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Intensive Care > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

Classify TBI

A

Primary (Irreversible)

  1. Focal (contusion, laceration)
  2. Diffuse (Concussion, Diffuse axonal injury)

Secondary (Preventable/treatable)
1. Intracranial haematoma
–> Extradural (16%)
–> Subdural (22%)
–> Intracerebral (54%)
2. Cerebral Swelling
3. Cerebral Ischaemia
4. Excitotoxicity
5. Herniation

Also

Mild GCS 13 - 15
Moderate 9 - 12
Severe 3 - 8

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2
Q

Differentiate diffuse brain injury and diffuse axonal injury

A

Diffuse brain injury
- Subtle CT Brain findings suggestive of diffuse axonal injury (deep white matter gliding contusions, cerebral swelling)

Diffuse axonal injury
- Pathologist viewing brain biopsy histology specimens: axonal cell bodies sheared from axons

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3
Q

What are the units of used on a CT scan? Give examples to demonstrate this scale of whiteness vs blackness

A

Hounsfield unit

Air = -1000
Water = 0
Dense calcified bone = + 1000

Can use specific measurements (e.g. fat vs blood vs bone vs pus vs fluid have specific numbers)

Can be measured on PACS

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4
Q

Why is new blood white on CTBrain

A

New blood has a high calcium content which increases the hounsfield units and makes it appear whiter and brighter than old blood where the calcium has been sequestered (Calcium in skull bone increases hounsfield units)

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5
Q

Where do most cerebral contusions occur and why?

A

Acceleration/Deceleration high velocity injuries
Anterior cranial fossa (frontal lobes) and the middle cranial fossa (Temporal lobes) are rough surfaces. So as brain moves over this –> contusions more commonly occur here in the frontal and temporal lobes

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6
Q

What are the key aspects of extradural hematoma

A
  1. Mostly laceration middle meningeal artery as it comes through the foramen spinosum at the base of the brain and into the middle cranial fossa
  2. Lucid interval after injury and before coning
  3. Lens shaped appearance (limited by the cranial vault sutures - dural attachment. Expansion limited.
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7
Q

What does hypodensity mean inside an extradural

A

Indicates ongoing active bleeding at the time scan was happening (not old blood)

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8
Q

What is the pathophysiology of subdural hematoma

A

Tearing of bridging veins in the subdural space during acceleration/deceleration. No dural attachment so expansion is not confined.

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9
Q

Why do acute subdural hematomas have worse prognostic sign vs extradural

A

The massive force required to shear bridging veins in the subdural space imply there is some form of diffuse brain injury associated with the mechanism. (Not in elderly patients –> larger space due to atrophy –> smaller knocks to the head)

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10
Q

What is the meniscus effect of subdural hematoma

A

Old blood separates into components (like in a test tube)

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11
Q

Why do we see subarachnoid haemorrhage in the basal cisterns

A

Because that where the circle of Willis is

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12
Q

What are the signs of subtle brain swelling on CTBrain

A

Slight lost of grey-white matter differentiation
“fattening of apperance of surface sulci”
Decreased size of appearance of cisterns/ventricles

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13
Q

Summarise the pathophysiology of secondary brain injury

A

Primary injury insights a cascade of events that bring about additional factors which further injure the brain tissue

  1. Oxidative Stress (free radicals)
  2. Disrupted BBB (hypoxia, ischaemia)
  3. Inflammation (cytokines, NO)
  4. Excitotoxicity (Glutamate, NMDA, Ca)
  5. Cell death
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14
Q

What is the different between a GCS M score of 3 and 4

A

3 - Abnormal flexion (spastic tone)

4 - Normal flexion (normal flexion –> almost localizing)

This is very NB as it makes a significant difference to prognostication

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15
Q

List the herniation syndromes and relevant clinical findings in each

A
  1. External herniation - (depends on area)
  2. Subfalcine herniation - Contralat. leg weak
  3. Transtentorial (uncal) herniation - Ipsilat. dilated pupil. contralat hemiparesis. midbrain
  4. Transtentorial (upward) herniation - N,V, obtundation
  5. Cerebellar (Tonsillar) herniation - HR and RESP
  6. Transforaminal herniation
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15
Q

What is the cushing reflex

A

Raised intracranial pressure
Hypertension
Bradycardia
Diminished respiratory effort

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16
Q

What are the indications for a CTB in TBI

A

Use western cape head injury guidelines

GCS < 15
Penetrating skull injury
Focal signas
CSF leak
Persisting headache after head injury
Seizures

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17
Q

When is ICP monitoring indicated

A

Majority of TBI patients will get a tissue oxygenation monitor and ICP monitor bolted to the skull.

Reserved for patients with severe head injury –> very sedated and flat therefore you cant monitor them clinically and the monitors have to go in.

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18
Q

Name and describe the two ICP monitors we use at GSH

A

Licox (PtO2)
- brain tissue oxygenation monitor
- intraparenchymal in the white matter

ICP monitor
- Intraparenchymal in the grey matter

Inserted into non-injured site

Use with A line to monitor CPP

And CVC to administer hypertonic saline

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19
Q

What is important with regard to autoregulation in TBI

A

Severe brain injury results in loss of autoregulation of brain perfusion in spite of variable perfusion pressures

20
Q

What is important about ICP waveforms

A

P1 - Percussion (arterial pulsation) wave
P2 - Tidal (brain compliance) wave
P3 - Aortic valve closure (dichrotic) wave

High P1 - High SBP patient (no action)
Low P1 - Low SBP

Large P2 (>P1) - Brain losing compliance (and ability to compensate for raised ICP)

Critically raised ICP –> merging of P1 to P3

21
Q

What are the Lundberg waveforms

A

Lundberg A
- Sustained pressure waves (50 - 80mmHg)
- Lasts 5 - 20 mins before returning to baseline
- Represents cerebral vasodilation due to decreased CPP
- Urgent treatment needed

Lundberg B
- High frequency oscillations (<50mmHg) 30s to 2 min
- Associated with normal breathing

Lundberg C
- Small oscillations (10 - 20 mmHg) ICPs 4 - 8 waves per minute
- Refelect changes in systemic arterial pressure
- Considered normal

22
Q

What is the treatment of TBI

A

Follow Brain Truama Foundation guidelines 2016.

Physical
- Head elevation (30 to 40 degrees)
- Head Straight + midline (dont occlude jug. v.)
- Neck collars (make sure not too tight as on propofol)
- ETT/Trachy tape: Check not occluding jugular venous drainage

Medical
- Steroids are BAD (unless another indication for low dose steroids like septic shock) They are talking about high doses.
- Prophylactic hypothermia (no clear benefit for mortality)
- Osmotherapy: mannitol still number 1 agent. May change to hypertonic saline (5%) in new BTF guidelines.
- Hyperventilation –> causes vasoconstriction which leads to reduced O2 delivery. Use Jugular venous saturation monitoring to ensure enough O2. (transient hernia prevention for a few minutes)
- Propofol: routine for ICP control
- Barbiturate coma (only for super refractory ICP
- Nutrition - full nutritional goals by day 5 -7
- Prophylactic antibiotics: No. Just Cefzol at surgery.
- DVT prophylaxis: VTE stockings/pumps. Wait to day 10 then repeat CTB. Risk assessment. If no change/new then start clexane.
- Seizure prophylaxis: Phenytoin 7 days. then individualise.

Surgical
- decompressive craniectomies (shorten ICU stay don’t alter outcome)
- draining CSF: Continuous drainage better than intermittent. Set height at 15 cm –> CSF will drain above this pressure.
- ICP monitor. GCS 3 - 8 and abnormal CTB. GCS 3 - 8 and normal CTB then any 2 of >40 yrs/motor posturing/SBP<90. ICP > 22 mmHG then treat with osmotherapy. CPP aim for 60 - 70
- Licox not recommended (or microdialysis catheters)

23
Q

How is osmotherapy administered at GSH

A

Follow Brain Trauma Foundation Guidelines

200 mls of 5% NaCl at 33 - 50 ml / hr (run in over 4 - 6 hours)

Mannitol can be given stat –> 1 - 1.5 g/kg body weight bolus. Then an additional 0.5 g/kg can be given in addition as a bolus if required.

24
Q

When and how do we use seizure prophylaxis in TBI

A

All patients get phenytoin 20 mg/kg loading dose (<50mg/minute)

Thereafter, 100mg 8hrly IV in ICU for seven days titrated to levels. (Give Folate to minimize gum hypertrophy)

Patients with seizures require treatment doses and levels etc.

25
Q

How should patients with TBI be anticoagulated

A

Unit and patient dependent

Severe TBI with high risk for bleeding - just VTE stockings and intermittent pneumatic compression devices.

Stable TBI and at GSH: VTE prophylaxis compression stockings, intermittent pneumatic compression devices. Re-scan after 10 to 14 days. If low risk bleeding complication –> start clexane/heparin.

26
Q

Are decompressive craniectomies effective for the treatment of TBI

A

They work to control ICPs
1. reduce ICU stay
2. Fewer ICP targeting strategies required (e.g. osmotherapy)

Have not been shown to improve overall outcome for patients (i.e. no increase in independent functioning patients)

27
Q

Does prophylactic hypothermia improve ooutcome

A

According to the Brain Trauma Foundation, outcomes in TBI are not effected by prophylactic hypothermia

28
Q

Describe osmotherapy administration recommended by Brain Trauma Foundation Guidelines

A

Mannitol (best) - 1.5 - 2g/kg over 30 - 60 minutes
- advantage is quicker bolus without infusion pumps i.e. in remote hospitals

Hypertonic Saline - NaCl 5% 200 ml at 50 ml/hour

29
Q

How does the brain trauma foundation recommend the CSF be drained in TBI if a EVD is in situ

A

Drain CSF for the first 12 hours for patients with GCS less than 6

Continuous is better than intermittent. I.e. set manometer to 10 to 15 and pressure higher than this will drain.

30
Q

Should a patient be hyperventilated to improve inctracranial pressure

A

No. The effect is transient

If it is done as a very brief temporising measure (e.g. on the way to theatre) then ensure jugular venous saturation monitoring is done to ensure the brain is being oxygenated (vasoconstriction could impair DO2)

31
Q

How should patient’s with TBI be sedated

A

Propofol is routine
Barbiturate coma only in very refractory patients

32
Q

Should steroids be administered to patients with TBI

A

NO. Steroids are bad (i.e. high dose)

Patients with accompanying indications for lower dose steroids –> can and should be administered

33
Q

How long should TBI patients be in antiepileptics if they develop seizures

A

6 - 12 months

34
Q

What is the target cerebral perfusion pressure and how is this calculated

A

CPP 60 - 70 mmHg

CPP = MAP - ICP(or CVP whichever is higher)

35
Q

How does the mechanism of action of mannitol and hypertonic saline differ in reducing intracranial pressure

A

Mannitol
- Increase osmolarity od glomerular filtrate –> Increased urinary volume–> decrease CSF production and mannitol present in plasma draws brain water into plasma to be excreted by the kidneys

Hypertonic Saline
- Increase plasma Na to 155 –> removes brain water into the plasma

36
Q

How is mannitol and hypertonic saline administered and what is the dose

A

Mannitol
- peripheral IV line ok
- 1 g/kg as a bolus (can then repeat 0.5g/kg)

Hypertonic saline
- CVC
- Need infusion pump
- Give 200ml of 5% at 50 ml/hour titrated to NA of 155 mmol/L

37
Q

What is the onset and duration of mannitol

A

Onset: minutes
Duration: 3 hours

38
Q

Summarise the key advantages and disadvantage of mannitol vs hypertonic saline

A

Mannitol

Advantages
- Rapid bolus (no infusion pumps)

Disadvantages
- Hypovolaemia and diuresis
- Electrolyte abnormalities

Hypertonic Saline

Advantages
- End point of therapy easily monitored and maintained with ABG
- Less likely to produce hypovolaemia

Disadvantages
- Need for CVC
- Hypernatraemia/Hyperchloraemic metabolic acidosis
- Central pontine myelinolysis

39
Q

When should mannitol therapy be discontinued

A

Sodium > 160
Osmolarity > 320

40
Q

Summarise the mechanism of action of the Phenytoin and Valproate

A

Phenytoin
- Blocks voltage gated sodium channels
- Promotes Na+ efflux and decreased Na influx
- Stabilizes neuronal membrane

Sodium Valproate
- Increased levels of GABA in the brain
- Enhances action of GABA / mimics GABA action at post synaptic receptor sites
- Blocks voltage-dependent sodium channels

41
Q

Classify and define seizures post TBI

A

Immediate < 24 hours
Early 24 hours to 7 days
Late > 7 days

42
Q

Describe the dosing of Epilim and Phenytoin

A

Phenytoin
Load: 20 mg/kg. So usually 1.2g IV in 200 mls over 20 minutes
Then: 300 mg daily
- 100mg IV 8 hourly
- 300mg PO nocte

(NB refractory hypotension / dysrhythmia so load slowly over 30 - 60 mins)

Epilim
Load: 10 - 15mg/kg 1 g IV in 200ml over 20 minutes.

Maintenance:
10 - 15 mg/kg daily
500 mg PO 12 hourly
(max 60 mg/kg/day)

43
Q

Name 3 adverse effects of phenytoin

A

Gum hypertrophy
Cardiac Arrythmias
Teratogenecity
GI symptoms

44
Q

Name 3 adverse effects of epilim

A

Thrombocytopaenia
GI symptoms

45
Q

Why is important to recognize evidence of BOS fracture

A

Risk of meningitis
(Translocation through sinuses)

Actions:
No specific actions –> will heal and seal by themselves

But if spike temps 5 days into ICU stay –> must cover for hospital acquired meningitis

46
Q

When and why is microdialysis used

A

At red cross hospital
Paediatric patients
TBI and TBM patients

Used to sample the ECF of the brain to look at lactate/pyruvate ratios and drugs levels (TB meds difference between serum and CNS drug levels)

Experimental treatment and extremely expensive

47
Q

How is recovery from TBI graded

A

Glasgow Outcome Score
1 - back to baseline fxn
2 - mild deficit
3 - deficit prevents return to employment
4 - Coma or completely dependent (vegetative state)
5 - Death

48
Q
A

Intensive Care (22 decks)

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