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Traumatic Brain Injury
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propofology.com
Dr. Barbara Stanley
Dr. Tom Dawes
Dr. David Lyness
1.4 million head injuries a year:
- 50,000 die.
- 90,000 permanently disabled.
- Primarily affects young adults.
- Hypotension alone increases mortality from 27% to 60%.
- Hypoxia, in addition to hypotension, is associated with a mortality of 75%.
- 50,000 die.
- 90,000 permanently disabled.
- Primarily affects young adults.
- Hypotension alone increases mortality from 27% to 60%.
- Hypoxia, in addition to hypotension, is associated with a mortality of 75%.
WHY IT MATTERS
- >60 yrs old
- Bilateral fixed dilated pupils
- Single BP reading <90mmHg systolic doubles mortality
- Tramatic SAH doubles mortality
- Midline shift
Direct worsening of outcome if transfer not executed correctly – physiology of raised ICP
- Bilateral fixed dilated pupils
- Single BP reading <90mmHg systolic doubles mortality
- Tramatic SAH doubles mortality
- Midline shift
Direct worsening of outcome if transfer not executed correctly – physiology of raised ICP
PREDICTORS OF POOR OUTCOME
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CORRELATES TO THE DEGREE OF HYPOXIA
Raised PaCO2 causes cerebral vasodilation (Aim PaCO2 4.5-5 kPa)
Hypoxia SPO2 <90% causes vasodilatation. (Aim PaO2 13 kPa)
Prevention of secondary cerebral injury relies on prevention of
Hypoxia SPO2 <90% causes vasodilatation. (Aim PaO2 13 kPa)
Prevention of secondary cerebral injury relies on prevention of
cerebral vasodilation which increases intracranial volume and thus pressure.
CORRELATES TO ADMISSION GCS
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Brighton and Sussex University Hospitals NHS Trust
WHICH INDUCTION AGENT?
Propofol, thiopentone, midazolam all can be used but reduce BP. Ketamine maintains BP, but associated with fears it raises ICP due to increasing the cerebral metabolic rate. But……
Ketamine does not lead to an elevation in ICP in severe TBI,
When utilized in bolus dosing, ketamine seems to provide a dramatic decrease in ICP, whether at baseline or during an episode of ICP elevation.
Consensus is that if BP is compromised but patient needs an anaesthetic to intubate/pain mx then
in the setting of an intubated and sedated patient.
In addition, bolus dose ketamine may provide a means of acute ICP reduction in these patients under IV sedation.
In addition, bolus dose ketamine may provide a means of acute ICP reduction in these patients under IV sedation.
When utilized in bolus dosing, ketamine seems to provide a dramatic decrease in ICP, whether at baseline or during an episode of ICP elevation.
Consensus is that if BP is compromised but patient needs an anaesthetic to intubate/pain mx then
KETAMINE is 1st choice in Prehospital setting around the world
The Ketamine Effect on ICP in Traumatic Brain Injury. F. A. Zeiler et al. Neurocrit Care (2014) 21:163–173
TBI & HAEMORRHAGIC SHOCK
RECOMMENDATIONS:
1. MAP ≥80mmHg maintained in patients with combined haemorrhagic shock and severe TBI (GCS ≤8) (Grade 1C)
2. Fluid therapy be initiated in the hypotensive bleeding trauma patient. (Grade 1A)
3. Crystalloids be applied initially to treat the hypotensive bleeding trauma patient. (Grade 1B)
4. Hypotonic solutions, such as Ringer's lactate, be avoided in patients with severe head trauma. (Grade 1C)
5. If colloids are administered, we recommend use within the prescribed limits for each solution. (Grade 1B)
1. MAP ≥80mmHg maintained in patients with combined haemorrhagic shock and severe TBI (GCS ≤8) (Grade 1C)
2. Fluid therapy be initiated in the hypotensive bleeding trauma patient. (Grade 1A)
3. Crystalloids be applied initially to treat the hypotensive bleeding trauma patient. (Grade 1B)
4. Hypotonic solutions, such as Ringer's lactate, be avoided in patients with severe head trauma. (Grade 1C)
5. If colloids are administered, we recommend use within the prescribed limits for each solution. (Grade 1B)
Management of bleeding and coagulopathy following major trauma: an updated European guideline Critical Care 2013, 17:R76 - Updated in 2016.
THERAPEUTIC HYPOTHERMIA? - NO
“ICP >20 mm Hg after TBI, therapeutic hypothermia plus standard care to reduce intracranial pressure did not result in outcomes better than those with standard care alone.”
Maintain NORMOTHERMIA (with active treatment of pyrexia)
(Eurotherm) Hypothermia for Intracranial Hypertension after Traumatic Brain Injury Andrews PJD, Sinclair HL, Rodriguez A, et al. N Engl J Med. DOI: 10.1056/NEJMoa150758 MUNRO-KELLIE DOCTRINE
Because the volume of the skull is fixed, the pressure is proportional to the volumes of the compartments within the skull.
Following trauma the volume within the skull can increase due to mass lesions, brain oedema, blocked venous or CSF drainage
Intracrainial hypertension will lead to:
Ischaemia – High ICP lowers the cerebral perfusion pressure (CPP=MAP-ICP).
Herniation – Developing pressure gradient pushes the brain through the foramen magnum disrupting the brainstem.
Because the volume of the skull is fixed, the pressure is proportional to the volumes of the compartments within the skull.
Following trauma the volume within the skull can increase due to mass lesions, brain oedema, blocked venous or CSF drainage
Can also increase due to vasodilation from hypoxia or hypercarbia.
As the volume of one compartment increases the other compartments can decrease to compensate preventing a raise in ICP.
If the volume change is rapid or the compensatory mechanisms of the other compartments are exhausted, the ICP will rise.
If the volume change is rapid or the compensatory mechanisms of the other compartments are exhausted, the ICP will rise.
Intracrainial hypertension will lead to:
Ischaemia – High ICP lowers the cerebral perfusion pressure (CPP=MAP-ICP).
Herniation – Developing pressure gradient pushes the brain through the foramen magnum disrupting the brainstem.
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Normally, cerebral autoregulation maintains cerebral blood flow (CBF) constant over a CPP range of 50-150mmHg.
In TBI the autoregulation can become totally disrupted and CBF becomes directly proportional to CPP.
Also note that as CPP decreases, resistance vessels dilate during normal autoregulation to maintain CBF. Therefore, maintaining an adequate MAP will improve CPP, allow the vessels to constrict, so reducing blood volume and ICP.
Maintaining a MAP 90-100mmHg will maintain CPP (protecting against ischaemia) and help control ICP.
In TBI the autoregulation can become totally disrupted and CBF becomes directly proportional to CPP.
Also note that as CPP decreases, resistance vessels dilate during normal autoregulation to maintain CBF. Therefore, maintaining an adequate MAP will improve CPP, allow the vessels to constrict, so reducing blood volume and ICP.
Maintaining a MAP 90-100mmHg will maintain CPP (protecting against ischaemia) and help control ICP.