11 - Traumatic Head and Spinal Injury Flashcards
Name for direct trauma to scalp
Laceration
Effects of direct trauma to meninges
Vascular injury, lacerations
Effects of direct trauma to brain or spinal cord
Contusions, lacerations, diffuse axonal injury, diffuse vascular injury
Concussion
1
2
3
- Instantaneous loss of consciousness, temporary respiratory arrest, loss of reflexes.
- Follows sudden change in the momentum of the head.
- Pathogenesis uncertain. Maybe effect is at brainstem level (reticular activating system).
Leading cause of death in Western countries, under 40 years old
Traumatic CNS injury
Two broad types of CNS trauma
1) Penetrating injury (direct disruption of tissue)
2) Closed injury (movement and compression of neural and vascular structures within bony confines)
Features of skull fractures 1 2 3 4 5
- Tend to radiate from the point of impact.
- Can be depressed.
- If communicate with surface called “open”. If not, “closed”.
- If splintering of bone – “comminuted”.
- Blood/CSF from nose and/or ears may result from basal fractures.
Significance of skull fractures
Indicates a high-energy transfer injury
Cause of epi- or extradural haematoma
Middle meningeal artery damage
Cause of subdural haemartoma
Subdural vein injury.
Can be acute or chronic
Why are extradurals more common in younger people?
With age, dura becomes more adherent to skull
More urgent type of haematoma
Extradural, because it is from an arterial bleed.
More common type of haematoma in elderly populations
Subdural.
Dura becomes more adherent to skull with age, stretching the dura out more. Venous sinuses are made up of walls of dura, these become more likely to rupture if they are under greater tension
Contusion
Haemorrhagic necrosis (bruise)
Coup
Contusion at the site of impact
Contrecoup
Occurs when head is not immobilised at the time of injury and involves the opposite side of the brain
Location of sterotypic contusions in head injury
At base of the brain
EG: inferior frontal lobes, inferolateral temporal lobes.
These often occur no matter where coup and contrecoup injuries are.
Occurs from brain dragging over uneven surface of cranial floor
Common finding with any sort of head injury
A degree of subarachnoid haemorrhage
Appearance of old cerebral contusions
Areas of depressed, shrunken brain tissue.
Brain rarely heals by fibrosis.
Gliotic brain with remains of haemosiderin.
Brain laceration
Penetration of brain by foreign body or skull fragment
Effect of missile brain injury
Eg bullet wound.
Injury not just at the area where the missile penetrated, but also sends out shockwaves through cerebral tissue that can be damaging.
If sufficient energy transfer, cerebral tissue can tear at vulnerable sites eg ponto-medullary junction.
Diffuse axonal injury
Axons can be mechanically shorn over a wide area.
What often accompanies diffuse axonal injury?
Diffuse vascular injury
Histological appearance of severed axon
Axoplasm continues flowing for a while out of severed axon, leading to a blob-like appearance at site of severance.
Can be visualised with silver stains
Long-term effects of diffuse axonal injury
Greatly-enlarged lateral and third ventricles.
This is because damaged white matter is removed, undergoes gliosis. This results in loss of tissue.
Effect of compression of spinal cord
‘Toothpaste’ effect, as cord is so soft. Can lead to a central haemorrhagic necrotic core either side of site of injury in spinal cord
Long-term sequelae of brain trauma 1 2 3 4`
1) Infections
2) Hydrocephalus
3) Epilepsy
4) Chronic traumatic encephalopathy
Chronic traumatic encephalopathy
1
2
3
1) Brain atrophy due to neuronal loss
2) Abnormal deposition of tau protein
3) Often diffuse deposition of A-beta plaques in cortex
Amounts of blood and CSF in cranial cavity
150mL of each
Initial response to swelling of brain
Expulsion of as much CSF as possible. Compression of ventricles. Expulsion of venous blood.
After this, ICP starts to rise
Effect of increasing ICP
Herniations of brain tissue through dural openings (EG foramen magnum).
As ICP approaches arterial pressure, brain perfusion ceases
Amount of CSF produced each day
~400mL
Potential causes of increased ICP 1 2 3 4 5 6 7
1) Trauma
2) Tumour
3) Infarction
4) Haemorrhage
5) Infection
6) Cerebral oedema (which can complicate any of the above)
7) Overproduction, diminished absorption of CSF
Two main subtypes of cerebral oedema
1) Vasogenic
2) Cytotoxic
Vasogenic cerebral oedema
From blood brain barrier disruption with increased vascular permeability.
Mostly involves white matter
Responds to steroid therapy
Cytotoxic cerebral oedema
Increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury.
Affects grey and white matter.
Doesn’t respond to steroid therapy.
Transtentorial herniation
Herniation of brain under tentorium cerebelli from a cerebral hemisphere lesion (eg: a haematoma).
Structure through which CSF drains
Aqueduct of Sylvius
Effect of subfalcine and transtentorial herniations
Brainstem is pushed downwards, vessels of brainstem are torn (as they are fixed in place).
Haemorrhage.