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IBSc PHEM Applied Science > TBI > Flashcards

TBI Flashcards

(66 cards)

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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
Causes of cellular damage in TBI
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
26
Normal ICP
5-15 mmHg
27
What ICP risks herniation
>25mmhg
28
Monro Kellie principal
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
What factors effect cerebral blood flow
Cerebral vascular resistance Cerebral perfusion pressure Autoregulated
30
CPP equation
CPP = MAP-ICP
31
CPP
Net pressure gradient driving blood flow through the cerebral circulation resulting in cerebral blood flow
32
At what MAP range can CBF be maintained via autoregulation
60-160mmhg
33
Normal CBF
50ml/100g/min (700ml/min)
34
What changes occur when CBF goes below 40ml, 30ml, and 20ml /100g/min
<40 ischaemic changes <30 cellular oedema <20 irreversible cell damage and cell death
35
Why does the brain develop ischaemic cellular damage quickly
Very limited capacity for anaerobic metabolism
36
Normal ICP CPP and MAP
ICP 5-15 CPP 60-70 MAP 70-100
37
Airway considerations in TBI
Recognise apnoea, impact brain apnoea, and dysventilation Airway adjuncts, definitive airway, manual vent
38
Breathing consideration in TBI
Optimise PO2 and PCO2
39
PaO2 and paco2 targets
PaO2 >8 PaCO2 4.5-5
40
CBF equation
CBF = CPP/CVR
41
Is hyperoxia or hypoxia more dangerous in TBI
Hypoxia
42
What is normal CPP What CPP causes ischaemia and irreversible brain damage
Normal 60-80 Ischaemia <40 Irreversible <25
43
How does autoregulation of CPP work
Dilation and constriction of cerebral blood vessels Autoregulation fails after cerebral vessels maximally dilated or constructed
44
What shape is the ICP pressure flow relationship between CBF and CPP
Sigmoid
45
What OOH factors are associated with mortality in severe TBI
Hypoxia hypotension
46
How to optimise ICP
Head up 30* Loosen tube ties Avoid tight fitting collar Consider hypertonic saline
47
Risks of hypo and hyper perfusion in TBI
Hypo - ischaemia Hyper - raised ICP
48
How does hypothermia affect clotting
Hypothermia alters enzyme kinetics causing a reduction in normal clotting factors
49
TBI coagulopathy tx
Give 2g TXA IS GCS <12 Aggressively correct
50
Seizure mx in TBI
Load with levetiracetam 40-60mg/kg, max 4.5g
51
Indications for levetiracetam in TBI
Seizures Consider in depressed skull fractures
52
What vaccination should be given to base of skull fracture pt
Pneumovax
53
Aspects of Neuroprotection
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
ICP monitoring modalities
Single ICP wire Triple bolt External ventricular device
55
What is measured by each probe in a triple bolt
ICP, CPP, and pressure reactivity index PBtO2 and temp Micro dialysis - lactate, pyruvate, glucose, glycerol, glutamate
56
Where does an EVD measure ICP
Lateral ventricle
57
Aim of ICP protocol
Prevent secondary damage ICP <20 CPP >60 PRx <0.2 LPR <25 PBtO2 >29 Brain temp <37 Brain glucose >0.5
58
Which patients should permissive hypotension not be used with
Polytrauma pt with TBI
59
Which aspect of GCS is most predictive
Motor score Important to know motor score before sedation/intubation
60
Which aspect of GCS is most predictive
Motor score Important to know motor score before sedation/intubation
61
DAI on CT
Initially normal Tiny punctate bleeds may be visible later
62
How can SAH lead to hydrocephalus
Blood gets into CSF -> enters ventricles and clogs vili
63
Most common type of herniation
Uncal
64
Uncal herniation sign
Blown pupil
65
Coning signs
Both pupils blown Cushing’s response
66
Hyperoxia in TBI
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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