Traumatic Brain Injury (TBI) Management Flashcards Preview

Y3S1 NEURO > Traumatic Brain Injury (TBI) Management > Flashcards

Flashcards in Traumatic Brain Injury (TBI) Management Deck (31)
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1
Q

Primary brain injury

A
  • Occurs at the moment of impact
  • Pattern & extent of damage depends in nature of impact
  • Nottreatable
  • Targetprevention (public health issue)
2
Q

Secondary brain injury

A
Focus of medical intervention is to minimise secondary brain injury
• Optimise oxygenation
• Optimise cerebral perfusion
• Blood glucose
• Hypo / hypercapnia
• Body temperature?
3
Q

Secondary processes which occur at the cell & molecular level to exacerbate neurological damage.

A
• Neurotransmitter release (glutamate) 
• Free radical generation
• Calcium mediated damage
• Inflammatory response
• Mitochondrial dysfunction 
• Early gene activation
8
4
Q

Monro-kellie Doctrine

A

That there is a solid box which is the cranium and there is intracranial compensation for expanding mass, as one thing grows the others must leak to somewhere causing an increase in cranial pressure

5
Q

Early Management of Head Injury

A
  • Assessment and identification of the patient at risk of secondary brain injury
  • Pre-emptive investigation (CT scan)
6
Q

Glasgow Coma Scale

A

EYES 1-4
VERBAL 1-5
MOTOR RESPONSE 1-6

7
Q

severe head injury GCS

A

8 OR LESS

8
Q

moderate head injury

A

9-12

9
Q

mild head injury

A

13-15

10
Q

Request CT scan immediately in adult patients if:

A
  • GCS <13 on initial assessment in A & E
  • GCS <15 2 hours after injury
  • Suspected open or depressed skull #
  • Any sign of basal skull #
  • Post traumatic seizure
  • 1 or more episode of vomiting (3 in kids)
  • Amnesia for events more than 30 mins before impact
11
Q

• Red flags:

A

– Loss of consciousness, drowsiness, confusion, fits
– Painful headache which doesn’t settle, vomiting or visual disturbance
– Clear fluid from ear or nose, bleeding from ears, new deafness (CSF rhinorrhoea test for glucose or beta 2 transferrin)
– Problems understanding or speaking, loss of balance, difficulty walking or weakness in arms or legs

12
Q

Breathing

A
  • Administer oxygen
  • Monitor SpO2
  • Monitor ABGs
  • GCS < 8 intubate
13
Q

• Minimise demand for oxygen

A

the need for O2 results in the dilation of blood vessels, allowing more blood to the brain, thus increasing intracranial pressure which = bad

– Convulsions occur in 15% of severe head injuries • Treat with phenytoin in early head injury
– Brain metabolic rate increases 6-9% for every degree rise in temperature
• Treat pyrexia

14
Q

what kind of sedation would be used

A

(propofol / midazolam)

15
Q

Carbon dioxide management

A

• Cerebralvessel diameter (and CBF) changes over a wide range of PaCO2
• Target directed therapy:
PaCO2 4.5 -5.0kPa

16
Q

circulation

A

CPP = MAP - ICP

cerebral perfusion pressure = mean arterial pressure (diastolic pressure + 1/3 pulse pressure) - intracranial pressure

17
Q

Cerebral Autoregulation

A
  • Cerebral arterioles react to local changes in the environment (pressure & chemical)
  • Normally autoregulation maintains a constant blood flow between MAP 50 mmHg and 150 mmHg.
  • Traumatised or ischaemic brain, CBF may become blood pressure dependent.
18
Q

After severe head injury what are the ideal maintenance targets

A

• Maintain CPP above 60 - 70mmHg
• Maintain systolic blood pressure higher than
90mmHg (preferably higher than 120mmHg)
• ICP less than 20mmHg (invasive pressure monitor)

19
Q

Hypotension

A
• Not due to head injury
• Look for other causes – Chest trauma
– Pelvic fracture
Stop bleeding
Intravenous fluids (n. saline)
20
Q

Encourage venous drainage

A
  • Nurse head up tilt (150 - 300 )

* Check straps and ties are not obstructing venous flow

21
Q

Identify features suggesting at

risk of intracranial mass in a patients history

A

high impact injury
significant retrograde amnesia
History of coagulopathy post traumatic seizure

22
Q

panda eyes

A

peri-orbital bruising

23
Q

Battles sign

A

petrous temporal bone fracture

24
Q

Extradural Haematoma

A
very uncommon but has good outcome if treated
• Strongly associated with
skull fracture
• Middle meningeal artery
• 1/3 due to venous bleeding
• Classically a lucid interval
25
Q

Subdural haematoma

A
• Common
• Complicates20-30%of
head injuries
• Ruptureoftheveins travelling from the brain surface to the saggital sinus
• Prognosis worse
26
Q

Subarachnoid Haemorrhage

A
  • Assoc. with ruptured aneurysm

* More commonly caused by head injury

27
Q

Intracerebral Haemorrhage

A
  • Stretching & shearing injury
  • Impact on inside of skull
  • Often contre coup injury
28
Q

Clinical signs of herniation

A
  • Dilated or unreactive pupil(s)
  • Extensorposturing
  • Decrease in GCS of 2 or more points
29
Q

Temporary hyperventilation can

A

decrease ICP and “buy time”

30
Q

Glucose

A

Tight control of blood glucose has been shown to improve outcome
• BUT
dangers of unrecognised hypoglycaemia…

31
Q

Drugs

A

• 20% Mannitol (0.25-1g/kg) – Decreases blood viscosity
– Osmotic diuretic
• Hypertonic saline
• Tranexamic Acid (CRASH-3 trial)