Head Injury

What is Head Injury

Literally refers to trauma to the head. This may or may not
include injury to the brain. However, the terms
traumatic brain injury and head injury are often used
interchangeably in the medical literature.
Brain injuries are common cause for morbidity and
mortality in trauma patients.
Patient can came presenting with from minimal cognitive
dysfunction to a vegetative state.
Primary injury occurs at time of trauma
Secondary injury occurs due to hypoperfusion (hypotension,
increased ICP), hypoxia, hyperglycemia, or anemia.
Common causes: traffic accidents, home and occupational
accidents, falls, and assaults.

Type of Head Injuries

Scalp injury

Scalp hematomas
Scalp laceration
Scalp avulsion

Skull fracture

Linear fracture
Depressed fracture

Craniocerebral
injury

Cerebral concussion
Diffuse axonal injury (DIA)
Contusion and laceration of the brain
Intracranial hematomas

Hamidah

APPROACH PATIENT WITH

HEAD INJURY

 The initial approach to the patient is the

rapid assessment of airway, breathing
and circulation, and appropriate
intervention if indicated.
Simultaneously, all patients with blunt
trauma require cervical spine
immobilization until injury is excluded.
This is typically accomplished by
applying a hard collar or placing
sandbags on both sides of the head
with the patient's forehead taped

 Breathing
Tension pneumothorax,open
pneumothorax,flail chest with
underlying pulmonary contusion

Circulation
Hemorrhagic shockMassive
hemothoraxMassive
hemoperitoneum, Mechanically
unstable pelvis fracture, Extremity
losses, Cardiogenic shock, Cardiac
tamponade, Neurogenic
shock,Cervical spine

Danger and disability

Environment

Assessment of injury
Primary survey
The first step in patient management
is performing the primary survey,
the goal of which is to identify and
treat conditions that constitute an
immediate threat to life. The ATLS
(Advanced Trauma Life Support)
course refers to the primary survey
as assessment of the "ABCs"
(Airway with cervical spine
protection,Breathing,
andCirculation)

1.Airway and cervical spine

Always assume that patient has cervical spine
injury
Place in hard collar and keep on until cervical
spine has been 'cleared'
If patient can talk then he is able to maintain
own airway
If airway compromised initially attempt a chin
lift and clear airway of foreign bodies
If gag reflex present insert nasopharyngeal
airway
If no gag reflex patient will need endotracheal
intubation
In the comatose patient, the tongue may fall
backward and obstruct the hypopharynx; this
may be relieved by either a chin lift or jaw
thrust.
If unable to intubate will require a

2. Breathing and ventilation

Check position of trachea, respiratory rate

and air entry, adequate oxygenation and
ventilation must be assured
Tension pneumothorax, open pneumothorax,
and flail chest with underlying pulmonary
contusion diagnoses should be made
during the initial physical examination
Tension pneumothorax is implied by
respiratory distress and hypotension in
combination with any of
tracheal deviation away from the affected
side, lack of or decreased breath sounds on
the affected side, and subcutaneous
emphysema on the affected side.
Patients may have distended neck veins due
to impedance of the superior vena cava,

 open pneumothorax or "sucking chest wound"

occurs with full-thickness loss of the chest
wall, permitting free communication between
the pleural space and the atmosphere.
This compromises ventilation due to
equilibration of atmospheric and pleural
pressures, which prevents lung inflation and
alveolar ventilation, and results in hypoxia and
hypercarbia.
Complete occlusion of the chest wall defect
without a tube thoracostomy may convert an
open pneumothorax to a tension
pneumothorax

Flail chest three or more contiguous ribs are

fractured in at least two locations. Paradoxical
movement of this free-floating segment of
chest wall may be evident in patients with
spontaneous ventilation, due to the negative
intrapleural pressure of inspiration.

3. Circulation and haemorrhage control

Assess pulse, capillary return and state of neck veins

Carotid pulse: systolic blood pressure at least 60mmHg
Femoral pulse: systolic blood pressure at least 70mmHg
Radial pulse: systolic blood pressure at least 80mmHg

At this point in the patient's evaluation, any episode of

hypotension (defined as a SBP <90 mmHg) is
assumed to be caused by hemorrhage until proven
otherwise.
Identify exsanguinating haemorrhage and apply direct pressure
Place two large calibre intravenous cannulas for IV fluids
Take venous blood for FBC, U+Es (urea and electrolites), and
Cross match
Take sample for arterial blood gasses
Give intravenous fluids
Crystalloid or colloid in adequate volume
Attach patient to ECG monitor
Insert urinary catheter
External control of hemorrhage should be achieved promptly
while circulating volume is restored. Manual compression of

4. DISABILITY
Glasgow Coma Scale (GCS) score
should be determined for all injured
patients. Assess level of
consciousness using AVPU method

A = alert
V = responding to voice
P = responding to pain
U = unresponsive

Assess pupil size, equality and

responsiveness

5. EXPOSURE
Fully undress patients
Avoid hypothermia

6. FLUID RESUSCITATION
Classic signs and symptoms of shock are
tachycardia, hypotension, tachypnea, mental
status changes, diaphoresis, and pallor
The goal of fluid resuscitation is to re-establish
tissue perfusion. Fluid resuscitation begins
with a 2 L (adult) or 20 mL/kg (child) IV bolus
of isotonic crystalloid, typically Ringer's
lactate.
Hypovolumic shock

Up to 15% blood volume loss (750ml)

15-30% blood volume loss (750 - 1500ml)
30-40% blood volume loss (1500 - 2000ml)
Loss greater than 40% (>2000ml)

 Radiology
With trauma and head injury, the
most immediate plain radiograph is
Skull
Cervical spine to exclude cervical
injury
Chest to identify lung contusion or
mediastinal injury, bony injury,
simple pneumthorax or heamatorax,
diaphragmatic injury and correct
placement of chest drain and CVP
line
Pelvis diagnose of pelvic fracture

 Secondary Survey
Once the immediate threats to life
have been addressed, a thorough
history is obtained and the patient is
examined in a systematic fashion.
The patient and surrogates should be
queried to obtain an AMPLE history
(Allergies,Medications,Past
illnesses or Pregnancy,Last meal,
andEvents related to the injury).

 Face, head and neck

Digital examination of the cranium,
facial skeleton, cervical vertebrae and
associated soft tissue to exclude
fracture

Central nervous system

Check the pupil, GCS score.

Chest
Detail chest examination with thoracic
spine

Abdomen and pelvis

Exclude any abdominal injury and pelvic
fracture
Do spring test for ribs n pelvis

Extremities
Presence of pain, pallor, pulselessnes,
coldness and poor capillary refill

GCS IN ADULT AND

PEDIATRIC PATIENT

Glasgow coma scale

A scale for measuring level of
consciousness, especially after a head
injury, in which scoring is determined by
three factors: amount of eye opening,
verbal responsiveness, and motor
responsiveness

GCS in Adult

Minimal head injury - ( GCS 15 , no loss of consciousness or amnesia )

Mild head injury - ( GCS 13 - 15 , amnesia or short loss of consciousness or
impaired alertness / memory )
Moderate head injury - ( GCS 9 - 12 , loss of consciousness longer than 5 minutes
or focal neurological deficit )
Severe head injury - ( GCS 5 - 8 , coma )
Critical head injury - ( GCS 3 - 4 , deep coma ).

GCS in paediatrics
Eye response

Verbal response

Motor response

CLOSE HEAD INJURY AND

PENETRATING INJURY

 Classification type of head injury are

Close head injury / blunt trauma
The dura still intact
Associated with multiple wide
distribution injuries

Penetrating head injury

Dura is breached
Damage is localize to the path of
bullet or knife

Brain injury
Secondary brain

Primary brain injury

results from the immediate

mechanical forces that
cause brain damage
Result of
Direct contact, such as a
blow to the head
Direct contact due to the
brain striking against
the internal surface of
the skull
Inertial forces originating
from rapid
acceleration/deceleratio
n such as that
experienced in a motor
vehicle collision.
Notably, contact forces
can also induce
acceleration of the brain
commonly leading to a
combination of focal

injury
delayed
pathophysiologica
l consequences of
TBI
Includes
Cerebral oedema
Increased
intracranial
pressure (ICP)
Haemorrhage
Seizures
Ischaemia due to
vasospasm,
vascular/brain
compression
Infection.

Zaizul

CLINICAL SIGN AND

SYMPTOMS OF HIGH ICP

Signs and Symptoms of

Increase
ICP
Symptoms
Signs
Headache.
Pupillary Dilatation, Abducens
Back Pain.
(Crn VI) Palsies,
Papilledema.
Cushing's Triad (Increased
Ringing In The Ears or Hearing Loss
Nausea And Vomiting
Systolic Blood Pressure, A
Vision Problems, Such As Blurry Vision Or
Widened Pulse Pressure,
Double Vision
Painful Eye Movements
Bradycardia, And An Abnormal
Neck Pain
Respiratory Pattern)
Feeling Tired And Wanting To Sleep
In Children, A Slow Heart Rate
Unsteadiness While Standing Or Walking,
Is Especially Suggestive Of High
Known As Ataxia
Altered Level Of Consciousness,
ICP.
Weakness, local or generalized.

Irregular Respirations
(Interference Of The Respiratory
Drive)
Hyperventilation (Brain Stem Or
Tegmentum Is Damaged)

Rusha

NEUROLOGICAL
EXAMINATION

History

Neurological
examination
Taking

Symptoms of neurological disorders;

1. Headache, back, neck or facial pain

(when asking about pain, include SOCRATES;

site, onset, character, radiation, assoc
symptoms, time (progression), exacerbating and
relieving factors, and severity)
2. Fits and faints
3. Dizziness or vertigo
4. Disturbances of vision, hearing or smell
5. Disturbances of gait
10.Loss of disturbed sensation, or weakness in
limb(s)
11.Disturbances of sphincter control (bladder,
bowels)
12.Involuntary movements or tremor

Past Medical History

-

Ask about head or spinal injuries

History of epilepsy or convulsions
Any previous operations
Treatment (anti-convulsants, contraceptive
pills, antihypertensive agents, steroids,
anticoagulants, antiplatelet agents
- Risk factors that may predispose
development of cerebrovascular disease
(Hypertension, DM, Hyperlipidemia,
smoking, MI)
- Previous dx of peripheral vascular disease
or of coronary artery disease ( risk of
29/9/2009
30
CV disease)

Social History
- Smoking history
- Occupation and exposure to toxins (e.g. heavy
metals)
- Alcoholism
o Blackouts
o Nutrition related conditions; e.g. peripheral
neuropathy due to thiamine deficiency
o Withdrawal syndrome; e.g. tremor, hallucination
o Cerebellar dysgeneration
o Alcoholic dementia
o Alcoholic myopathy
o Autonomic neuropathy

Fa m i-ly H isto ry

A n y h isto ry o f n e u ro lo g ica lo r m e n ta l
d ise a se sh o u ld b e d o cu m e n te d

29/9/2009

31

Physical examination
Head
Scalp- inspect & palpate for laceration,
swelling, bony depression and distortion
Orbits- palpate the margins of the orbits
for depression/irregularities
Eyes- size, reflex, movement & visual
acuity

- Panda eyes subconjuctival

hemorrhage

- Diplopia fracture of floor of orbit

Panda eye

Signs of intracranial
hemorrhage
Face palpate cheek bone for a step & asymmetry, loss of

sensation facture of
cheek bone due to damage of infra-orbital nerve
Jaw & temperomandibular joint malocclusion & open bite
deformityfractured
jaw & numbness of lower
lip
Mouth, teeth & gums - record no of missing/damaged teeth xray exclude
possibility inhaled & lodged to the
lung
Nose palpate and detect any bloody/fluid dischargeanterior
cranial fossa
fracture
Ear blood/fluid discharge bruising behind ears (Battles
sign)post cranial fossa
fracture
Neck palpate for bruising, deformity & any subcutaneous
surgical emphysema

 Chest inspect for flail chest multiple contiguous rib

fractures resulting in free-floating ribs with
paradoxical motion on respiration)

- Rib fracturesinjuries to great vessles, lung,

spleen & liver

- Sternal fracturecardiac injuries

- Increase width of mediastinum aortic

dissection

- Check for hemothorax, pnuemothorax and

cardiac temponade
Abdomen - intra-abdominal hemorrhage

- Increase abdominal distension, tenderness &

guarding are significant signs

-Skin bruising, penetrating wounds & assoc. rib

fracture possibility organ damag - Blood from
urethra/frank hematuria kidney, bladder/urethral
damage

 Upper & lower limbs palpate all major bones to

detect any bony deformity & swelling
Circulation palpate radial & pedal pulses
asymmetrical pulses indicate vascular injury

- Persisting pallor in one limb severe ischemia

- Compartment syndrome(pain, tenderness &

swelling over ant. shin/calf muscle) ischemia,
obliterate the pulses, muscle and nerve death
Nerves examine both upper and lower limbs of
peripheral nerves

-Test power, tone, strength, coordination, sensation,

and reflexes
Back (thoraco-lumbar spine) paralysis/muscle

weakness spinal cord injury

Ilyas

SKULL FRACTURE

Skull Fracture
Break in the bone in the skull, caused
by head injury
Fragments
Lacerate or bruise brain
Damage blood vessels
Intracranial hematomas
Epidural hematomas

Dissection of cerebral arteries

Classifications

 Simple linear fracture is by far the most

common type of fracture, especially in
children younger than 5 years.
Temporal bone fractures represent 15-48%
of all skull fractures.
Basilar skull fractures represent 19-21% of
all skull fractures.
Depressed fractures are frontoparietal
(75%), temporal (10%), occipital (5%),
and other (10%).
Most of the depressed fractures are open
fractures (75-90%).

Linear fracture
Most common 69%
Low-energy blunt trauma, widely distributed force
Little significance unless runs thru vascular
channel, venous sinus groove or a suture:
Vascular channel Epidural hematoma
Venous sinus groove Venous sinus thrombosis
Suture Sutural diastasis

Growing fracture brain swelling

Most patients are asymptomatic and present
without LOC. Swelling occurs at the site of
impact, and the skin may or may not be
breached.

Width

Fracture

Suture

>3mm

<2mm

Widest at centre and narrows Same width throughout

at end
On X-ray Appear darker
Lighter
Site
Pattern

Usually over temporoparietal Specific anatomical sites

area
Usually straight line
Not in straight line

Turns

Angular

Curvaceous

Basilar fracture

Linear fracture at the base of the skull

Associated with dural tear
Require > force, thus rare 4%
Characteristic

Blood in sinuses
CSF leak nose/ear
CSF rhinorrhea
Raccoon eyes
Battles sign clotting behind ear
Cranial nerve palsy
Hemotympanum
Ocular nerve entrapment: 1-10%

Likely to get meningitis

HANS device usage in high risks

Temporal fracture
Temporal bone fracture.
75% of all skull base fractures.
3 subtypes of temporal fractures are
longitudinal, transverse, and mixed.

Tra n sve rse

Lo n g itu d in a l

 Longitudinal fracture
Occurs in the temporoparietal region and involves
the squamous portion of the temporal bone, the
superior wall of the external auditory canal, and
the tegmen tympani.
These fractures may run either anterior or posterior
to the cochlea and labyrinthine capsule, ending in
the middle cranial fossa near the foramen
spinosum or in the mastoid air cells, respectively.
Longitudinal fracture is the most common of the 3
subtypes (70-90%).

Transverse fractures
Begin at the foramen magnum and extend through
the cochlea and labyrinth, ending in the middle
cranial fossa (5-30%).

Mixed fractures
Have elements of both longitudinal and transverse
fractures.

 Petrous temporal bone fracture

Battle sign.

CSF otorrhea and bruising over the mastoids

Anterior cranial fossa fractures

Raccoon eyes
CSF rhinorrhea and bruising around the eyes

Longitudinal temporal bone fractures

Conductive deafness
Ossicular chain disruption and of
Greater than 30 dB that lasts longer than 6-7
weeks.

Temporary deafness
Resolves in less than 3 weeks is due to
Hemotympanum and mucosal edema in the middle
ear fossa.
Facial palsy, nystagmus, and facial numbness are
secondary to involvement of the VII, VI, and V
cranial nerves, respectively.

Transverse temporal bone fractures

Involve the VIII cranial nerve and the labyrinth,
resulting in nystagmus, ataxia, and permanent
neural hearing loss.

Occipital condylar
fracture
High-energy blunt trauma with axial compression,
lateral bending, or rotational injury to the alar
ligament.
3 types based on the morphology and mechanism
of injury with alternative classification into
displaced and stable, ie, with and without
ligamentous injury.
Type I - secondary to axial compression resulting in
comminution of the occipital condyle. This is a
stable injury.
Type II results from a direct blow, and, despite
being a more extensive basioccipital fracture, type
II fracture is classified as stable because of the
preserved alar ligament and tectorial membrane.
Type III an avulsion injury as a result of forced
rotation and lateral bending. This is potentially an
unstable fracture.

 Very rare and serious injury.

Most of the patients with occipital
condylar fracture, especially with
type III, are in a coma and have
other associated cervical spinal
injuries.
These patients may also present with
other lower cranial nerve injuries
and hemiplegia or quadriplegia

Clivus fractures
High-energy impact sustained in motor
vehicle accidents.
Longitudinal, transverse, and oblique
types have been described in the
literature.
A longitudinal fracture carries the worst
prognosis, especially when it involves
the vertebrobasilar system.
Cranial nerves VI and VII deficits are
usually coined with this fracture type.

Nerve involvement of basilar

fracture
Vernet syndrome or jugular foramen
syndrome
Involvement of the IX, X, and XI cranial
nerves with the fracture.
Difficulty in phonation and aspiration and
ipsilateral motor paralysis of the vocal
cord, soft palate (curtain sign), superior
pharyngeal constrictor,
sternocleidomastoid, and trapezius.

Collet-Sicard syndrome
glossolaryngoscapulopharyngeal hemiplegia
occipital condylar fracture with IX, X, XI, and
XII cranial nerve involvement.

Depressed skull fracture

High-energy direct blow small
surface area with a blunt object
such as a baseball bat
Comminution of fragments starts
from the point of maximum impact
and spreads centrifugally
Most are over the frontoparietal
region because the bone is thin and
the specific location is prone to an
assailant's attack.

 Very serious - 11% of severe head

injury
Comminuted fractures, bone
displaced inward
High risk of increasing ICP
Crush delicate tissue
Complex torn dura matter
May require surgery to lift

the bone

 Approximately 25% of patients with

depressed skull fracture do not
report LOC, and another 25% lose
consciousness for less than an
hour. The presentation may vary
depending on other associated
intracranial injuries, such as
epidural hematoma, dural tears,
and seizures.

Zaizul

INDICATION FOR CT SCAN

CT vs MRI
CT
M RI
S u fficie n t to d e te ct clin ica lly
S e n sitive to
S u p e rio r in d e te ctin g sku ll
im p o rta n t b le e d a n d a b le to su b tle le sio n
M a y D e m o n stra te fin d in g s o f
fra
g u ictu
d e re
m .a n a g e m e n t.
D
A I (to
d iffu
se bone,
a xo n soft
a lintissue
ju ry )and
Able
image
su
ch vessels
a s m icro
h athe
e msame
o rrhtime.
a g e s.
blood
all at

More on CT
Sensitive
D e te ctin g Pa th o lo g y T h a t
DAdvantages
isto rts T h e N o rm a lA n a to m y
O f T h e B ra in
D iffe re n tia tin g a n isch a e m ic
H a e m o rrh a g e s ,
i n fa rct fro m a ce re b ra lb le e d .
N e o p la sm s,
Id e n tifyin g sp a ce o ccu p yin g
A b sce sse s .
le sio n s ( su ch a s tu m o u rs a n d
a b sce sse s)
D e te ctin g h yd ro ce p h a lu s .

Less Sensitive
B ra in In fa rctio n ,
A rte rio ve n o u s M a lfo rm a tio n s ,
Disadvantages
A n e u rysm s ,
S m a llle sio n s (< 1 cm ) o r
Le ss S e n sitive S tillFo r
b ra in ste m le sio n s m a y b e
D e te ctin g W h ite M a tte r D ise a se
m isse d
A n d Le p to m e n in g e a lD ise a se .
E a rly in fa rctio n (< 6 -8 h o u rs)
m a y n o t b e se e n .

Indications for CT.

History.
Construct a Focused history.
Witnesses of the trauma or
individuals who know the patient
may be helpful in ascertaining the
details of the traumatic event and
other valuable patient information.
Past medical and surgical history,
drug/alcohol use and allergies are
important.

 PE
GCS and Pupillary reflexes,
Full neurological examination.
Evidence of basilar skull fracture:
blood in the middle ear cavity
(haemotympanum), raccoon eyes
(periorbital ecchymosis), post-auricular
ecchymosis, CSF leakage (rhinorrhoea
or otorrhoea).
Associated spinal injury: spinal
tenderness, paraesthesias,
incontinence, extremity weakness,
priapism.
Carotid dissection: carotid bruits
Abnormal eye findings: papilledoema,
retinal haemorrhage.

 Investigations.
Arterial blood gas.
FBC including platelets.
Serum electrolytes and urea.
Serum glucose.
Coagulation status: PT, INR, activated
PTT.
Blood alcohol level and toxicity
screening if indicated.
Urine analysis: specific gravity,
osmolality (to detect endocrine
complications such as diabetes
insipidus or Syndrome of
Inappropriate Antidiuretic Hormone).

Rules of Standard Guidance.

The Canadian CT Head Rule.
The New Orleans Criteria.

* Both guidelines contain 7 criteria to

guide the use of CT in patients with mild
injury and have been validated.
* Patients under 16 years of age were not
included in the initial Canadian CT rule
derivation or validation.

The Canadian CT Head Rule.

CT is required for patients with minor
head injuries (minor head injury is
defined as witnessed LOC, definite
amnesia or witnessed disorientation in
patients with a GCS score of 13 to 15)

with any one of the following.

High Risk (for neurologicaol

intervention)

Medium Risk (for brain

injury for CT scan)

Amnesia more than 30

GCS less than 15 at 2 hours
after injury
minutes before impact

Suspected open or depressed

(retrograde amnesia)
skull fracture

Any sign of basal skull fracture Dangerous mechanism

(pedestrian struck by
(haemotympanum , raccoon eyes
[periorbital ecchymosis ], CSF
motor vehicle, occupant
otorrhoea/rhinorrhoea, Battle
ejected from motor
sign [ecchymosis of the
vehicle, fall from
mastoids])

2 or more episodes of vomiting height more than 3 feet

Aged 65 years or above
or 5 stairs).

New Orleans Criteria.

CT is required for patients with minor
head trauma (minor head injury was
defined as LOC in patients with normal
findings on a brief neurological
examination and a GCS score of 15, as
determined by a physician upon arrival
at the emergency department) with

any one of the following:

High Risk (for neurolsurgical

intervention)
Headache

Vomiting
Aged more than 60 years
Drug or alcohol intoxication
Persistent anterograde amnesia
(deficits in short-term memory)
Evidence of traumatic soft-tissue or
bone injury above clavicles
Seizure (suspected or witnessed)

The derivation set for the

criteria also contained a
history of coagulopathy as a
clinical parameter, although
this was not included in the
final validation.
Where possible this history
should be obtained and
considered with respect to
CT scanning.

Interpretation of CT.
Basic Interptetation
Most of the picture are non-specific.
CT picture are depending on the
density of the structure.

 Principle
Pre-Contrast Study.
Hypo- Density
Comparison with CSF and Brain
Tissue
Higher than CSH and lower
than Brain Tissue
(Protein, Blood , Debris)
Tumor, Abcess,Resolving
Hematoma, Evolution
Infarct.
Lower that CSF
Fat or cholesterol ;
Congenital Tumor ;
dermoir , epidermoid,
lipoma.
Air ; Head injury,

 Hyper- Density
Comparison with Cranium Bone
Iso or higher than bone
Ossification, calcification,
metallic iatrogenic, blood
pooling.
Less than bonebut higher that brain
tissues
Haemorrhage, compected
cellurity.

Iso- Density
As brain Parenchyma.
Iso-density to CSF (Water like
congtent)
Chronic haematoma, chronic
infarct, porencephaly,
congenital cycts ,

 Post Contrast CT.

Gyral, ribbon, cortical.
Solid.
Rim or Ring.
Mural Nodular.
Linear and Dot.
Heterogeneous.
No Enhancement.

Changes in adjacent tissue

Edema pattern in CT
Vasogenic Edema
Tumors, infection, late infarct aling
white matters, fingerlike.

Interstitial edema,
periventricular white matter,
ependymitis granularis

Cytotoxic edema
Ischemia or infarct, gray matter

Bone
Ventricles, Sulci and cistern

Classification of Cerebral Edema

Type
Location
Site
Vasogenic Extracellular White
Cytotoxic Intracellular White or
gray
Ischemic Intra- and
White and
extracellular
HydroExtracellular gray
White and
static
HydroExtracellular gray
White
cephalic
Osmotic Intra- and
White and
extracellular gray

BloodBrain
Disrupted
Barrier
Intact
Disrupted
Disrupted
Intact
Intact

Probable Mechanism
Increased vascular
permeability
Cellular failure
Anoxia
Increased blood
pressure
Impaired CSF outflow
or
absorption
hangindent1em
Relative plasma hypoosmolality

Examples
C T sca n o f a 1 6 ye a r- o ld p a tie n t
w ith a typ ica l
d iffu se h e a d in ju ry.
T h e p a tie n t's G C S
a t a d m issio n to
h o sp ita lw a s 4 .
T h e re is a sm a ll
a m o u n t o f b lo o d in
th e trig o n e a n d
o ccip ita lh o rn o f
th e rig h t la te ra l
ve n tricle ( lower
arrow). There is a
small punctate
hemorrhage in the
left internal
capsule (upper

CT scan of a 50year-old man

injured in a fall.
There is a large
mixed-density
lesion in the left
temporal lobe
(lower arrow) and a
similar, smaller
lesion in the left
orbitofrontal
cortex (upper
arrow). The
appearance is
typical of cerebral
contusions.

CT scan of a large
acute epidural
hematoma (arrows).
Epidural (or
extradural)
hematomas have a
convex medial
border, which
produces the lens
shape that
distinguishes
epidural from
subdural hematomas.

CT scan of a large
acute subdural hematoma
(horizontal arrows). The
hematoma spreads over
the entire convexity of
the hemisphere, so that
the medial border of
the hematoma is
concave. Note also the
large amount of midline
shift. The occipital
horn of the left
lateral ventricle is
acutely enlarged as a
result of trapping of
CSF by ventricular
distortion and
obstruction of CSF flow
(vertical arrow).

CT scan of a
confluent traumatic
intracerebral
hematoma in the left
frontal lobe of a
patient struck by a
motor vehicle (lower
arrow). There is
overlying scalp
swelling and
contusion at the
site of the blow to
the head (upper
arrow).

An unenhanced CT of
the brain in a
patient with the
complications of
hypertensive
encephalopathy. The
arrows are pointing
to the end-arterial
border zones with
changes consistent
with ischemic and
hemorrhagic changes.

A schematic diagram demonstrating the concept of evolving pressure

differentials with regional brain swelling from large supratentorial
hemispheric infarction. Note that the clinical worsening in its early
states correlates with brain tissue displacement.

Rusha

INTRACRANIAL
HAEMORRHAGE

Intracranial Hemorrhage
1. E xtra d u ra l ( e p id u ra l)
H e m a to m a
2. S u b d u ra lH e m a to m a
3. S u b a ra ch n o id H e m a to m a
4. In tra ce re b ra lH e m o rrh a g e

1. Extradural Hematoma
(epidural)

Very common in children, adolescents and young adult

Blood between skull & dura d/t rupture of meningeal
artery
Usually a/w skull fracture in temporal region
Symptoms within 24 hours of trauma:
- Loss of conciousness
- Lucid interval with severe headache & drowsiness
- Fixed & dilated pupil on the side of injury
- hemiparesis on the opposite side
Lucid intervalfollowed by acutely progressive
evidence of increased ICP compression of brain
stem coma death
Morphology: Smooth inner contour (dura), biconvex.
Need urgent diagnosis through CT scan
Mx: immediate surgery to remove clot

# Lucid interval=> a period of consciousness after the

injury before the patient became unconscious

CT scan of extradural hematoma

Extradural hematoma. Such a

location for hemorrhage is
virtually always the result of
trauma that causes a tear in
the middle meningeal artery.

2. Subdural Hematoma
Blood between dura & arachnoid d/t rupture of
bridging veins
More common (30%) than extradural (10%)
Underlying primary brain injury and 50% mortality
Manifest within 48 hrs.
Lateral aspect of cerebral hemispheres, 10% bilateral.
Volume of the haematoma increases ICP increase
herniation (Coning=> herniation of cerebellar into
foramen magnum compressing medulla
cessation of respiration & death
S/S: Headache & confusion. Rarely focal signs.
Types:
- Acute due to major brain injury

s/s: deeply unconscious & develop

neurological localizing

 Morphology:
- Clot along brain surface contour without extension
into the
depth of sulci. (crescent)
- Hematoma surrounded by fibrous membrane
(organising), attached to dura only.
Rebleeding greatest risk in 1st few months.
Mx: Craniotomy

Subdural hematoma

3. Subarachnoid haematoma
Most cases of traumatic SAH are a/w
parenchymal haematoma
In subarachnoid space
Due to ruptured of berry aneurysm blood
flows into the subarachnoid space increase
in ICP + destructive and toxic effects of
blood on brain parenchyma and cerebral
vessels
S/S: meningeal irritation, headache, neck
stiffness, Kernigs sign +ve (inability to
completely extend the leg when sitting or
lying with the thigh flexed upon the
abdomen)

#Berry aneurysm a small saccular aneurysm

of a cerebral artery, usually at the junction of

Kernigs sign

Subarachnoid hematoma

4. Intracerebral Hematoma
Common after a severe head injury.
Caused by a cerebral contusion fluid
accumulation in the damaged brain
(cerebral edema)deaths.
S/S: severe headache, nausea, seizures,
and coma or death
Mx: surgery is usually avoided because it
usually does not restore brain function.

Zaizul

HYDROCEPHALUS

Hydrocephalus.
Definition
Disturbances in CSF circulation or
absorption which results in the continuous
increase in the ICP which leads to
hydrocephalus.

Classification
Obstructive - ; CSF circulation is blocked
within the ventricular system, and there is
enlargement in the ventricles proximal to
the obstruction.
Communicating ; CSF absorption is
blocked at the level of the arachnoid
granulations.
Rarely, hydrocephalus may be due to the

Pathophysiology
Increase pressure
in expandable
compartment

Menifestations
Neonates and infants whose anterior fontanelle
is still open,
Symptoms includes tense or bulging
fontanelle, apneic and bradycardic episodes,
engorgement of the scalp veins, upward gaze
palsy, gaps between the cranial sutures, rapid
increases in head circumference, irritability,
poor head control, and poor oral intake.

Increase pressure Children with closed fontanelle

Symptoms includes lethargy or excessive
in rigid
compartment
sleepiness, papilledema, headache, nausea,
vomiting, gait disturbance, increased fussiness,
or upgaze or lateral gaze palsy

Treatments Modalities.
Ventriculoperitoneal shunting,
creating a shunt between the cerebral
ventricles and the peritoneal cavity.
Ventriculoatrial shunt,
Right Atrium Shunt
Ventriculopleural shunt
Pleural Cavity Shunt
Endoscopic third ventriculostomy
Children with obstructive type.
Involves fenestration of the floor of the third
ventricle, thereby creating an alternative
CSF pathway.
Shunt Failure OR Delayed treatment may leads to
irreversible neurologic injury, including
herniation, blindness, or death.

DIFFUSE AXONAL INJURY

 hx rapid acceleration/deceleration of
the head, or direct impact to head;
DAI may be responsible for mild
forms of cognitive impairment seen
acutely with concussions;
severe DAI: generally no lucid
interval, presents with immediate
and persistent LOC

 Diffuse axonal injury is caused by

damage to axons throughout the
brain, due to rotational acceleration
and then deceleration.
Axons may be completely disrupted
and then retract, forming axon
balls.
Small hemorrhages can be seen in
more severe cases, especially on
MRI.
Hemorrhage is classically seen in the
corpus callosum and the
dorsolateral midbrain.

Management
Rapid intervention with particular attention
to ABCs to minimize secondary brain
injury.
Treat elevated ICP only if symptomatic
Sedate patient and elevate head of bed 300
Brief hyperventilation may be performed
acutely to cause cerebral vasoconstriction
Mannitol for osmotic diuretics and free
radical scavenging
Surgical decompression of deteriorating
patients via trephinaton or
ventriculostomy

 Intracranial bleeds require seizure

prophylaxis e.g. phenytoin and may
require surgical drainage
Check coagulation studies (PT/aPTT/INR)
immediately and correct any
coagulopathy to minimize intracranial
bleed
Depress skull fractures and penetrating
trauma may require surgical repair