HEAD INJURYBy - 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.

SCALPThe 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.

SCALP

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

LACERATION OF SCALP

AVULSION OF SCALP

Involves large are of scalp

Occurs in :

- traffic accident

- hairs entangled in machinery

Avulsion of scalp

INJURIES TO FACE

Bleeding is more in facial

wounds

EYESBlunt 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.

Black Eye

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

EARSA blow may produce -1.Rupture of the tympanum2.Deafness3.Labyrinth may injured

FACIAL BONESA 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.

TEETHA 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.

SKULLThe 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.

LOCAL DEFORMATION

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 SKULLA. 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 Fracture2.Depressed Fracture3.Comminuted Fracture4.Ponds or Indented Fracture5.Gutter Fracture6.Ring or Foramen Fracture7.Perforating Fracture8.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

FISSURED FRACTURE

FISSURED FRACTURE

FISSURED FRACTURE

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.

DEPRESSED FRACTURE

DEPRESSED FRACTURE

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.

COMMINUTED FRACTURE

COMMINUTED FRACTURE

POND OR INDENTED FRACTUREThis 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.

POND FRACTURE

POND FRACTURE

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.

GUTTER FRACTURE

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.

PERFORATING FRACTURE

PERFORATING FRACTURE

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 AUTOPSY1.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 ConcussionFEATURES 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.

BehaviorUncooperative, 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 lacerationIn 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

CONTUSION

TYPES OF CONTUSION1.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)

LACERATION

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 & SDHCerebral hemorrhageInfarction of brainTumour or AbscessDural Sinus ThrombosisLeptomeningitisDiffuse 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

CEREBRAL OEDEMA

CEREBRAL OEDEMA

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 HAEMORRHAGE1.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

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

EDH

EDH

EDH

EDH

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 ± FractureCommonly seen in older children and

young adultsSymptoms are noted 2 to 3 days after

injurySudden 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 / #

SDH

SDH

SDH

Types of SDH 1.Acute

2.Subacute

3.Chronic

ACUTE SDHD/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

AUTOPSYCerebral 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 SDH24 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

SAH

UNRUPTURED BERRY ANEURYSM

RUPTURED BERRY ANEURYSM

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

CAUSES1.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 objectBleeds from - choroid plexuses

- veins of septum pelucidum

- rupture of an AV fistulaAlso d/t extension of non traumatic ICHDeath - rapid or delayed for several days

INTRA CEREBRAL HEMORRHAGE

INTRACEREBRAL HEMORRHAGE

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. OnsetDistinct 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. ConcussionMay be seen, may become conscious before clinical effect appear

Not present

8. Coma Spontaneous variation Deep unconciousness

Questions

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