No one can confidently say that he will still be

living tomorrow.  ~Euripides

Nearly 1.5 to 2 million persons are injured


and 1 million succumb to death every

year in India.

of TBIs
followed by
falls (20%-
25%) and
violence
(10%).
Alcohol
involvemen
t is known
to be
present
among
15%-20% of
TBIs at the
time of
injury.
Thirty-eight
per cent of injured persons had a serious injury

to the head
and face region.


Head Injury
S1 Unit
 DEFINITION & TYPES OF HEAD INJURY
 PATHOPHYSIOLOGY
 Clinical Features
 PRIMARY BRAIN INJURIES
 EXTRADURAL HAEMATOMA
and
SUBDURAL HAEMATOMA
 ASSESSMENT OF SEVERITY OF HEAD INJURY
 INVESTIGATION
 CONSERVATIVE MANAGEMENT
OF HEAD INJURY
 SURGICAL MANAGEMENT OF HEAD INJURY
 C O M P LIC A T IO N S O F H E A D
IN JU R Y
DEFINITION & TYPES
OF HEAD INJURY
NITHA.J
Head injury
Traumatic insult to the head that may result in
any injury to the soft tissue bony structures
and/or brain.
TRAUMATIC BRAIN
INJURY[TBI]
Traumatic brain injury (TBI) is a
nondegenerative, noncongenital insult to the
brain from an external mechanical force,
possibly leading to permanent or temporary
impairment of cognitive, physical, and
psychosocial functions, with an associated
diminished or altered state of consciousness.
CLASSIFICATION OF
HEAD INJURY
Based on the Severity
GCS: Best predictor of neurological outcome
GLASGOW COMA SCALE


EYE OPENING SCORE

SPONTANEOUS 4
TO SPEECH 3
TO PAIN 2
NIL 1
MOTOR RESPONSE SCORE

OBEYS 6
LOCALISES 5
WITHDRAWS 4
ABNORMAL FLEXION 3
EXTENSION 2
RESPONSE 1
NIL
VERBAL RESPONSE SCORE
ORIENTED 5
CONFUSED CONVERSATION 4
INAPPROPRITE WORDS 3
INCOMPREHENSIBLE SOUNDS 2
NIL 1
Severity of TBI
Severity GCS

Minor 15

Mild 14-15

Moderate 9-12

Severe 3-8
OPEN HEAD
INJURY
Implies

communication
b/w the intra dural
contents & outside
CLOSED HEAD

INJURY
Scalp is intact and

there is no

communication
between the OPEN HEAD INJURY

intradural contents
and the
atmosphere

PATHOLOGICAL
CLASSIFICATION
 FOCAL  DIFFUSE
Confined to specific Distributed in a more
areas general manner
Cerebral laceration Cerebral edema
Contusion Concussion
Intracranial Diffuse axonal injury
hemorrhage 
Based on the time of
onset
Primary Brain Secondary Brain
Injury Injury
ØDiffuse axonal injury Ø Brain swelling
ØCerebral concussion Ø Intracranial
Haemorrhage
ØCerebral contusion
Ø Infection
ØCerebral laceration

ØTraumatic
subarachnoid
haemorrhage

CLASSIFICATION OF SKULL
FRACTURE
 COMMINUTED
FRACTURE
DEPRESSED FRACTURE
SCALP LACERATION
 GCS
The scale was published in 1974 by Graham
Teasdale and Bryan J. Jennett, professors of
neurosurgery at the University of Glasgow.
The pair went on to author the textbook
Management of Head Injuries (FA Davis 1981,
ISBN 0-8036-5019-1), a celebrated work in
the field.
The University of Glasgow is the fourth-
oldest university in the English-speaking
world and one of Scotland's four ancient
universities

PATHOPHYSIOLOGY
Nithin Humayoon
Neuronal Injury
Chromatolysis
Wallerian Degeneration
Retrograde Degeneration
Transneural degeneration
Regeneration
Brain metabolism
Ø CMRO2: 3.5 ml/100g/min

Cerebral Blood flow
Ø 55ml/100g/min




Cerebral Autoregulation








Cushing’s Reflex

ICP and brain herniation
The addition of mass lesion is compensated
by displacement of CSF and venous blood
out of cranial cavity.



As further expansion of mass occur quite
small rise in volume result in large
increase in ICP and Brain herniation can
occur
MECHANISM of brain
injury
Distortion of the brain
Mobility of the brain in relation to the skull and
membrane
Configuration of interior of skull
Deceleration and acceleration of injury
Cerebral Concussion
Cerebral Contusion
Cerebral Laceration
Primary brain injury
Diffuse neuronal damage
Shearing lesions
Contusion
Lacerations
Traumatic SAH
Ø Extent of primary injury is reflected by state of
consciousness and presence of focal
neurological deficit
Secondary brain injury
Brain swelling: odema, venous congestion,
hypoxia
Intra cranial hemorrhage:Extradural, subdural,
intracerebral
Infection
Ø Open head injury: Generalized meningitis,
subdural empyema, brain abscess
Ø Closed head injury: Infection of sub pericranial
blood clot
Causes of secondary brain
injury
Hypoxia:PO2 < 8kPa
Hypotension: Systolic BP<90mm Hg
Raised ICP: >20mm Hg
Low cerebral perfusion pressure:<65mm Hg
Pyrexia
Seizures
Metabolic Disturbance
Raised ICT Cerebral compression
Decreased Cerebral perfusion Brain
ischaemia

Pressure on motor cortex C/l hemiparesis
Herniation of cingulate gyrus:
Subfalcine herniation

Temporal lobe herniation

Compress ipsilateral
IIIrdnerve …
Dilation of ipsilateral pupil

Central Herniation and

Tonsillar herniation
Compress Brain stem
Increase in BP, Bradycardia,
Abnormal resp.pattern

Coup and Contrecoup injury
Causes of death in head
injury
Brain hypoxia
Coning
Diffuse severe irreversible neuronal injury
Metabolic changes
Aspiration in unconscious patients






"father of modern neurosurgery"
Harvey Williams Cushing, M.D. (April 8,
1869 - October 7, 1939) was an American
neurosurgeon and a pioneer of brain surgery.
He is widely regarded as the greatest
neurosurgeon of the 20th century and often
called the "father of modern neurosurgery".
 Cushing's triad
is the triad of widening pulse pressure (rising
systolic, declining diastolic), change in
respiratory pattern (irregular respirations),
and bradycardia.

It is sign of increased intracranial pressure, and
it occurs as a result of the Cushing reflex.
Clinical Features
Philip Daniel
Clinical Features
Altered consciousness
Pupillary changes
Symptoms and Signs of raised ICT
Signs of skull fracture
Signs of meningeal irritation
Signs of focal neurological deficit
Signs of coning
Altered consciousness
Assessed by Glasgow Coma Scale
Used to assess severity of head injury

 y
change
s
1. Change in
pupil size
2. Change in light

response


 Normal pupil
size: 2.5-5mm

 Anisocoria &
asymmetrical
sluggish light
response- 3rd
CN
compression on
side of mass
lesion
(hematoma)
Pinpoint pupil
<1mm
Pontine hemorrhage

Bilateral dilated unreactive pupil
Severe midbrain compression


Symptoms and Signs of
raised ICT
Normal upper limit: 15mm Hg
SYMPTOMS
Ø Impairment of consciousness
Ø Headache
Ø Vomiting
Ø Convulsions
SIGNS
Ø Papilloedema
Ø Bradycardia
Ø Hypertension
Ø Changes in respiration
Ø B/l Babinski’s sign
Fracture skull
Signs of base of skull fracture
Bilateral periorbital edema (racoon eyes)
Battle’s sign (bruising over mastoid)


Skull fracture
CSF
rhinorrhoea/CSF
otorrhoea
Hemotympanum

Signs of meningeal
irritation
Neck stiffness
Kernig’s sign
Straight leg raising test
Brudzinski’s sign
Focal neurological deficit
Cortical involvement
Ø Frontal lobe-
C/l paralysis(monoplegia),Gaze palsy,Changes in

mentality,personality, behaviour, bowel and bladder

involvement
If dominant hemisphere is involved Motor aphasia, agraphia

Ø Parietal lobe- C/l cortical sensory loss. If dominant

hemisphere involved alexia, apraxia, jargon’s aphasia
Ø Temporal lobe- Hearing impairment, auditory agnosia
Ø Occipital lobe- Homonymous hemianopia, visual agnosia
Cranial nerve involvement

IIIrd N. Dilated non reacting pupil, ptosis,

diplopia, divergent paralytic squint
VII N. Facial Palsy
IV N. Diplopia on downward gaze(SO
Paralysis)
VI N. Diplopia on looking outwards to
paralysed side(LR Paralysis)
VIII N. Loss of hearing, vertigo, nystagmus
I N. Anosmia
II N. Blurring of vision, field defects
Coning
Supratentorial
herniation
Deterioration in
level of
consciousness
Dilatation of pupil
on side of
compressing
mass
Hemipareisis on
ipsilateral side


Coning
Infratentorial
herniation
Further damage to
brain function
Loss of vital
functions









RACOON!!!
PRIMARY BRAIN INJURIES


BY
POOJA P S
PRIMARY BRAIN INJURIES
Diffuse axonal injury
Cerebral concussion
Cerebral contusion
Cerebral laceration
Traumatic subarachnoid haemorrhage (SAH)

DIFFUSE AXONAL INJURY
Acceleration deceleration type of forces causes
mechanical shearing at the grey white matter
interface (due to differential brain
movement).
This causes disruption and tearing of axons
myelin sheath and blood capillaries over an
extensive area.
Can present as mild confusion followed by
recovery or coma or death
Cerebral concussion
It is a clinical diagnosis
A brief temporary physiological paralysis of
function with out organic structural damage
with amnesia/transient loss of consciousness
followed by complete recovery .
Brady cardia, hypotension and sweating may
be present.

CEREBRAL CONTUSION
Circumscribed areas of brain tissue destruction
accompanied by extravasation of blood into
the affected tissues.
Produced by blunt force.
Most common in frontal and temporal lobe.
FEATURES OF
CONTUSION


Bruising
Swelling of cortical gyri
Brain edema
Shearing damage to nerve cells and
axons.
Bleeding due to tearing of small blood
vessels in the brain.
Focal neurological deficit ( > 24 hrs )
may be present
Recovery may/may not occur.
Cerebral laceration

A cerebral laceration is a similar to contusion
except that, the pia-arachnoid membranes
are torn over the site of injury in laceration
Focal deficits are the rule.



Subarachnoid
hemorrhage
Bleeding into the subarachnoid space—the
area between the arachnoid membrane
and the piamater surrounding the brain
(containing blood vessels)
WFNS(World Federation of Neurological
Surgeons) grading of SAH





SUBARACHNOID
HAEMORRHAGE
SYMPTOMS


Thunderclap headache "like being kicked in the

head", or the "worst ever“; This headache often
pulsates towards the occiput
Vomiting
Seizures
Confusion
Decreased level of consciousness or coma
Neck stiffness, Fever
Hemi paresis
Rarely back pain and radicular pain
SIGNS


Raised blood pressure (adrenaline Release due

to bleeding )
Positive kernig’s sign.
Fundoscopy-subhyaloid hemorrhage , vitreous
hemorrhage and papilloedema
Isolated dilation of a pupil and loss of the
pupillary light reflex may reflect brain
herniation as a result of rising intracranial
pressure.







Subdural hemorrhage is a classic finding in
shaken baby syndrome
EX TR A D U R A L
H A EM ATO M A
and
SU BD U RAL
H A EM ATO M A
BY
PRAJI.S.PRASAD
SUBDURAL HAEMATOMA
Ø 70%-due to falls, 25% due to vehicle accidents.
Ø Classical finding in battered baby syndrome
Ø Mostly venous and capillary haemorrhage.
Ø Common in older age group.
Ø

 Divided into 3 types based on the time of onset
of symptoms.
1.Acute-immediately and rapidly after the
trauma
2.Subacute-several days to 2-3 weeks after the
injury due to the pressure of hematoma.
3.Chronic-weeks to months.
4.
Acute Subdural
Hematoma


Most lethal of all head injuries.

High mortality rate if not rapidly treated.
Closely resembles extra dural haemorrhage .
Symptoms develop 24 to 48 hours.
Longer lucid interval.

Chronic Subdural Haematoma

Affects older individuals.

Minor injury causes subclinical hematoma.
Clot liquefaction over next 2-4 weeks results in
clot expansion and development of signs and
symptoms of mass.
Effects may resemble brain tumor or stroke.
EXTRADURAL
HAEMATOMA
Neurosurgical emergency.
Exclusively due to trauma.
Skull # + tearing of middle meningeal artery.
Commonest site –temporal bone.
Not always arterial.
Mostly seen in young adults.
Lucid interval-present in typical cases.

Clinical features
Ø Concussion
Ø Lucid interval
Ø Confused and irritable
Ø Drowsiness and evidence of hemiparesis.
Ø Compression of third nerve-initial constriction
followed by dilatation of pupil on the side of
haemorrhage
Ø Hemiparesis of same side of haematoma
Ø
Ø
ASSESSMENT OF SEVERITY OF
HEAD INJURY
AND CASUALTY MANAGEMENT
Prathibha Raj M R
 ASSESSMENT OF SEVERITY OF
HEAD INJURY
vInitial assessment is by Advanced Trauma
and Life Support (ATLS)
Ø Primary survey
Ø Resuscitation
Ø Secondary survey
Ø Definitive management
 GENERAL PRINCIPLES
Ø Team work
Ø Patients are more likely to die from airway
obstruction than from any remediable intra
cranial lesions
Ø Surgically remediable intra thoracic and intra
abdominal lesions take precedence over any
intra cranial procedures
Ø Compressing intra cranial hematomas are unlikely to
be present when patient is first seen
Ø The initial GCS assessment is of crucial importance
Ø The immediate institution of the correct care of
unconscious patient does lower the morbidity and
mortality from major head injury
v
INITIAL ASSESSMENT
Ø RECORD
Blood pressure
Pulse rate
Respiratory rate
Type of breathing


NEUROLOGICAL
ASSESSMENT
ØGCS
ØPUPIL
§ Size and equality
§
ØLIMBS
§ Reflex limb movements
§ Stroke may be due to primary cerebral
damage; is very rarely due to a compressing
intra cranial hematoma
§ Spinal injury - Paraplegia,quadriplegia

Rule out associated skull fractures
Presence of CSF rhinorrhoea or otorrhoea
Mandibular or facial fracture
 HISTORY
Ø Loss of consciousness
Ø Post traumatic amnesia
Ø Skull fracture
Ø Focal neurological signs
Ø Persistent headache
Ø Vomiting
Ø Other medical conditions like patients on
anticoagulants,hemophiliacs
Ø alcohol intoxication
Ø Cause and circumstances of injury
Ø

RESUSCITATION
Airway
Breathing
Circulation
Disability
Exposure
Airway assessment
Respiratory rate
Stridor and dyspnoea
Air entry
Intactness of rib cage

AIRWAY MANAGEMENT
üImmediate measure in an unconscious
patient
üRemoval of loose dentures
üPositioning prone or on one side with the
head low
üMouth suction
üInsertion of Endotracheal tube
ü
Endotracheal
Intubation:Indications
Unconscious patient
GCS<8
Oropharyngeal bleeding

vEmergency tracheostomy-crushed larynx,massive
posterior pharyngeal bleeding
v
vIndication of ventilatory support
§ Extensive Chest injury
§ Generalized brain swelling
§ Status epilepticus
§ Acute reduction in intra cranial pressure
§ For CT scanning in unconscious patient
§ For all surgery
§ or extensive pulmonary soiling
Circulation Assessment
Pulse
BP

CIRCULATION


Control of bleeding and restoration of blood
volume
Examination of whole body to assess other
injuries and bleeding into body cavities
Fracture of major long bones-shock,reflex
lowering of BP---correct splintage
Treatment of oligaemic shock is replacement
of circulating volume(iv fluids-NS,Plasma
expanders, blood transfusion)
Haemodynamic status stabilised and
monitored with pulse,BP,Urine output and
CVP

 Neuroassessment
Vitals
GCS
Pupils
Symptoms: Drowsiness, recurrent
vomiting,seizures,headache
CSF leak
Disability
Assessment of focal neurological deficit



E xp o su re


Intactness of skull and spine are assessed
Fracture stabilised

Management
Neuro observation
Monitor vitals
Catheterisation
Antibiotics
Antiedema measures
Antacids
Intravenous fluids



 Triage
Triage originated and was first formalized in
World War I by French doctors treating the
battlefield wounded at the aid stations behind
the front. Much is owed to the work of
Dominique Jean Larrey during the Napoleonic
Wars.
INVESTIGATION
PRIYANKA P.G
SKULL XRAY
CT
CEREBRAL ANGIOGRAPHY
LUMBAR PUNCTURE
SKULL XRAY
INDICATION


Laceration or contusion of scalp

Obvious depression of skull
Compound fracture
Suspected penetrating injury
 COMPUTERISED TOMOGRAPHY
 INDICATION
MILD HEAD INJURY
 NICE CRITERIA
1.GCS < 13 at any point
2.GCS 13 or 14 at 2 hours
3.Focal neurological deficit
4.Suspected open depressed or basal skull
fracture
5.Seizure;Vomiting > 1 episode
OTHER INDICATIONS
Age > 65
Coagulopathy
Dangerous mechanism of injury
Anterograde amnesia > 30 mts

MODERATE TO SEVERE
AIMs


To identify intra cranial haematoma

Scalp soft tissue injury
Skull fracture
Intracerebral contusion
CT FINDINGS
Extra dural haematoma – Lentiform
hyperdense lesion b/w skull & brain

Acute subdural haematoma – hyperdense
areas giving a diffuse & concave
appearance
Subacute subdural haematoma – isodense
areas
Chronic subdural haematoma – hypodense
area
Cerebral contusion - heterogenous

Subarachnoid
Haemorrhage
FIRST WEEK
Repeat scan at 3 days
Post op
Investigation of CSF leak
Intracranial infection
FIRST MONTH
Intracranial infection
c/c subdural haematoma
Hydrocephalus
CEREBRAL ANGIOGRAPHY- subarachnoid
haemorrhage


LUMBAR PUNCTURE – subarachnoid

haemorrhage, meningitis
 CONSERVATIVE
MANAGEMENT
OF HEAD INJURY
By
Priyanka R Nair
OBJECTIVES
Nursing of the patient in the period of
unconsciousness.
Repeated observation of the patient to detect
the development of complications at the
earliest.
Measures
Position-head of the patient should be placed
30 degree up, it is the known as REVERSE
TRENDELENBERG.
Collar must not be too tight This
is to avoid obstruction of venous drainage
from the head.
Tracheostomy -indications
If the patient is ventilator dependent.
To facilitate tracheobronchial toilet.
To prevent respiratory infections.
Advantages:

 Decreases dead space by half

 Work of breathing is decreased
 Tracheobronchial toilet is facilitated
 Incidence of resp.infection is decreased

Patient should be ventilated to a pCO2 of 4.5-5
kPa.
If the arterial pCO2 increases the intracranial
pressure will increase since the normal auto
regulation of the brain is disturbed in head
injury.
The central venous pressure should be
maintained at 3-8 cm of water to prevent
hypotension, so a central line should be
started.
Intracranial pressure (ICP) and cerebral
perfusion pressure (CPP) should be constantly
monitored.

 CPP=Mean arterial pressure(MAP) -ICP

CPP should be maintained >65mm Hg in a

severely head injured patient. So if the ICP is
20mm Hg the MAP should be >85mm Hg.
If needed ionotropes can be used to support
the CPP and the blood pressure.
 ICP MONITORING

A tunnelled parenchymal ICP monitor can be inserted through a

twist drill burr hole
MEASURES TO DECREASE
THE ICP
Sedation with/without muscle relaxants
Patient is sedated using Propofol or
Midazolam. Muscle
relaxants like Atracurium can be used.
Diuretics- Frusemide and Mannitolcan be used
to decrease the cerebral swelling and raised
ICP.
Mannitol an osmotic diuretic is used mainly in
subarachnoid haemorrhage.It is
contraindicated in extradural haematoma.
Seizure control-


Seizures will increase the brain metabolic rate

and thereby increase the ICP. So prophylactic
anticonvulsants can be used in the first week
to decrease the incidence of seizures.
Phenobarbitone 60mg Q8H or Phenytoin
100mg Q8H can be used.
If the ICP cannot be controlled it can lead to
status epilepticus. Here EEG burst
suppression therapy with Lorazepam or
Thiopentone may be used.
Normothermia should be maintained-
 Pyrexia may decrease the cerebral blood
flow so this should be avoided.Active cooling
may be used to decrease the metabolic rate.
Maintaining fluid and electrolyte balance-
Severely brain injured people are
susceptible to disturbances in sodium
homeostasis like Diabetes insipidus and
Syndrome of inappropriate antidiuretic
hormone(SIADH). SIADH can
lead to dilutional hyponatremia will in turn
can precipitate seizures.
IV fluids should be administered until
nasogastric feeding can be commenced .If
patient is conscious, oral feeding can be
started .
If the patient is in pain analgesics like Fentanyl
or Codeine may be used.
Pantoprazole 40mg iv OD may be given to
avoid gastritis
If fever occurs due to meningitis following
basal skull fracture lumbar puncture should
be done and empirical treatment for
meningitis should be started.

Any other source of infection should be ruled

out
Antimeningitic prophylactic regimen(CP 20lakh
unit iv Q6h, Chloromycetin 500mg Q6h iv,
Metronidazole 500 mg iv Q8h):Indications-
Comminuted fractures, otorrhoea,
rhinorrhoea, pneumocephalus
Care of the unconscious
patient
Nasogastric tube feeding.
Care of the eyes by padding.
Urinary catheter for drainage of urine and to
monitor the urine output. Urinary
incontinence may occur in frontal lobe
lesions.
Change of position of the patient to avoid bed
sores.

Limb physiotherapy to prevent deep vein
thrombosis.
Chest physiotherapy to prevent respiratory
infections.
Care of the endotracheal tube.

Indications for ICU admission
Ø if severely injured
Ø if requiring ventilatory assistance






Repeat CT scan should be considered:


If there is deterioration of the mental state of

the patient.
If there is a continued rise in the ICP.
If there is a failure to improve over 24 hours .

 SURGICAL
MANAGEMENT OF HEAD
INJURY
Rachana Chandran
Discussed as under

Scalp injuries

Skull injuries

Cerebral injuries
SCALP INJURIES

§Scalp haematoma
Aspiration,compression bandage &
antibiotic coverage

§Scalp Laceration
Clean-excision of devitalised
tissue-irrigation-suture
SKULL FRACTURES

Linear fractures
No specific treatment required

Depressed fractures
1)Small and shallow without any focal
signs-no indication for surgery
2)Compound
Compound depressed fractures-

Small-conservative management
Large-
1.Wound enlarged
2.Saline irrigation
3.Creation of burr hole
4.Elevation of depressed bone
HAEMATOMAS

Extradural haematoma

Aspiration done surgically to remove

mass & decrease the intracranial
pressure

Neurosurgically evacuated through a

burr hole or craniotomy
Acute Subdural haematoma

Small haematomas-conservative management

>10mm thickness or a midline shift in CT >5mm

regardless of GCS
Craniotomy done with or without bone flap
removal

Factors- GCS, pupillary reaction, age & presence

of anticoagulants
Chronic Subdural Haematoma
Evacuation with burr hole or craniotomy

Subarachnoid Haemorrhage
Indication for surgery- CT large
haematoma, decreased consciousness, focal
neurological deficit
Clipping & coiling done
Clipping via craniotomy to locate aneurysm

Traumatic Subarachnoid haemorrhage- managed

conservatively

Intracerebral haemorrhage
Surgery indicated-haematoma >3cm,presence of
structural vascular lesion in a young patient
CRANIOTOMY

Definition

Indications- mainly for brain

lesions, traumatic brain injury

Done under general anaesthesia

Preceded by an CT scan
CRANIOTOMY
urgical management of raised intracranial
ressure:-
)Early evacuation of focal haematomas
)Cerebrospinal fluid drainage by ventriculostomy
Delayed evacuation of swelling contusions
)Decompressive craniectomy
COMPLICATIONS OF
HEAD
INJURY
BY
Radhika.V
P o st C o n cu ssio n a l S y n d ro m e

Commonest among complications

Includes neuropsychological symptoms

Most Important- post traumatic

headache

Most often associated with WHIPLASH

INJURIES
Post Traumatic Epilepsy

Occurs in < 5% people

Intradural haematoma- 18% chances
Extradural haematoma- 2% chances

Risk increased in the following

states:-

a)Post traumatic amnesia of > 24

hours
b)Cases of dural penetration
c)Missile injuries
Two types- early and late (true)

I. Early- occurs within a week of the

injury
Cause- bruising & oedema near
injury
II. Late- after a week
Cause- scar formation in the
brain

Post traumatic epilepsy is mainly of

JACKSONIAN type
Treatment

Ø Phenytoin & Phenobarbitone can be used

the first week to decrease incidence of
seizures

ØLong term beneficial effects are not prove

Infections

Associated with delayed operation

Causes Bacterial Infections- mainly

MENINGITIS
Treatment- Empirical treatment with
Broad Spectrum Antibiotics until
culture reports are obtained

Rarely; osteomyelitis, brain abcesses

etc
Cerebrospinal fluid fistula

Common in fractures of base of skull

Diffic ult to detect due to increased

bleeding
from nose & mouth

Presents as Rhinorrhoea and/or

otorrhoea

Diagnosis by skull films to detect

fractures
Treatment

Øsuspected/diagnosed cases are treated with

Broad spectrum antibiotics after culture of
normal flora of nose,ear & mouth
ØMeningitic cover given

ØNormally resolves within 48 hours, if lasts

>48 hours, indication for dural repair
ØExact site of fracture must be found to
determine approach of surgery
Ø
CSF LEAK THROUGH FISTULA
Hydrocephalus

Occurs due to ventricular dilatation

after injury

Acute situations- burr

hole/ventricular drainage

Not detected until weeks or months

 Evidence of hydrocephalus-

Ø Rate of recovery slows down

Ø Giddiness, urinary and gait
disturbances develop

Treatment
Immediate-measures to reduce intracranial
pressure
Longterm- monitoring of ICP
CSF shunt may be
required
Cranial Nerve Palsies

Most common- 3rd & 6th nerves

Treatment of appropriate cause

Craniofacial injuries

Injury to orbit and paranasal

sinuses
Rehabilitation

Concerted efforts of medical,

nursing, physiotherapy, speech &
occupational therapies
PROGNOSIS
Assessed by Glasgow Outcome Score(GOS)
Good Recovery 5
Moderate disability 4
Severe disability 3
Persistent vegetative state 2
Dead 1

Other factors include: age, presence of

other
injuries
BELONGED TO???
 PREVENTION IS BETTER THAN CURE!!!

If the unpreventable happen however..

Let us Doctors do the job!!!

THANK YOU