Traumatic Brain Injury Flashcards
(49 cards)
Classify TBI
Primary (Irreversible)
- Focal (contusion, laceration)
- 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
Differentiate diffuse brain injury and diffuse axonal injury
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
What are the units of used on a CT scan? Give examples to demonstrate this scale of whiteness vs blackness
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
Why is new blood white on CTBrain
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)
Where do most cerebral contusions occur and why?
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
What are the key aspects of extradural hematoma
- Mostly laceration middle meningeal artery as it comes through the foramen spinosum at the base of the brain and into the middle cranial fossa
- Lucid interval after injury and before coning
- Lens shaped appearance (limited by the cranial vault sutures - dural attachment. Expansion limited.
What does hypodensity mean inside an extradural
Indicates ongoing active bleeding at the time scan was happening (not old blood)
What is the pathophysiology of subdural hematoma
Tearing of bridging veins in the subdural space during acceleration/deceleration. No dural attachment so expansion is not confined.
Why do acute subdural hematomas have worse prognostic sign vs extradural
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)
What is the meniscus effect of subdural hematoma
Old blood separates into components (like in a test tube)
Why do we see subarachnoid haemorrhage in the basal cisterns
Because that where the circle of Willis is
What are the signs of subtle brain swelling on CTBrain
Slight lost of grey-white matter differentiation
“fattening of apperance of surface sulci”
Decreased size of appearance of cisterns/ventricles
Summarise the pathophysiology of secondary brain injury
Primary injury insights a cascade of events that bring about additional factors which further injure the brain tissue
- Oxidative Stress (free radicals)
- Disrupted BBB (hypoxia, ischaemia)
- Inflammation (cytokines, NO)
- Excitotoxicity (Glutamate, NMDA, Ca)
- Cell death
What is the different between a GCS M score of 3 and 4
3 - Abnormal flexion (spastic tone)
4 - Normal flexion (normal flexion –> almost localizing)
This is very NB as it makes a significant difference to prognostication
List the herniation syndromes and relevant clinical findings in each
- External herniation - (depends on area)
- Subfalcine herniation - Contralat. leg weak
- Transtentorial (uncal) herniation - Ipsilat. dilated pupil. contralat hemiparesis. midbrain
- Transtentorial (upward) herniation - N,V, obtundation
- Cerebellar (Tonsillar) herniation - HR and RESP
- Transforaminal herniation
What is the cushing reflex
Raised intracranial pressure
Hypertension
Bradycardia
Diminished respiratory effort
What are the indications for a CTB in TBI
Use western cape head injury guidelines
GCS < 15
Penetrating skull injury
Focal signas
CSF leak
Persisting headache after head injury
Seizures
When is ICP monitoring indicated
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.
Name and describe the two ICP monitors we use at GSH
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
What is important with regard to autoregulation in TBI
Severe brain injury results in loss of autoregulation of brain perfusion in spite of variable perfusion pressures
What is important about ICP waveforms
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
What are the Lundberg waveforms
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
What is the treatment of TBI
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)
How is osmotherapy administered at GSH
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.