HEAD_INJURY_.........................3.ppt

introduction, mechanism of injury, classification and management

1. HEAD INJURY
By -Dr. RAJA RUPANI

2. DEFINITION
Headinjuryisamorbidstate,resultingfromgrossor
subtlestructuralchangesinthescalp,skull,and/orthe
contentsoftheskull,producedbymechanicalforces.
Thebluntforcemayresultininjurytothecontentsof
theskull,eitheraloneorwithafractureoftheskull.
Theextentanddegreeofaninjuryisnotnecessarily
proportionaltotheamountofforceappliedtothe
head.

3. SCALP
The thicknessof 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 contusionsor lacerations.

4. SCALP

5. CONTUSIONS OF SCALP
May occur in the superficial fascia, in the
temporalis muscleor loose areolar tissue
Contusions in the superficial fascia appears as
localized swellingand 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)

6. Bruisingofthescalpisbetterfeltthanseen
Itsfirmedgefeelslikedepressedfracture
Ascalpwoundbyabluntweaponfrequently
resemblesanincisedwoundandassuch
theedgesandendsshouldbecarefully
examinedwithamagnifyinglens.

7. LACERATIONS OF SCALP
If the scalp is lacerated by a blow, blood is driven out
of the vessels due to compression and considerable
bleedingoccurs
With further blows, blood is projectedabout the scene
With repeated blows, blood is splatteredover
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

8. LACERATION OF SCALP

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

10. Avulsion of scalp

11. INJURIES TO FACE
Bleeding is more in facial
wounds

12. 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

13. BLACK EYE
(PERIORBITAL BRUISING)
Itiscausedby:
1.Directblowinfrontoforbits,bruisinglids.
2.Injurytotheforehead,thebloodtracking
downunderthescalp.
3.Fractureintheanteriorcranialfossa,
thebloodleakingthroughcrackedorbital
plates.

14. Black Eye

15. NOSE
1.Maybebittenorcutoffduetosexual
jealousyorenemity.
2.Ablowmaycausenasalbleedingdueto
partialdetachmentofmucousmembrane
EARS
Ablowmayproduce-
1.Ruptureofthetympanum
2.Deafness
3.Labyrinthmayinjured

16. FACIAL BONES
Ablowoftenfracturesthenasalboneandalsoethmoid
bonewithradiatingfracturesintosupraorbitalplates,if
theforceissevere.
Ablowmayfracturemaxillaandmalarbone.
Pulpingoffacemayresultfromstrikingwithaheavystone.
Themandibleisfracturedbyablowfromafist,stickorby
fallfromheight.
Aheavyblowonthejawsdrivesthecondylesagainstthe
baseofskullproducingafissuredfracture.
TEETH
Afallorablowwithabluntweaponmaycausefractureor
dislocationofteeth,withcontusionorlacerationonlips
orgumsandbleedingfromthesockets.

17. SKULL
The outer table is twicethe 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.

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

19. 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.

20. LOCAL DEFORMATION

21. 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

22. 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.

24. 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

25. FISSURED FRACTURE
These are linearfractures 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.

26. •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.

27. •Linear fractures do not tend to cross bony
buttresses (an architectural structure built against
or projecting from a wall which serves to support or
reinforce the wall), 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.

28. 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

29. FISSURED FRACTURE

30. FISSURED FRACTURE

31. FISSURED FRACTURE

32. 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 hammeris used ,the fracture is circularor
an arcof a circle, having the same diameter as the
striking surface.

33. DEPRESSED FRACTURE

34. DEPRESSED FRACTURE

35. 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.

36. COMMINUTED FRACTURE

37. COMMINUTED FRACTURE

38. POND OR INDENTED FRACTURE
This is simple dentof the skull –
-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.

39. POND FRACTURE

40. POND FRACTURE

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

42. GUTTER FRACTURE

43. RING FRACTURE
It occurs in the baseof 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.

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

46. PERFORATING FRACTURE
These are caused by firearmsand 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.

47. PERFORATING FRACTURE

48. PERFORATING FRACTURE

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

51. •ELEVATED FRACTURE
•It is a rare compound skull fractures in which
the fractured segment is elevated above the
level of remaining skull topography.
•BLOW OUT FRACTURE
•It is a break of one or more of the 7
bones that surround the eye.

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

53. Blow on the chin or mandibleproduces:
-fracture of glenoid fossa
-fracture of cribriform plateof ethmoid
Fracture of roof of orbit occurs due to :
-Fall on backof the head
-Blow on topof head
-Sudden violent increase in internal pressure

54. 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

55. 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

56. COMPLICATIONS
1.Fracture of anterior cranial fossamay 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 -inflammation of the subarachnoid
space.
4. Cranial pneumatocele –thin walled, air filled cysts/
lesions that develop within the lung parenchyma.

57. 5.Middle fossa fracturethrough 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

58. 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

59. 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.

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

61. AGE OF SKULL INJURY
Healingoccurswithouttheformationofvisible
callus,asperiostealbloodvesselsaredamaged
1stweek-
-Edgesoffissuredfracturesticktogether
14days-
-Edgesareslightlyeroded
-Innersurfaceoftheskullshowspittingordeposition
ofsalt
3-5week
-Edgesbecomeslightlysmoothandbandsof
osseoustissuerunacrossthefissure.

62. 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

63. 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.

64. 3Acceleration / Deceleration injuries:
Suddenmovementofthehead→intracranial
pressuregradients→shearingandtensileforces.
Animpactingforcetotheheadcanproduce:
-linearaccleration,
-rotational(angular)acclerationor
-combinitionofboth

65. 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)

66. MECHANISM OF CEREBRAL INJURIES
Damagemaybecausedwithoutactualbloworfall
onthehead,e.g.byshakingtheinfantasinchild
abusemaycausesubduralhemorrhage.
Ablow→linearorrotationalchangeinvelocity
Forcesinvolved-linearacceleration/deceleration
-centrifugal&rotationalvelocity.

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

68. Sudden arrest of moving skull →decelaration of the skull
first, but momentum of braincauses 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 wallof the skull → diffuse contusion
of cortex
Cerebellum d/t small size and light weight is less liable to
damage from rotatory movement of head

70. Contrecoup lesion
•Coup-located beneath the area of impact
•Contrecoup-in an area oppositethe 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 vaccumon opposite
side

71. Blow on Occipital–injures Frontal lobe & tip of
Temporal lobe
Blow on Frontof head –damages inner & lower part
of back of brain or Brain stem
Fall on side–contusion of opposite side
Fall on topof head –contusion of ventral surface of
cerebral hemisphere
Blow on parietalarea –lesion on opposite hemisphere
or medial side of same hemisphere

74. 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

75. MECHANISM
Occursduetoacceleration/decelerationof
thehead
Theviolentheadmovementcausesshearing
orstreachingofthenervefibersandaxonal
damage.
Severeinjuriesoccurincoronalheadmotion
only.
Sagittalheadmotionproducesmildor
moderateinjury

76. Atlowlevelofaccleration/decelaration,
thereisphysiologicaldysfunction.
Withincreasedphysicalforce,thereis
immediatestucturaldamageofaxonsand
immediatestoppageofallactivites.
Mildconcussion
-consciousnessisnotlost
-noconfusionordisorientation(±amnesia)
Severeconcussion
-amnesiaandlossofconsciousness

78. Cerebralconcussionmaybeproducedby
1.Directviolencetohead
2.Indirectviolence
a)falluponthefeetorbuttocks
b)anunexpectedfallonthegroundin
trafficorindustrialaccidents

79. Duringestablishedconcussion:-
a)muscles-flaccid
b)pupils-dilatedandunreacting
c)pulse-weakandslow
d)respiration-shallow
Asconsciousnessreturns,thereisperiod
duringwhichthepersonappearstobe
lucidandintouchwithsurrounding

80. 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 comadevelops later

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

82. CAUSE OF CONCUSSION
Mostacceptablecauseis-
“Diffuseneuronalinjury“-afunctional
abnormalityofnervecellsandoftheir
connection.

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

84. FeaturesofDAI-
1.Focallesionin-corpuscallosum
-theparasagittalwhitematter
-septum
-wallofIIIVentricle
-dorsolateralbrainstem
2.Microscopicevidenceofnumerousaxonal
swellingandaxonalbulbs

85. ON AUTOPSY
1.Petechial hemorrhages (tiny round, brown purple spots due
to bleeding under the skin) in
-cortex(at the junction of grey and white matter)
-in roofof IV ventricle
-piamaterof 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 axonsin white matter of cerebral hemisphere,
corpus callosum and upper brainstem
-focal hemorrhagein corpus callosum and dorsolateral
rostral brain stem

86. 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

87. 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% )

88. 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
rememberedindistinctly → latercomplete amnesia
occurs
Such patients may make false accusation

89. 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 remembersthem
afterwards
Post traumatic automatism

90. HEAD INJURY AND ACUTE ALCOHOLIC
INTOXICATION
Apersonmaybeconfusedanddisorientated
afteraheadinjurysimulatesacutealchohlic
intoxication
Intoxicatedpersonsustainingheadinjury→
impossibletoassesstowhatdegreehis
conditionisduetoheadinjuryorintoxication
Suchpersonshouldbeadmittedinahospital
forobservation.

91. Difference b/w Drunkenness and Concussion
FEATURES DRUNK CONCUSSED
Face Suffused, flushed, warmPale, 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, eructatesShallow, irregular, slow
Memory Confused
Retrograde amnesia
unrelieved by time.
Behavior
Uncooperative, abusive,
unresponsive, insolent,
talkative
Cooperative quiet.

92. Contusion of brain
Localiseddeformationofskull→shearstrain
developsinthebraintissue→azoneofcontusion
inthesurfacelayer
Whenheadisrotated→layerofbraintissueslide
overeachotheratdifferentdepthsincortex→
damagetothebloodvessles
Contusionmayoccuronsurfaceofcortexordeeper
downwithouttearingoftissue
Mayoccurwithoutinjurytotheskull
Theperiodofunconsciousness=30minutesto
severaldays

93. CONTUSION
Circumscribed area of brain tissue destruction ＋
extravasation of blood into affected tissue.
Produced by blunt force
Found in greyand white matter
Due to injury of blood vesselsby mechanical stress.
Most often found in frontaland 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

94. 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.

95. 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-
brownarea known as plaque jaures

96. 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)

97. CONTUSION NECROSIS
Foundatconvolutions
Formsmallclefts,irregularly-shapedholesor
trencheswithsharplyoutlinedwalls
Usuallybrownincolour.
Theycommunicatewithsubarachnoidspace
anddonotcontainanybloodvessles

98. CONTUSION

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

100. 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 injuryproduce laceration of brain.
Blunt trauma, without fracture skull lacerates the
corpus callosum or septum pallucidum in younger
individual

101. In severe hyperextentionof 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)

102. LACERATION

103. CEREBRAL OEDEMA
Itoccursduetolocalisedordiffuse
accumulationofwaterandsodium→increases
thevolumeofthebrain
Itiscauseddueto:-
-↑intravascularpressure
-↑permeabilityofthecerebralvessels
-↓plasmacolloidalosmoticpressure
Contusionandlacerations→Focaloedema

104. OEDEMA OF BRAIN AND SWELLING
Inbrainswelling,oedemaismainlyintracellular.
Theorganisenlargedandfirmandhasrelatively
drycutsurface.
Inoedemaofbrain,thefluidcollectionisinterstitial.
Theorganisenlargedandsoftandhasavery
waterycutsurface

105. Swelling of brain
Mayoccurfollowingsignificantheadinjury
Maybefocalordiffuseinvolvingoneorbothcerebral
hemispheres
Within20minutes
Headinjury---------→Massivecerebralswelling
Swellingofonecerebralhemisphere＋Ipsilateralacute
subduralhaematoma
Vasodilation→Increaseinintravascularcerebralbloodvolume
oranabsoluteincreaseinwatercontentofthebraintissue→
Brainswelling

106. Cerebral oedema
Occursdueto↑watercontentofthebrain
↑Intravascularbloodvolume(forsometime)
↓
Brainswelling
↓
↑Vascularpermeability
↓
Cerebraloedema

107. Haemorrhageand Necrosisat site of pressure
Severe oedema
presses down cerebral
hemispheresupon the
tentorium
Herniatethrough the
midbrain opening
The hippocampal gyrus
may impactin the
opening
Groovingof unci.

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

109. 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

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

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

112. 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)

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

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

115. DURET HAEMORRHAGE
Secondary tear drophaemorrhage of mid
brain and pons
Ranging from small streaksto massive
confluent haemorrhage in the midline
Occurs with asymmetrical herniationof brain
stem

116. 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

117. CEREBRAL OEDEMA

118. CEREBRAL OEDEMA

119. 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

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

121. 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

122. 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

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

124. INTRACRANIAL
HAEMORRHAGES

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

128. 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

129. 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. Occiputor 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.

130. 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 2
nd
Haemorrhage

131. 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 cmsin diameter & 2 to 6 cmsthick
Weight = 30 to 300 gms
Area -Tempero-parietal
-Fronto-temporal
-Parieto-occipital
100 mlis fatal

133. EDH

134. EDH

135. EDH

136. EDH

137. 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

138. 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

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

140. CHRONIC EDH
Rare
±Fracture
Commonly seen in older childrenand
young adults
Symptoms are noted 2 to 3 daysafter
injury
Sudden deathmay occurs after several
days

141. SUBDURAL HEMORRHAGE
(SDH)
Arachnoidis -
-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

142. 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.

143. SDH may occur from relatively slight traumawith
unconsciousness or fracture
May be associated with contrecoup contusion
May occur after fight or falls
Found in alcoholics, old personsand children
100 to 150 mlis fatal
Rapid SDH causes -compression of brain stem
-secondarybrain haemorrhage

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

145. SDH

146. SDH

147. SDH

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

152. ACUTE SDH
D/t-ruptureof-largebridgingveins
-corticalartery
-laceration
Spreadsfreelyinsubduralspace
Bloodisusuallyliquidorsemi-liquid
Varyfrom1mmto2to3cmthickness
Commonlyaffectedareaisfronto-tempero-parietal
regions
FreshSDH-easilywashedoff(butnotSAH)

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

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

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

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

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

158. Chemical changesmay cause further hemorrhage
↓ Further trauma
Second Hemorrhage (Sealed off)
↓
New Blood vesselspenetrate for healing
↓
Successive hemorrhage
↓
Increase volume
↓
Unconsciousness or Death
(PACHYMENINGITIS HEMORRHAGICA INTERNA
CHRONICA)

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

161. DATING OF SDH
24 Hours -Layer of fibrin is deposited beneath the dura
36 hours -Fibroblastic activityat junction of clot & dura
4-5 days -2 to 5 cells thicklayer of fibroblast
(after 4 days -red cells lose their shape)
5-10 days -capillaries &fibroblasts invaded
-Haemosiderin-laden macrophagesseen
At 8 days-A membrane of 12 to 14 cells thickpresent

162. 14 days -The membrane enclosing the arachnoid
begins to form
-Dural membraneattain 1/3–1/2dural 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 hyalinisedon both sides
↓
large capillaries invade → complete resorption
↓
Gold coloured membrane
(adherent to the dura)

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

164. SUBARACHNOID HAEMORRAHAGE
(SAH)
Piamaterisasurfacefeltworkofglialfibres,
inseperablefromunderlyingbrain
Subarachnoidspacecontains:
-bloodvesslesofthebrain
-itscranialnerves
-anetworkofconnectivetissuefibres
-ItisfilledwithCSF

165. Causes
1. Rupture of bridging veinsnear sagittal sinus
2. Laceration and contusion of brain and pia-arachnoid
3. Rupture of saccular berry aneurysm (in95% 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

166. 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

167. InacutealchoholictraumaticSAHismorecommon
dueto:
-lossofmuscularcoordination→↑rotationalforce
-↑bleedingfromcongestedvessels
Mostcommon formoftraumaticIntracranial
haemorrhage
U/LorB/L
Localised/Diffuse
Areas–Frontal,ParietalorTemporal(Ant.1/3)
Itismostlyvenous

168. Subdural blood washesaway 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 discolourationof leptomeninges is seen in
older SAH

169. SAH

170. UNRUPTURED BERRY ANEURYSM

171. RUPTURED BERRY ANEURYSM

172. SAH

173. C/F
Headache with rapid onset (thunderclap headache)
Stiff neck
Photophobia
Deterioration of consciousness
ARTEFACT
Producedatautopsyd/t-
a)damagetocerebralveinandthearachnoid
b)decompositionwith:
-lysisofbloodcells
-lossofvascularintegrity
-leakageofbloodinSAspace

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

176. 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)

177. 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

178. 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

179. INTRA CEREBRAL HEMORRHAGE

180. INTRACEREBRAL HEMORRHAGE

181. 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 agedand elderly

182. 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
Ganglionicregion
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 variationDeep unconciousness

183. Questions

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

185. 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

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

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

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

189. 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.

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

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

192. 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.

193. 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

194. 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

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

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

197. 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

198. 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

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

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

201. 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

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

203. 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