Traumatic Brain Injury Flashcards
What is a traumatic brain injury?
- Severe head trauma associated with high mortality in humans and animals
- Dogs and cats remarkable ability to compensate for loss of cerebral tissue
- Important not to reach hasty prognostic conclusions based on initial appearance
- Many pets go on to have a functional outcome and recover from injury
What is a primary traumatic brain injury?
–Damage caused by the trauma
- Haemorrhage and oedema
- Little we can do about this
- Will happen before these patients get to us
What is a secondary brain injury?
What does it lead to?
•Secondary injury
–Excitatory neurotransmitters
–Reactive oxygen species
–Pro-inflammatory cytokines
:
•Leads to
–Cerebral oedema formation
–Increased intracranial pressure
–Compromised to the blood-brain barrier
–Alterations in cerebrovascular reactivity
What is a common and potentially deadly sequel to traumatic brain injury?
Increased intracranial pressure
What happens if the ICP increases?
•Brain within a box
–If brain parenchyma swell, vessels must shrink à parenchyma becomes hypoxaemia
–CSF
- Perfusion decreases if brain enlarges
- Systemic contributions to secondary brain injury include hypotension, hypoxia, hypo- or hyperglycaemia, hypo- or hypercapnia, and hyperthermia
–Don’t want any of these extremes
What should be included in the patient assessment and management?
•Hypovolaemia and hypoxaemia must be recognised and treated
–strongly correlated with increased ICP and increased mortality in human TBI victims
•Initial neurologic assessment
–consciousness
–breathing pattern
–pupil size and responsiveness
–ocular position and movements
–skeletal motor responses
Before giving fluids to the TBI patient, initial extracranial stabilisation takes place first. How is this done?
–Correction of tissue perfusion deficits, typically as a result of hypovolaemia
–Optimising systemic oxygenation and ventilation
What do goals for intracranial stabilisation include?
•Goals for intracranial stabilisation include:
–Optimising cerebral perfusion
–Decreasing ICP
–Minimising increases in cerebral metabolic rate
What fluid therapy should you use for treatment of a TBI?
Restrict fluids or nah?
What to use?
–Fluid restrictions in these cases are contra-indicated
- It does not reduce or prevent cerebral oedema
- Equally don’t want to flood with fluids so we cause oedema of the brain and other tissues
–What to use
•Either ¼ aliquots of ‘shock’ rates
–15-20ml/kg boluses of Hartmann’s, reassess and then give more if needed – easier to give more than take away
–2.5-5ml/kg Colloids
–Smaller volumes of shock rate fluids
•Evidence that 7.2% hypertonic saline good option
–Rapidly restores circulating volume
–Also increased osmolarity draws fluid from interstitium thus decreasing oedema
–4ml/kg over 3-5 mins
–Follow with crystalloids
As part of the treatment of TBI, what should we supplement?
•Oxygen supplementation
–SpO2 >95% or PaO2 >90mmHg
–<89% likely severe hypoxaemia with marked consequences
–<75% life-threatening hypoxaemia
As part of the treatment of TBI, how can you minimise increases in ICP?
–Raise head and neck by 15-30o from horizontal
- Use stiff board under the chest
- Increases venous drainage
–Remove collars and check any wraps on venous catheters
What is hyperosmolar therapy for the treatment of TBI?
–Hypertonic saline is hyperosmolar therapy (?)
–Mannitol for severe TBI and progressive neurologic deterioration
–First-line therapy for decreasing ICP and improving CPP
–0.5 to 1.5 g/kg as a slow bolus over 15–20 minutes
–Relatively high-dose (1.4 g/kg) for a better neurologic improvement compared with low-dose (0.7g/kg)
–Hypertonic saline may be better
- 4ml/kg 7.2% over 3-5 mins
- Lasts longer then mannitol and reduces ICP more
As part of the treatment of TBI, how do you deal with hyperglycaemic?
Why is hyperglycaemia bad?
–Associated with increased mortality rates or worsened neurologic outcomes in human patients with head trauma
•Hard to know if its cause of effect as with disease more stressed, higher glucose concentrations but is also associated with poor neurological output
–Reflection of brain injury or a cause of worsened secondary injury?
–Increases with sympatho-adrenal response so probably reflection of severity of injury
–Increases free radical production, excitatory amino acid release, cerebral oedema and cerebral acidosis, and alters the cerebral vasculature
–Associated with severity of TBI, but not outcome in small animals
–Insulin infusions may help prevent detrimental effects
–Can be caused by steroid administration à causes hyperglycaemic state, often why steroids aren’t used with TBI
As part of the treatment of TBI, how can you induce hypothermia and why?
–Thought to decrease brain metabolic demands leading to decreased cerebral oedema and ICP
–Induced hypothermia thought to provide beneficial results through reduction in the release of excitatory neurotransmitters e.g. glutamate
–May also reduce secondary brain injury by inhibition of posttraumatic inflammatory response including reduction in release of inflammatory cytokines and preservation of the BBB
–We will never have monitoring in veterinary that will allow us to safely cool out patients. In humans they do whole body cooling. But in children, they will do selective brain cooling
As part of the treatment for TBI, what are the disadvantages to inducing hypothermia?
•Disadvantages to induced hypothermia
–coagulation disorders
–increased susceptibility to infections
–hypotension
–bradycardia
–dysrhythmias
•Complications occur with more severe hypothermia (<3OoC)
