HEAD INJURY
Presentation by Wasid Wajid Khan
Skull
fracture
• Head injuries derive importance
bcoz,the many patients who die
or are disabled belong to
younger age group
• Head injury accounts to one
fourth deaths due to trauma
• And half the deaths from RTA
OPEN SKULL #
A type of injury where fracture of skull is
associated with tear of dura & arachnoid matter
resulting in leak of CSF into ext environment or
base of skull
CLOSED SKULL #
There is no leakage of CSF
*This classification helps to recognise patients who can develop infective
complications post trauma
BLUNT INJURIES
It can lead to open or close head injury
it can be due to Acceleration or deceleration
There can also be rotational deceleration
MISSILE INJURIES
Missile injuries result in penetrating cranial cerebral
trauma with focal brain damage and hemorrhages. In
contrast, nonmissile injuries usually are more likely to
produce widespread brain injury.
CLASSIFICATION
1. # of vault of 2. # of Base of
skull skull
CLASSIFICATION
1. # of vault of 2. # of Base of
skull skull
1.Linear 1.# of Ant
#(crack or Cranial
fissure Fossa
2.Simple & 2.# of Middle
Comminuted # Cranial
3. Depressed # Fossa
3.# of Post
LINEAR
FRACTURE/CRACK
• Caused by
compression of
sphere
• Very common #
• This fracture may
continue at base of
skull
SIMPLE & COMMINUTED
#
• It can be caused by
acceleration or
deceleration
• There may be
subdural or
extradural
haemorrhage
DEPRESSED FRACTURE
• Open depressed #
poses risk of infection
• It is significant when
degree of depression is
more than the depth of
inner table of skull
• Complications - Dural
tear, pressure on
cerebral cortex,
Underlying
haemorrhage, Epilepsy,
Pressure on Venous
sinuses
• Linear # without displacement - no spl treatment
• Comminuted # - detached # which are contaminated
should be removed
• compound #- start prophylaxis antibiotic
• Depressed # -
1.If depression is more than the depth of inner table,skull should be
elevated
2.(DIgging Burr hole & using Adisons elevator)
3.if dural tear - sutured with non abosorbable sutures e.g. fine
silk(interrupted sutures)
4.If dural loss- transplant with fascia lata or pericranium
5.If associated with hemorrhage
Cauterisation, if large vein involved - muscle graft ,skull
reconstruction(tantalum plates,acrylic inlàys)
• # of Ant Cranial Fossa
• Clinical features-
• Epistaxis
• Csf rhinorrhoea
• Brain matter escape through
nose
• ecchymosis around
eyes,subconjunctival
haemorrhage(Racoon eyes)
• Olfactory nerve injury- partial
anosmia
• optic nerve injury- partial/
total loss of vision
• Dilated pupils -3rd nerve palsy
• Middle Cranial fossa
fracture
• Epistaxis due to injury
to venous/sphenoid
sinuses
• CSF Otorrhoea
• 7th- Facial nerve palsy
• 6th nerve injury-
strabismus
• 8th nerve injury-
deafness
• Battle sign
• # of Post Cranial
fossa
• Extravasation of
blood in suboccipital
region causing boggy
swelling at nape
• battle sign
• 9,10,11th cranial
nerves may be
It must be noted that even if skull
fracture is of little isignificant
surgically its importance for
medicolegal reasons should not be
ignored
Head
Injury
PRIMARY LESIONS
Secondary
Injury inflicted on the lesions
Due to brain
brain at moment of swelling/edema/intracrani
injury al hemorrhage
• Swelling
• Cerebral Concussion Haemorrhage
• Cerebral Contusion • Extradural Hematoma
• Cerebral laceration • Subdural,
• Cerebral irritation intracerebral
haematoma
Primary
Lesions
CEREBEAL CONCUSSION
Brief temporary physiological
Paralysis of function
WITHOUT STRUCTURAL
DAMAGE
Symptoms - Transient loss or
impairment of conciousness,
dizziness, mild confusion followed by
complete recovery
PTA(post traumatic amnesia),
spasticity of limbs,sweating, pulse
drops thenbecomes full
Many Theories to explain- 1. Cerebral
anemia 2. Molecular disturbance of
hypothalamus & brain stem 3. Transiet
ischemia due to streching of delicate
arteries 4. Pressure transmission through
csf on 4th ventricle
CEREBRAL CONTUSION
• Shearing damage to nerve cells &
axons,superficially or deep in the
cortex
• Brain edema is present
• haemorrhage from small blood
vessels, & congestion is present, thus
bruising & swelling present
CEREBRAL LACERATION
• Brain surface is torn or lacerated with
effusion of blood into cerebrospinal fluid
• Damage to nerve cells, axons & brain
oedema are present
• laceration is most severe on opposite
side of trauma "counter coup injury '
• Damaged part shrinks fluid accumulates
in subarachnoid space--traumatic
epilepsy
CEREBRAL IRRITATION
• This is vague term
• It may occur within 48hr of injury
• Cerebral irritation is due to localised
oedema which occurs around area of
contusion or laceration in the bone
• Patient curls up on side with knees
drawn up & arms flexed,avoids
light,irritability
CLINICAL FEATURES
• Cerebral Irritation
• Headache
• photophobia
• nausea ,vomitting
• depression
• lack of concentration
• Delerium
• all of above is - POST CONTUSIONAL
SYNDROM
CLINICAL FEATURES
• Post traumatic epilepsy
• According to site of injury - Anosmia/
blindness/ ataxia/ nystagmus
• symptoms of cerebral compression
CLINICAL FEATURES
• PTA- Post traumatic Amnesia
PTA is best guide to assess severity of
head injury ,its time between head injury&
return to continous memory
less than 1hr- minor, 1 to 24hr - moderate,
1 to 7 days- severe
• RTA -(Retrograde traumatic amnesia)
Loss of memory for events before
accident
Secondary
Lesions
SECONDARY PATHOLOGIES
Brain Swelling - Brain often reacts to any insult by swelling due to
oedema,Initialy oedema is localised to damaged part of brain then
gradually extends throughout one or both cerebral hemespheres, thus
rise in intracranial pressure can cause cerebral compression
Haemorrhage - After brain injury there may be extradural or
subdural or subarachnoid or subcortical haemorrhage
Brain Necrosis - In cerebral contusion or laceration ischemia to
localised part may occur (temporal or frontal lobe)
Coning - This means herniation of contents of brain. When contents
of the supratentorial compartment herniate through tentorial
hiatus due to compression in supratentorial compartment is called
coning
Intracranial
Haemorrhages
INRACRANIAL
HAEMORRHAGES
It van be above Tentorium Cerebelli
Or below Tentorium Cerebelli
This can lead to Brain Compression
Lucid Interval
It requires some time for accumulation of
blood causing cerebral Compression
In this period patient remains concious,
This is called "Lucid Interval"
SUPRA TENTORIAL HAEMORRHAGE
INTRA CEREBRAL HAEMORRHAGE
SUBDURAL HAEMORRHAGE
EXTRA DURAL HAEMORRHAGE
INTRA CEREBRAL HAEMORRHAGE
• Intra Cerebral Haemorrhage
• This is produced by arterial.bleeding from
area of surface laceration
• Intracerebral haemorrhage hardly causes
cerebral compression of considerable
magnitude
• If intraventricular haemorrhage occurs
main symptom is hyperthermia, epilepsy
• other symptoms - epileptic fits, localised
paralysis
• Symptoms develop from 1 to 10 days
after head injury
• Subdural Haemorrhage
• Most common haemorrhage
• most common in Elderly(As brain atrophies
& thus more space for brain to move within
skull
• Causes 1. Laceration of cortex with venous
or arterial haemorrhage 2. Rupture of
superior cerebral veins ,in 50% cases this
condition is bilateral
• Mechanism - veins fixed at one end & loose
and moving near sagital sinus, thus prone
to rupture when impact from front or back
CLINICAL FEATURES OF SUBDURAL HAEMORRHAGE
• Lucid interval may or may not be
present
• If associated with primary brain
injury it will be absent
• Uncociousness manifests quickly
than extra dural haemorrhage
• In bilateral cases signs &
symptoms are seen on both sides
• Subacute Subdural Haemorrhage-
(symptoms are delayed)
symptoms - headache, mental
apathy, slowness to respond, coma if
mid brain pressure cone
EXTRADURAL HAEMORRHAGE
• Bleeding is OUTSIDE DURA MATTER
• Patient saved if surgery is performed in time
• More common in children & young
adults.Commonly seen in footballers
• Bleeding - 1. Mostly from 'middle meningeal
artery' 2. Post meningeal artery 3. Middle
meningeal vein
• Mechanism - Relatively trivial injury from lateral
side(on Thin Temporal bone plate) e.g. hit on
head by cricket/foot ball
• After trauma blood escapes in 3 directions
• 1. if it passes outward- boggy swelling under
temporal mussle seen
EXTRADURAL HAEMORRHAGE
• 2. If it gravitates down - blood gravitates to middle cranial
foss
• 3.If blood moves upward - It seperates Dura matter, theis a
lethal problem
• When a large hematoma is formed Intracranial pressure
rises
• Uncus may herniate from tentorial hiatus
• Clinical Features - h/o laterally directed
trauma ,immediately there may or may not be short period
of unconciousness,after he recovers from unconciousness
he complains of headache, drowsiness followed by
unconciousness
• Lucid interval not present if associated with primary injury
CLINICAL FEATURES OF CEREBRAL COMPRESSION
(All secondary pathologies may lead to cerebral
compression)
1.Patient passes into profound unconciousness
2.Pulse becomes slow & bounding
3.Respiration becomes slow & deep
4.Face becomes flushed
5.Temprature becomes unequal(higher on paralysed
part)
6.Hemiparesis on opposite side of injury
7.Pupil on the side of lesion is dilated with poor
reaction to light(Hutchinson's pupil)
CEREBRAL CONCUSSION Cerebral
• Uncociousness from • Compression
Two periods of
time of injury Uncociousness with lucid
• Pulse is quick & interval inbetween
thready • Pulse is slow & bounding
• BP is normal or slightly • BP is raised
lowered • Pupils are typically
• Pupils are slightly 'Hutchinson's Pupils
dilated,equal & • Respiration becomes slow&
reacting to light deep,later Chyne Stokes
• RRespirationbecomes breathing
slow & shallow
Treatment
Main aim - to detect & evaxuate haematoma
before it causes secondary damage
1.Exploratory burr hole
2.Craniotomy for decompression of brain
