11 - Traumatic Head and Spinal Injury Flashcards

1
Q

Name for direct trauma to scalp

A

Laceration

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2
Q

Effects of direct trauma to meninges

A

Vascular injury, lacerations

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3
Q

Effects of direct trauma to brain or spinal cord

A

Contusions, lacerations, diffuse axonal injury, diffuse vascular injury

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4
Q

Concussion
1
2
3

A
  • 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).
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5
Q

Leading cause of death in Western countries, under 40 years old

A

Traumatic CNS injury

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6
Q

Two broad types of CNS trauma

A

1) Penetrating injury (direct disruption of tissue)

2) Closed injury (movement and compression of neural and vascular structures within bony confines)

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7
Q
Features of skull fractures
1
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4
5
A
  • 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.
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8
Q

Significance of skull fractures

A

Indicates a high-energy transfer injury

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9
Q

Cause of epi- or extradural haematoma

A

Middle meningeal artery damage

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10
Q

Cause of subdural haemartoma

A

Subdural vein injury.

Can be acute or chronic

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11
Q

Why are extradurals more common in younger people?

A

With age, dura becomes more adherent to skull

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12
Q

More urgent type of haematoma

A

Extradural, because it is from an arterial bleed.

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13
Q

More common type of haematoma in elderly populations

A

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

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14
Q

Contusion

A

Haemorrhagic necrosis (bruise)

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15
Q

Coup

A

Contusion at the site of impact

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16
Q

Contrecoup

A

Occurs when head is not immobilised at the time of injury and involves the opposite side of the brain

17
Q

Location of sterotypic contusions in head injury

A

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

18
Q

Common finding with any sort of head injury

A

A degree of subarachnoid haemorrhage

19
Q

Appearance of old cerebral contusions

A

Areas of depressed, shrunken brain tissue.
Brain rarely heals by fibrosis.
Gliotic brain with remains of haemosiderin.

20
Q

Brain laceration

A

Penetration of brain by foreign body or skull fragment

21
Q

Effect of missile brain injury

A

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.

22
Q

Diffuse axonal injury

A

Axons can be mechanically shorn over a wide area.

23
Q

What often accompanies diffuse axonal injury?

A

Diffuse vascular injury

24
Q

Histological appearance of severed axon

A

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

25
Q

Long-term effects of diffuse axonal injury

A

Greatly-enlarged lateral and third ventricles.

This is because damaged white matter is removed, undergoes gliosis. This results in loss of tissue.

26
Q

Effect of compression of spinal cord

A

‘Toothpaste’ effect, as cord is so soft. Can lead to a central haemorrhagic necrotic core either side of site of injury in spinal cord

27
Q
Long-term sequelae of brain trauma
1
2
3
4`
A

1) Infections
2) Hydrocephalus
3) Epilepsy
4) Chronic traumatic encephalopathy

28
Q

Chronic traumatic encephalopathy
1
2
3

A

1) Brain atrophy due to neuronal loss
2) Abnormal deposition of tau protein
3) Often diffuse deposition of A-beta plaques in cortex

29
Q

Amounts of blood and CSF in cranial cavity

A

150mL of each

30
Q

Initial response to swelling of brain

A

Expulsion of as much CSF as possible. Compression of ventricles. Expulsion of venous blood.
After this, ICP starts to rise

31
Q

Effect of increasing ICP

A

Herniations of brain tissue through dural openings (EG foramen magnum).

As ICP approaches arterial pressure, brain perfusion ceases

32
Q

Amount of CSF produced each day

A

~400mL

33
Q
Potential causes of increased ICP
1
2
3
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5
6
7
A

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

34
Q

Two main subtypes of cerebral oedema

A

1) Vasogenic

2) Cytotoxic

35
Q

Vasogenic cerebral oedema

A

From blood brain barrier disruption with increased vascular permeability.

Mostly involves white matter

Responds to steroid therapy

36
Q

Cytotoxic cerebral oedema

A

Increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury.

Affects grey and white matter.

Doesn’t respond to steroid therapy.

37
Q

Transtentorial herniation

A

Herniation of brain under tentorium cerebelli from a cerebral hemisphere lesion (eg: a haematoma).

38
Q

Structure through which CSF drains

A

Aqueduct of Sylvius

39
Q

Effect of subfalcine and transtentorial herniations

A

Brainstem is pushed downwards, vessels of brainstem are torn (as they are fixed in place).
Haemorrhage.