Head Injuries

Head Injuries
Dr. S.R. Hulathduwa
MBBS, DLM.MD. DMJ(Path) (Lond.) DMJ(Clin)(Lond.)
Dip.Crim. MFFLM(UK)
Senior Lecturer
Department of Forensic Medicine
University of Sri Jayewardenapura
Regional Injuries
• This includes
Head injuries
Neck injuries
Facial injuries
Chest injuries
Abdominal injuries
Musculoskeletal injuries
Head Injuries
 An important topic in clinical forensic medicine
and forensic pathology.
 Commonly encountered in traffic accidents,
assaults and falls.
 Any weapon may be used (cluds, swords, sticks,
stones, firearms, bombs..etc.)
Force applied may be
Direct trauma
(force directly applied to head)
e.g. assaults, accidents, falls
Indirect trauma
(transmitted force)
e.g. fall off height landing on feet or buttocks,
blow to chin, hitting the ground of a motor cyclist
in RTA
e.g. violent shaking(shaken body syndrome)
• The force may be
e.g fall
e.g. blows, shaking, etc..
• The following anatomical peculiarities
modify the nature and the extent of head
- hair, scalp, skull, meninges, brain and
base of skull
e.g. scalp bruises are better felt than seen.
-Bleed profusely even PM.
-Easy spread of infection.
-Sinus thrombosis.
Types of head injuries
 Hair – cuts, crushed bulbs and burns.
 Scalp – abrasions, lacerations, bruises
incised wounds, stabs, burns
 Sub scalpar haematoma
 Pericranial haemorrhages.
 Skull-fractures, suture diasthesis, cuts, deficiencies.
 Extra dural heamorrhages(EDH)
 Dural tears
 Sub dural haemorrhages (SDH)
- acute, sub acute, chronic
• Pia-arachnoid tears.
• Sub arachnoid heamorrages (SAH)
• Brain-contusions, lacerations, cuts, stabs,
intra cerebral haemorrhages,
intra ventricular haemorrhages.
• Brain stem – primary and secondary brain
stem heamorrhages.
• Damage to cerebral blood vessels.
• Raised intracranial pressure
Scalp injuries
• Layers of scalp
• Are rare due to presence of head hair.
• May also be unidentified/ missed due to
presence of head hair.
• May indicate severe friction unless the person
is bald.
eg. RTA, fall off height. etc..
Bruises / Contusions
 May be hidden by hair.
 Occurs between the aponeurosis and skin.
 Better felt than seen
 Felt as a boggy mass, swelling or a bump,
specially when associated with a sub-scalpar
 Well seen in autopsy when the scalp is reflected.
• May give the false sense of a fracture of
the underlying skull on external palpation.
• May gravitate to appear at a distant site
(eg. Black eye)
• May become confluent with time so that
it will not accurately indicate the actual
number of blows dealt.
 Usually spilt lacerations due to compression of
scalp between a blunt object and underlying
skull: thus resembling incised wounds.
How to differentiate?
 Depending on the offending object/ weapon,
there may be other types of lacerations too
(crush / perforating / blast lacerations)
 May sometimes give a clue to the shape of the
offending weapon.
eg. Stellate – blunt rods /falling backwards.
Incised wounds
- Usually slashed cuts.
-usually on an area where the skull is thin.
E.g. temporal bone.
-also can penetrate the orbit.
 Could be due to flame / high tension
electrocution / corrosives.
 Flame burns may cause singeing of hair,
which is of value in,
a)Deciding the approximate range of fire arm
b) Deciding the proximity of the victim to the
c) Differentiating dry heat from scalds (moist
burns) and corrosive burns
Fire arm injuries
-perforating and/or blast lacerations.
Blast injuries
-blast and/or perforating lacerations.
Skull fractures
• A fall through one meter (or even lesser) can
cause a skull fracture in an adult.
• Usually a substantial force in needed to cause
a skull fracture.
• May involve one or both tables of the skull.
• Common on the vault than the base of the
Types of skull fractures
Linear / fissured
Depressed comminuted
Linear/fissured #
-usually falls.
-also by blows with blunt weapons on an
unsupported head.
-may represent the forward and downward
components of the force applied, thus
indicating the direction of the blow/position
of the victim. (pointer #)
Depressed #
- When the inner table is disrupted and driven
- Usually due to blows with a heavy weapon
with a relatively small striking surface. E.g.
head of a hammer
- Common with supported head.
- May usually indicate the shape of the striking
surface, thus known as “signature fracture”
- Damage to meninges and brain is common.
- If the force is severe enough, can end up with
a deficiency of the skull.
- Can be a focus of post traumatic epilepsy at a
later time.
Comminuted #
- When the skull is broken in to more than
two fragments.
- May take the shape of a “cob-web” )cobweb/mosaic #)
e.g. RTA, falls, blunt heavy weapon with a
large striking surface.
Depressed comminuted #
Guttered #
- An elongated depressed #
e.g. long, heavy, thin, blunt weapon.
Elevated #
- When a cutting/stabbing weapon is
withdrawn from the skull, the fractured
fragments may be elevated.
Pond #
- In infants the skull may bend / indent
inwards without “ cracking”
Growing #
- If the soft tissue/meninges are caught in
between the two edged of a fracture, in
an infant, the # will widen with time
delaying healing. Brain tissue may even
herniate through the defect with time.
Ring #
- Around the foramen magnum.
- Usually due to transmitted force along
the spine (fall off height landing on
- Rarely when landing on the top of head.
Compression #
- Due to lateral compression of head.
- The fracture line may encircle the head.
Hinge #
- Fracture line runs across the middle
cranial fossa and pitutary fossa dividing
the base of the skull in to two.
- Seen when motorcyclists land on the road
chin first (motorcyclist’s #)
- Also in boxers.
Contre-coup #
- Orbital plate of the frontal bones (orbital
roofs) and ethmodial plate may be
fractured due to occipital impact.
Eg. Fall on the back of the head.
 Any of the above can be compound
internally or externally.
Factors modifying the nature of
a skull fracture
 Nature of the weapon/agent
(blunt, sharp, cutting, stabbing, firearm,
 Striking surface
 Pliability of the weapon
 Force used
 Thickness of the skull
 Area of the head involved
(e.g temporal Vs occipital)
 Whether the head was supported or free
to move.
 Other factors related to the victim
(eg. Age, bone diseases, etc..)
Forensic information that may be
gathered from skull fractures.
 Nature of the weapon/agent.
 Force used(a crude approximation only).
 Whether the head was supported or free to
 Direction of the blow(by studying the pointer #)
 Possible external injuries
 Possible internal injuries
 Volitional activities.
Period of survival
Evidence of infection/healing
Is it fall or a direct blow?
e.g. depressed # on the vertex are usually
due to a direct blow while a linear # in
occipital area. Extending in to base of
skull is more suggestive of a fall
Intra cranial haemorrhages
This includes,
• Extra dural haemorrhages (EDH)
• Sub dural haemorrhages (SDH)
(acute, sub acute, chronic)
• Sub arachnoid haemorrhages (SAH)
• Intra cerebral haemorrhages
• Ventricular haemorrhages
Cerebral injuries
The following can be included as cerebral injuries,
- Cerebral concussion
- Diffuse axonal injuries (DAI)
- Diffuse vascular injuries
- Coup injuries
- Contre-coup injuries
- Intra cerebral haemorrhages
- Brain stem haemorrhages
- Ischaemic brain damage (hypoxic ischaemic
Extra Dural Haemorrhage (EDH)
• Collection of (clotted) blood in the potential
space between the inner table of the skull and
the dura.
• Commonest site is the temporal area as the
skull is thin and the meningeal vessels run in
this area.
• Parietal is the second commonest.
• Can rarely be infra tentorial in the posterior
cranial fossa
• Symptoms occur rapidly in temporal and
parietal EDH, enabling early diagnosis.
• Can present in 3 ways.
1.) classical presentation (yet rare)
immediate loss of consciousness
Spontaneous recovery with lucid interval
Gradual deterioration of level of
consciousness until death
2).No LOC initially gradually deteriorates
until death
3). Unconscious from the beginning
Dies without regaining consciousness
• Prognosis is poor in frontal EDH as onset
of symptoms is delayed.
• EDH in posterior cranial fossa can cause
brainstem compression (infra-tentorial
 EDH is considered to be always traumatic
in origin; 85% are associated with skull #
 Source of bleeding could be either arterial
(middle meningeal) or venous (diploic
veins, superior sagittal sinus and other
venous sinuses)
 Onset is rapid arterial bleeds and in most
cases the bleed is arterial.
 In an adult, approximately 100-150 ml is
considered to be fatal if not removed.
• After established cerebral oedema due to
increased intracranial pressure, EDH will
have a poor prognosis, though
successfully evacuated.
• Usually considered as FIOCN.
• Rare in extremes of age: why?
• Bilateral EDH can occur with compression
# though this is very rare.
• “heat haematoma” is a post mortem
artifact due to burns, which will resemble
an ante-mortem EDH
 When the skull of the dead body is subjected
to intense heat, blood will seep from the
diploe and collect above the dura.
 Usually seen underneath an area of
extensive burns: may be bilateral and
chocolate brown in colour (or even cherry
pink due to carboxy-haemoglobin), Honeycomb/cavernous in appearance:
 But problem may occur when associated
with other heat artifacts such as ruptures as
heat ruptures and heat fractures.
Subdural haemorrhage (SDH)
• A collection of blood between dura and
pia arachnoid.
• Commoner than EDH.
• Less commonly associated with skull
fractures when compared with EDH
• May occur over convexities of the brain as
well as in all three cranial fossa.
• Almost always traumatic. Rarely non
traumatic due to rupture of an aneurysm
in the posterior communicating artery;
• Also burst lobe following a spontaneous
intra cerebral haemorrhage, is also non
• Bleed is mainly venous (bridging veins,
dural sinuses, extension of an intracerebral haemorrhage as a burst lobe).
• Clinically can be,
-sub acute
• Usually does not occur as an isolated
injury, thus category of hurt is not clear
• Chronic SDH (an organized sub dural
blood clot) can be an incidental finding in
the elderly at the autopsy.
• Clinical effects of a chronic SDH can be
misinterpreted as those due to neuropsychiatric disorders.
 A chronic SDH will be seen as a brownish,
cystic, gelatinous mass containing fluid of
various colours (red/brown/yellow),
adherent to dura and covered with a neo
 This membrane usually grows from the dural
surface. The degradation of blood pigments
gives the different colours.
 Munro has devised a dating system (ageing
of the chronic SDH) by histological
examination of the neo membrane.
• SDH is common in extremes of age. E.g.
infants – shaken baby syndrome
-elderly – due to shrunken brain with
widened sub dural space.
• Also in,
-chronic alcoholics
punch drunk syndrome
• Category of hurt is variable
-may be FIOCN
• In a criminal trial (eg. Assualt case) it may
be important to prove/disprove the
causative relationship of the assualtive
event and the SDH, which has resulted in
death. This may be attemped by
histoligical ageing of the neo membrane.
Sub archonoid haemorrhage (SAH)
 Collection of blood between pia and
 Can be spontaneous or traumatic.
 Spontaneous;
1. Rupture of berry aneurysm (read path notes)
2. Extension of a spontaneous intacerebral or
an intraventricular haemorrhage in to sub
arachonoid space as a burst lobe or through
the normal path of CSF flow.
 Traumatic
1. Primary traumatic
due to diffuse rotational trauma to brain,
bridging vessels are ruptured. The SAH is
diffuse. There may be other associated
injuries such as SDH, contre-coup injuries.
2. Secondary traumatic
due to localized trauma to brain (eg. A
cerebral contusion or a laceration). There will
be localized SAH in that area.
3. Extension of a traumatic intra-cerebral
or/and intra ventricular haemorrhage in to
sub arachonoid space.
4. Basal SAH can occur due to lateral neck
trauma resulting in the rupture of vertebral
vessels (how to demonstrate a vertebral
artery damage in the autopsy?)
5. Sudden fluctuation of the pressure in the
neck arteries without actual trauma to
vessels in the neck.
e.g. sudden compression of the neck in
manual strangulation.
• Categorization of hurt is difficult when
associated with other injuries. May depend
on the individual case.
• It may be an important (yet very difficult)
issue to link a rupture of berry aneurysm
causing a traumatic SAH following an
assaultive event.
Read clinical presentation.
 An increasingly important topic in clinical
forensic medicine and sports medicine.
 Different authors classify concussion in to
different grades.
Eg. CANTU classification
Colarado classification
AAN classification
 Grade I,II,III etc.
 As a crude generalization, it is
conventionally defined as
“transient loss of consciousness
immediately following blunt trauma to
head, with spontaneous recovery,
usually associated with retrograde
amnesia, with no demonstrable
macroscopic brain damage.”
 Thus it is a retrospective diagnosis
• Usually complete recovery will occur.
• But may at times be associated with
altered brain function for some time.
• It is transient state of paralysis of brain
function (pathology is at the level of
metabolism of neuro-chemicals, Details
not needed.)
 After spontaneous recovery the person
may show,
1. Features of post concessional syndrome
(e.g. retrograde amnesia, headache,
giddiness, nausea, vomiting, irritability,
confusion etc.)
NB : some times these features may persist
for a considerable time. eg. rupulsion for
alcohol, personality changes
(read compensation neurosis)
2. Post traumatic automatism
(legal validity of statement)
NB:- brain stem concussion – category of
• Cerebral concussion is commoner with
rotational injury when the head is free to
Diffuse axonal injury
 Diffuse axonal damage in the white
matter may occur (without an ICH or a
mass lesion) due to shearing force
occurring in the brain due to acceleration
or deceleration.
e.g. RTA, falls and assaults
Rarely can occur due to violent shaking
without an impact injury on the head.
• Has a spectrum of clinical presentation.
Commonly the victims are deeply
unconscious and in a vegetative state
(intact brain stem)
• In the autopsy, minute haemorrhages
may be found in the midline structures of
white matter eg. Corpus callosum, parasagittal white matter, Intra ventricular
septrem, rostral brain stem, thalamus,
internal capsule, cerebellar peduncles etc.
• DAI is ideally a histological diagnosis, if the
patient had survived for few days,
retraction bulbs (axonal bulbs) may be
seen in H&E, Silver/Gold stain and Beta
A.P.P. may show early changes.
Coup injuries – discuss
Contre coup injuries – discuss
 Define
 When the head is free to move
 Common in frontal and temporal areas
 Mainly due to rotational force
(acceleration declaration injury)
 can be contusions, lacerations or rarely
Intra cerebral haemorrhages
• Primary
• Secondary (secondary traumatic apoplexy)
“Bollinger haemorrhages”
Brain stem haemorrhages
 Usually in mid brain and pons
 Primary – at the moment of impact/trauma.
- usually with occipital impact
e.g. # of base of skull – posterior cranial fossa
brain stem Impinges on the free margin of
Forward movement when the brain stem
impact with bone.
- Contre coup mechanism
• Appearance
- small, peripheral, circular, solitary (or few
in number) usually between the aqueduct
and outer end of Substantia Nigra.
• Clinical presentation
Immediate loss of consciousness
Rapid deterioration of unconscious state to
end up in an early death.
Volitional activities are not possible
 Secondary
- Not due to direct trauma but to effects of
raised intracranial pressure, (supra tentorial
or infra tentorial) which leads to brain stem
compression and herination.
- Appearance
 Multiple, streaky, centrally located and large.
 Associated with other features of increased
intracranial pressure.
 Usually no evidence of primary injury around
brain stem.
Secondary brain stem haemorrhages are
also called “Duret haemorrhages”
• Clinical presentation
- discuss
Diffuse vascualr injury
 Can go hand in hand with DAI
 Due to shearing of small blood vesseles
following acceleration decleration injuries.
 Present as multiple petecheal haemorrhages
in white matter
 Poor prognosis
 Usually instant or early death.
Ischaenic brain damage
(hypoxic ischaemic encephalopathy)
 Due to reduction in oxygen tension in
cerebral blood flow.
e.g. 1. closed head injury resulting In raised ICP.
2. severe crush injury to chest, resulting in
inadequate chest movements.
3. focal reduction of cerebral blood flow
leading to infracts. (common sites are
hippocampus and basal gangila)
 Depending on aetiology, the ischamic
damage can be focal or global.
Volitional activities following
head injuries
• discuss
Head injuries and category of
• discuss
Complication / sequelae of head injuries
 Complete uneventful recovery.
 Post concussional syndrome.
 Post traumatic automatism.
 Disfiguration of head or face.
 Cranial nerve palsies.
 Functional deformities.
e.g: eyes, ear, mouth, nose, jaw, etc..
 Infection (meningitis, cerebral abscess
formation) Hydrocephalus
 Arterio-venous fistula formation e.g. carotid –
cavernous sinus fistula
 Sinus thrombosis
• Post traumatic epilepsy ( pre disposing
factors are prolonged unconscious state,
depressed #, hematoma formation,
surface brain injury, infection)
• Neurological deficits other than cranial
nerve palsies e.g. due to structural
damage to specific areas of brain
• Prolonged unconscious/ vegetative state
complications of unconsciousness leading
to death
• Immediate / rapid or early death due to
structural brain damage.
• ? Tumour formation (Ewing's postulate)
Effects of raised ICP – what is seen at
 The cause for the increased ICP
e.g. head injury, haemorrhages, global
Ischaemia etc.
say an EDH for example
 External injuries (scalp lacerations, Linear # of
parietal or temporal area + EDH
 Dura is shiny, tensed and stretched over the
• Brain is heavy, oedematous, and water
logged, Sulci are flattened and gyri are
• Local compression of brain with dilatation
and compression of ipsilateral ventricle –
internal hydrocephalus.
Also midline shift / pushed
(initially contra lateral lateral ventricle is
• Midline shift causes distortion / compression
of third ventricle.
• This leads to internal hydrocephalus and
further increases ICP
• Cingulate gyrus herniates under the falx.
(sub falcine herniation / supra callosal
- compression of anterior cerebral artery
(supra callosal branches)
- Frontal lobe infarcts
 Further cerebal oedema and further Increase
in ICP
 Compression of perforating vessels supplying
basal ganglia, thalamus and hypothalamus
leads to infarction of these area.
 Trans tentorlal herniation e.g. uncal
herniation (uncus of parahippocampul gyrus
herniates in to infra tentorial compartment.)
 Compression of post. Cerebral artery leading
to calcarine infarction of occipital lobe
 Now the mid brain is compressed against
the free margin of tentorium resulting in
an indentation called “Kernohons Notch”
 Downward shift of brain stem leads to
compensation of blood supply by basillar
artery resulting in secondary brain stem
 Compression of,
CN III – fixed dilated pupil
CN VI – paralysis of lateral rectus
• Cerebral tonsillar herniation through
foramen magnum.
• With Infarction of brain stem respiration is
 Worsens hypoxia and Ischaemia to brain.
 Further cerebral oedema
 Further rise in ICP
 Further aggravation of the condition
 (hypoxic ischaemic encephalopathy)
 (Anoxic cycle of Jaques)
 Death
 COD can be given as “cranio-cerebral
Not mere cerebral lacerations or other
specific structural injury to brain.

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