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 across the
bags to the backboard.

 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 cricothyroidotomy
. Give 100% oxygen through a Hudson mask

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, but the neck veins may be flat
due to systemic hypovolemia

 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 open wounds with
ongoing bleeding should be done with a single gauze and a gloved hand.

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 diagnose of acute ischemic

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)

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
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/deceleration 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 anddiffuseinjuries.

Secondary brain
injury
delayed
pathophysiological
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

Pupillary Dilatation, Abducens

(Crn VI) Palsies,
Cushing's Triad (Increased
Systolic Blood Pressure, A
Widened Pulse Pressure,
Bradycardia, And An Abnormal
Respiratory Pattern)
In Children, A Slow Heart Rate Is
Especially Suggestive Of High ICP.
Irregular Respirations
(Interference Of The Respiratory
Drive)
Hyperventilation (Brain Stem Or
Tegmentum Is Damaged)

Headache.
Back Pain.
Papilledema.
Ringing In The Ears or Hearing Loss
Nausea And Vomiting
Vision Problems, Such As Blurry
Vision Or Double Vision
Painful Eye Movements
Neck Pain
Feeling Tired And Wanting To Sleep
Unsteadiness While Standing Or
Walking, Known As Ataxia
Altered Level Of Consciousness,
Weakness, local or generalized.

Rusha

NEUROLOGICAL
EXAMINATION

Neurological
examination

History 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
6. Loss of disturbed sensation, or weakness in limb(s)
7. Disturbances of sphincter control (bladder, bowels)
8. Involuntary movements or tremor
9. Speech and swallowing disturbances
10.Altered cognition

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 CV
29/9/2009
30

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

Family History
Any history of neurological or mental
disease should be documented
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
- Pain & local tendernesscervical fracture

 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.

Fracture

Suture

>3mm

<2mm

Widest at centre and

narrows at end

Same width throughout

On Xray

Appear darker

Lighter

Site

Usually over
temporoparietal area

Specific anatomical sites

Pattern

Usually straight line

Not in straight line

Turns

Angular

Curvaceous

Width

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.

Transverse

Longitudinal

 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

 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
MRI
Sufficient to detect clinically Sensitive to
important bleed and able to subtle lesion
guide management.
Superior in detecting skull
fracture.
Able to image bone, soft
tissue and blood vessels all
at the same time.
May Demonstrate findings
of DAI (diffuse axonal injury)
such as microhaemorrhages.

More on CT
Sensitive

Less Sensitive

Detecting Pathology That

Distorts The Normal Anatomy
Of The Brain
Haemorrhages,
Neoplasms,
Abscesses.

Brain Infarction,
Arteriovenous Malformations,
Aneurysms,
Less Sensitive Still For
Detecting White Matter
Disease And Leptomeningeal
Disease.

Advantages

Disadvantages

Differentiating an ischaemic
infarct from a cerebral bleed.
Identifying space occupying
lesions (such as tumours and
abscesses)
Detecting hydrocephalus.

Small lesions (<1 cm) or

brainstem lesions may be
missed
Early infarction (<6-8 hours)
may not be seen.

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), postauricular 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)

GCS less than 15 at 2 hours

after injury
Suspected open or depressed
skull fracture
Any sign of basal skull fracture
(haemotympanum, raccoon
eyes [periorbital ecchymosis],
CSF otorrhoea/rhinorrhoea,
Battle sign [ecchymosis of the
mastoids])
2 or more episodes of
vomiting
Aged 65 years or above

Medium Risk (for brain

injury for CT scan)

Amnesia more than

30 minutes before
impact (retrograde
amnesia)
Dangerous
mechanism
(pedestrian struck
by motor vehicle,
occupant ejected
from motor vehicle,
fall from height
more than 3 feet 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 shortterm 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

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, pneumocephaly.
Myxoid (mucus like)

 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 ,
encephalomalacia change.

Hetero- Density.
Difference density as compared to the
contralateral part.

 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
BloodProbable
Brain
Mechanism
Barrier
Vasoge Extracellul White
Disrupt Increased
nic
ar
ed
vascular
permeability
Cytotoxi Intracellula White or Intact
Cellular failure
c
r
gray
Ischemi Intra- and White
Disrupt Anoxia
c
extracellul and gray ed
ar
HydroExtracellul White
Disrupt Increased blood
static
ar
and gray ed
pressure
HydroExtracellul White
Intact
Impaired CSF
cephalic ar
outflow or
absorption
Osmotic Intra- and White
Intact
hangindent1em

Examples
CT scan of a 16year-old patient
with a typical
diffuse head injury.
The patient's GCS
at admission to
hospital was 4.
There is a small
amount of blood in
the trigone and
occipital horn of
the right lateral
ventricle (lower
arrow). There is a
small punctate
hemorrhage in the

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

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 endarterial 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

Rusha

INTRACRANIAL
HAEMORRHAGE

Intracranial Hemorrhage
1.Extradural (epidural)
Hematoma
2.Subdural Hematoma
3.Subarachnoid Hematoma
4.Intracerebral Hemorrhage

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 vessels in the
circle of Willis, having a narrow opening into the artery

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 overproduction
of CSF, as is the case in certain choroid plexus tumors.

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

in rigid
Symptoms includes lethargy or excessive
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