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
What head position should all patients post TBI be placed at?
30 degrees
26
What is the last option in increased ICP if there is no surgical management and everything has been done to manage it medically?
Decompressive craniectomy
27
What is the consequence of loss of autoregulation of BP seen in TBI?
Direct changes in BP will directly influence the cerebral blood flow
28
What is every 10 kcal/kg decrease in caloric intake associated with in TBI?
30-40% increase in mortality rate
29
What are the different mechanisms of DAI?
Stretched axon Sheared axon Twisted axon Compressed axon
30
What are the toxic effects of DAI?
Excitotoxicity Apoptosis Inflammatory mediator release
31
Where is DAI most likely to happen?
Grey/ white interface
32
What is the basic pathogenesis of excitotoxicity?
Increased glutamate release Activates NMDA receptors Calcium mediated activation of proteases and lipases Secondary cell death
33
Which interleukin is released in TBI?
6- acute phase and fever
34
What should you ensure before attempting to carry out a brainstem assessment?
No drugs that will alter consciousness Normothermic; cannot perform on a hypothermic patient, need to be warm No severe metabolic or endocrine disrutbances
35
What is carried out in a brainstem death assessment?
``` No pupillary response No corneal reflex No gag reflex No VOR No motor response No respiration ```
36
How is respiration assessed in brainstem death?
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
How many doctors need to carry out a brainstem death assessment?
2 - at least one a consultant
38
When is time of death recorded in brainstem death?
1st set of tests positive | 2nd set is confirmatory