Treatment of Traumatic Brain Injury Flashcards
What is the first thing to do in TBI?
Extracranial stabilisation
What is extracranial stabilisation?
○ Correction of tissue perfusion deficits - often as a result of hypovolaemia
○ Optimising systemic oxygenation and ventilation
* Goals include:
○ Optimising cerebral perfusion
○ Decreasing Intracranial Pressure
○ Minimising increases in cerebral metabolic rate
Fluid therapy and contra-indications?
With-holding fluid is contra-indicated
○ It does not reduce or prevent cerebral oedema
○ Can actually help reduce cytokines and ROS
What fluid therapy can you use?
Small boluses of hartmann’s
Small boluses of colloids (Careful)
7.2% hypetonic saline (Acts like colloid but better)
Why is 7.2% hypetonic saline good for TBI?
Rapidly restores circulating volume
Increases osmolarity
□ Draws fluid from interstitium - decreasing oedema
Very small volumes
□ 4ml/kg over 3-5 mins
Follow with crystalloids (Hartmann’s) as needed
What levels do you want SpO2 and PaO2
- SpO2 >95% or PaO2 >90mmHg
○ <89% likely severe hypoxaemia with marked consequences
○ <75% life-threatening hypoxaemia
Monitor with pulse ox or blood gas machine
How does PaCO2 affect TBI
- High PaCO2 leads to vasodilatation and worsening of ICP
- Don’t want to reduce PaCO2 too much:
○ Leads to vasoconstriction and reduced intra-cerebral perfusion - Aim for 38-40mmHg (normal level)
How else can you reduce increases in ICP?
Raise head and neck by 15-30 from horizontal
Remove collars
Check wraps on venous catheters aren’t restricting blood flow
Hyperosmolar therapy
- Mannitol is a hyperosmolar drug for severe TBI and progressive neurologic deterioration
- Used as first-line therapy for decreasing ICP and improving Cerebral Perfusion Pressure
○ 0.5 to 1.5 g/kg as a slow bolus over 15–20 minutes - High-dose is better neurologic improvement compared with low-dose
- Hypertonic saline may be better than mannitol?
○ 4ml/kg 7.2% over 3-5 mins
○ Lasts longer then mannitol and reduces ICP more
Can be cheaper
How does hyperglycaemia affect TBI
- Worsens secondary injury:
○ Increases with sympatho-adrenal response
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 (cortisol)
How does hypothermia affect TBI
- Thought to decrease brain metabolic demands
○ Leading to decreased cerebral oedema and ICP - Induced hypothermia is thought to reduce release of excitatory neurotransmitters
○ E.g. glutamate
○ May also inhibit posttraumatic inflammatory response including reduction in release of inflammatory cytokines and preservation of the BBB
Disadvantages of induced hypothermia
Only when severe (<30)
○ Coagulation disorders
○ Increased susceptibility to infections
○ Hypotension
○ Bradycardia
○ Dysrhythmias
How does hyperthermia affect TBI?
Increases cellular metabolism and vasodilation leading to increased ICP
Causes of hyperthermia in TBI
○ Direct trauma to the thermoregulatory centre
○ Excitement
○ Seizure activity
○ Pain
○ Iatrogenic
Risks of TBI causing seizures
○ Severity of injury
○ Depressed skull fractures
○ Epidural, subdural and intra-cerebral haematomas
○ Penetrating head wounds
○ Seizure within the first 24 hours following injury
Adverse effects of seizures
○ Hyperthermia
○ Hypoxaemia
○ Cerebral oedema
Exacerbate increased ICP
Anti-convulsant therapy
Shown to improve outcome
Diazepam as treatment
Phenobarbitone as prevention
Corticosteroid use in TBI?
Don’t do it! - increases mortality
Associated with:
○ Hyperglycaemia
○ Immunosuppression
○ Delayed wound healing
○ Gastric ulceration
○ Exacerbation of a catabolic state
Why do we use gastric protectants?
To reduce the risk of GIT bleeding
Not appropriate in equine
Why are TBI patients not tolerant to enteral feeding?
○ Abdominal distension
○ Increased gastric residuals
○ Ileus
○ Delayed gastric emptying
○ Diarrhoea
Why do TBI patient shave delayed gastric emptying?
○ Increased ICP
○ Sympathetic nervous system stimulation
○ Cytokine release
○ Hyperglycaemia
○ Opioid use
Effects of delayed gastric emptying
○ Poor nutrition
○ Bacterial colonisation of GIT
○ Gastro-oesophageal reflux
○ Increased prevalence of aspiration pneumonia
How can we treat gastric emptying problems
Intra-gastric enteral feeding with prokinetic agent
Nutrition factors in TBI
Patient is in hypermetabolic and catabolic state
Start enteral nutrition early to maintain GI mucosa
* If unconscious and enteral is not practical us parenteral feeding
50% glucose for up to 48 hrs with IV fluids
Then partial or total
NOT 5% DEXTROSE!
Needs combination with prokinetic
