TBI Flashcards
TBI
Disruption to the normal function of the brain caused by an external force
Ways to classify a head injury
Anatomically
Blunt vs penetrating
Primary vs secondary injury
Open vs closed
GCS severity
Mild moderate and severe TBI by GCSE
Mild 13-15
Mod 9-12
Severe 3-8
Anatomical classifications of TBI
EDH
SDH
ICH
SAH
IVH
DAI
What injury can have talk and die presentation
EDH
EDH location, shape, assoc injuries
Bleed between dura mater and skull
Convex shape contained within suture lines
Typically assoc s skull fracture
Trauma to What region of the skull and which vessel most commonly leads to EDH
Temporal parietal region
Middle meningeal artery
Typical presentation of EDH
LOC -> lucent period -> acute deterioration
Skull fracture
EDH mx
Haematoma evacuation
SDH location, shape, source
between dura and arachnoid mater
Crescent/concave shape
Caused by rupture of bridging veins
SDH risk factors
Elderly
Alcoholic
Anticoagulant
2 types of SDH
Acute - brighter more hyperechoic blood on CT
Chronic - gradual deterioration
SDH Mx
Haematoma evacuation
ICH location, types, CT appearance, cause
Haematoma within brain parenchyma
Contusion, coup, contrecoup
Hyperattenuation in brain parenchyma
Haemorrhagic stroke
ICH mx
ICP directed therapy
Is ICH caused by blunt or penetrating injury
Both
Signs of SAH on CT
Blood in subarachnoid cisterns
Blood in Sylvian fissures
Enlarged temporal horns
Intra ventricular blood
DAI
Shearing of axons at white-grey matter interface
ICH presentation
Sudden onset of neuro defecits
SAH location, CT appearance, cause
Between arachnoid and pia
Hyperattenuation around circle of Willis
Rupture of berry aneurism
SAH presentation
Thunderclap headache
Sudden sx onset
Primary brain injury in TBI
Skull fractures or lacerations
Contusions
Cerebral laceration
ICH
DAI
Causes of secondary brain injury in TBI
Incr ICP
Hypoxia
Hypotension
Hypothermia
Electrolyte disturbance
Toxic amino acids
Oxygen radicals
What factors are important in TBI management to preserve tissue
Maintenance of cerebral blood flow
Sufficient glucose and oxygen delivery
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
Normal ICP
5-15 mmHg
What ICP risks herniation
> 25mmhg
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
What factors effect cerebral blood flow
Cerebral vascular resistance
Cerebral perfusion pressure
Autoregulated
CPP equation
CPP = MAP-ICP
CPP
Net pressure gradient driving blood flow through the cerebral circulation resulting in cerebral blood flow
At what MAP range can CBF be maintained via autoregulation
60-160mmhg
Normal CBF
50ml/100g/min (700ml/min)
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
Why does the brain develop ischaemic cellular damage quickly
Very limited capacity for anaerobic metabolism
Normal ICP CPP and MAP
ICP 5-15
CPP 60-70
MAP 70-100
Airway considerations in TBI
Recognise apnoea, impact brain apnoea, and dysventilation
Airway adjuncts, definitive airway, manual vent
Breathing consideration in TBI
Optimise PO2 and PCO2
PaO2 and paco2 targets
PaO2 >8
PaCO2 4.5-5
CBF equation
CBF = CPP/CVR
Is hyperoxia or hypoxia more dangerous in TBI
Hypoxia
What is normal CPP
What CPP causes ischaemia and irreversible brain damage
Normal 60-80
Ischaemia <40
Irreversible <25
How does autoregulation of CPP work
Dilation and constriction of cerebral blood vessels
Autoregulation fails after cerebral vessels maximally dilated or constructed
What shape is the ICP pressure flow relationship between CBF and CPP
Sigmoid
What OOH factors are associated with mortality in severe TBI
Hypoxia
hypotension
How to optimise ICP
Head up 30*
Loosen tube ties
Avoid tight fitting collar
Consider hypertonic saline
Risks of hypo and hyper perfusion in TBI
Hypo - ischaemia
Hyper - raised ICP
How does hypothermia affect clotting
Hypothermia alters enzyme kinetics causing a reduction in normal clotting factors
TBI coagulopathy tx
Give 2g TXA IS GCS <12
Aggressively correct
Seizure mx in TBI
Load with levetiracetam
40-60mg/kg, max 4.5g
Indications for levetiracetam in TBI
Seizures
Consider in depressed skull fractures
What vaccination should be given to base of skull fracture pt
Pneumovax
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
ICP monitoring modalities
Single ICP wire
Triple bolt
External ventricular device
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
Where does an EVD measure ICP
Lateral ventricle
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
Which patients should permissive hypotension not be used with
Polytrauma pt with TBI
Which aspect of GCS is most predictive
Motor score
Important to know motor score before sedation/intubation
Which aspect of GCS is most predictive
Motor score
Important to know motor score before sedation/intubation
DAI on CT
Initially normal
Tiny punctate bleeds may be visible later
How can SAH lead to hydrocephalus
Blood gets into CSF -> enters ventricles and clogs vili
Most common type of herniation
Uncal
Uncal herniation sign
Blown pupil
Coning signs
Both pupils blown
Cushing’s response
Hyperoxia in TBI
Evidence of harm >26kpa
Short periods of hyperoxia doesn’t effect autoregulation
Low sats worse than high sats
