HEAD INJURIES

DR DIVYA(PG)
OUTLINE
Introduction
Epidemiology
Anatomy
Causes
Classification
Diagnosis
Management
Complication
INTRODUCTION

 Head injury is a broad term that describes

a vast array of injuries that occur to the
scalp, skull, brain, and underlying tissue
and blood vessels in the head.

The injuries can range from a minor bump on the

skull to severe brain injury
EPIDEMIOLOGY
Number one killer in trauma

25% of all trauma deaths

50% of all deaths from MVA

200,000 people in the world live with the

disability caused by these injuries

50% in ages b/n 15 and 35
ANATOMY
 Anatomy of the ’’SCALP’’
Skin
firmly bound to the 3rd layer by
perpendicular fibers
Connective tissue
contain blood vessels of the scalp
Aponeurosis
 fibrous sheet, found over much of
the vertex
attaches occipitalis to frontalis m
Loose connective tissue
accounts for the mobility of the scalp
blood tracks freely in this layer bilateral orbital
edema following sever head injury or cranial operation

Periosteum
adheres to the suture lines of the skull
collection of blood beneath this layer  outlines the
affected bone  cephalohematoma (children)
Anatomy of the meninges
Dura
endosteum and true meningeal layer
forms falx, tentorium, diaphragm
Arachinoid
vascular membrane
arachinoid granulations
Pia
highly vascular
dips into sulci and fissures
carries cortical vessels
ANATOMY
CAUSES OF HEAD INJURY
Road traffic accident
65% of deaths following severe
head injury
Falls
Injuries at work place, during
sport, or at home
Assaults
CLASSIFICATIONS OF HEAD INJURY

1. Blunt Vs Penetrating

2. Primary Vs Secondary

3. Mild, Moderate, or Severe

PRIMARY INJURY TO SCALP
Hematoma - Usually do not require Rx
- If large aspiration when it liquefies

Wounds
Abrasions - Cleaned & exposed
- Dressed - if hemorrhagic or serous
exudates

Lacerations - Cleaned & sutured( LA or GA)

- LA infiltrated into scalp
- Wound closure without tension
PRIMARY INJURY TO SKULL

Linear fractures - Do not require Rx

- At temporal area  tear
MMAEDH

Depressed #s - Simple Vs Open

Surgery indicated in:
ocompression (large plate of bone)
ocosmetic area
o compound/open wound:
 wound debridement
 elevate the depression
 suture dural laceration
 Fractures of the skull base

Diagnosis
oHistory - nasal bleeding,…
oPhysical examination
Raccoon eyes
Battle sign
Rhinorrhea,......

Management:
conservative, advise on danger Sn
closure of dura - persistent CSF leak
 PRIMARY BRAIN INJURY
The damage caused to the brain at the moment of
impact
Concussion
 temporary neuronal dysfunction after blunt head trauma
 head CT is normal, & deficits resolve over minutes to hours

Contusion/laceration
 bruise of the brain
 breakdown of small vessels and extravasation
of blood into the brain

Diffuse axonal injury

 damage to axons throughout the brain
 most frequent finding in patients who die from severe head injury
Mechanisms
Coup & counter-coup injuries

 Common sites:-
undersurface of frontal lobe
tip of temporal lobe
SECONDARY BRAIN INJURY

 Injurysustained by brain after

the impact
 Often preventable
Extracranial
 hypoxia
 hypotension

Intracranial
 hematoma
 brain edema
 raised ICP
 infection
Traumatic Parenchymal Injury

 Concussion (most common

type)
 Reversible altered consciousness from head
injury in the absence of contusion
 Brain receives trauma from an impact or a
sudden momentum or movement change
 May remain conscious, but feel dazed
 Caused by direct blows to the head, gunshot
wounds, violent shaking of the head or force
from whiplash type injury
 Skull fracture, brain bleeding, or swelling may
or may not be present
 Defined by exclusion, considered as a complex
neurobehavioural syndrome
 Contusion
 Bruise on the brain
 Wedge-shaped, with the widest aspect closest to
the point of impact
 Further divided into coup, contrecoup and coup-
contrecoup according to the site of bruise
 Coup - at the site of the impact
 Contrecoup - opposite the site of the impact on
the other side of the brain
o The force moves the brain and cause it to slam
into the opposite inner skull table
 Coup-contrecoup - both at the site of the impact
and on the complete opposite site of the brain
 Diffuse Axonal Injury
• Caused by shaking or strong rotation
of head, as with Shaken Baby
Syndrome
• Or by rotational forces, such as with
car accident
• Rapid displacement of the head and
brain can tear axons
• Disrupt axonal integrity and function,
causing immediate severe,
irreversible neurologic deficits
• Lesions are asymmetric, most
commonly found near the angles of
the lateral ventricles and in the brain
stem
• Axonal swelling appears within hours
of injury
• Temporary or permanent widespread
brain damage, coma, or death
Traumatic Vascular
Injury
Directly disrupt vessel walls, leading to
haemorrhage
The accumulated blood volume causes
increased intracranial pressure, which in
turn damages the brain and can lead to
permanent neurologic deficit or death
Depending on the location of affected
vessels, can be divided into epidural,
subdural and subarachnoid
Skull Fractures
 Any break in the skull
 Type of skull fracture depends on :

- the force of the blow

- the location on the skull at which the
impact occurs
- the shape of the object making impact
with the head
 Only one cause: an impact or a blow to the
head that is strong enough to break the bone
 Two major types of skull fractures :

- Linear
- Depressed
Linear Skull Fractures
 The most common type of skull fracture
 Result from low-energy blunt trauma over a
wide surface area of the skull
 Run through the entire thickness of the bone
 Can be further divided into vault and basilar
skull fractures
 Basilar skull fracture
Linear fracture at the base of the skull
It is usually associated with a dural tear
Found at specific points on the skull base
Temporal, sphenoid and occipital condylar
fractures
Depressed Skull Fractures
 Result from a high-energy direct blow to a small
surface area of the skull with a blunt object such as a
baseball bat
 Part of the skull is actually sunken in from the trauma
 Most common in the frontal and parietal region
 May be open or closed
 Open fractures
 have either a skin laceration over the fracture
 or the fracture runs through the paranasal sinuses
and the middle ear structures, resulting in
communication between the external environment
and the cranial cavity
 Closed fractures
 Simple fractures
 Skin is not broken or cut
Skull fracture
Exploration, debridement and
elevation of fragment
Compound fracture has high
incidence of infection,
neurological deficit and late onset
epilepsy hence antibiotic,
antiepilectics are indicated
Skull base fracture may
associated with CSF leak hence
pneumococcal vaccination is
Scalp Injury
Scalp is the highly vascular skin
that cover and protect the skull
may manifest as abrasion,
bruising, laceration, or a burn
may lead to bleeding or tissue
damage
EPIDURAL HEMATOMA

Usually from torn middle meningeal artery

and/or vein
Other causes:
torn dural sinuses(e.g: saggital sinus)
oozing from diploe bone & stripped dura
Uncommon but serious,1- 4% of TBI
Highest among adolescents and young adults
Skull fractures in 75-95%
 Neurosurgical emergency
 Nearly always associated with a skull
fracture
o skull fracture is associated with tearing of a
meningeal artery and a haematoma
accumulates in the space between bone
and dura meter
 Most common site: temporal
◦ As pterion is the thinnest part of the skull
◦ Overlies the largest meningeal artery – the
middle meningeal artery
 Other regions: frontal and in the posterior
fossa
Clinical presentation
lucid interval (in 1/3 of cases) associated with
headache vomiting, drowsiness, confusion,
aphasia, seizures and hemiparesis
-epidural hematoma due to venous bleeding
neurologic decline is slower
-posterior fossa EDH - elevated ICP
◦ Rapid deterioration (after minutes or
hours)
 contralateral hemiparesis
 reduced conscious level
 ipsilateral pupillary dilatation
Diagnostic evaluation
 CT scan - lens shaped collection
- hematoma volume
estimation
 Unilateral
 Biconvex (lentiforms or lens
shaped)
 Hyperdense lesion
 Sharply demarcated
 Does not cross suture line
 Associated with mass effect
on underlying brain
 With or without midline shift
Swirlsign ( Fresh/ non clotted
blood)
◦ Less hyperdense/ isodense
Management
• In infants, traumatic displacement of the easily
deformable skull may tear a vessel, even in the
absence of a skull fracture
• In children and adults, by contrast, typically
associated with skull fractures
• Lucid for several hours between the moment of
trauma and the development of neurologic signs
 Immediate transfer to neurosurgical unit
 Immediate evacuation in deteriorating or comatose
patient or those with large bleeds with burr holes or
craniotomy
 Close observation with serial imaging
Prognosis-mortality -10%
SUBDURAL HEMATOMA
 Pathophysiology
 result from the tearing of bridging veins crossing the subdural
space or hemorrhage from severe cerebral contusions
 Differs from EDH in terms of pathophysiology,
presentation and prognosis
 Accumulates in the space between the dura
and the arachnoid
 Disruption of a cortical vessel or brain
laceration
 Nearly always associated with a significant
primary brain injury
Spread more diffusely over the hemisphere
than extradural and are often associated
with diffuse swelling of the underlying
hemisphere

Clinical manifestations - depends on type

◦ impaired conscious level from the
time of injury
◦ further deterioration as the
haematoma expands
ACUTE SUBDURAL HEMATOMA

1-2 days after onset

coma in (56%)
lucid interval (12-38%)
posterior fossa SDH - signs of increased ICP

Result from:
torn bridging veins
cortical lacerations
torn dural sinuses
CT SCAN FEATURES
clot is bright or mixed-density
crescent-shaped (lunate)
HYPERDENSE(ACUTE BLOOD)
may have a less distinct border
does not cross the midline due to
the presence of falx

Signs of mass effect:

ventricular compression, midline
shift and reduction in the size of
the basal cisterns
SUBACUTE SUBDURAL HEMATOMA
After approximately 1-2 weeks the subdural
collection become isodense to grey matter

detection may be challenging & recognized when:

 effacement of cortical sulci
 deviation of lateral ventricle
 midline shift

Contrast enhancement will often define cortical-

subdural interface
CHRONIC SUBDURAL HEMATOMA
after 2 weeks usually post trivial injury
due to injury of small bridging veins
headache, cognitive impairment, apathy,
seizures and focal deficits
symptoms are transient and fluctuating
proximal, painless and intermittent
paraparesis
CT features

 After 2 weeks, hypodense

crescentic collections

 Acute-on-chronic SDHs can

further complicate the images,
with hyperdense fresh
haemorrhage intermixed, or
layering posteriorly, within the
chronic collection

 Do not cross the midline

Management
Acute SDH - Surgery for symptomatic & unstable pt
 Surgery
burr hole
Craniotomy
Smaller bleeds can be managed
conservatively with ICP monitoring

 Nonoperative Mx
clinically stable
clot thickness <10mm
no clinical or CT signs of herniation
repeat CT scans 6-8 hrs after initial scan
Chronic SDH

Surgery - burr hole

signs of increased ICP

clot thickness >10mm
cognitive impairment
motor impairment
Cerebral contusion
Rarelyrequires surgery unless to
reduce mass effect
Subarachnoid
haemorrhage
• Spontaneous arterial bleeding in the
subarachnoid space which is in between
arachnoid mater and pia mater
• Often associated with a cerebral aneurysm
(stroke)
• Can also caused by a skull fracture

• Endure some degree of life-long

impairment or chronic headache
Acquired Brain Injury
Damage to the brain not necessarily
caused by an external force
Examples :

- strokes
- tumors
- anoxia
- hypoxia
- toxins
- degenerative neurological diseases
- near drowning
Anoxia – when brain does not receive any oxygen
a) Anoxic anoxia
 no oxygen supplied to brain
b) Anemic anoxia
 blood does not carry enough oxygen
c) Toxic anoxia
 toxins or metabolites that block oxygen in the blood from
being used

2) Hypoxic – when brain receives some, but not enough

oxygen
a) Hypoxic ischemic brain injury
 Stagnant hypoxia or ischemic insult
 Lack of blood flow to brain because of a critical reduction
in blood flow or blood pressure
 RAISED INTRACRANIAL PRESSURE
The three normal contents
of the cranial vault are brain
tissue (80%), blood (10%),
and CSF (10%)

Normal state - ICP normal

4-14 mmHg - normal
>20mmHg – abnormal
The Monro-Kellie doctrine states that ’’the cranial
vault is a rigid structure, and therefore, the total
volume of the contents determines ICP ’’

Cerebral Perfusion Pressure (CPP) can be

determined by the following formula:
CPP = MAP – ICP
Symptoms & Signs of increased ICP

 Diminishing level of consciousness

 Headache, vomiting, seizures
 Cushing’s Triad:
 bradycardia
 hypertension
 abnormal respiration
 Pupillary changes
 Papilledema
Effects of raised ICP:

brain herniation
1. subfalcine herniation
2. uncal herniation
3. central transtentorial

herniation
4. tonsillar herniation

reduced cerebral perfusion

Management of raised ICP
includes airway protection and adequate
ventilation (intubation may be required)
a bolus of Mannitol 0.25-1g/kg causes:
free water diuresis
increased serum osmolality and extraction
of water from the brain
require rapid neurosurgical evaluation
ventriculostomy or craniotomy may be
needed for definitive decompression
Signs of Head Injury
Dilation of one or both pupils of the
eyes
Leakage of clear fluid which is
cerebrospinal fluid (CSF) into the ear
(otorrhea) or nose (rhinorrhea)
Ecchymosis over the mastoid process
(Battle's sign)
Bruising around the tissue of
periorbital area (Raccoon eyes)
SYMPTOMS
Physical symptoms
 Loss of consciousness for a few seconds to a
few minutes
 No loss of consciousness, but a state of
being dazed, confused or disoriented
 Headache
 Nausea or vomiting
 Fatigue or drowsiness
 Difficulty sleeping
 Sleeping more than usual
 Dizziness or loss of balance
 Sensory symptoms
• Blurred vision
• Ringing in the ears
• A bad taste in the mouth or
 changes in the ability to smell
• Sensitivity to light or sound

 Cognitive or mental symptoms

• Memory or concentration
 problems
• Mood changes or mood swings
• Feeling depressed or anxious
Symptoms of Head Injury
(Moderate to Severe)
Physical symptoms
Loss of consciousness from several
minutes to hours
Persistent headache or headache that
worsens
Repeated vomiting or nausea
Convulsions or seizures
Inability to awaken from sleep
Weakness or numbness in fingers and
toes
Loss of coordination
Cognitive or mental symptoms
• Profound confusion
• Agitation, combativeness or other
 unusual behavior
• Slurred speech
• Coma and other disorders of
 consciousness
DIAGNOSIS
History
 Age
 Loss of consciousness
 Cause, circumstance and mechanism of
injury
 Presence of headache & vomiting
 Seizures
 Anticoagulant use,….
HISTORY TAKING
 After initial resuscitation and management of
ABCDs, a focused history should be
performed on every patient with a TBI or
unknown cause of altered mental status.
 A detailed description of the traumatic event
should be solicited from the patient, family
members, first responders, or police.
 Witnesses or individuals who know the
patient may be helpful in ascertaining the
details of the traumatic event and
environment, as well as the patient’s normal
level of functioning.
 It is important to keep the differential
diagnoses broad to avoid making an error of
Common or concerning
symptoms
• Headache
 - ask about location, severity,
duration and any associated
symptoms, such as visual changes,
weakness, or loss of sensation?
 - ask if coughing, sneezing, or
sudden movements of head affect
the headache
• Dizziness
 - ask is the patient lightheaded or
feeling faint? Is there unsteady
gait from disequilibrium or perception
• Generalized weakness
 - are associated symptoms
present such as double vision,
difficulty in forming words,
difficulty with balance?
• Loss of sensation
 - is there any loss of
sensation, difficulty in moving
limb?
• Seizure, confusion
 Drug or alcohol use
◦ current intoxication: shown to have an
increased association with intracranial
injury detected on CT scan
◦ chronic: associated with cerebral atrophy,
thought to increase risk of shearing of
bridging veins
 Past medical history, including any CNS
surgery, past head trauma, haemophilia, or
seizures
 Current medications including anticoagulants
 Age: TBI in older age has a poorer outcome
in all subgroups.
Physical Examination
A thorough physical examination must
be performed after the initial ABCDs
have been addressed.
In addition to vigilance for occult
injuries, the physician should perform
the physical examination with careful
attention to the following:
Serial GCS and pupillary examinations
should be performed every 15 minutes
until the patient is stable, to
immediately identify deterioration in
neurological function
Head and Neck
◦ Inspection for cranial nerve deficits, periorbital or
postauricular ecchymoses, CSF rhinorrhoea or
otorrhoea, haemotympanum (signs of base of skull
fracture)
◦ Fundoscopic examination for retinal haemorrhage
(sign of abuse) and papilloedema (sign of increased
ICP)
◦ Palpation of the scalp for haematoma, crepitance,
laceration, and bony deformity (markers of skull
fractures)
◦ Auscultation for carotid bruits (sign of carotid
dissection)
◦ Evaluation for cervical spine tenderness,
paraesthesias, incontinence, extremity weakness,
priapism (signs of spinal cord injury)
◦ Obvious foreign bodies or impaled objects should
Cardiovascular status requires
continuous cardiac and serial blood
pressure monitoring. Any episodes of
hypotension must be addressed
immediately.
Respiratory status requires continuous
pulse oximetry and, in intubated
patients, continuous end-tidal CO2
capnography. Any episodes of hypoxia
must be addressed immediately.
Extremities should receive motor and
sensory examination (for signs of
GLASCOW COMA SCALE
The GCS is widely used to assess the
level of consciousness in patients with
TBI, and provides fairly good
prognostic information (when score is
very low or very high) that allows the
physician to plan for expected
diagnostic and monitoring
requirements.
GCS has 3 components: best eye
response (E), best verbal response (V),
and best motor response (M). Scoring
for each component should be
ASSESSMENT OF NEUROLOGICAL FUNCTION
AND OF CONSCIOUSNESS LEVEL
Glasgow Coma Score

Best Eye Response (4)

No eye opening……………………………1
Eye opening to pain..…………………….2
Eye opening to verbal command.……...3
Eyes open spontaneously…...………….4
Best Verbal Response (5)
No verbal response ………………………1
Incomprehensible sounds. ……………..2
Inappropriate words. …………………….3
Confused …………………………………..4
Orientated …………………………………5
Best Motor Response (6)
No motor response.…………………..…..1
Extension to pain.…………………….…..2
Flexion to pain.……………………….…...3
Withdrawal from pain..……………….…..4
Levels of Brain Injury
Mild
Glasgow Coma Scale (GCS) score
13-15
Stunned or dazed for a few
seconds or minutes
Remains alert without post-
traumatic amnesia (PTA)
Headache can follow
Complete recovery is usual
Levels of Brain Injury

Moderate
 GCS score 9-12
 Usually result from a non-penetrating blow to
the head, and/or a violent shaking of the
head
 A loss of consciousness lasts from a few
minutes to a few hours
 Confusion lasts from days to weeks
 Physical, cognitive, and/or behavioral
impairments last for months or are
permanent
 Good recovery with treatment or successfully
Levels of Brain Injury
Severe
GCS score 3-8
Usually result from crushing
blows or penetrating wounds to
the head
PTA of more than 24 hours
Coma with no meaningful
response and no voluntary
activities lasts days, weeks, or
months
Exclude other causes of depressed
conscious level (causes of coma)
No focal signs
drugs (alcohol, opiate)
circulatory collapse
hypothermia / hyperthermia
concussion
meningitis, encephalitis
subarachinoid hemorrhage

Focal signs present

cerebral abscess ,infarction, tumor
intracranial hemorrhage
Pupil reflex
 Pupillary reflexes function as an indication of
both underlying pathology and severity of
injury, and should be monitored serially.
 Pupils should be examined for size,
symmetry, direct/consensual light reflexes,
and duration of dilation/fixation.
 Abnormal pupillary reflexes can suggest
herniation or brainstem injury.
 Orbital trauma, pharmacological agents, or
direct cranial nerve III trauma may result in
pupillary changes in the absence of
increased ICP, brainstem pathology, or
herniation
Pupil Size
The normal diameter of the pupil
is between 2 and 5 mm, and
although both pupils should be
equal in size, a 1-mm difference
is considered a normal variant.
Abnormal size is noted by
anisocoria defined as >1 mm
difference between pupils.
Pupil Symmetry
Normal pupils are round, but can
be irregular due to
ophthalmological surgeries.
Abnormal symmetry may result
from compression of CNIII can
cause a pupil to initially become
oval before becoming dilated and
fixed
Direct Light Reflex
Normal pupils constrict briskly in
response to light, but may be
poorly responsive due to
ophthalmological medications.
Abnormal light reflex may be
seen in sluggish pupillary
responses associated with
increased ICP. A non-reactive,
fixed pupil has <1 mm response
to bright light and is associated
with severely increased ICP.
CRANIAL NERVE TEST
Investigations

Skull radiograph
CXR and X-ray of cervical spines
CT-Scan - first line investigation
MRI
Indication for CT-scan
 GCS<13 at any stage
 GCS =13 or 14 at 2 hours following injury
 Suspected open or depressed #
 Any sign of basal skull # (haemotympanum,
'panda' eyes, cerebrospinal fluid leakage from the
ear or nose, Battle's sign).
 Post-traumatic seizures
 Focal neurologic deficit
 Post-traumatic amnesia of >30 minutes
 Persistent vomiting
 Coagulopathy
 Significant mechanism of injury
CT Cervical Scan
For adults who have sustained a head injury
and have any of the following risk factors,
perform a CT cervical spine scan within 1
hour of the risk factor being identified:
 GCS less than 13 on initial assessment.
 The patient has been intubated.
 Plain X-rays are technically inadequate (for
example, the desired view is unavailable).
 Plain X-rays are suspicious or definitely
abnormal.
 A definitive diagnosis of cervical spine injury
is needed urgently (for example, before
surgery).
MRI
MR imaging is indicated if there
are neurological signs and
symptoms referable to the
cervical spine.
If there is suspicion of vascular
injury (for example, vertebral
malalignment, a fracture
involving the foramina
transversaria or lateral
processes, or a posterior
circulation syndrome), CT or MRI
MRI
More sensitive and detail imaging
study
Demonstrate: anatomic &
vascular structures, myelination
process & detection small
hemorrhages
Disadvantage: time consuming,
sensitivity to patient motion and
incompatibility with various
medical devices
Angiogram
An angiogram is a test used to
examine blood vessels. When
diagnosing a brain injury, the test
involves injecting dye into an
artery that supplies blood to the
brain, usually through a catheter
inserted in the groin.
The dye highlights the blood
vessels on x-ray, and can show
any leakage from those vessels.
ICP MONITOR
An ICP monitor is a device used to
measure intracranial pressure, or
pressure within the skull. One of the
reasons this pressure can increase is
when an injury to the brain causes
swelling.
The ICP monitor consists of a small
tube, placed into or on top of the brain
through a small hole in the skull. This
tube is connected to a transducer that
registers the pressure, which is
displayed on a monitor.
Blood test
All patients with multiple injuries and
those with severe head injuries,
should have blood samples analysed
for baseline estimations - full blood
count, electrolytes and urea,
coagulation screen, blood gases,
alcohol level and blood group (and
save).
Electrolyte abnormalities and
haemoglobin deficiencies should be
corrected, if present, whilst clotting
disorders should be corrected if
Other diagnostic method
Electroencephalograph (EEG)
Single-photon emission
computed tomography (SPECT)
Positron emission tomography
(PET)
Diffusion tensor imaging (DTI)
Transfer to hospital
Patients who have sustained a head injury
should be refered to a hospital emergency
department, using the ambulance service if
deemed necessary, if any of the following
are present:
 Glasgow coma scale (GCS) score of less than
15 on initial assessment.
 Any loss of consciousness as a result of the
injury.
 Any focal neurological deficit since the injury.
 Any suspicion of a skull fracture or
penetrating head injury since the injury.
 Amnesia for events before or after the injury
Emergency Management
Remember that the priority for all
emergency department patients
is the stabilisation ABCDE before
attention to other injuries.
Airway
Breathing
Circulation
Disability
Exposure
AIRWAY
Handle Neck With Caution:
Assume C-spine Injury
Attempt full cervical
immobilisation
Avoid Obstruction of Venous
Drainage
Do oral intubation if GCS < 8
May Need to Protect Airway Due
to Seizures or Trauma
BREATHING
Even a small rise in PaCO2 causes
a significant rise in ICP
“Adequate” breathing may not
be enough- aim for PaCO2 of 35-
40 mmhg
Hyperventilation is the quickest
way to lower ICP if there are signs
of herniation
CIRCULATION
Blood pressure must be
optimized to help maintain
adequate CPP (Cerebral perfusion
pressure)
Prevent increased ICP by
administering Mannnitol IV
Only use isotonic fluids for
volume expansion
May need inotropic or pressor
support
DISABILITY
Neurological examination begins
with assessment of the patient’s
conscious level using the GCS.
The severity of the head injury
can be based on this initial GCS
score.
 A patient with a GCS of 8 or less
is in need of urgent anaesthetic
assessment as airway
compromise and/or reduced lung
Assessment of pupil and
reaction to light
 Asymmetrical pupil size and reduced
reaction to light may indicate brain injury
from either diffuse injury or an intra-cranial
hematoma. It may also, however, indicate an
isolated injury to the orbit and associated
with cranial nerves
Asymmetry of limb movement
may help in diagnosing an
underlying intra-cranial lesion.
Observations on the blood
pressure, pulse and respiratory
rate are also essential, not only
to ensure cardio respiratory
stability of the patient, but also to
indicate possible
brainstem compromise.
Pain Management
Manage pain effectively because
it can lead to a rise in intracranial
pressure.
Provide reassurance, splintage of
limb fractures and catheterisation
of a full bladder, where needed.
Treat significant pain with small
doses of intravenous opioids
titrated against clinical response
and baseline cardio respiratory
measurements
GENERAL MANAGEMENT OF HEAD INJURY
ABC rule
stabilization of airway, breathing and circulation
IV access - maintain normovolemia
- hypotonic/glucose containing fluids
should not be used
endotracheal intubation (e.g: GCS ≤ 8, hypoxia,…)
Head end elevation - 300
Treat co-existing injuries
chest drain - tension pneumothorax
cervical collar - # of cervical spine,….
 Anticonvulsants
may decrease early posttrauma seizures but

no benefit in long term epilepsy prevention

Phenytoin
 Loading dose = 18 - 20 mg/kg
 Maintenance dose = 100 mg q 8 hrly
Regular observation at half hourly interval:

GCS
BP, HR, RR, and Temperature
oxygen saturation
pupil size & reactivity
limb movement
COMPLICATIONS HEAD INJURY
Meningitis & brain abscess
CSF rhinorrhea and otorrhea
Epilepsy - about 80% arise in 2yrs
Hydrocephalus- usually due to atrophied white
matter
Amnesia (PTA)
Postconcussional Sx
Posttraumatic encephalopathy
Cranial nerve injury - in up to 30% pts
Indications for surgery
1. Penetrating injuries or blunt injuries
with breach of the calvarium/skull
2. Presence of expanding intracranial
hematoma
a) Epidural Hematoma
b) Subdural Hematoma
3. Malignant cerebral edema
Decompressive Craniotomy -
Decreases ICP, improves cerebral
perfusion, prevents ischemia
◦ EPIDURAL HEMATOMA
◦ Surgery is Indicated – If volume >
30 cm3
Clot evacuation with or without
ligation of bleeding vessel
SUBDURAL HEMATOMA
◦ Surgery is Indicated – If size > 10
mm on CT or if 5 mm shift
◦ 1st line – Irrigation/evacuation via burr
twist drill and burr hole craniostomy
Indications for surgery
 New, surgically significant abnormalities on
imaging
 Persisting coma (GCS 8 or less) after initial
resuscitation.
 Unexplained confusion which persists for
more than 4 hours.
 Deterioration in GCS score after admission
(greater attention should be paid to motor
response deterioration).
 Progressive focal neurological signs.
 A seizure without full recovery.
 Depressed skull fracture
 Definite or suspected penetrating injury.

Principal Management of
Head Trauma
 Can be divided into:

1. Initial management
2. Early Neuro-assessment
3. Neuro-surgical management
INITIAL MANAGEMENT
Early Neuro-assessment
1. Assess for the conscious level by using
Glasgow Coma Scale
2. Cranial nerves examinations if possible
3. Assessment of pupillary size & reaction
4. Search for CSF leaks from nose, mouth &
ears
5. Examine scalp for laceration and
fractures
6. Assessment of maxillofacial skeleton
7. Monitor neurological symptoms
◦ Vomiting
◦ Altered behaviour (confusion)
◦ Severe & persistent headache
Discharge criteria in mild head
injury
 GSC 15/15 with no focal deficits
 Normal CT brain
 Not under influence of drugs or alcohol
 Accompanied by a responsible adult
 Verbal and written head injury advice to seek
medical attention if:
◦ Persistent/worsening headache despite
analgesia
◦ Persistent vomiting
◦ Drowsiness
◦ Visual disturbance
◦ Limb weakness and numbness
Observe for few hours especially
when there is history of LOC at
time of injury
Evaluate if patient need
admission or not
Investigations:
◦ Imaging (CT scan of brain)
◦ Other baseline investigations (FBC,
coagulation profile, GXM)
Treatment/intervention