Ray Often with fracture, Normal
luxation or listesis
MRI (Ramon, 1997, 55 patients with Hemorrhage (54%), Edema (62%),
SCI, 28 complete and 27 incomplete) Compression (25%), Contusion (26%),
Contusion (11%) Normal (15%)
 Medical
Management
of SCI

Immediate acute pain

Management
Improper Always Assume in back or neck radiate
handling SCI

damage and loss of Immobilize

functioning Prevent flexion,
rotation or extension
Avoid twisting patient

Aim: preventing further injury and observing for progression of

Neurological deficits (A-B-Cs)
 Algorithm of X Ray Examination
Conscious no Specialist Evaluation
and Cooperative
yes
Neurological no
Intact X Ray:
•Cervical AP/lat/ Continue
yes SC ?
odontoid/obliq Indication
yes •Th &L/S AP/lat
Spinal Pain

no
yes
SC Abnormality
Immobilisation

no
SC (-)
 Breathing
C1
partial to complete diaphragmatic paralysis (C3-5)
Above C5
Below C5 Allow full diaphragmatic movement, but intercostal
muscles (T1) and abdominal muscles (T12) are
affected.
Th1

Below T12 Airway Compromise

L1
 Circulation
Cardiac output

external or internal hemorrhage neurogenic shock

abdominal pain muscular rigidity signs of shock

(may be masked  sensory-motor deficits)

absence of urine and/or classic

signs of shock (decreased BP and
increased HR)
Evaluation of Circulation
Access
circulation

Pulse no Perform
present ? CPR
yes
Pulse no 0.5-1.0 mg
> 40 bpm ? Atropine iv
yes
Administer volume
SBP >90 no
Trendelenburg position
mmHg ?
Moderate MAST trousers
yes
MAST : military anti-shock trousers
transport
Spinal Cord Fixation

X-ray C1-C7
Spinal Cord Fixation (cont’)

C1
Segmen yg
paling mudah
cedera

C7
 Spinal Cord Fixation (cont’)

Cause of Tetraplegia Minimal moving of Cervical spine

“in-line” position with stabilization of neck
 Management of SCI

Prevention of Resuscitation Steroid

Secondary Trauma and Electrolite Monitoring

CVP Neurological Deficit in < 3 hours

30mg/Kg bw in 10 – 15’
5,4mg/Kgbw/ hrs – 23hrs
Urine Catheter
If Deficit 3-8 hours following -47 hrs

X –Ray
NGT