Traumatic Brain Injury Flashcards
what are the most common age groups of TBI
0-4
15-19
75+
what are the major causes of TBI
falls
road traffic accidents
assaults
what is the commonest cause of death and disability in 1-40 years
head injury
which gender is is it more common in
men 1.5
what are traumatic brain injuries
external forces causing damage
mild-moderate-severe
what is primary brain injury
the instant injury
-happens at the instant of trauma
-pattern and extent of damage depends on nature of impact
-not treatable
-TARGET PREVENTION (PUBLIC HEALTH)
-there is more happening around that area
what is shaken baby syndrome
occurs when a baby or toddler gets shaken violently
they have very flexible necks
brain hits skull at each movement due to hyperextension and hyperflexion
what is coup contrecoup injury
“blow” and “counterblow”
two separate brain injury occur at same incident
coup- directly under first impact (hit dashboard)
countercoup- (hit headboard)
what is the early management of head injury
-manage at site
-assessment in EandR
-investigating pre-emtive investigations (eg. ct)
who gets sent to hospital (this is post ABC)
under 5 years, over 65 years
amnesia
loss of consciousness
high energy injury
vomiting
seizure
bleeding/clotting disorders
what to do when in contact with TBI patient straight away
ABC
Disability: GCS
Optimise oxygenation
why do you need to optimise oxygenation in TBI patients
50% patients pre admission have SpO2 <90%
the airway should be open BUT could have cervical spine injury– stabalise while intubating and mobilising
why do you do GCS
to find out degree of consciousness
differentiate mild, moderate, severe injury
what are the different levels of GCS in regards to mild moderate and severe
mild– 13-15
moderate– 9-12
severe– 8 or less
what is secondary brain injury
secondary processes which occur at the cell and molecular level to EXACERBATE neurological damage
what happens in secondary brain injury
once inflammation occurs after primary injury
NT release (glutamate)
oedema- increases intracranial pressure
free radical generation
calcium mediated damage
mitochondrial dysfunction
inflammatory response
ischaemia, excitotoxicity
neuronal death cascades
how can you minimise secondary brain injury
stop bleeding
optimise oxygenation
optimise cerebral perfusion
blood glucose- dont want hypoglycaemia trying to stop hyperglycaemia
hypocapnia/hypercapnia
HYPERTONIC solution to reduce oedema and intracranial pressure
body temperature control- every degree increase increase metabolic rate– give paracetamol if pyrexic
what is the monro kellie doctrine/ PRINCIPAL
there is a balance in the skull between
1. venous/arterial volume of blood
2. volume of brain
3. volume of csf
the sum of these three components remain constant, if one increases all other areas have to decrease
intracrainial bleeding
increase intracranial pressure
csf squished out of brain to compensate
compensatory mechanisms wont last long– therefore uncompensated phase
different stages:
-NORMAL BRAIN
-COMPENSATED BRAIN
-UNCOMPENSATED AND RAISED ICP
what is a physiological principle (not monro-kellie doctrine)
CPP=MAP-ICP
cerebral perfusion pressure
mean arterial pressure
intracranial pressure
MAP= diastolic pressure + 1/3 pulse pressure
or
MAP= DP + 1/3 (SP-DP)
identify some features that suggest risk of intracranial mass
history:
high impact injury
significant retrograde amnesia
history of coagulopathy
post traumatic seizure - increase metabolic rate
exam:
GCS
-12/15 or less
-13/15 or 14/15 and failing to improve within two hours of injury
-clinical signs of skull fracture
-leaking fluid from nose or ears
rhinorrhoea, otorrhea
what are some red flag to not discharge
-loss of consciousness, drowsiness, confusion, fits
-painful headache which doesnt settle, vomiting, visual disturbance
-rhin/otorrhea (to check if CSF do glucose test or beta 2 transferrin)
-problems understanding or speaking, loss of balance, walking difficulties, weakness in arms or legs
what do you do in hospital in regards to breathing
administer oxygen
monitor SpO2
monitor ABGs
GCS <8 INTUBATE
What is the investigation of choice
X-ray
often CT cervical spine
what drug should you use to control bleeding
Tranexamic Acid (CRASH-3 trial)
stops fibrinolytic activity
what is the target co2 pressure
what happens if co2 is increased
PaCO2 4.5-5.0kPa
if co2 increases
vasodilation as tissue wants more o2
vascular volume increases
icp increases
oedema increases
cerebral vessel diameter and CBF changes over a range of PaCO2
discuss supply vs demand
optimise oxygen supply
convulsions occur in 15% of severe head injuries
-phenytoin
brain metabolic rate increases 6-9% for every degree rise in temperature
sedation-propofol/midazolam
how do gene influence the TBI
some are more prone to a negative outcome after traumatic brain injury
What should u let the neurosurgeon know
mechanism of the injury
age
resp and cardiovascular status
GCS score and pupil response
alcohol/druh
associated injuries
CT scan results
what is cushings triad
indicative of increased intracranial pressure
- low heart rate
- irregular respiration
- widened pulse pressure (great different between S and D)
what is involved in ICU management of intracranial hypertension
ICP monitoring
osmolar therapy
decompressive craniotomy
hypothermia cases vasoconstriction, oedea wont increase but circulation will be less – CPP less
- we dont want that
venous thromboembolism prophylaxis
stress ulcers prophylaxis
seizure prophylaxis
nutrition
how can you decreases the patient’s arterial pCO2
increase rate of ventilation
what does peri-orbital bruising show
basal skull fracture?
anterior cranial fossa fracture?
it shows blood tracking into peri-orbital fissure
what could battles sign indicate
bruising over the mastoid process
petrous temporal bone fracture?
csf leaking from ear might also be associated
when should you immediately request CT
GCS<13 on initial
GCS<15 2 hours after injury
open or suspected depressed skull
any sign of basal skull injury
post traumatic seizure
1+ episodes of vomiting (3 in kids)
–shows increase in intracranial pressure
amnesia for events more than 30 mins before impact
describe extradural haematoma
- collection of blood in the potential space– between dura mater and skull
-usually with skull fracture
-middle meningeal artery damaged from fracture
-wont pass suture line so expand towards brain and herniation.
-1/3 due to venous bleeding
-relatively uncommon
describe a subdural haematoma
-common
-complicates 20-30% of head injuries
-rupture of veins travelling from brain to saggital sinus
-prognosis worse
-blood within dura and subarachnoid space
describe an epidural haematoma
-collection of blood that forms between your skull and the dura mater
-The cause is usually an artery that gets torn by a skull fracture.
describe a subarachnoid haemorrhage
-associated with ruptured aneurysm (berry aneurysm)
-more commonly caused by head injury
-bleeding in area between arachnoid membrane and pia mater
describe a scalp haematoma
swelling of scalp tissue, damage to external skin and muscles
describe an intracerebral haemorrhage
-stretching and shearing injury
-impact on inside of skull
-often contre coup injury
-bleeding into tissues or ventricles
-AXONAL INJURY
What is a diffuse axonal injury
occurs when the brain rapidly shifts inside the skull as injury occurs
-white matter of the axons-neuronal tracts
what are some signs of herniation
dilated or unreactive pupil
extensor posturing
decrease in GCS of 2 or more points
discuss the pathophysiology of primary and secondary brain injury
decrease in CPP= increase in ICP and vasodilation
increase cerebral blood volume
activation of biomolecular mediators of injury
causes neuronal damage
causes cytotoxic oedema
cerebral vessel damage- opening of BBB
causes increased interstitial fluid and tissue pressure
causes vasogenic oedema
