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IBSc PHEM Applied Science > TBI > Flashcards

TBI Flashcards

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1
Q

TBI

A

Disruption to the normal function of the brain caused by an external force

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2
Q

Ways to classify a head injury

A

Anatomically
Blunt vs penetrating
Primary vs secondary injury
Open vs closed
GCS severity

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3
Q

Mild moderate and severe TBI by GCSE

A

Mild 13-15
Mod 9-12
Severe 3-8

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4
Q

Anatomical classifications of TBI

A

EDH
SDH
ICH
SAH
IVH
DAI

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5
Q

What injury can have talk and die presentation

A

EDH

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6
Q

EDH location, shape, assoc injuries

A

Bleed between dura mater and skull
Convex shape contained within suture lines
Typically assoc s skull fracture

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7
Q

Trauma to What region of the skull and which vessel most commonly leads to EDH

A

Temporal parietal region
Middle meningeal artery

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8
Q

Typical presentation of EDH

A

LOC -> lucent period -> acute deterioration
Skull fracture

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9
Q

EDH mx

A

Haematoma evacuation

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10
Q

SDH location, shape, source

A

between dura and arachnoid mater
Crescent/concave shape
Caused by rupture of bridging veins

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11
Q

SDH risk factors

A

Elderly
Alcoholic
Anticoagulant

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12
Q

2 types of SDH

A

Acute - brighter more hyperechoic blood on CT
Chronic - gradual deterioration

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13
Q

SDH Mx

A

Haematoma evacuation

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14
Q

ICH location, types, CT appearance, cause

A

Haematoma within brain parenchyma
Contusion, coup, contrecoup
Hyperattenuation in brain parenchyma
Haemorrhagic stroke

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15
Q

ICH mx

A

ICP directed therapy

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16
Q

Is ICH caused by blunt or penetrating injury

A

Both

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17
Q

Signs of SAH on CT

A

Blood in subarachnoid cisterns
Blood in Sylvian fissures
Enlarged temporal horns
Intra ventricular blood

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18
Q

DAI

A

Shearing of axons at white-grey matter interface

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19
Q

ICH presentation

A

Sudden onset of neuro defecits

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20
Q

SAH location, CT appearance, cause

A

Between arachnoid and pia
Hyperattenuation around circle of Willis
Rupture of berry aneurism

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21
Q

SAH presentation

A

Thunderclap headache
Sudden sx onset

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22
Q

Primary brain injury in TBI

A

Skull fractures or lacerations
Contusions
Cerebral laceration
ICH
DAI

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23
Q

Causes of secondary brain injury in TBI

A

Incr ICP
Hypoxia
Hypotension
Hypothermia
Electrolyte disturbance
Toxic amino acids
Oxygen radicals

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24
Q

What factors are important in TBI management to preserve tissue

A

Maintenance of cerebral blood flow
Sufficient glucose and oxygen delivery

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25
Q

Causes of cellular damage in TBI

A

Cerebral oedema
Hypoxia and ischaemia
Cerebral metabolic impairment
Cerebral Vasospasm
Incr ICP
Cell death
Incr glutamate
Mitochondrial dysfunction
Impaired glucose metabolism
BBB damage
Excitotoxicity
Complement activation and inflammation
ROS generation

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26
Q

Normal ICP

A

5-15 mmHg

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27
Q

What ICP risks herniation

A

> 25mmhg

28
Q

Monro Kellie principal

A

the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two

29
Q

What factors effect cerebral blood flow

A

Cerebral vascular resistance
Cerebral perfusion pressure
Autoregulated

30
Q

CPP equation

A

CPP = MAP-ICP

31
Q

CPP

A

Net pressure gradient driving blood flow through the cerebral circulation resulting in cerebral blood flow

32
Q

At what MAP range can CBF be maintained via autoregulation

A

60-160mmhg

33
Q

Normal CBF

A

50ml/100g/min (700ml/min)

34
Q

What changes occur when CBF goes below 40ml, 30ml, and 20ml /100g/min

A

<40 ischaemic changes
<30 cellular oedema
<20 irreversible cell damage and cell death

35
Q

Why does the brain develop ischaemic cellular damage quickly

A

Very limited capacity for anaerobic metabolism

36
Q

Normal ICP CPP and MAP

A

ICP 5-15
CPP 60-70
MAP 70-100

37
Q

Airway considerations in TBI

A

Recognise apnoea, impact brain apnoea, and dysventilation
Airway adjuncts, definitive airway, manual vent

38
Q

Breathing consideration in TBI

A

Optimise PO2 and PCO2

39
Q

PaO2 and paco2 targets

A

PaO2 >8
PaCO2 4.5-5

40
Q

CBF equation

A

CBF = CPP/CVR

41
Q

Is hyperoxia or hypoxia more dangerous in TBI

A

Hypoxia

42
Q

What is normal CPP
What CPP causes ischaemia and irreversible brain damage

A

Normal 60-80
Ischaemia <40
Irreversible <25

43
Q

How does autoregulation of CPP work

A

Dilation and constriction of cerebral blood vessels
Autoregulation fails after cerebral vessels maximally dilated or constructed

44
Q

What shape is the ICP pressure flow relationship between CBF and CPP

A

Sigmoid

45
Q

What OOH factors are associated with mortality in severe TBI

A

Hypoxia
hypotension

46
Q

How to optimise ICP

A

Head up 30*
Loosen tube ties
Avoid tight fitting collar
Consider hypertonic saline

47
Q

Risks of hypo and hyper perfusion in TBI

A

Hypo - ischaemia
Hyper - raised ICP

48
Q

How does hypothermia affect clotting

A

Hypothermia alters enzyme kinetics causing a reduction in normal clotting factors

49
Q

TBI coagulopathy tx

A

Give 2g TXA IS GCS <12
Aggressively correct

50
Q

Seizure mx in TBI

A

Load with levetiracetam
40-60mg/kg, max 4.5g

51
Q

Indications for levetiracetam in TBI

A

Seizures
Consider in depressed skull fractures

52
Q

What vaccination should be given to base of skull fracture pt

A

Pneumovax

53
Q

Aspects of Neuroprotection

A

Airway, gas exchange, MAP, ICP, temp, glucose

Secure airway
Optimise pO2 and pCO2
Maintain MAP
Head up 30*
Loosen ETT ties
Hypertonic saline
Normothermia
Normoglycaemia

54
Q

ICP monitoring modalities

A

Single ICP wire
Triple bolt
External ventricular device

55
Q

What is measured by each probe in a triple bolt

A

ICP, CPP, and pressure reactivity index
PBtO2 and temp
Micro dialysis - lactate, pyruvate, glucose, glycerol, glutamate

56
Q

Where does an EVD measure ICP

A

Lateral ventricle

57
Q

Aim of ICP protocol

A

Prevent secondary damage
ICP <20
CPP >60
PRx <0.2
LPR <25
PBtO2 >29
Brain temp <37
Brain glucose >0.5

58
Q

Which patients should permissive hypotension not be used with

A

Polytrauma pt with TBI

59
Q

Which aspect of GCS is most predictive

A

Motor score
Important to know motor score before sedation/intubation

60
Q

Which aspect of GCS is most predictive

A

Motor score
Important to know motor score before sedation/intubation

61
Q

DAI on CT

A

Initially normal
Tiny punctate bleeds may be visible later

62
Q

How can SAH lead to hydrocephalus

A

Blood gets into CSF -> enters ventricles and clogs vili

63
Q

Most common type of herniation

A

Uncal

64
Q

Uncal herniation sign

A

Blown pupil

65
Q

Coning signs

A

Both pupils blown
Cushing’s response

66
Q

Hyperoxia in TBI

A

Evidence of harm >26kpa
Short periods of hyperoxia doesn’t effect autoregulation
Low sats worse than high sats

IBSc PHEM Applied Science (21 decks)

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