Clinical Management of TBI Flashcards
Define primary and secondary brain injury and the treatment
Primary brain injury refers to the sudden and profound injury that is complete at the time of impact. It is not treatable.
Secondary brain injury refers to the changes that evolve over a period of hours-days after the primary brain injury. It involves a series of steps that contribute to further destruction of brain tissue. The treatment is medical intervention to minimise brain injury;
- optimise oxygenation
- optimise cerebral perfusion
- stabilise blood glucose
- resolve any hypo/hypercapnia (CO2)
- stabilise body temperature
- monitor ABGs
What are the processes that occur during the stages of secondary brain injury?
- NT release (glutamate)
- free radical generation
- Ca2+ mediated damage
- inflammatory response
- mitochondrial dysfunction
- early gene activation
Explain the Monroe-Kellie Doctrine
In normal cranial physiology, 3 components exist in equilibrium; blood (mostly venous in dural sinuses), CSF, and brain tissue. The volumes are restricted by the fixed space within the cranium. Therefore any increase in volume of any of the components causes an increase in ICP (pressure within the skull).
Pathology can cause the equilibrium to be disrupted (eg. a tumour). Initially when the mass is small and growing, the volume of this new component may be small enough for the brain to be able to accommodate for it and compensatory mechanisms can be used to maintain normal ICP (by increasing drainage of blood/CSF from the cranial cavity to create space).
However, if the tumour continues to grow to a certain size to which compensatory mechanisms become exhausted, this will disrupt the equilibrium. Without intervention, the ICP can rise to such a degree that it can cause the brain tissue to become displaced (herniation).
What is the early management of a head injury?
Assess GCS and identify if the patient is at risk of a secondary brain injury
Do a CT scan if;
* GCS <13 on initial assessment in A and E
* GCS <15 2 hours after injury
* suspected open/depressed skull or basal skull fracture
* seizure
* 1 or more episodes of vomiting (3 in children)
* amnesia for events more than 30mins before impact
Describe the components of the Glasgow Coma Scale
Eye opening: 4-spontaneously, 3-to speech, 2-to pain, 1-don’t open, NT-unable to open eyes due to swelling/bandages
Verbal response: 5-orientated, 4-confused, 3-inappropriate words, 2-incomprehensible, 1-no response on verbal/physical stimuli, NT-dysphasic, T-intubated
Motor response: 6-obeys commands, 5-localises to central pain, 4-normal flexion towards pain, 3-abnormal flexion, 2-extension to pain, 1-no response
Explain the scoring of GCS in the context of a head injury
- minimal injury = 15 (and no LOC)
- mild = 13-15
- moderate = 9-12
- severe = 8 or less (requires intubation)
What are the red flags for a head injury?
- LOC, drowsiness, confusion, fits
- painful headache that doesn’t settle, vomiting, visual disturbance
- clear fluid from ear/nose, bleeding from ears, new deafness
- problems understanding or speaking, loss of balance, difficult walking/weakness in limbs
What are some possible consequences of a brain injury?
- convulsions (treat with phenytoin early)
- peri-orbital bruising (possible anterior cranial fossa bruising)
- brain metabolic rate increasing (treat with propofol/midazolam - sedation)
- battle’s sign (possible petrous bone fracture)
- extra-dural/sub-dural haematoma
- subarachnoid haemorrhage
- intracerebral haemorrhage (stretching and shearing injury, contre-coup injury)
How would you calculate cerebral perfusion pressure and describe the factors that affect cerebral perfusion
CPP = MAP (diastolic pressure + 1/3 pulse pressure) - ICP
In TBI, ICP is increased (from swelling/bleeding) so if systemic BP is low then this limits blood flow to the brain.
Hypercapnia (CO2) causes dilation of arteries and increased blood flow.
Hypoxia can cause MAP to increase as it can cause narrowing of arteries.
Control of blood glucose is important as hyperglycaemia can increase BBB permeability and promote inflammation of the brain. It also promotes hypovolaemia which will in turn decrease MAP and CPP
Describe the volume-pressure curve in the context of a patient with an intracranial pathology
As the pathology increases in size the patient will enter a decompensated state, where small increases in intracranial volume results in large increases in ICP resulting in a steep upward curve of the volume-pressure curve
What are the clinical signs of herniation of the brain
- dilated/unreactive pupils
- extensor posture (involuntary extension of arms, knee and plantar, flexion of hands)
- decrease in GCS of 2 or more points
How would you treat a hypercapnic patient?
Drugs:
- mannitol
- hypertonic saline
- tranexamic acid
