Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

what are the most common age groups of TBI

A

0-4
15-19
75+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the major causes of TBI

A

falls
road traffic accidents
assaults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the commonest cause of death and disability in 1-40 years

A

head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which gender is is it more common in

A

men 1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are traumatic brain injuries

A

external forces causing damage
mild-moderate-severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is primary brain injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is shaken baby syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is coup contrecoup injury

A

“blow” and “counterblow”
two separate brain injury occur at same incident
coup- directly under first impact (hit dashboard)
countercoup- (hit headboard)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the early management of head injury

A

-manage at site
-assessment in EandR
-investigating pre-emtive investigations (eg. ct)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

who gets sent to hospital (this is post ABC)

A

under 5 years, over 65 years
amnesia
loss of consciousness
high energy injury
vomiting
seizure
bleeding/clotting disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what to do when in contact with TBI patient straight away

A

ABC
Disability: GCS
Optimise oxygenation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why do you need to optimise oxygenation in TBI patients

A

50% patients pre admission have SpO2 <90%
the airway should be open BUT could have cervical spine injury– stabalise while intubating and mobilising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why do you do GCS

A

to find out degree of consciousness
differentiate mild, moderate, severe injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the different levels of GCS in regards to mild moderate and severe

A

mild– 13-15
moderate– 9-12
severe– 8 or less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is secondary brain injury

A

secondary processes which occur at the cell and molecular level to EXACERBATE neurological damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens in secondary brain injury

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can you minimise secondary brain injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the monro kellie doctrine/ PRINCIPAL

A

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

19
Q

what is a physiological principle (not monro-kellie doctrine)

A

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)

20
Q

identify some features that suggest risk of intracranial mass

A

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

21
Q

what are some red flag to not discharge

A

-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

22
Q

what do you do in hospital in regards to breathing

A

administer oxygen
monitor SpO2
monitor ABGs
GCS <8 INTUBATE

23
Q

What is the investigation of choice

A

X-ray
often CT cervical spine

24
Q

what drug should you use to control bleeding

A

Tranexamic Acid (CRASH-3 trial)

stops fibrinolytic activity

25
Q

what is the target co2 pressure
what happens if co2 is increased

A

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

26
Q

discuss supply vs demand

A

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

27
Q

how do gene influence the TBI

A

some are more prone to a negative outcome after traumatic brain injury

28
Q

What should u let the neurosurgeon know

A

mechanism of the injury
age
resp and cardiovascular status
GCS score and pupil response
alcohol/druh
associated injuries
CT scan results

29
Q

what is cushings triad

A

indicative of increased intracranial pressure

  1. low heart rate
  2. irregular respiration
  3. widened pulse pressure (great different between S and D)
30
Q

what is involved in ICU management of intracranial hypertension

A

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

31
Q

how can you decreases the patient’s arterial pCO2

A

increase rate of ventilation

32
Q

what does peri-orbital bruising show

A

basal skull fracture?
anterior cranial fossa fracture?

it shows blood tracking into peri-orbital fissure

33
Q

what could battles sign indicate

A

bruising over the mastoid process
petrous temporal bone fracture?

csf leaking from ear might also be associated

34
Q

when should you immediately request CT

A

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

35
Q

describe extradural haematoma

A
  • 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
36
Q

describe a subdural haematoma

A

-common
-complicates 20-30% of head injuries
-rupture of veins travelling from brain to saggital sinus
-prognosis worse
-blood within dura and subarachnoid space

37
Q

describe an epidural haematoma

A

-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.

38
Q

describe a subarachnoid haemorrhage

A

-associated with ruptured aneurysm (berry aneurysm)
-more commonly caused by head injury
-bleeding in area between arachnoid membrane and pia mater

39
Q

describe a scalp haematoma

A

swelling of scalp tissue, damage to external skin and muscles

40
Q

describe an intracerebral haemorrhage

A

-stretching and shearing injury
-impact on inside of skull
-often contre coup injury
-bleeding into tissues or ventricles
-AXONAL INJURY

41
Q

What is a diffuse axonal injury

A

occurs when the brain rapidly shifts inside the skull as injury occurs
-white matter of the axons-neuronal tracts

42
Q

what are some signs of herniation

A

dilated or unreactive pupil
extensor posturing
decrease in GCS of 2 or more points

43
Q

discuss the pathophysiology of primary and secondary brain injury

A

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

Medicine (54 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions