HEAD INJURIES

& GLASGOW COMA

SCALE
• Any degree of injury to the head ranging from
scalp laceration to loss of conciousness to focal neurological deficits.
AEITIOLOGY
• Motor vehicle accidents
• Falls
• Assault
• Sports related injuries
• Firearm related injuries
• Highest among adolescents, young adults and those older than 75 yrs
• 50% of major trauma deaths are due to TBI
• Vehicle causes are the leading causes of brain injuries. Falls are
second leading cause.
LAYERS OF SCALP
CLASSIFICATION OF HEAD INJURY
1) Injury to scalp
2) Injury to vault of skull
3) Injury to base of skull
4) Injury to duramater
5) Injury to brain
6) Injury to blood vessels
7) Escape of cerebrospinal fluids
8) Injury to cranial nerves
INJURY TO VAULT OF SKULL
INJURY TO BASE OF SKULL
INJURY TO DURAMATTER
DIFFERENTIAL DIAGNOSIS
INJURY TO THE VAULT OF SKULL
• Causes:
1. Compression of Sphere
2. Local Indentation
3. Tangential Force
1. Compression of Sphere

• If, the head is compressed against

a hard flat surface, the Spherical
Shape of the skull becomes more
Oval(Ovoid).
• As a result a Linear Fracture Lines
is formed which starts from the
point of maximum Convexity
through the thin areas of the skull.
• The fracture line often deflects
from the Vault towards the base of
the skull and hence, may also
cause Base Of Skull Fracture
2. Local Indentation
i. By Large Round Object
• May produce Closed Pond depressed
Fractures.
• Scalp may be bruised but intact.
• Skull may be indented but not indriven
• Dura remain intact.
• Underlying Brain Area may be bruised
but intact.
ii. By Small Round Object
• May produce Compound Depressed
Facture
• Scalp is Lacerated
• Skull is indriven
• Dura and underlying brain Lacerated
• Immediate Risk of Infection due to
open wound and later risk of Epilepsy
due to contracting scar on healing.
3. Tangential
Force
• Rare
• May be caused by a Tangentially directed force which grips the skull
and lifts it up.
• Appears as a Horse-shoe shaped fracture surrounding the calvarium
INJURY TO BASE OF THE
SKULL
• TYPES:
1. Fracture of Anterior Cranial Fossa
2. Fracture of Middle Cranial Fossa
3. Fracture of Posterior Cranial Fossa
ANTERIOR CRANIAL FOSSA
FRACTURE
• Presents with:
 Epistaxis
 CSF through nose
 Brain Matter through nose
 Ecchymosis which starts in the lower eyelid and
spreads to upper eyelid( Raccoon/Panda Eyes)
 Sub-conjuctival hemorrhage with possible
Proptosis.
• Cranial Nerves:
 1st( Anosmia)
 3rd,4th ,1st division of 5th and 6th due to injury at
sphenoidal fissure.
 3rd Nerve involvement may produce pupillary
dilation
MIDDLE CRANIAL FOSSA FRACTURE
• Presents with:
 Bleeding from Ear or Mouth
 Escape of CSF or Brain Matter
through Ear or Mouth
 Epistaxis if Nasal Sinuses are involved
• Cranial Nerves:
 7th (Paralysis of Facial Muscles); May
occur Early or Late
 8th (Deafness)
 6th (Internal Strabismus); Occassional
POSTERIOR CRANIAL FOSSA
FRACTURE
• Presents with:
 Extravasation of blood in sub occipital
region and swelling in neck
 CSF Otorrhea
 Ecchymosis posterior to mastoid process.
• Cranial Nerves:
• 9th, 10th and 11th Nerve at Jugular
Foramen
INJURY TO BRAIN
• TYPES:
1. Cerebral Concussion
2. Cerebral Contusion
3. Cerebral Irritation
4. Cerebral Laceration
CEREBRAL CONCUSSION
• Mild Traumatic Brain Injury
• Temporary Physiological Paralysis of Function without Structural
Damage.
• It is a condition of shock.
• Symptoms:
 Short period of Unconsciousness( Stupor)
 Pulse: Rapid, Hypovolumic
 Blood Pressure: Slightly Reduced
 Respiration: Quick and Shallow
 Temperature: Subnormal
 Muscles: Flaccid.
 Recovery is complete and Perfect
CEREBRAL CONTUSION
• Petechial Hemorrhages and Rupture of White Fibres Of
Brain.
• Hemorrhages:
i. Petechial
ii. Ring shaped(by Bleeding into Perivascular VRS.
iii. Hemorrhages in Corpus Callosum and Substantia
Nigra
• Symptoms:
 More prolonged Unconsciuosness
 Initial Recovery: Imperfect. Results in Post-Contusional
State with defective memory and personality
change.Patient has confusion, irritability, delirium etc.
 Intracranial Pressure is reduced.
 During unconsciousness:
o Pulse Rate: Increased, Hypovolumic
o Blood Pressure: Reduced
o Respiration: Shallow
o Muscles Relaxed
o Facial Pallor
 Following this the patient recovers:
o Pulse Rate: Increases in Volume
o Blood Pressure: Reduced
o Respiration: Deeper
o Face becomes flushed.
o Patient complains of Headache, irritation and may vomit
CEREBRAL IRRITATION
• Starts 2-3 days after Head Injury.
• Cause: Cerebral Edema.
• Symptoms:
 Patient conscious but not interested in surroundings.
 Attitude: Attitude of Flexion. Remains curled up with Knees drawn up
arms flexed
 Resists interference.
 May show Headache, depression, memory loss, Personality change
etc.
CEREBRAL LACERATION
• The tearing of Brain Surface along with
effusion of blood into CSF.
• Leads to Subarrachnoid Hemorrhage.
• Cause: Injury of Brain surface against Bony
ridges and edges of Dural septa.
• These are common on the inner aspect of
hemisphere under surface of the frontal Lobe
and tip of the temporal lobe.
• Impact may be on the same side(Coup) or
opposite(Contre-coup)
• Symptoms( Mostly Similar to Cerebral
Contusion)
 Anosmia
 Change of Personality
INJURY TO BLOOD VESSELS
• Injury to any Intra-Cranial Vessel causes
Hemorrhage.
• It results in Cerebral Compression
• Cerebral Compression takes time to develop.
• This time varies with the type of Vessel(Artery
or Vein) and the caliber of vessel.
• During this period the patient remains
conscious and it is hence known as Lucid
Interval.
• Depending on whether the bleeding is above
or below Tentorium Cerbelli, the hemorrhage
is:
1. SupraTentorial
2. InfraTentorial
SUPRATENTORIAL
HEMORRHAGE
• It includes:
1. Subcortical Hemorrhage
2. Subdural Hemorrhage
3. Extradural Hemorrhage

• The effect produced is due to

o Local Pressure on Underlying Brain
o Herniation of Uncus Of Temporal Lobe
through Tentorial Hiatus causing Mid Brain
Compression
• Cerebral Compression Symptoms:
 Irritable followed by unconsciousness
 Pulse: Slow and Bounding
 Respiration: Slow and Deep. May show Stertorous Respiration. Cheeks flap with respiration
 Temperature Higher on side of Lesion.
 Pupil: Contract initially then dilation of same side then both sides with non-reactivity.
• Contribution of MidBrain Compression:
 Consciousness: Deteriorate because of damage to Reticular Activating System
 Pupillary Changes due to effect on Occulomotor Nerve
 Hemiplegia due to compression of opposite crus of MidBrain
• Damage to Pons:
 BP: Increase
 Pulse: Slow
 Respiration: Irregular
SUBCORTICAL
HEMORRHAGE
• Cause: Arterial Bleed; due to Brain Surface
Laceration or Rupture of Central Artery.
• Symptoms may take 1-10 days to develop. LOBAR BASAL GANGLIA

• Symptoms: Epileptic Fits with Localized

Paralysis.
• It becomes fatal when bleeding reaches
Ventricles leading to Intraventricular
Hemorrhage.
• Main symptom Hyperthermia.
• Old blood clots produce symptoms
mimicking Cerebral Tumors
SUBDURAL HEMORRHAGE

• More common than Extradural

Hemorrhage
• Cause: Rupture of Superior Cerebral Veins;
Most commonly due to injury to back of
head.
• Mechanism: Cerebral Hemisphere moves
with sinus while Superior Veins draining
them remain fixed
• About 50% cases are Bilateral
• Symptoms:
 Acute:
o Cerebral Compression; Fatal requires
immediate Surgery
o No definite lucid interval. Rapid onset of
unconsciousness.
 SubAcute/Chronic:
o Prolonged severe headache,
o Mental apathy,
o Slowness in responding to questions,
o Coma when Midbrain Pressure Cone
develops
SUB-ACUTE SDH

CHRONIC SDH
EXTRADURAL
HEMORRHAGE
• Cause: Most commonly Lateral Blow leading
to fracture of Temporal Bone causing Injury to
Anterior or Posterior Branch of Middle
Meningeal Artery.
• Anterior Bleeding is more significant and is
associated with injury to Pterion.
• Hemorrhage is mostly Unilateral
• Symptoms:
o Concussion
o Followed by Lucid Interval during which
Hemorrhage develops and compression starts.
o Followed by Confusion and Irritability
o Followed by Drowsiness
o Followed by twitching and then Paralysis of
the opposite side of Face, Arms and
Legs(Contralateral Hemiplegia). This is
caused by Hematoma pressing the Motor
Cortex of One Side.
o At the same time Temporal Lobe shifts
medially and presses on the 3rd Nerve causing
Rapid Contraction and then Dilation
o Following, this Ipsilateral Hemiplegia occurs.
This is due to Opposite Crus of Brain Stem
pressing against the opposite crus of Brain
Stem.
o Finally, Mid Brain Cone impaction leads to
fixed Dilation of Pupils and Decerebrate
Rigidity.
• The side of Middle Meningeal
Hemorrhage is diagnosed by
i. Side of Skull Fracture
ii. Side of Boggy Swelling
iii. Side of initial Dilation of pupil
• EDH can also be from Anterior Cranial
Fossa Fracture leading to Anterior
Meningeal or Maxillary Bleed
 Extradural Hemorrhage Sub Dural Hemorrhage
Incidence Less Common More Common

Onset Signs of compression appear Later Appear Earlier

Lucid • Present. • Very less or absent.

Interval • Occurs after Initial Loss of • Blood Accumulates rapidly.
consciousness(Concussion). • No compensation of Pressure occurs.
• Increase in Pressure due to blood accumulation
between Dura and skull is balanced by flowing of
CSF into Spinal Canal.
• When this fails Uncal Herniation occurs and then
Unconsciousness sets.

Paralysis • Contralateral Hemiplegia followed by Ipsilateral • Contralateral Hemiplegia followed by Ipsilateral

Hemiplegia Hemiplegia
• The time interval between these is more • The time interval between these is less

X-Ray Skull • May show fracture line in temporal bone May not show

CT Scan • Lens-Shaped Hematoma Banana/Crescent Shaped Hematoma

Laterality • Mostly Unilateral Usually Bilateral

INFRATENTORIAL HEMORRHAGE
• Compression of Cerebellum, Pons and Medulla
• Initially, no Midbrain Compression so no Loss of
Consciousness.
• Symptoms:
 BP: Increase
 Pulse: Slow
 Respiration: Irregular
 Ataxia
 Nystagmus
 Lower CN Palsies
COMPLICATIONS
• Most common Complications:
 Post-traumatic Headache
 Post-traumatic epilepsy
 Hydrocephalus
 Metabolic Disorders like Uraemia, Diabetes Insipidus,
 Caroticocavernous fistula
 Fat Embolism
• Post-Traumatic headache may also be due to injury to Upper Cervical Vertebra pressing on the
Greater Occipital and Posterior Auricular Nerves
• Such a headache is characterized by Pain on Flexion of Cervical Spine and Tenderness at Upper
Cervical Spine Region.
• Post-traumatic epilepsy is of 2 types:
 Early:
o Seen in first 24 hours.
o Due to bruising and Edema of Brain Near Site of Injury.
 Late(True Post-Traumatic Epilepsy):
o Takes upto 6 months to develop.
o Due to Scar tissue formation in Brain
o Jacksonian Type(Unilateral)
o First, twitching of Thumb or hand.
o Then Muscles of Arm, Shoulder and Face.
o Then Aura may be seen.
o Finally, it may become a generalized fit
History taking and
investigation
Type of accident
• Whether road accident or fall from height
• Whether acceleration injury or deceleration injury
• If injured with a weapon, the type of weapon used-whether sharp or
blunt
• The exact site of injury should be noted
Level of consciousness
• Time of onset of unconsciousness
• Duration of unconsciousness
• Lucid interval: short period of consciousness between initial
unconsciousness which occurs immediately after accident and
unconsciousness at later stage after the lucid interval .
Post-traumatic amnesia
• Time between the head injury and return of continuous memory.
• A) if 1-24 hrs: moderate injury
• B) if 1-7dys: severe injury
• C) if>1 week: almost fatal injury
Retrograde traumatic amnesia
• Loss of memory for events before the occurrence of the accident
vomiting
• Ensure whether the patient vomited since the accident or not.
• If yes, note quantity and type of vomitus
• A) if blood mixed: middle cranial fossa fracture
• B) persistent vomiting: increased intracranial tension
Epileptic fits or seizures
• The nature of epileptic fits may give a clue to localization of site of
trauma
• A) bilateral in case of hemorrhage from the superior longitudinal sinus
• B) jacksonian epilepsy: unilateral-due to middle meningeal
hemorrhage
Swelling and pain in the head
• Swelling due to hematoma or fracture of the skull
• Headache is a common symptom following head trauma
• Persistent and localised headache may be due to
• i) progressive extradural hematoma
• ii) subdural hematoma
Other complaints
• bleeding from the nose, ear or mouth
• 1) CSF rhinorrhoea indicates anterior cranial fossa
fracture
• Also associated with raccoon eyes(subaponeurotic bleeding)
Middle cranial fossa fracture
• CSF otorrhoea indicates fracture of petrous part sof temporal bone
i.e. middle cranial fossa fracture
• Also associated with battle sign(discoloration over mastoid process)
Posterior cranial fossa fracture
• Visual problems
• 6th nerve injury leading to diplopia
Past history

• Whether patient had fits in the past

• Similar type of head injury
• High blood pressure
• Renal disease
• diabetes
Personal history
• Alcohol
• Apoplexy
• Uraemia
• Diabetic coma
• Opium poisoning
Family history
• Epilepsy
• Diabetes
• Hypertension
Often run in family
Special investigations
• 1) blood: for diabetes and grouping and cross matching
• 2) x-ray: to know the fractures of skull
Lumbar puncture
• Pressure raised in cerebral compression
• Crystal clear fluid in case of haemorrhage outside the membranes
• Blood stained fluid with increased pressure in case of cerebral
contusion or laceration.
•s
 Carotid angiography
• Used to demonstrate the site of lesion(subdural,extradural or
subtemporal)
• Technique- Injection OF DYE (10 ml of 35%diodone)into common
carotid artery followed by skiagraphy immediately
• It takes 2 hours so its done when the patient condition is not so acute
Electro encephalography(EEG)
• It shows areas of suppressed activity of the cortex due to injury or
haemorrhage by pressure
Echo encephalography
• Indicates the presence of haematoma by indicating a shift of the
midline structure
• Not much helpful in subdural haematoma as half of the caese are
bilateral with no midline shift
ultrasonography
• Useful in locating the
site of haemorrhage
Brain scan
• Important investigation in case of head injury and space occupying
lesions
• Head is scanned from above downwards in a series of transverse
planes
• In the report brain substance
appear grey ventricular fluid
black and blood clot white
• Particular in chronic subdural
haematoma
Magnetic resonance imaging(MRI)
• Supercedes other investigations in accuracy
• Gives a clear picture of brain
injury and injury of the skull,
subdural and extradural
haematoma
GLASGOW COMA SCALE
Historical Background
• The scale was published in 1974 by Graham Teasdale and Bryan J.
Jennett, professors of neurosurgery at the University of Glasgow’s
Institute of Neurological Sciences at the city’s Southern General
Hospital.
• A patient is assessed against the criteria of the scale, and the resulting
points give a patient score between 3 (indicating deep
unconsciousness) to 15 (full consciousness).
What is GCS?
• The Glasgow coma scale (GCS) is a neurological scale which aims to
give a reliable way of recording the conscious state of a person.
• The scale is based on Behaviour-Response score.
• Behaviour: It includes:
• Eye opening response
• Best verbal response
• Best motor response
• Response: This is based on grades of behaviour with minimum score
of 1.
Glasgow Coma Scale Scoring Criterion
Assessment of GCS in a patient with head
injury
• General Assessment:
• GCS score 13-15: Mild head injury
• GCS score 9-12: Moderate head injury
• GCS score <8 : Severe head injury
• Baseline score should be calculated before giving any sedative agents.
• Serial GCS monitoring should be done to evaluate if the patient is improving.
• Every 30 minutes for 1st 2 hours
• Every 1 hour for next 4 hours
• Every 2 hours after 6 hours
• The GCS score should be charted there after.
Notes on GCS
• Non testable should be
mentioned wherever
appropriate.
• GCS-P Score
• GCS –P score is better
indicator of outcome than
GCS Score
Example:
• You are asked to assess a seriously head injured patient.
• They make no eye, verbal or motor movements, either spontaneously
or in response to your spoken requests; when stimulated with fingertip
pressure their eyes do not open, they make no sounds, but their arms
flex normally.
• This translates to scores of E1V1M4 giving a sum score of 6 which
carries a likelihood of death of 29%.
• Neither pupil is reactive to light; this gives a Pupil Reactivity Score (PRS)
of 2. The GCS-P score (GCS-PRS ) is 6-2 = 4.
• The likelihood of mortality is increased to 39%.