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CRS2 > Management of traumatic brain injury > Flashcards

Management of traumatic brain injury Flashcards

1
Q

What is primary brain injury?

A
  • Damage caused by the trauma
  • Haemorrhage and oedema
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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
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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
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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
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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
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6
Q

Disadvantages to induced hypothermia?

A
  • coagulation disorders
  • increased susceptibility to infections
  • hypotension
  • bradycardia
  • dysrhythmias
  • Complications occur with more severe hypothermia (<3OoC)
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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
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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
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9
Q

Adverse effects of seizure activity in patients with brain injury?

A
  • hyperthermia, hypoxaemia, and cerebral oedema
    • Exacerbate increased ICP
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10
Q

What drugs can be used to control seizures?

A
  • Diazepam regarded as drug of choice for stopping seizures
  • Use phenobarbitone for prevention
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11
Q

How do barbiturates (including phenobarb) work?

A
  • Decreases metabolic needs of the brain
  • Also causes vasoconstriction and decreased blood flow
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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
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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
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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
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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
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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
Q

How is hyperosmolar therapy used in TBI?

A
  • 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
Q

What is hyperglycaemia associated with in TBI?

A
  • 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
Q

How can you manage hyperglycaemia in TBI?

A
  • 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
Q

Initial treatment of TBI?

A
  • Analgesia
  • Anti-convulsant therapy
    • Seizures complicate between 4% and 42% of cases of severe TBI in human patients so often used prophylactically
29
Q

Should corticosteroids be used in TBI?

A
  • 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
Q

What can enteral feeding intolerance be secondary to?

A
  • Abdominal distension
  • Increased gastric residuals
  • Ileus
  • Delayed gastric emptying
  • Diarrhoea
  • Documented in human TBI patients
31
Q

Delayed gastric emptying attributable to multiple factors, what are these?

A
  • Increased ICP
  • Sympathetic nervous system stimulation
  • Cytokine release
  • Hyperglycaemia
  • Opioid use
32
Q

Implications of delayed gastric emptying?

A
  • implications for increased morbidity and mortality
    • poor nutrition
    • bacterial colonisation of GIT
    • Gastro-oesophageal reflux
    • increased prevalence of aspiration pneumonia
33
Q

How can you provide nutrition to a TBI case when enteral feeding is not an option?

A
  • 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
Q

Preferred imaging for TBI?

A
  • CT preferred modality
    • rapid scan times
    • better visualisation of fractures and peracute haemorrhage
35
Q

Prognosis of TBI?

A
  • 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

CRS2 (64 decks)

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