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Neurology Y2 > L20 - Traumatic Brain Injury > Flashcards

L20 - Traumatic Brain Injury Flashcards

- Risk factors for head injury and markers of severity - Difference between primary and secondary brain injury. - Delivery of medical intervention affects latter - Understand complications of head injury - Importance of rehabilitation

1
Q

State some examples of causes of Brain injury?

A 
RTC (road traffic collisions) 
Falls 
Assaults 
Sports Injuries 
Firearms
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2
Q

What are risk factors for brain injury?

A 
Alcohol.
Recreational drugs. 
Young adults. 
Elderly. 
Younger children.
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3
Q

Define a primary brain injury?

A

The initial insult to the brain at the time of injury.

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4
Q

State some examples of primary brain injury?

A
  • Bleeding within skull
  • Contusions (bruising) of the brain tissue
  • Contracoup injury
  • Diffuse axonal injury
  • Penetrating injury
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5
Q

What is a contracoup injury?

A

Coup injury
- occurs under site of impact with an object
Contracoup
- occurs on the side opposite the area that was hit

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6
Q

What is a diffuse axonal injury?

A

Result of traumatic shearing forces that occur when head is rapidly accelerated or decelerated.
- Immediate disconnection of axons

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7
Q

Describe an extradural haematoma

A

Convex, inwards.
Spread limited by dural adhesion to skull.

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8
Q

Describe a subdural haematoma

A

Area of increased density spreading around surface of cerebral hemisphere.

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9
Q

Describe a secondary brain injury?

A

Occurs from insults to the brain after the initial injury.

- Hypoxia, hypovolaemia and cerebral oedema.

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10
Q

Define hypovolaemia?

A

Volume depletion.

Can be due to a loss of both salt and water or just a decrease in BV.

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11
Q

Describe what may occur in the presence of a brain oedema?

A
  • Raise in ICP
  • Cerebral herniation
  • raised ICP may lead to hypoperfusion (inadequate delivery oxygen and nutrients) of brain
  • may cause cerebral ischaemia
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12
Q

What causes an extradural haematoma?

A

Middle meningeal artery bleeds into extradural space.

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13
Q

Describe diffuse axonal injury?

A
  • Results from widespread axonal shearing
  • often no signs on inital CT head
  • can result in raised ICP from swelling
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14
Q

Briefly state the different types of skull fractures?

A

Simple
Depressed
Basal fractures
- more difficult to see on X-ray

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15
Q

What particular physical signs are associated with Basal skull fractures?

A 
Battle's sign, periorbital bruising. 
Produce bleeding into middle ear. 
CSF rhinorrhoea (clear fluid coming out of nose, contains glucose unlike mucus)
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16
Q

Describe penetrating trauma?

A

Damage occuring directly from object piercing skull and disrupting brain tissue.

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17
Q

State some causes that may lead to secondary brain injury?

A

Hypoxaemia
Hypotension
Raised ICP

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18
Q

During the pre-hospital care of a patient suffering a suspected brain injury it is important too…

A

Ensure adequate oxygenation and blood pressure to prevent hypoxic-ischaemic brain injury.

19
Q

Describe what may occur during the pre-hospital care of a brain injury patient?

A

ABCDE assessment
Sedation, tracheal intubation with ventilation if GCS < 8
Control of bleeding
IV access and IV fluids / blood to maintain BP and cerebral perfusion.

20
Q

Describe the Monro-Kellie

hypothesis

A

Sum of volumes of brain, CSF, and intracranial blood is constant.
Once skull reaches critical volume - any further expansion in the size of space-occupying lesions will result in a dramatic rise in ICP.

21
Q

The pressure gradient driving blood flow to the brain is known as the…

A

Cerebral perfusion pressure CPP.

- often tightly controlled through autoregulation, despite variations in arterial BP.

22
Q

Significant increases in ICP may result in…

A

Reduced CPP

- potentially causing further hypoxic-ischaemic damage

23
Q

What is the formula for calculating cerebral perfusion pressure?

A

Mean arterial pressure - ICP

24
Q

What are some signs of raised ICP?

A

Reduced conscious level.
Pupillary abnormalities e.g. dilation, bilateral ptosis.
Cushing’s triad
- late sign, often pre-terminal

25
Q

What is Cushing’s triad?

A
  1. High BP
  2. Bradycardia
  3. Irregular breathing pattern
26
Q

What two component’s can adapt most easily to accommodate an increase in the volume of intracranial contents?

A

Intracranial blood
- esp in the venous compartment
- CSF
Once these compensatory mechanisms are exhausted. further increases in vol result in large rises in ICP.

27
Q

What are simple measures to help prevent / treat raised ICP?

A

Elevation of head of bed to 30 degrees

- improves jugular venous outflow, lowers ICP.

28
Q

What is CVP?

- Central Venous Pressure

A

Circulating blood flows into the RA via inferior and superior vena cava.
Pressure in the right atrium is known as the central venous pressure.

29
Q

Give an example of how Diuretics can be used to decrease ICP?

A

e. g. Mannitol
- intravascular osmotic agent, can draw fluid fro both normal and abnormal brain.
- decreased ICP through cerebral autoregulation,

30
Q

Give examples of further treatment for raised ICP?

A
  • Osmotic therapy
  • Hyperventilation
  • Sedation
  • Craniectomy
31
Q

How may Mannitol aid in decreasing a raised ICP?

A

Decreased blood viscosity

- resulting in reflex vasoconstriction and decreased cerebrovascular volume.

32
Q

How may hyperventilation lead to a decreased ICP?

A

Reduced PaCO2

  • vasoconstriction
  • reduced ICP
33
Q

Give problem with using hyperventilation to treat raised ICP?

A

Vasoconstriction can cause cerebral ischaemia therefore this is not generally recommended.

34
Q

Once ICP of patient has stabilised what are the next steps?

A 
Begin to withdraw sedation.
Assess ventilatory needs. 
Assess neurological deficits. 
Other less acute injures via tertiary survey (e.g. broken fingers) 
Rehab
35
Q

What are the categories of traumatic brain injury?

A

Mild / moderate / severe

36
Q

What are the measures for severity of traumatic brain injury?

A
  1. Post traumatic amnesia
  2. Glasgow coma score
    - <8 is very severe
  3. Loss of consciousness
37
Q

Describe post traumatic amnesia?

A

Reduced ability to lay down new memory.
Confusion, agitation, wandering of patient.
Requires supportive care.
Lasts from hours to months.
GOAT assessment helps identify improvements.

38
Q

Frontal Lobe

A 
Problem solving 
Emotional traits 
Reasoning (judgement) 
Speaking 
Voluntary motor activity
39
Q

Temporal lobe

A

Understanding language
Behaviour
Memory
Hearing

40
Q

Brainstem

A 
Breathing 
Body temp 
Digestion 
Alertness / sleep 
Swallowing
41
Q

Cerebellum

A

Balance
Coordination and control of voluntary movement
Fine muscle control

42
Q

Occiptal lobe

A

Vision

Colour perception

43
Q

Parietal lobe

A 
involved in sensory
Knowing right from left 
Sensation 
Reading 
Body orientation
44
Q

How may the brain recover after injury?

A 
Neurons do not regenerate. 
Neuroplasticity 
- brain can reorganise itself 
- new pathways develop 
- undamaged areas of brain take over from damaged areas

Neurology Y2 (24 decks)

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