Head Injury

Scalp injury
Skull injury
Meningeal injury
Traumatic Brain Injury

WHAT
IS THE DEFINITION OF A
TRAUMATIC BRAIN INJURY
(TBI)?

Congenital brain injury

Pre-birth

During birth

Acquired Brain Injury

After birth process

Traumatic Brain Injury

(external physical force)
Closed
Head
Injury

Non-traumatic
Brain Injury
Open Head
Injury

an acquired injury to the brain

caused by an external physical force
resulting in total or partial functional
disability or psychosocial impairment
or both that adversely affects a
childs educational performance.

Stroke
Brain Infection
Tumor
Anoxia
Exposure to Toxic Substances

Important note:
Brain injuries
that result from either an
external
or internal force
may have similar effects.

Epidemic in Indonesia
Major cause of death and permanent
disability
70% of all road fatalities
50% of trauma death
10-20% of head injury: death on arrival
Degree
10% mild head injury
10% moderate head injury
80% severe head injury

Severity of primary injury

Intracranial complications
Hypoxaemia
Hypercarbia
Hypotension
Anaemia
Multiple injuries, proportional to Injury
Severity Score (ISS)
Age

Prolonged prehospital time

Admission to inappropriate hospital
Delayed or inappropriate interhospital
transfer/retrieval
Delay in definitive surgical treatment

Traumatic Brain Injury

Blunt(Closed)
Explosion
Blast

Fall

Penetrating
GSW
Stab
Fragment

Motor vehicle crashes (MVC)

Injury forces applied to particular anatomical areas produce a

pattern of injury for the individual, e.g.
Acceleration/deceleration
Appiled to the entire head, evident as disordered
consciousness from the time of impact resulting from
concussion, often with diffuse axonal injury and/or cerebral
contusions (coup or contreceup)
Local impact
Coup injuries to scalp, skull, meninges, brain
Penetrating
Pathway of injury velocity and nature of projectile
Crush injury
Scalp, skull and cranial nerve injuries

Coup-Contra Coup

Diffuse Axonal Injury

Rotational forces on
the brain cause the
stretching and snapping
of axons

Axon

1.
2.
3.
4.

Headache
Vomiting
Papilloedema occur in chronic condition
Cushing response
Bradicardia
Hipertension
Alteration of ventilatory pattern

5. Herniation
- ipsilateral dilated pupil
Uncal
- contralateral hemiparesis
- ipsilateral hemiparesis
(Kernohans notch phenomenom)
Central - rostrocaudal sign
Subfalcine
Tonsiller herniation

Mild GCS 14-15

Patient typically mildly lethargic, disoriented
Moderate GCS 9-13
Patient typically sleepy or obtunded, able to follow
commands with arousal.
Confused.
Severe GCS 3-8
Patient comatose, unable to follow command or
perform purposeful motor activity.
Range of motor activity: localizes, withdraws,
decorticate posturing, decerebrate posturing, nil.

Severity

GCS

LOC

PTA

Mild
Moderate

1415

<20 min-1 hr

<24 hr

913

1 24 hrs.

> 24 hrs.
- <7days

Severe

38

>24 hrs.

>7 days

GCS = Glasgow Coma Scale

LOC = Loss of consciousness
PTA = Posttraumatic amnesia

Primary Injury: Function of energy transmitted to brain

Very little can be done by health care providers to
influence
Cerebral concussion, contusion and degeneration, Diffuse
Axonal Injury (DAI)

Secondary Injury: Function of damage to brain from

systemic physiology
Systemic
Hypotension: Acute and easily treatable
Hypoxia: Acute and easily treatable
Fever and Electrolyte Imbalances
Seizures
Intracranial Pressure Can Lead to Herniation

Primary
Scalp
contusion, abrasion, laceration

Skull fracture
open, closed (note-compound base of skull fracture
without a scalp laceration), linier, depressed

Meningeal injury
dural tear

Brain injury
concussion
contussion
diffuse axonal
focal contusion
laceration and penetration

Secondary
Intracranial haemorrhage
Cerebral swelling
cerebral hypoxia
CSF leakage and pneumocephalus
methabolic disorders
infection
epilepsy

Dorsolateral prefrontal cortex

(executive function, including sustained and
complex attention, memory retrieval, abstraction,
judgement, insight, problem solving)

Orbitofrontal cortex
(emotional and social responding)

Anterior temporal cortex

(memory retrieval, sensory-limbic integration)

Amygdala (emotional learning and

conditioning, including fear/anxiety)

Ventral brainstem

Hippocampal-Entorhinal
Complex (declarative
memory)

(arousal, ascending activation of

diencephalic, subcortical, and
cortical structures)

Viewed on coronal MRI

Postconcussion Symptoms (PCS)

SOMATIC
Headache
Dizziness
Fatigue for
physical and
mental
Visual
Disturbances
Sensitivity to Noise
and Light

COGNITIVE
Decreased Concentration
Memory Problems
NEUROPSYCHIATRIC
Anxiety
Depression
Irritability
Mood Swings
Sleep Disturbances

Natural history is recovery within

weeks/months (Levin 1987)

A small percentage will have persistent

symptoms (Alexander, Neurology 1995)

Repeat concussions more morbidity

(Collins, et al, Neurosurgery 2002)

Educational interventions effective in

reducing symptoms (Ponsford, et al. 2002)

Attention/Concentration
Speed of Mental Processing
Learning/Information Retrieval
Executive Functions (e. g., Planning,
Problem Solving, Self Monitoring) May see
judgment problems, apathy, inappropriate
behaviors

Factors influencing outcome

- airway
-

breathing
control of haemorrhage
prevention and shock treatment
avoidance of factors ICP

head down position

hypoxia
hypercarbia

vomiting

recognition of serious associated injury

- effective communication and transport

Lateral position for airway control

in Px with susp spinal injury

The face in turned slightly down words

the tongue to fall forwards
saliva and vomit will drain out

The indication:
Airway is inadequate
GCS 8
Herniation
Rapid deterioration

Should be performed only by a competent

medical practitioner

Gambar COB dgn ETT

Early management of severe trauma

The management plan is based on:
1. Primary survey
2. Resuscitation
3. Secondary survey
4. Definitive care

Primary survey
Airway with cervical spine immobilized in neutral

position
Breathing pattern and adequacy
Circulation and haemorrhage
Disability, minineurological examination:
GCS
Pupils
Motor deficit

Exposure: completely expose the patient for an

adequate examination but protect against

hypothermia

Resuscitation
Airway
Ensure patient airway
Unconscious patient: intubated if skilled
Note: maintain cervical spine immobilization
until radiological examination excludes
spinal injury
Breathing and oxygenation
Ensure adequate ventilation
Mechanically ventilate if intubated
Give supplemental oxygen initially

 Circulation support and control haemorrhage

Treat shock aggressively to improve tissue

perfusion
Control external haemorrhage
Assess response to resuscitation using
physiological parameters: pulse, blood
pressure, skin colour, capilary refill and urine
output
Nasogastric tube and urinary catheter unless
contraindicated

 Head injury alone, without scalp injury,

does not cause hypotension. If hypotension

is present, identify the cause, e.g.:
Hypovolaemic shock,
spinal injury.
Rarely, may be due to medulallary failure.
Blood loss from a scalp or head injury may
cause hypotension (hypovolaemic shock)
in children

Secondary survey
Special neurosurgical assessment including

Glasgow Coma Score (GCS) and external sign

of injury to the head
Record the pulse, blood pressure, respiratory
rate and temperature
Systematically examine each region of the
body, i.e. head-to-toe examination
Connect to monitors as available
Re-evaluate the GCS
Radiological examination-lateral X-ray spine,
chest, pelvis, other areas as indicated, skull Xray and CT head scan

History
Cause of injury. This will help in determining

the mechanism and pattern of head injury

Loss of consciousness at the injury site
Has the patient talked before becoming
unconscious? If so, there is some secondary
cause of a poor neurological state, e.g.
Hypoxia, hypotension, intracranial
haematoma
Pupillary response

 Were the pupils equal or unequal at the

scene of the injury? Initial equality with

change to inequality suggest a lateralised
mass lession
Cardiorespiratory status at the injury site
and response to resuscitation
History of drugs or alcohol, both prior to
and at the time of injury
Other medical disease, previous head
injury and ocular conditions

CNS examination
Glasglow Coma Scale (GCS)
Pupillary responses

are they equal or unequal? Were the pupils equal

at the time of the incident (report from ambulance
officer) and have they the same response now?
Motor pattern
hemiparesis, quadriparesis
flexion or extension to pain (from supraorbital,
trapezius or tendo achilles pressure)
Inspection of the face and scalp
Palpation of the face and scalp and any laceration
for a depressed fracture
Palpation of the spine for the tenderness and
deformity

Glasgow Coma Scale (GCS)

This scale examines three areas of behaviour: eye
opening, response to voice and motor responses.
The score can be quantitative with 3 being the
lowest score and 15 normal

Eye opening

Orientated
V5
Confused conversation
Inappropriate words
Incomprehensible sound
Nil
1

4
3
2

Best motor response

E4

Verbal response

Spontaneous
To speech3
To pain 2
Nil
1

Obeys
M6
Localizes 5
Withdraws
4
Abnormal flexion 3
Extension
2
Nil
1

Coma Score (E+V+M) = 3-15

CT head scan guidelines

GCS < 15 after resuscitation
Neurological deterioration, i.e 2 point or more on

the GCS, hemiparesis, squint

Drowsiness or confusion (GCS 9-14 persisting>2 h)
Persistent headache, vomiting
Focal neurological signs
Fracture known or suspected
Penetrating injury known or suspected
Age over 50 years of age
Post-operative assessment

Comment
A CT scan is the investigation of choice
where available. Except for an
uncomplicated minor head injury, all
patients ideally should have a CT scan.
As lesions may develop after an initial
normal scan, serial CT scans may be
required if neurosurgical deterioration
occur

Skull X-ray guidelines

In rural area where a CT scan is not
available or readily accessible, a plan skull
X-ray can provide useful information. The
pictures required are AP, lateral, Townes
view and tangential to the point of impact
for demonstrating a depressed fracture

Indications
Loss of consciousness, amnesia
Persisting headache
Focal neurological signs
Scalp injury
Suspected penetrating injury
CSF or blood from nose or ear
Palpable or visible skull deformity
Difficulty in clinical assessment
Patient with GCS 15, essntially asymptomatic

but at risk bacause of a defect blow or fall

onto a hard surface, etc, especially in a patient
over 50 years of age

Comment
The presence of a skull fracture may influence
treatment, i.e.
A skull fracture is associated with an increased risk of

intracranial haemorrhage and a CT scan is indicated

A compound fracture, including base of skull can be associated

with an increased risk of infection and a depressed fracture with

an increased risk of epilepsy especially if associated with dural
penetration
A fracture indicates the site for surgery particularly in a rapidly

deteriorating patient in whom an extradural haematoma is

suspected
Pneumocephalus presence and volume is a consideration in

aerial transport

Criteria for admission to hospital with head injury:

Confusion or any other decreased level of consciousness

Neurological symtoms or sign including persistent
headache, vomiting
Difficulty in clinical assessment, e.g. alcohol, epilepsy
Other medical condition, e.g. coagulation defects, diabetes
mellitus
Skull fracture
Abnormal CT brain scan
Responsible observation not available outside the hospital
Age patients over 50 years of age
Children under 5 years of age

Minor head injury

A minor head injury is defined as one where the

Glasgow Coma Score is 14-15

Admit and observe the patient if:
a). There has been loss of consciousness or a period of
post-traumatic amnesia
b). The patient remains confused
c). The patient is under 5 years of age or over 50 years
of age
d). Presence or development of focal neurological signs
e). Severe headache with or without vomiting

Discharge of minor head injury patient

Orientated in time and place
No focal neurological signs
No skull fracture
A responsible person is available to continue

observation of the patient

Discharge check list advise to report back to hospital
immediately if there is:
a)
b)
c)
d)

Vomiting
Complains of severe headache or dizziness
Becomes restless, drowsy or unconscious
Had a convulsion or fit

Definitive management of traumatic brain

injury
Immediate surgery for evacuation of

hematoma, if necessary
Monitor ICP with implanted pressure gauge
Medically manage cerebral edema to maintain
cerebral perfusion pressure > 70 mmHg
Perform serial head CT Scans
20% of cerebral contusions may enlarge to
surgical hematoma

Concussion
Brief loss of consciousness with normal

head CT Scan, normal neuro exam

Patient may have mild lethargy and/or
confusion
Treatment: observation
In sport, avoid any risk of reinjury until any
sxs have completely resolved
Second impact before full recovery may
be fatal

Skull fracture
May or not have associated underlying brain injury
Linier or non-depressed-observe
Open or compound-irrigate, close, antibiotic coverage
Depressed-require surgical repair

Any associated dural tear or brain laceration requires

surgical repair
Basilliar skull fracture-fracture around orbital roof,
sphenoid bone, or petrous or mastoid portion of temporal
bone.
Signs:
Battles or Racoons eye signs May be associates with
injury to cranial nerves 2,7 or 8 or CSF leak into nose
(rhinorhea) or ear (otorhea)- these require special
attention. Seldom life threatening

Cerebral contusion / intracranial

hematoma
Area of focal tissue injury. Neurological

deficit depends on area injured.

Commonly occur in coupe / contra coupe
pattern eg. Frontal / occipital
20% of contusions may expand into
surgical hematoma
Observe patients in ICU, repeat head CTScan within 24 hours

Epidural Hematoma EDH

Lens shaped hematoma between dura and skull
Associated with skull fracture and laceration of
dural artery (e.g. Middle meningeal artery)
Urderlying brain is ussually not injured
Arterialized bleeding result in rapid expansion
of hematoma and neurological decline
Often present with brief loss consciousness,
followed by lucid interval of minute to hours,
before rapid neurological decline into coma
Extreme neurosurgical emergency. Timely
diagnosis and surgery is often followed by
excellent recovery

Subdural hematoma SDH

Crescent shaped hematoma lying between brain and dura,

conforming to brain surface

Indicative of high acceleration / deceleration injury with tearing

of bridging veins or cortical arterioles

Usually associated with severe diffuse injury, immediate deep

coma from moment of impact

Extreme neurosurgical emergency
30% mortality, 30% good outcome

DAI diffuse axonal injury

Also known as shear injury or brain stem contusion
High acceleration/deceleration injury with shock waves and

momentary tissue distortion causing microscopic tearing of nerve

fibers
radiographically consist of small petechial hemorrhages in white

matter tracts
Cause immediate deep coma
Often associated with severe cerebral edema and ICP elevation
Mortality is 30-40%, good outcome 20-30%

Gunshot wound-GSW
Cause mixtures of skull fracture, DAI,

intracerebral hemorrhage, epidural and

subdural hematomas, in addition to direct
tissue injury. May also couse injury to
major cerebral vessels.
High velocity weapons cause extreme

diffuse injury from tissue cavitation

Chronic subdural hematoma

Usually found in older patients with cerebral

atrophy
Minor trauma causes small, often minimally
symptomatic subdural hemorrhage. As clot
liquifies over next 1-3 weeks, the hemorrhage
may expand into a significant mass.
CT apperance, hypodense crescent shaped
mass between dura and brain
Presenting symptoms: elevated ICP often
associated with hemiparesis. May also cause
TIA-like episodes or seizures
Treatment consists of surgical drainage of
hematoma via burrholes and irrigation. Most
patients make excellent recovery

Intubate & ventilate with GCS<9

the goal: PaO2=100mmHg, PaCO2 35mmHg, O2 sat
96%,
hyperventilation (PaCO2< 30mmHg) should be
avoided
Cerebral perfusion
the goal: CPP>70mmHg, MAP>90mmHg
hypotension (systolic BP<90mmHg) must be avoided
Intravenous fluid electrolites
normovolaemic is the goal,
avoid dehydration on or ever hydration
normal serum electrolyte should be maintaned
Head posture: should be elevated to 20-30
Corticosteroid: are not recommended
Transfer to CT and / or neurosurgical unit

Active treatment of intracranial pressure

Only be under taken of there is evidence of
- rapid neurological deterioration
- signs of uncal herniation
- ICP from the ICP monitoring
- modality (should be decided by neurosurgeon)
CSF drainage
intravenous mannitol
hyperventilation
barbiturate
mild hypothermia
decompressive craniectomy

Prevention of intracranial infection

This can result from basal skull fracture or from a
penetrating craniocerebral injury. CSF
rhinorrhoea or otorrhoea, intracranial aerocele or
a known or suspected penetrating injury require
careful assessment. The indication for
prophylactic antibiotic therapy is controversial. A
neurosurgical consultation is indicated.
1. CSF rhinorrhoea or otorrhoea swab for culture
and sensitivity and observe
2. Intracranial aerocele antibiotic therapy
3. Penetrating craniocerebral injury surgical repair
and antibiotic therapy

Restlessness and analgesia

o

Before prescribing analgesia, it is important to determine the cause of

restlestness, e.g.:
cerebral hypoxia from airway inadequacy or poor ventilation or poor perfusion,
raised intracranial pressure,
pain,
alcohol intoxication or a
full bladder.

oDrugs other than paracetamol or codeine phosphate require

neurosurgical consultation

Post traumatic epilepsy

The risk factors for epilepsy are:

intradural haematomas,
dural laceration with cortical injury,
depressed fractures,
a post-traumatic amnesia period of 24 h early post traumatic
epilepsy

The indication for prophylactic anti-convulsant therapy is

controversial. A neurosurgical consultation is indicated
both for the cause of the epilepsy and for consideration for
anti-convulsant therapy.

Scalp Wounds
1. shave at least 3 cm around the wound
2. gently palpate the laceration with a gloved finger.
This may provide information regarding an
underlying fracture
3. if a fracture is found unexpectedly, do not remove
bone fragments: contact your neurosurgeon at
once.
4. Scalp wounds may bleed profusely and cause
hypertension. Secure haemostasis by pressure or
suturing early
5. if the wound edges are badly torn, excise non
viable scalp and where possible suture the scalp in
two layers

Airway-protect cervical spine

Breathing-oxygenation
Treat shock-control haemorrhage
Maintenance fluids after resuscitation
Full neurological examination early and establish a working
diagnosis
Prevent secondary brain injury
Assess and treat non cerebral injuries
X-ray (or CT-Scan if available) when cardiorespiratory
stability achieved
Consult early with a neurosurgical unit and consider
transfer, particularly in the multiple injured patient (after
stabilization of extracranial injuries)
Continually re-assess neurological status