Management of traumatic brain injury Flashcards
(35 cards)
1
Q
What is primary brain injury?
A
- Damage caused by the trauma
- Haemorrhage and oedema
2
Q
What is secondary brain injury?
A
- Excitatory neurotransmitters, reactive oxygen species and pro-inflammatory cytokines (a result of the primary damage) lead to:
- Cerebral oedema formation
- Increased intracranial pressure
- Compromised blood-brain barrier
- Alterations in cerebrovascular reactivity
3
Q
What fluids should be used in traumatic brain injury?
A
- Either ¼ aliquots of ‘shock’ rates
- 15-20ml/kg boluses of Hartmann’s and/or…
- 2.5-5ml/kg Colloids
- Reassess and give more if needed
- OR 7.2% hypertonic saline
- Rapidly restores circulating volume and decreases oedema
- 4ml/kg over 3-5 mins
- Follow with crystalloids
4
Q
How can you minimise increases in ICP in traumatic brain injury?
A
- 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
5
Q
Benefits of hypothermia in traumatic brain injury?
A
- 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
6
Q
Disadvantages to induced hypothermia?
A
- coagulation disorders
- increased susceptibility to infections
- hypotension
- bradycardia
- dysrhythmias
- Complications occur with more severe hypothermia (<3OoC)
7
Q
Why do we need to avoid hyperthermia?
A
- direct trauma to the thermoregulatory centre
- excitement
- seizure activity
- pain
- Increases cellular metabolism and vasodilation leading to increased ICP
8
Q
Risk factors for seizures with traumatic brain injury?
A
- severity of injury
- depressed skull fractures
- epidural, subdural and intra-cerebral haematomas
- penetrating head wounds
- seizure within the first 24 hours following injury
9
Q
Adverse effects of seizure activity in patients with brain injury?
A
- hyperthermia, hypoxaemia, and cerebral oedema
- Exacerbate increased ICP
10
Q
What drugs can be used to control seizures?
A
- Diazepam regarded as drug of choice for stopping seizures
- Use phenobarbitone for prevention
11
Q
How do barbiturates (including phenobarb) work?
A
- Decreases metabolic needs of the brain
- Also causes vasoconstriction and decreased blood flow
12
Q
When should barbiturates be used?
A
- ONLY use when all other treatments fail
- Decreases metabolic demands of the brain
- May worsen outcome, although beneficial when nothing else works
- Pentobarbitone treatment of choice in this category
13
Q
Recommendations for nutrition in TBI?
A
- Hypermetabolic and catabolic state
- Especially with animals that are seizuring
- Early enteral nutrition maintains integrity of GI mucosa
- beneficial effects on immunocompetence
- improves the metabolic response to stress
- parenteral nutrition asap if enteral not possible
14
Q
Advantages of urinary catheters?
A
- Reduce urine scalding
- Especially if the animal is seizuring
- Measure urine output and assess success of fluid therapy
15
Q
Disadvantages of urinary catheters?
A
- >50% dogs with indwelling catheters end up with UTI’s
- Less likely with intermittent catheterisation than with permanent indwelling
16
Q
Complications of traumatic brain injury?
A
- coagulopathies, pneumonia, sepsis, transient or permanent central diabetes insipidus (transient well reported in dogs) and seizures
- Delayed seizures months to years later
17
Q
What is a common and potentially deadly sequel to traumatic brain injury, and why?
A
- Increased intracranial pressure
- Perfusion decreases if brain enlarges - hypoxaemia
18
Q
What systemic contributions are there to secondary brain injury?
A
hypotension, hypoxia, hypo- or hyperglycaemia, hypo- or hypercapnia, and hyperthermia
19
Q
Which type of brain injury can be manage?
A
Secondary
(primary brain injury has already occurred before they get to us so we can do nothing about it)
20
Q
How should you assess the traumatic brain injury patient initially?
A
- Hypovolaemia and hypoxaemia must be recognised and treated (strongly correlated with increased ICP and increased mortality in human TBI victims)
- Initial neurologic assessment (still give oxygen, make sure they can breathe and give fluids)
- consciousness
- breathing pattern
- pupil size and responsiveness
- ocular position and movements
- skeletal motor responses
- A modified Glasgow coma scale (MGCS) has been proposed for use in veterinary medicine and evaluated with respect to survival over a 48-hour period
- Higher scores correlate with a better prognosis
- Level of consciousness most reliable measure of impaired cerebral function
- Validated for use in dogs and cats, not appropriate for horses
21
Q
What is the first issue that is managed first in traumatic brain injury cases?
A
- Initial extracranial stabilisation takes place first (sort circulation first)
- Correction of tissue perfusion deficits, typically as a result of hypovolaemia
- Optimising systemic oxygenation and ventilation
22
Q
Goals for intracranial stabilisation include…?
A
- Optimising cerebral perfusion
- Decreasing ICP
- Minimising increases in cerebral metabolic rate
23
Q
What levels are oxygen saturation are we aiming for and which levels are dangerous?
A
- SpO2 >95% or PaO2 >90mmHg
- <89% likely severe hypoxaemia with marked consequences
- <75% life-threatening hypoxaemia
24
Q
What does high PaCO2 lead to with traumatic brain injury patients?
A
- High PaCO2 leads to vasodilatation and worsening of ICP
- However hyperventilation contra-indicated
- Leads to vasoconstriction and reduced intra-cerebral perfusion
- Aim for 38-40mmHg
25
How is hyperosmolar therapy used in TBI?
* 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
* Hypertonic saline may be better
* 4ml/kg 7.2% over 3-5 mins
* Can be given much more quickly
* Lasts longer then mannitol and reduces ICP more
26
What is hyperglycaemia associated with in TBI?
* Associated with increased mortality rates or worsened neurologic outcomes in human patients with head trauma
* 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
27
How can you manage hyperglycaemia in TBI?
* Insulin infusions may help prevent detrimental effects
* Note - Can be caused by steroid administration
* If you give these animals steroids, you are creating a hyperglycaemic state
28
Initial treatment of TBI?
* Analgesia
* Anti-convulsant therapy
* Seizures complicate between 4% and 42% of cases of severe TBI in human patients so often used prophylactically
29
Should corticosteroids be used in TBI?
* Now contraindicated in human medicine for TBI
* Should fall out of favour in veterinary medicine
* Associated with
* Hyperglycaemia
* Immunosuppression
* Delayed wound healing
* Gastric ulceration
* Exacerbation of a catabolic state
30
What can enteral feeding intolerance be secondary to?
* Abdominal distension
* Increased gastric residuals
* Ileus
* Delayed gastric emptying
* Diarrhoea
* Documented in human TBI patients
31
Delayed gastric emptying attributable to multiple factors, what are these?
* Increased ICP
* Sympathetic nervous system stimulation
* Cytokine release
* Hyperglycaemia
* Opioid use
32
Implications of delayed gastric emptying?
* implications for increased morbidity and mortality
* poor nutrition
* bacterial colonisation of GIT
* Gastro-oesophageal reflux
* increased prevalence of aspiration pneumonia
33
How can you provide nutrition to a TBI case when enteral feeding is not an option?
* Parenteral
* 50% glucose for up to 48 hrs with IV fluids
* Then partial or total
* NOT 5% DEXTROSE
* Probably needs combining with pro-kinetic
* If unable or unwilling to eat on his/her own
* nasogastric tube
34
Preferred imaging for TBI?
* CT preferred modality
* rapid scan times
* better visualisation of fractures and peracute haemorrhage
35
Prognosis of TBI?
* Predicting outcome difficult
* Prognostic indicators in veterinary medicine scarce
* MGCS correlated with probability of survival in the first 48 hours after TBI in dogs
* predicted a 50% probability of survival with score of 8 out of a total of 18
