Head (Brain) Injury
This Session
•
•
•
•
•
•
Skull
CSF
Circulation
Brain stem
Head injury
Assessment
Structure of the Skull
• Bones fused
• Openings allow passage of blood vessels
and nerves
• Largest opening is the foramen magnum
Production and Circulation of
Cerebrospinal Fluid (CSF)
• Production from choroid plexus
• One in each ventricle
• CSF provides buoyancy, protection &
chemical stability to Brain
Production and Circulation of
CSF
• CSF circulates through the subarachnoid
spaces and ventricles
• CSF is reabsorbed from the arachnoid villi
into the Sagittal Sinus
Circulation of the Brain
• Arterial supply (arterial pressure)
• Venous sinuses and veins
Brain Stem
•
•
•
•
Respiratory centres
Cardiac centres
Cranial nerves
Reticular Activating System
Head Injury Risk
•
•
•
•
•
Males, ages 15 to 30 years
Low/median income
Peak - evenings, nights weekends
Alcohol
Causes: motor vehicle accident, falls,
assaults, sport-related injuries
Injury
• Primary injury – from the impact
• Secondary injury – hypoxia, hypercapnia,
hypotension (ischaemia), intracranial
hypertension (high ICP)
• Acceleration - deceleration
• Rotational injuries
Injury
• Primary Injury
– Direct tissue damage from traumatic
mechanism (eg. Contusion, tissue shearing,
haemorrhage)
• Secondary injury
– Occurs minutes to hours after the primary
injury
– Ischemia from elevated ICP and/or systemic
hypotension
– Metabolic toxins
Open Head Injury
• Fractures associated with Open Head Injury
–
–
–
–
Depressed
Open
Comminuted
Basilar - CSF leakage from nose and ears (i.e.
rhinorrhea and otorrhea)
– Most often from bullet or knife wounds
Closed Head Injury
• Caused by ‘blunt’ trauma
– Concussion
– Contusion
– Laceration
• Acceleration & Deceleration Injuries
Concussion
• Mild Concussion – cortical dysfunction
• Classic Concussion – loss consciousness
• No physical evidence
Cerebral Contusion
• Cortical bruise
• Usually due to violent anterior - posterior
displacement
• Contusion at point of contact is “coup”
• Contusion opposite is “contre coup”
Brain Stem Injury
• Poor prognosis
• Immediate dysfunction, loss of
consciousness, pupillary changes, posturing,
cranial nerve deficits, changes in vital
functions
Diffuse Axonal Injury
• Shear damage is microscopic
• Common cause of brain damage after
Traumatic Brain Injury
How things evolve after a Head
Injury
• Brain is enclosed
• Blood, brain tissue and CSF contribute to
ICP
• Normal = 10 - 15 mm Hg in lateral
ventricles
• Brain Oedema, Brain tumour or bleeding
increases ICP
Monroe Kellie Hypothesis
BRAIN 80%
BLOOD 10%
CSF
10%
80%
10%
10%
As ICP increases
• Initially compensated by displacement of
CSF
• ICP increases ⇒ cerebral blood flow
decreases ⇒ tissue hypoxia ⇒ decrease in
pH and increase in CO2 level
• This leads to cerebral vasodilation, oedema
& further increases in ICP. This cycle
continues
As ICP increases
• CNS ischaemic response
• Ultimately, brain can herniate
Signs and Symptoms of
Increased ICP
•
•
•
•
•
LOC change
Pupil change
Motor dysfunction
Headache
Change in Breathing Pattern
Signs & Symptoms of Increased
ICP
•
•
•
•
•
•
Vomiting
Positive Babinski reflex
Blurred vision, diplopia
Seizures
Loss of brain stem reflexes
Cushing reflex
Treatment
• Reduce ICP surgically or with mannitol
(osmotic diuretic)
Types of
Haematoma
• Epidural
• Subdural
• Intracerebral
Epidural Haematoma
•
•
•
•
•
Between skull & dura
Usually due to torn middle meningeal artery
Skull usually fractured
Dura slowly separates
Arterial bleed
Intracerebral Haematoma
•
•
•
•
•
2/
3
ruptured aneurysms
Also caused by penetrating injuries
CSF often contains blood
Rapid progression as arterial bleed
More frequent in older persons and
alcoholics
Subdural Haematoma
•
•
•
•
•
Between dura and arachnoid
Common in victims of child abuse
Dura attached to skull, pia to Brain
Bridging veins shear
Bleeding is slower than epidural
Subdural Haematoma
• Absence of blood in CSF doesn’t negate
subdural haematoma
• Clinically manifest as:
– Acute
– Chronic
Acute & Chronic Subdural
Haematomas
• Based on time interval until appearance of
symptoms after injury
• Acute (within 24 hr)
• Subacute (2-10 days)
• Chronic (possible weeks)
Acute Subdural Haematoma
• Symptoms seen within 24 hours
• Progresses rapidly and carry high mortality
due to secondary injuries from inc. ICP
• Similar symptoms to Epidural haematoma
due to ICP
Chronic Subdural Haematoma
• Develop weeks after injury
• Clot is encapsulated by fibroblasts
• Encapsulated cells gradually lyse and the
contained fluid develops high osmotic
pressure
• Draws fluid from surrounding tissue,
increasing volume (& ICP)
Chronic Subdural Haematoma
• Affects older persons with cerebral atrophy
• Minor fall causes subdural haemorrhage - often
subclinical
• Clot liquification over next 2-4 weeks results in a
process of clot expansion and development of
signs and symptoms of a mass
• Effects may resemble brain tumour or stroke
Chronic Subdural Haematoma
• Treatment usually surgical
• Most patients make excellent recovery
unless elevated ICP leads to secondary
injury or herniation
Characterization of TBI
• Clinical severity is graded using GCS
– Mild, GCS 13-15
• normal to lethargic, mildly disoriented
– Moderate, GCS 9-12
• lethargic to obtunded, follows commands with arousal,
confused
– Severe, GCS 3-8
• comatose, no eye opening or verbalization.
• does not follow commands
• motor exam: ranges from localizing to posturing
Glasgow Coma Scale
Eye Opening Response
•
•
•
•
Spontaneous--open with blinking at baseline
To verbal stimuli, command, speech
To pain only (not applied to face)
No response
4
3
2
1
points
points
points
point
5
4
3
2
1
points
points
points
points
point
Verbal Response
•
•
•
•
•
Oriented
Confused conversation, but able to answer questions
Inappropriate words
Incomprehensible speech
No response
Motor Response
•
•
•
•
•
•
Obeys commands for movement
6 points
Purposeful movement to painful stimulus
5 points
Withdraws in response to pain
4 points
Flexion in response to pain (decorticate posturing)
3 points
Extension response in response to pain (decerebrate posturing)
2 points
No response
1 point