HEAD_INJURY_RUPANI3.ppt

HEAD INJURY
By - Dr. RAJA RUPANI

DEFINITION
 Head injury is a morbid state, resulting from gross or
subtle structural changes in the scalp, skull, and/or the
contents of the skull, produced by mechanical forces.
 The blunt force may result in injury to the contents of
the skull, either alone or with a fracture of the skull.
 The extent and degree of an injury is not necessarily
proportional to the amount of force applied to the
head.

SCALP
The thickness of scalp in adult is variable,
ranging from a few mm to 15 mm.
Most wounds are caused by blunt force to
the head, like falls or blows
Wounds are contusions or lacerations.

CONTUSIONS OF SCALP
 May occur in the superficial fascia, in the
temporalis muscle or loose areolar tissue
 Contusions in the superficial fascia appears as
localized swelling and are limited in size because
of dense fibro-fatty tissue of the fascia.
 Extensive hematoma spreads beneath galea
(Sub galeal hemorrhage)
 Deeper bruising occurs in fibrous galea
 Infected wounds may result in thrombophlebitis
(through emissary veins)

Bruising of the scalp is better felt than seen
Its firm edge feels like depressed fracture
A scalp wound by a blunt weapon frequently
resembles an incised wound and as such
the edges and ends should be carefully
examined with a magnifying lens.

LACERATIONS OF SCALP
 If the scalp is lacerated by a blow, blood is driven out
of the vessels due to compression and considerable
bleeding occurs
 With further blows, blood is projected about the scene
 With repeated blows, blood is splattered over
assailant
 Flat surface or object causes ragged split (linear,
stellate or irregular)
 Temporal arteries spurt freely, as they are firmly
bound and unable to contract and a fatal blood loss
can occur

AVULSION OF SCALP
Involves large are of scalp
Occurs in :
- traffic accident
- hairs entangled in machinery

INJURIES TO FACE
Bleeding is more in facial
wounds

EYES
Blunt trauma on the eye causes
a) Permanent injury to :
- cornea
- iris
- lens
b) Vitreous hemorrhage
c) Detachment or rupture of retina
d) Traumatic cataract

BLACK EYE
(PERIORBITAL BRUISING)
It is caused by:
1.Direct blow in front of orbits, bruising lids.
2.Injury to the forehead, the blood tracking
down under the scalp.
3.Fracture in the anterior cranial fossa,
the blood leaking through cracked orbital
plates.

NOSE
1. May be bitten or cut off due to sexual
jealousy or enemity.
2. A blow may cause nasal bleeding due to
partial detachment of mucous membrane
EARS
A blow may produce -
1.Rupture of the tympanum
2.Deafness
3.Labyrinth may injured

FACIAL BONES
A blow often fractures the nasal bone and also ethmoid
bone with radiating fractures into supraorbital plates, if
the force is severe.
A blow may fracture maxilla and malar bone.
Pulping of face may result from striking with a heavy stone.
The mandible is fractured by a blow from a fist, stick or by
fall from height.
A heavy blow on the jaws drives the condyles against the
base of skull producing a fissured fracture.
TEETH
A fall or a blow with a blunt weapon may cause fracture or
dislocation of teeth, with contusion or laceration on lips
or gums and bleeding from the sockets.

SKULL
The outer table is twice the thickness of
inner.
In young males,the thickness of -
Frontal and parietal bone = 6 to 10 mm
Occipital bone =15 mm.
Temporal bone = 4 mm.
Skull is thicker in midfrontal, midoccipital,
parieto-sphenoid and parieto-petrous
buttresses.

Force required to fracture a cadaver skull –
• Covered by an intact,hair-bearing scalp
= 400 to 600 pounds per square inch
• Empty human skull =
25 inch-pounds energy is sufficient to

MECHANISM OF FRACTURE
OF SKULL
1.FRACTURE DUE TO LOCAL DEFORMATION
 A local impact will drive inwards a piece of
bone,shaped a cone like indentation
 At the apex, the inner table will get streched &
fractures first.
 If the force continue to act,fracture of outer table
follows
 complete fracture line runs from the central point
radially.
 At the periphery of indentation the convexity of
the bend is outwards,the outer table fractures
first.

2.FRACTURE DUE TO GENERAL
DEFORMATION
 Whenever the skull is compressed laterally, the
vertical and longitudinal diameters are increased
(and vice versa) due to which parts of skull at distant
get bulged and may fracture by bending.
 The head may be compressed between
a) two external objects,such as the ground
and a wheel of a car
b) an external object and spinal column

FRACTURES OF SKULL
A. Direct injuries may be caused by:
1. Compression- as midwifery forceps or crushing of
head under the wheel of a vehicles.
2. An object in motion striking the head e.g. bullet,
bricks, masonary, machinery, dagger, etc.
3. Head in motion striking an object, as in falls and
traffic injuries.
B. Indirect injury occurs from fall from height and
landing on feet or buttocks.

Types of Fractures of Skull
1.Fissured Fracture
2.Depressed Fracture
3.Comminuted Fracture
4.Ponds or Indented Fracture
5.Gutter Fracture
6.Ring or Foramen Fracture
7.Perforating Fracture
8.Diastatic or Sutural Fracture

FISSURED FRACTURE
These are linear fractures as cracks in the
bone
Involving the inner table or outer table or
both.
They are caused by forcible contact with a
broad resisting surface like –
• the ground
• an agent having a broad striking surface
• fall on the feet or buttocks.

• Runs parrallel to the direction of force .
• May start at the counter pressure, e.g.,
in the bilateral compression.
• The line of fracture runs parallel to the
axis of compression.
• Fracture line tends to follow an irregular
course and is usually no more than hair's
breadth.

• Linear fractures do not tend to cross bony
buttresses, such as glabella, frontal and
parietal eminance, petrous temporal bone,
and occipital protuberance.
• They tend to cross points of weakness, such
as frontal sinuses, orbital roof, parietal and
occipital squama.
• Fracture lines stop when the energy dissipates
or when they meet a foramen, a suture or a
preexisting fracture.

OSSA TRIQUETRA :
In skull, small portion of brim ossify from
irregular independent centres and remain for
variable period of time as small bone know as
OSSA TRIQUETRA

DEPRESSED FRACTURE
• They are produced by local deformation of the
skull.
• The outer table table is driven into diploe, the inner
table is fractured irregularly.
• Also called “fracture a ala signature” (Signature
fracture) as their pattern often resembles the
causing weapon or agent .
• Caused by blows from heavy weapon with small
striking surface e.g. stone, sticks, axe, chopper,
hammer etc..
• When a hammer is used ,the fracture is circular or
an arc of a circle, having the same diameter as the
striking surface.

COMMINUTED FRACTURE
• It has two or more intersecting lines of
fracture which divide the bone into three or
more fragments.
• They are caused by fall from height on hard
surface, vehicles accidents and from blows
from weapons with broad striking surface,
e.g. heavy iron bar, thick sticks, etc.
• When there is no displacement of the
fragment of fragments, it resembles a spider's
web or mosaic.

POND OR INDENTED FRACTURE
This is simple dent of the skull –
d/t - an obstetrics forceps blade,
- a blow from a blunt object or
- forcible impact against protruding object.
They occur only in skulls which are elastic
i.e, skull of infants.
Fissured fractures may occur in outer table
around the periphery of the dent.

GUTTER FRACTURE
They are formed when part of thickness
of bone is removed so as to form a gutter,
e.g, in oblique bullet wounds.

RING FRACTURE
It occurs in the base of skull
The anterior 1/3 is separated at its junction
with the posterior 2/3.
It runs at about 3 to 5 cm. outside foramen
magnum and passes forward through the
middle ears and roof of the nose
The skull is separated from the spine.

It occurs due to :
1.Fall from height
2.Blow to the vertex
3.Blow on the chin
4.Sudden violent turn of head

PERFORATING FRACTURE
These are caused by firearms and pointed
sharp weapons like - daggers knives or
axe.
The weapon passes through both the table
of skull leaving a clear-cut opening, the size
and shape of which corresponds o the
cross-section of the weapon used.

DIASTATIC OR SUTURAL
FRACTURE
Seperation of sutures, due to a blow on
head with blunt weapon.
Occurs only in young persons

• ELEVATED FRACTURE
• BLOW OUT FRACTURE

FRACTURE BASE OF SKULL
 May be produced by
1. Force applied directly at the level of the base
2. General deformation of the skull
3. Extention from the vault
4. Through spinal column or face
 Most basal fracture tend to meet at and overrun the
pitutary fossa
 Fracture line usually opens into basal foramina
 Sphenoidal fissure is most commonly affected

 Blow on the chin or mandible produces:
- fracture of glenoid fossa
- fracture of cribriform plate of ethmoid
 Fracture of roof of orbit occurs due to :
- Fall on back of the head
- Blow on top of head
- Sudden violent increase in internal pressure

FRACTURES OF BASE OF SKULL
1.Longitudinal
May results from -
a) Blunt impact on face and forehead or back of head
b) In front-to-back or back-to-front compression
2.Transverse
Results from an impact on either side of head or side
to side compression
3.Ring fracture

Anterior fossa fracture are due to
direct impact on chin.
Middle fossa fractures are due to
direct impact behind ear.
Posterior fossa fractures are due to
direct impact on back of head

COMPLICATIONS
1.Fracture of anterior cranial fossa may involve frontal,
ethmoidal and sphenoidal sinuses with loss of blood
from nose or mouth
2. In cribriform fracture, CSF and even brain tissue can
leak into nose (CSF Rhinorrhoea)
3. Leptomeningitis
4. Cranial pneumatocele

5.Middle fossa fracture through basioccipit or
sphenoid → bleeding from mouth
6.Fracture of sellaturcica communicates with airway via
sphenoid sinus → blood passing into bronchial tree
7.Fracture of petrous temporal bone
→ blood and CSF escape from ear (CSF Otorrhoea)
→ blood may pass to mouth via eustachian
tube
→ bleeding from ear due to tearing of posterior branch
of middle meningeal artery

8. In posterior fossa fracture
→ bleeding occurs behind mastoid process
→ large haematoma at the back of neck
9.Fracture foramen magnum → cerebellar
contusion & oedema → fatal herniation of
cerebellar tonsils
- Cranial nerve injury (streched or bruised)
10. Damage to surrounding structures
11. Shock
12. Portal of entry of bacteria
13. Fat and bone marrow embolism
14. Deprssed fracture → severe dysfunction,
coma and death

Contrecoup fracture
• Fracture of skull occuring opposite to site of force
is known as contrecoup fracture.
• Usually occurs when head is not supported.
• There is sudden disturbance in fluid brain content
which transmits the force recieved to opposite side &
impacts against the cranial wall.

THE CIRCUMSTANCES OF
FRACTURE OF THE SKULL
1. Accident - Fall or an injury by a motor
vehicles
2. Homicide - Multiple localised and depressed
fracture
3. Suicide - by insane

AGE OF SKULL INJURY
 Healing occurs without the formation of visible
callus, as periosteal blood vessels are damaged
1st week-
- Edges of fissured fracture stick together
14 days-
- Edges are slightly eroded
- Inner surface of the skull shows pitting or deposition
of salt
3-5 week
- Edges become slightly smooth and bands of
osseous tissue run across the fissure.

INJURIES OF BRAIN & MENINGES
1. Open injuries - if dura is lacerated,
e.g. by bullet or fragment of bone
2.Closed injuries - if dura remains intact,
whether skull is fractured or not :-
e.g. a)Blunt force to head
b)fall
c)head striking a flat surface

BRAIN INJURY
May be caused by:
1. Penetration by a foreign body - knife, bullet or skull
fragments etc.
2. By Distortion of skull -
- a localised segment undergoes deformation
→ shear strain in the brain tissue → contusion in
surface layer
- fractured bone may penetrate the dura → laceration.

3 Acceleration / Deceleration injuries:
 Sudden movement of the head → intracranial
pressure gradients → shearing and tensile forces.
 An impacting force to the head can produce :
- linear accleration,
- rotational (angular) accleration or
- combinition of both

Linear acceleration
- The force passes through the centre of head,
acclerating it in a stright line.
- Impact to the front and back of head
Rotational or angular accleration
- Head will rotate about its centre.
Impact to the side → linear + angular acceleration
(is more injurious)

MECHANISM OF CEREBRAL INJURIES
 Damage may be caused without actual blow or fall
on the head, e.g. by shaking the infant as in child
abuse may cause subdural hemorrhage.
 A blow → linear or rotational change in velocity
 Forces involved - linear acceleration / deceleration
- centrifugal & rotational velocity.

 Linear accleration forces → compressional or
rarefactional forces
 Acceleration or decelaration ＋ rotational element →
brain damage
 Deceleration or accleration → the head in rotation →
transmitted to brain → brain glides within dura →
gliding or shear strain → moves adjacent strata of
tissue laterally.
 The area of the skull depressed → compression and
typical cone-shaped contusion.

 Sudden arrest of moving skull → decelaration of the skull
first, but momentum of brain causes continuous motion.
 The skull and brain cannot change their velocities
simultaneously
 The brain is restraint by the falx and tentorium → damage
to base of cerebrum, corpus calosum and brain stem.
 Impact against the wide wall of the skull → diffuse contusion
of cortex
 Cerebellum d/t small size and light weight is less liable to
damage from rotatory movement of head

Contrecoup lesion
• Coup-located beneath the area of impact
• Contrecoup-in an area opposite the side of
impact
• D/t
-Local distortion of skull and sudden rotation
of head resulting from blow, which causes
shear strain
- Acceleration or Deccelaration injury
- Formation of cavity or vaccum on opposite
side

 Blow on Occipital – injures Frontal lobe & tip of
Temporal lobe
 Blow on Front of head – damages inner & lower part
of back of brain or Brain stem
 Fall on side – contusion of opposite side
 Fall on top of head – contusion of ventral surface of
cerebral hemisphere
 Blow on parietal area –lesion on opposite hemisphere
or medial side of same hemisphere

CONCUSSION OF BRAIN
Head injury (Blunt trauma)
↓
Partial / complete paralysis of cerebral function
↓
Concussion- State of temporary unconciousness
↓
Tends to spontaneous recovery.
↓
Post-traumatic Retrograde Amnesia

MECHANISM
Occurs due to acceleration / deceleration of
the head
The violent head movement causes shearing
or streaching of the nerve fibers and axonal
damage.
Severe injuries occur in coronal head motion
only.
Sagittal head motion produces mild or
moderate injury

 At low level of accleration / decelaration,
there is physiological dysfunction.
 With increased physical force, there is
immediate stuctural damage of axons and
immediate stoppage of all activites.
 Mild concussion
- consciousness is not lost
- no confusion or disorientation (± amnesia)
 Severe concussion
- amnesia and loss of consciousness

Cerebral concussion may be produced by
1. Direct violence to head
2. Indirect violence
a) fall upon the feet or buttocks
b) an unexpected fall on the ground in
traffic or industrial accidents

During established concussion:-
a) muscles - flaccid
b) pupils - dilated and unreacting
c) pulse - weak and slow
d) respiration - shallow
As consciousness returns, there is period
during which the person appears to be
lucid and in touch with surrounding

 Post traumatic amnesia
- ranges from minutes to days
- duration is usually proportional to severity
of the injury
 Concussion can be ruled out if :
a) unconsciousness is prolonged
b) unconciousness does not occur
immediately after blow
c) If coma develops later

COMMOTIO CEREBRI
Severe movement of head
↓
Shearing stress in brain
↓
Small or punctate hemorrhages through
out the brain (Commotio cerebri )

CAUSE OF CONCUSSION
 Most acceptable cause is-
“Diffuse neuronal injury“ - a functional
abnormality of nerve cells and of their
connection.

DIFFUSE AXONAL INJURY
Occurs when head acceleration occurs over a
long period, as in a traffic accident and fall
from a considerable height.

Features of DAI -
1. Focal lesion in - corpus callosum
- the parasagittal white matter
- septum
- wall of III Ventricle
- dorsolateral brainstem
2. Microscopic evidence of numerous axonal
swelling and axonal bulbs

ON AUTOPSY
1.Petechial hemorrhages in
- cortex (at the junction of grey and white matter)
- in roof of IV ventricle
- piamater of the upper segments of the cervical cord
2.Oedema
3.Foci of myelin degeneration
4.In mild DAI, some axons may be damaged.
In severe DAI there is
- shearing of axons in white matter of cerebral hemisphere,
corpus callosum and upper brainstem
- focal hemorrhage in corpus callosum and dorsolateral
rostral brain stem

Microscopic examination :
 up to 12 hours - no axonal injuries
 After 12 hours - the axons appear
Dilated
↓
Club shaped
↓
Retraction balls
↓
no. decreases after 2 to 3 weeks
↓
Microglial cells
↓
Astrocytosis
↓
Demyelinisation

DAI is clinical condition :
- Mild DAI - coma for 6 to 24 hrs
- Moderate DAI - coma for > 24 hrs
- Severe DAI - coma for > 24 hrs + brain stem
dysfunction
Occurs due to - vehicles accidents (90%)
- falls and assaults (10% )

AMNESIA FOLLOWING HEAD INJURIES
 Amnesia usually associated with concussion
 The memory of distant events tends to return before
recent events
 Permanent retrograde amnesia - seconds up to 7 days
 Person recovering from concussion, events which
occured just before the injury are sometimes
remembered indistinctly → later complete amnesia
occurs
 Such patients may make false accusation

Is intimately associated with amnesia, after
accident
Is a behaviour in which person is unaware that
the act is taking place
The patient may speak and act in purposive
manner, but does not remembers them
afterwards
Post traumatic automatism

HEAD INJURY AND ACUTE ALCOHOLIC
INTOXICATION
A person may be confused and disorientated
after a head injury simulates acute alchohlic
intoxication
Intoxicated person sustaining head injury →
impossible to assess to what degree his
condition is due to head injury or intoxication
Such person should be admitted in a hospital
for observation.

Difference b/w Drunkenness and Concussion
FEATURES DRUNK CONCUSSED
Face Suffused, flushed, warm Pale, clammy
Pulse Fast, bounding Slow, feeble
Pupils
Contracted in coma,
dilate on external stimuli and
contract again,
reaction to light -sluggish
Contracted or unequal
Breathing Sighs, puffs, eructates Shallow, irregular, slow
Memory Confused
Retrograde amnesia
unrelieved by time.
Behavior
Uncooperative, abusive,
unresponsive, insolent,
talkative
Cooperative quiet.

Contusion of brain
 Localised deformation of skull → shear strain
develops in the brain tissue → a zone of contusion
in the surface layer
 When head is rotated → layer of brain tissue slide
over each other at different depths in cortex →
damage to the blood vessles
 Contusion may occur on surface of cortex or deeper
down without tearing of tissue
 May occur without injury to the skull
 The period of unconsciousness = 30 minutes to
several days

CONTUSION
 Circumscribed area of brain tissue destruction ＋
extravasation of blood into affected tissue.
 Produced by blunt force
 Found in grey and white matter
 Due to injury of blood vessels by mechanical stress.
 Most often found in frontal and temporal lobes
 Deeper structures,e.g.,basal ganglia,midbrain,and
brain stem may be contused from impact to forehead
and vertex
 Most haemorrhages occur at the crest of convolution
facing the dura of flax and tentorium

 Haemorrhage is first seen in the perivascular space
along the shrivelled and collapsed blood vessles
 At the crest
 Columnar arrangement perpendicular to the surface
of the convolutions
 A larger haematoma may be formed by their union
 Blow to the top of the head → prominent contrecoup
subtemporal or uncal contusion.

Blow to the side
→ a lateral coup lesion
→ prominent contrecoup contusion or
laceration (on lateral aspect of opposite
hemisphere)
Blow to the front of head usually do not
produce cerebral contusion or laceration
In severe frontal injury → coup laceration
Old contusion appear as shrunken yellowish-
brown area known as plaque jaures

AGE OF CONTUSION
• 1hour - Ischaemic changes
• 5-10 days - Capillary proliferation
• 2 weeks - Macrophage containing fat
• Few weeks - Astrocyte proliferation
• 2 months - Scar (pale or golden yellow)

CONTUSION NECROSIS
Found at convolutions
Form small clefts, irregularly-shaped holes or
trenches with sharply outlined walls
Usually brown in colour.
They communicate with subarachnoid space
and do not contain any blood vessles

TYPES OF CONTUSION
1.Fracture contusion
2.Intermediary coup contusion
3.Gliding contusion
4.Herniation contusion

CEREBRAL LACERATION
 There is loss of continuity of the substance of brain.
 Surface lacerations are accompained by ruptures of
pia matter and subarachnoid haemorrhage
 When parenchyma is completly disorganised it is
termed pulpefaction
 Usually seen underneath skull fractures
 In depressed fractures the bone fragments tear the
brain surface
 All penetrating injury produce laceration of brain.
 Blunt trauma, without fracture skull lacerates the
corpus callosum or septum pallucidum in younger
individual

 In severe hyperextention of head -
At pontomedullary junction, there may be -
→ laceration in the pyramid
or
→ avulsion of the brain stem
 Usually associated with fractures of the base of the
skull and upper cervical vertebrae.
 Slit-like or irregularily shaped
 Contain very little blood
 Adhesions may develop between the brain and dura
mater due to healing of surface laceration → causing
Secondary epilepsy
 Healing of deep laceration involving ventricles may
produce large glial cyst, filled with CSF (Traumatic
Porencephalic Cyst)

CEREBRAL OEDEMA
 It occurs due to localised or diffuse
accumulation of water and sodium → increases
the volume of the brain
 It is caused due to : -
- ↑ intravascular pressure
- ↑ permeability of the cerebral vessels
- ↓ plasma colloidal osmotic pressure
 Contusion and lacerations → Focal oedema

OEDEMA OF BRAIN AND SWELLING
 In brain swelling, oedema is mainly intracellular.
 The organ is enlarged and firm and has relatively
dry cut surface.
 In oedema of brain, the fluid collection is interstitial.
 The organ is enlarged and soft and has a very
watery cut surface

Swelling of brain
 May occur following significant head injury
 May be focal or diffuse involving one or both cerebral
hemispheres
Within 20 minutes
 Head injury ---------→ Massive cerebral swelling
 Swelling of one cerebral hemisphere＋Ipsilateral acute
subdural haematoma
 Vasodilation → Increase in intravascular cerebral blood volume
or an absolute increase in water content of the brain tissue →
Brain swelling

Cerebral oedema
 Occurs due to ↑ water content of the brain
 ↑Intravascular blood volume (for some time)
↓
Brain swelling
↓
↑ Vascular permeability
↓
Cerebral oedema

Haemorrhage and Necrosis at site of pressure
Severe oedema
presses down cerebral
hemispheres upon the
tentorium
Herniate through the
midbrain opening
The hippocampal gyrus
may impact in the
opening
Grooving of unci.

↑ Intracranial pressure → ↓VR from intracranial sinuses
Arterial flow is not impaired → ↑ swelling
Cerebral oedema ↔ Hypoxia

AUTOPSY
 The dura is stretched and tense
 Brain is bulging with increase in weight
 Gyri are pale & flattened with thinning of grey
matter.
 Sulci are filled & cerebral surface is smooth.
 Cerebral hemispheres and uncus may herniate
 Cerebellar tonsils may be impacted or coned into
foramen magnum

INCREASED INTRACRANIAL PRESSURE
Causes:
EDH & SDH
Cerebral hemorrhage
Infarction of brain
Tumour or Abscess
Dural Sinus Thrombosis
Leptomeningitis
Diffuse cerebral oedema

CEREBRAL COMPRESSION
 D/t - ↑Size of brain (Swelling or ICSOL)
 Compression → ↓CSF amount
↓ Blood supply
 Types : 1. Supratentorial
2. Infratentorial

Supratentorial
Squeezing of Uncus or Temporal Lobe (inner margin)
through hiatus
↓
Squeezing of Mid brain (A-P lenghthening)
↓
Streching of Paramedian & Nigral blood vessels
↓
Rupture
↓
Hemorrhage in Midline & Substantia Nigra (Fatal)

Infratentorial
Rise in pressure
↓
Forces cerebellar lobe and tonsils
through foramen magnum
↓
Compresses medulla oblongata
↓
Respiratory failure

P. M. Findings
1. Uncal grooving
2. Foraminal indentation of cerebellar tonsils

DURET HAEMORRHAGE
 Secondary tear drop haemorrhage of mid
brain and pons
 Ranging from small streaks to massive
confluent haemorrhage in the midline
 Occurs with asymmetrical herniation of brain
stem

Suggestive evidence of cerebral compression
 Flattening of gyri
 Narrowing of sulci
 Apparent decrease of CSF
 Deep grooved marking around uncus of
temporal lobe and cerebellar pressure cone

Supratentorial compression of mid brain
against the free edge of tentorium may cause
unilateral grooving of cerebral peduncle
(Kernohan's notch)
When symmetrical, the oedema forces
against the tentorium, so that hippocampal
gyrus is squeezed into the opening

LOSS OF CONSCIOUSNESS
D/t-
 Destruction of Reticular activating system
↓
Reduced affarent activity
↓Stimuli → Normal sleep
↓Enzyme system → Irresistible sleep
 Toxic agents

BRAIN STEM
May be injured by -
1.Streching of peduncles
2.Decelaration against basisphenoid & dorsum sellae
3.Lateral shift of peduncle against tentorial margin
4.Strech or avulsion of cranial nerves
5.Traction on its vascular supply

PONTINE HAEMORRHAGE
1.Spontaneous - single
- 1/3 to 1/2 of pons involved
2.Traumatic - in different foci, which may unite
(Both rupture in IVth ventricle)
C/F - Pinpoint pupil not reacting to light with Head injury
 Primary small hemorrhage occur near walls of III or IV
ventricles & aquaduct
 Numerous & severe hemorrhage in rostral brain stem are fatal

CAUSE OF DEATH IN HEAD INJURY
 Damage to vital cerebral centres -
- posterior hypothalmus
- mid brain
- medulla
 Respiratory failure or paralysis
 Vital centres - compression or concussion or
secondary changes
 Others - Infection, hypostatic pnemonia,
pulmonary embolism or renal infarction

INTRACRANIAL
HAEMORRHAGES
1.Extradural Haemorrhage
2.Subdural Haemorrhage
3.Subarachnoid Haemorrhage
4.Intracerebral Haemorrhage

EXTRADURAL HAEMORRHAGE
(EDH)
 Exclusively due to trauma
 On impact → skull moves relative to the bone →
empty extradural space → blood vessels get injured
 Emmissary veins pass through Extradural space

Vessels injured (depend upon the site of trauma)
A blow over -
1. Lateral convexity of head may injure :
- Middle meningeal artery (Posterior branch)
- Meningeal vein
- Posterior Meningeal artery
- Anterior Meningeal artery
2. Forehead → anterior ethmoidal artery
3. Occiput or low behind the ear → transverse sigmoid sinus
→ posterior fossa hematoma
4. Vertex → sagittal sinus
5. Venous extradural hemorrhage accompanies fracture of skull
and is due to bleeding from the diploic vein.

 It is least common type of meningeal bleeding
 Rare below 2 years (d/t greater adherence of dura to the skull)
 Common in adults between 20-40 years
 Occurs due to :
- fall from height
- hit by a moving object
- after a minor accident
 If fracture found - fissured type (90% cases)
 Coup
- Contre-coup in gross deformity
- B/L in B/L trauma
 50% with 2nd Haemorrhage

Blood Clot :-
 Sharply defined
 Presses the dura inward → localized concavity of
external surface of the brain
 Oval or circular
 Rubbery in consistency
 Reddish-purple
 Size = 10 to 20 cms in diameter & 2 to 6 cms thick
 Weight = 30 to 300 gms
 Area -Tempero-parietal
- Fronto-temporal
- Parieto-occipital
 100 ml is fatal

C/F
 History of head injury
 Temporary unconciousness
 Followed by Lucid interval of few hrs to a week
(in 30 to 40 % cases)
 C/L Hemiparesis
 I/L Dilation of Pupil, not reacting to light (Anisocoria)
 If B/L – Both pupils dilated + Decerebrate rigidity

Age of EDH
 Recent effusion-Bright red
 4th day - Bluish black to brown
 12 to 25 days - Pale brownish yellow
 Few months - Coagulum becomes
firm and laminated

 Death d/t –
- Respiratory failure
- Cerebral oedema
- Secondary haemorrhage in pons
- Tentorial herniation
 PM Findings-
- Fisssured fracture
- Break in vessels

CHRONIC EDH
Rare
± Fracture
Commonly seen in older children and
young adults
Symptoms are noted 2 to 3 days after
injury
Sudden death may occurs after several
days

SUBDURAL HEMORRHAGE
(SDH)
 Arachnoid is -
- thin, vascular meshwork and is intimately applied to
the inner surface of the dura
- attached to the dura by venous sinuses and
arachnoid granulations
 Subdural space is very narrow and contains fluid
 The cerebral vein (bridging veins) cross this space to reach
the sinuses

CAUSES
1. Rupture of bridging or communicating veins.
2. Rupture of inferior cerebral vein entering the
sinuses at the base of skull.
3. Rupture of dural venous sinuses.
4. Injury to cortical veins.
5. Laceration or contusion of the brain and dura.
6. Reinjury of old adhesions between brain and the
dura.
7. Secondary to disease e.g. cerebral neoplasm,
cerebral aneurysm or blood disorder
8. Drugs such as dicoumarol,warfarin and heparin.

 SDH may occur from relatively slight trauma with
unconsciousness or fracture
 May be associated with contrecoup contusion
 May occur after fight or falls
 Found in alcoholics, old persons and children
 100 to 150 ml is fatal
 Rapid SDH causes - compression of brain stem
- secondary brain haemorrhage

 Haematoma causes - displacement of cerebral hemisphere
- flattening of the convolutions of the
opposite hemisphere
 Most commonly supratentorial
 U/L or B/L
 Fatal with – Contusion / Laceration / #

Types of SDH
1.Acute
2.Subacute
3.Chronic

ACUTE SDH
D/t - rupture of - large bridging veins
- cortical artery
- laceration
 Spreads freely in subdural space
Blood is usually liquid or semi-liquid
Vary from 1mm to 2 to 3 cm thickness
Commonly affected area is fronto-tempero-parietal
regions
Fresh SDH - easily washed off (but not SAH)

 C/F- resembles EDH
- delayed for 24 to 48 hours
 ± Lucid interval (longer than EDH)
 Almost always of traumatic origin
 Initially no cerebral compression, but secondary changes may
increase the size
 Death d/t secondary pressure upon the brain stem
 Infarction d/t
a) SDH - underneath
- recent
b) Stroke - Not underlies
- as old as oldest portion of haemorrhage

SUBACUTE SDH
 D/t bleeding from smaller bridging veins
 ± Brain injury
 Blood – thin & watery d/t – haemolysis
or
- dilution with CSF
 May appear like that of chronic type

AUTOPSY
Cerebral oedema
Secondary haemorrhage in pons
Tentorial herniation d/t pressure of blood
clot and brain swelling
Break in the vessels and fissured
fracture of nearby skull

CHRONIC SDH
 Presents 3 to 6 weeks after the injury
 Usually seen over - the parietal lobe
- near the midline
- may be B/L
 Often spreads over the temporal or frontal lobe and
may extend to the base
 Localised / Deep / Widespread

 The fluid is reddish brown (often with fibrin clots)
↓
Darker
↓several weeks
Brownish
 Small hematoma replaced by fibrous tissue
 Hemorrhage gets rapidly sealed off

 Chemical changes may cause further hemorrhage
↓ Further trauma
Second Hemorrhage (Sealed off)
↓
New Blood vessels penetrate for healing
↓
Successive hemorrhage
↓
Increase volume
↓
Unconsciousness or Death
(PACHYMENINGITIS HEMORRHAGICA INTERNA
CHRONICA)

 More space in old age d/t atrophy
 SDH = small to 100 - 150 ml
 ± Neurologic symptoms
 Gradually encapsulated
 Presses on gyri → flattens → deforms brain surface
(without shifting)

DATING OF SDH
24 Hours - Layer of fibrin is deposited beneath the dura
36 hours - Fibroblastic activity at junction of clot & dura
4-5 days - 2 to 5 cells thick layer of fibroblast
(after 4 days - red cells lose their shape)
5-10 days - capillaries & fibroblasts invaded
- Haemosiderin-laden macrophages seen
At 8 days - A membrane of 12 to 14 cells thick present

14 days -The membrane enclosing the arachnoid
begins to form
- Dural membrane attain 1/3–1/2 dural thickness
3-4 wks - covered by fibrous membrane (grows inwards)
4-5 wks - Arachnoid membrane has 1/2 dural thickness
- Clot is liquified completely
- Haemosiderin-laden macrophages
1-3 Months -The membrane is hyalinised on both sides
↓
large capillaries invade → complete resorption
↓
Gold coloured membrane
(adherent to the dura)

SUBDURAL HYGROMA
When arachnoid is torn
↓
CSF may pass into subdural space
↓
large collection of fluid
↓
cerebral compression
↓
Cerebral hygroma

SUBARACHNOID HAEMORRAHAGE
(SAH)
 Piamater is a surface feltwork of glial fibres,
inseperable from underlying brain
 Subarachnoid space contains:
- blood vessles of the brain
- its cranial nerves
- a network of connective tissue fibres
- It is filled with CSF

Causes
1. Rupture of bridging veins near sagittal sinus
2. Laceration and contusion of brain and pia-arachnoid
3. Rupture of saccular berry aneurysm (in 95% of aneurysms)
4. Angiomas and AV malformations
5. Asphyxia
6. Diseases : Blood dyscrasias, leukaemias
7.Tears of the ventricular ependyma
8. Rupture of an intracerebral haemorrhage of non traumatic
origin (apoplectic haemorrhage or stroke)
9. A kick or heavy blow on neck beneath the ear → rupture of
vertebro - basilar artery

Spontaneous Hypertensive SAH
 D/t - ruptue of microaneurysyms (Charcot-Bouchard
aneurysm)
 ↑ in no. in arteries of brain with age & length of H.T.
 Major sites are - putamen / internal capsule (55%)
- lobar white matter (15%)
- thalamus (10%)
- pons (10%)
- cerebellar cortex (10%)
 > 50% are d/t Intracranial aneurysms
 Berry aneurysms are found at -
- Bifurcation of Middle cerebral Artery (90%)
- Anterior cerebral artery
- Posterior communicating arteries

 In acute alchoholic traumatic SAH is more common
due to :
- loss of muscular coordination → ↑rotational force
- ↑bleeding from congested vessels
 Most common form of traumatic Intracranial
haemorrhage
 U/L or B/L
 Localised / Diffuse
 Areas – Frontal, Parietal or Temporal (Ant. 1/3)
 It is mostly venous

 Subdural blood washes away under gently running,
while subarachnoid blood imparts a red colour to the
brain that does not wash
AUTOPSY
 In mild forms - splashes of haemorrhage over the
areas of contusion
 In most cases - diffuse overlying the cerebral
hemispheres
 Rarely causes scarring within SA space (esp. over
brain stem and basal cisterns)
 Yellow discolouration of leptomeninges is seen in
older SAH

C/F
 Headache with rapid onset (thunderclap headache)
 Stiff neck
 Photophobia
 Deterioration of consciousness
ARTEFACT
 Produced at autopsy d/t -
a) damage to cerebral vein and the arachnoid
b) decomposition with:
- lysis of blood cells
- loss of vascular integrity
- leakage of blood in SA space

INTRACEREBRAL HAEMORRHAGE
(ICH)
Found on surface or in the substance of the
brain
Haemorrhage into brain due to trauma usually
occurs near surface

CAUSES
1.Capillary haemorrhage found in softening of brain d/t:
- anoxia or arterial thrombosis
- sinus thrombosis
- blood dyscrasias
- fat embolism
- asphxial deaths
2.Spontaneous haemorrhage in region of basal
ganglion by rupture of lenticulostriate artery
(common in middle aged and elderly)

3. Angioma or malignant tumor of the brain
4. Hypertensive cerebro-vascular disease -
Haemorrhage occurs in thalmus, external capsule,
pons and cerebellum
5. Laceration of brain
6. Blow on head ± fracture of skull → coup-contrecoup
mechanism
7. Intraventicular haemorrhage

INTRAVENTRICULAR
HAEMORRHAGE
D/t head striking firm object
Bleeds from - choroid plexuses
- veins of septum pelucidum
- rupture of an AV fistula
Also d/t extension of non traumatic ICH
Death - rapid or delayed for several days

NON TRAUMATIC ICH
 In hypertensive cerebrovascular disease
 With physical exercise or excitement
 D/t rupture of lenticulostriate artery
 Spontaneous hemorrhage in basal ganglia,
thalamus, external capsule, pons or
cerebellum
 Common in middle aged and elderly

Difference B/W Post-traumatic ICH & Apoplexy
Trait
Po st-traumatic
haemorrhage
Apoplexy
1. Cause Head injury
Hypertention,
atherosclerosis, aneurysm
2. Age Young individuals Adults past middle age
3. Onset
Distinct interval (few min
to several hrs) b/w
violence and symptoms
Sudden
4. Position of head In motion Any position
5. Region
White matter of temporo-
occipital or frontal region
Ganglionic region
6. Contrecoup haemorrhage May be present Not present
7. Concussion
May be seen, may become
conscious before clinical
effect appear
Not present
8. Coma Spontaneous variation Deep unconciousness

1. Contre coup injuries are seen in :
A) Heart
B) Brain.
C) Lungs
D) Uterus

2. Depressed fracture of skull is produced
by:
A) A light weight blunt object
B) A heavy weight blunt object with small
striking surface.
C) A heavy weight blunt object with big
striking surface
D) Fall on the road

3. Sutural surface of skull is also known
as :
A) Diastatic fracture.
B) Fissured fracture
C) Depressed fracture
D) Comminuted fracture

4. Spider web fracture of skull is other
name for:
A) Diastatic fracture
B) Fissured fracture
C) Depressed fracture
D) Comminuted fracture.

5. Gutter fracture of skull is due to:
A) Sharp pointed weapon
B) Fire arm injury.
C) Blunt weapon
D) Heavy cutting weapon

6. Contre coup injuries of the brain are seen
at:
A) Adjacent to site of impact
B) Away from the site of impact
C) Anywhere in the brain
D) Just opposite to the site of impact.

7. Punch drunk syndrome is commonly
seen in :
A) Tailors
B) Cobblers
C) Boxers
D) Cricket players

8. Ring fracture is a type of fracture of :
A) Mandible
B) Skull.
C) Humerus
D) Femur

9. Fracture of the base of the skull may
result from:
A) Fall from feet
B) Blow over chin
C) Blow over vertex
D) All of the above.

10. Contre coup injuries are usually
seen, when head is :
A) Not supported
B) Supported.
C) Covered with a heavy object
D) Moving at a great speed

11. Bevelling of inner table of the skull
bone is suggestive of :
A) Burr hole
B) Penetrating wound
C) Fire arm entry wound.
D) Perforating wound

12. Commonest type of intracranial
haemorrhage is :
A) Subarachnoid .
B) Subdural
C) Intracerebral
D) Extradural

13.Rupture of berry aneurysm leads to :
A) Subarachnoid haemorrhage.
B) Subdural haemorrhage
C) Extradural haemorrhage
D) All of the above

14. Ring fracture of skull is produced by :
A) A blow on the front of head with blunt
object
B) A blow on the side of head with blunt
object
C) Fall from height landing on buttocks.
D) A hit with a small bullet over the head

15. CHF ottorrhea is caused by:
A) Fracture of cribriform plate
B) Fracture of parietal bone
C) Fracture of petrous temporal bone.
D) Fracture of tympanic membrane

16. Most common site for fracture
mandible :
A) Condyle.
B) Angle
C) Body
D) Symphysis

17. Lucid interval is classically seen in:
A) Intracerebral hematoma
B) Acute subdural hematoma
C) Chronic subdural hematoma
D) Extradural hematoma.

18.True about CSF rhinorrhoea:
A) Commonly occurs due to break in
cribriform plate.
B) Contains less amount of proteins
C) Decreased glucose content confirms
diagnosis
D) Immediate surgery is required

19. Characteristic of anterior cranial
fossa fracture :
A) Black eye.
B) Pupillary dilatation
C) CSF otorrhea
D) Hemotympanum

20.Orbital blow out fracture involves :
A) Lateral wall and floor of orbit
B) Medial wall and floor of orbit
C) Lateral wall and roof of orbit
D) Medial wall and roof of orbit

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