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Neurology > Traumatic Brain Injuries > Flashcards

Traumatic Brain Injuries Flashcards

1
Q

What is the definition of a head injury?

A

TBI is a non-degenerative, non-congenital insult to the brain from an external mechanical force, possibly leading to temporary or permanent impairment of cognitive, physical and psychosocial function

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2
Q

What are the high risk groups for a TBI?

A 
Young men
Elderly
Previous head injuries
Residents of inner cities
Alcohol and drug abuse
Low-income
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3
Q

What are the mechanisms of injury for a TBI?

A 
Assault
Falls
RTCs
Sports 
OVER HALF DUE TO ALCOHOL
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4
Q

When are the peaks in head injury in deaths?

A

Initially within the 1st hour
Around 7 hrs due to secondary effects
3rd peak later on due to medical complications such as pneumonia, DVT, PEs

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5
Q

What is ATLS?

A

Airway with C-spine control
Breathing
Circulation

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6
Q

What are the categories for GCS?

A

Eye opening
Motor
Verbal

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7
Q

What are the different levels within eye opening of GCS?

A

Open spontaneously = 4 points
Eyes open to verbal command, speech or shout = 3 points
Eyes open to pain = 2 points
No eye opening = 1 point

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8
Q

What are the different levels within verbal response of GCS?

A 
Oriented = 5 points
Confused = 4 points
Inappropriate responses, words discernible = 3
Incomprehensible sounds = 2 
No verbal response = 1
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9
Q

What are the different levels within motor response of GCS?

A

Obeys commands = 6
Purposeful movement to painful stimuli/localising = 5
Withdraws from pain/ flexing = 4
Abnormal (spastic) flexion, decorticate = 3
Extensor (rigid) response, decerebrate = 2
No motor response = 1

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10
Q

Which section of the GCS scale is MOST important?

A

Motor

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11
Q

Describe the head injury severity scale

A

Mild: 14/15, brief LOC
Mod: 9-13
Severe: 3-8

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12
Q

What are the nice guidelines for CT scanning?

A 
GCS under 13 on initial assessment
GCS under 15 at 2 hours after injury 
Suspected open or depressed skull fracture
Any sign of basal skull fracture
Post traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting
Suspicion of NAI
Age over 65 
Coagulopathy
Dangerous mechanism of injury
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13
Q

What are signs of a basilar skull fracture?

A

Lacunar eyes
Battle’s sign (bruising over mastoid)
Any blood of CSF leakage from ear canal

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14
Q

What are the different types of traumatic haematomas?

A

Extradural haematoma
Subdural haematoma
Intracerebral haematoma

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15
Q

Will an extradural haematoma cross the suture lines?

A

No - lens shape or biconvex shape

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16
Q

What is the classic presentation for an extradural haematoma?

A

Injury with LOC
Recovery “lucid interval”
Rapidly progressing neurological symptoms; deteriorating GCS, hemiparesis, unilateral fixed and dilated pupil then ultimately apnoea and death

17
Q

Who is likely to get an acute subdural haematoma?

A

Elderly patients due to atrophy of brain

Bridging veins rupture

18
Q

What is the differences on CT scan from an acute and a chronic subdural haematoma?

A

Acute; hyperdense

Chronic; hypodense

19
Q

What is the management of a diffuse axonal injury?

A

Medical management to control ICP as there is nothing surgical to remove

20
Q

What secondary insults do neurosurgeons aim to prevent?

A

Hypoxia
Hypotension
Mass lesions
Control ICP and CCP

21
Q

How is CCP calculated?

A

MAP - ICP
THEREFORE
If you keep MAP up and ICP down you will have good cerebral perfusion

22
Q

What occurs if the ICP gets too high?

A

Herniation; subfalcine, uncal or tonsillar

23
Q

What is the medical management of a raised ICP?

A

Sedation; propofol, benzodiazepines or barbiturates
Venous drainage; tilt head, remove any compression of the neck e.g. cervical collars or ET tube ties
CO2 control
Osmotic diuretics (mannitol, hypertonic saline)
CSF release - external ventricular drain

24
Q

What pCO2 do you aim for post TBI?

A

4.5; not too high as to increase ICP further but not so low as to reduce blood flow to the brain

25
Q

What head position should all patients post TBI be placed at?

A

30 degrees

26
Q

What is the last option in increased ICP if there is no surgical management and everything has been done to manage it medically?

A

Decompressive craniectomy

27
Q

What is the consequence of loss of autoregulation of BP seen in TBI?

A

Direct changes in BP will directly influence the cerebral blood flow

28
Q

What is every 10 kcal/kg decrease in caloric intake associated with in TBI?

A

30-40% increase in mortality rate

29
Q

What are the different mechanisms of DAI?

A

Stretched axon
Sheared axon
Twisted axon
Compressed axon

30
Q

What are the toxic effects of DAI?

A

Excitotoxicity
Apoptosis
Inflammatory mediator release

31
Q

Where is DAI most likely to happen?

A

Grey/ white interface

32
Q

What is the basic pathogenesis of excitotoxicity?

A

Increased glutamate release
Activates NMDA receptors
Calcium mediated activation of proteases and lipases
Secondary cell death

33
Q

Which interleukin is released in TBI?

A

6- acute phase and fever

34
Q

What should you ensure before attempting to carry out a brainstem assessment?

A

No drugs that will alter consciousness
Normothermic; cannot perform on a hypothermic patient, need to be warm
No severe metabolic or endocrine disrutbances

35
Q

What is carried out in a brainstem death assessment?

A 
No pupillary response 
No corneal reflex
No gag reflex 
No VOR 
No motor response
No respiration
36
Q

How is respiration assessed in brainstem death?

A

Pre-oxygenate
Look for a change in pCO2 levels
Must rise to 6 pKa for it to be a positive test of lack of respiration

37
Q

How many doctors need to carry out a brainstem death assessment?

A

2 - at least one a consultant

38
Q

When is time of death recorded in brainstem death?

A

1st set of tests positive

2nd set is confirmatory

Neurology (48 decks)

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