Brain Resuscitation

1
Brain Resuscitation

• Dr Neil Orford
• Oct 2006

2
Introduction

• Cerebral resuscitation ?
• Situations where primary brain insult occurs.
• Management directed towards prevention of
  secondary brain insult

3
Cerebral Insults

• TBI (traumatic brain injury)
• Hypoxic brain injury
• Cardiac surgery
• Status epilepticus
• Metabolic encephalopathy
• others

4
Secondary Injury

• Brain injury not due to primary insult
• multiple insults all end up in reduced cellular
  perfusion
• hypoxia
• hypotension
• cerebral oedema
• intracellular changes
• metabolic

5
Physiology

• CDO2 CBF x CaO2 (Hb, SpO2)
• CBF CPP
• CVR
• CPP MAP - ICP (or CVP)

MAP
ICP,CVP
CVR
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Physiology

• Cerebral DO2 twiddling
• MAP
• CVP
• ICP
• CVR
• O2 content

ICP,CVP
MAP
Hb,SpO2
CVR
7
Physiology - ICP

• Monro-Kellie doctrine rigid cranial vault,
  fixed volume.
• Contents
• Brain - 1350 mls
• Blood volume - 75 mls
• CSF volume - 75 mls
• Increase volume one of these must be associated
  with decrease in others (squeezing out hole in
  bottom)

8
Physiology- CVR

• Controlled by
• Autoregulation
• CO2
• O2
• Metabolism - cerebral metabolic rate

9
Brain Resuscitation - Aims

• To maintain perfusion of viable brain and thereby
  prevent secondary injury
• Achieve this by trying to control
• SpO2
• MAP
• ICP
• CVP
• CVR
• CMRO2

ICP,CVP
MAP
SpO2
CVR
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Traumatic Brain Injury

• Major cause morbidity and mortality in
  industrialised countries
• Statistics
• 150 000 trauma death/yr US
• 50 000 TBI/yr die
• 15-35 males(2.51) highest risk
• RTAs biggest cause
• Devastating social problem

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TBI
12
TBI
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TBI Classification Severity
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TBI classification Morphology Primary Injury
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TBI classification - CT Head
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CT Brain
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CT Brain
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TBI - Cerebral Circulation

• Triphasic response to TBI
• Hypoperfusion 24-72 hrs
• Hyperaemia D3 - D5
• Vasospasm gtD5

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Stage 1 Hypoperfusion

• Mechanism
• Intra-cerebral
• Vasoconstriction
• Intravascular thrombosis
• External microvascular compression
• Extra-cerebral
• Hypotension
• Hypovolaemia
• Hyperventilation

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Stage 1 Hypoperfusion

• Early restoration CBF may reduce cerebral oedema
  in 1st 24 hrs

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TBI - What to do?

• Guidelines
• Brain Trauma Foundation (USA) - evidence based
  guidelines, looked at 13 areas and published
• Standards
• Guidelines
• Options
• European Brain Injury - expert opinion

22
TBI - management

• Trauma systems - insufficient data
• Blood pressure and oxygen - G/O
• ICP monitor - G
• Intracranial hypertension - G
• Hyperventilation - S/G/O
• Barbituates - G
• Anticonvulsants - S/O
• Enteral feed- G/O
• Mannitol - G/O
• Glucocorticoids - S

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Hypoxia/hypotension
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TBI - BP and PaO2

• Current recommendations are
• Guidelines
• SBP gt 90 mmHg
• PaO2 gt 60 mmHg
• Options
• CPP gt 70 mmHg or MAP gt 90 mmHg
• Practice
• Fill
• Noradrenaline
• What fluid, which inotrope to resuscitate with

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TBI - Fluid resusc
Cooper,Myles,McDermott,Bernard et al. JAMA, 2004.
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TBI - Fluid Resusc

• SAFE (ANZICS CTG)
• Overall equivalent outcomes N.Saline vs 4
  albumin used for fluid resuscitation
• TBI subgroup
• Subgroup analysis show outcome approach
  significance for better outcome with N.Saline
• Currently reviewing charts to see if bias, etc.
• Should we avoid albumin for fluid resusc in TBI

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Vasopressors
CCM April 20041049-1060. Direct comparison of
cerebrovascular effects of noradrenaline and
dopamine in head injured patients CPP adjusted
65,75,85 mmHg, measured TCD Dopamine more
variable and inconsistent Noradrenaline may be
more predictable and efficient to augment
cerebral perfusion in patients with TBI.
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Vasopressors
Catecholamines in anaesthetised sheep. Myburgh
etal. AIC 2002
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TBI - ICP monitor

• GCS lt 8
• Abnormal CT 50-60 ICH
• Diffuse injury Gr II-IV
• Mass lesion with shift
• Normal CT 13 ICH
• gt40 yrs
• Uni/bilateral posturing
• SBPlt90
• If 2 of above, gt50 risk ICH

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TBI - ICP elevation

• Clinical
• Uni/bilateral pupil dilate
• Asymmetric pupil reactivity
• Abnormal posturing
• Deteriorating neurological state

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TBI - ICP elevation

• ICP monitor
• Normal 0-10 mmHg
• gt20 mmHg - major predictive factor for worse
  outcome

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TBI - ICP elevation

• Management - aim to maintain CBF
• Evacuate mass (?ICP)
• Prevent venous obstruction
• Drain CSF (?ICP)
• CPP gt 70 (?CPP ? ?CBF)
• Sedate, paralyse (?CMRO2,CBF,ICP)
• Hyperosmolar therapy (?Brain volume ? ?ICP)
• Acute hyperventilate (?blood volume? ?ICPgtCBF)
• Decompress take the lid off (?ICP)

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Hyperosmolar therapy

• Intracranial hypertension
• Aim to increase intravascular osmolality and suck
  water out of brain, reduce volume, reduce ICP
• Choices
• Mannitol
• Hypertonic Saline
• Problems
• Osmotic diuresis?hypovolaemia
• Cross BBB ? increase oedema, neurotoxicity
• Recommended for intracranial hypertension

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TBI - CO2

• Prophylactic hyperventilation NOT indicated
  (level 1 evidence BTF)
• First 24 hrs reduced CBF
• CO2 lt30mmHg further decrease, associated with
  worse outcome
• Hyperventilationrestrict for brief periods when
  clinical or direct evidence of ICH.

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TBI - CVP

• 30 head up
• Neutral head position
• No neck ties
• Prevent cough, strain
• Minimal PEEP

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TBI-seizure prophylaxis

• Seizures
• Increase ICP, CVP, CMRO2,CO2
• Early day 0-7
• Late gt day 7
• Current recommendation phenytoin in SHI reduce
  early seizure incidence, but no effect on outcome

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Early surgery

• Surgery
• Surgery hypotension and hypoxia
• Non-urgent surgery - avoid any non life or limb
  threatening surgery
• First 24 hrs patch up surgery only, delay
  definitive

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Take the lid off

• Decompressive craniectomy long use as salvage for
  intractable ICH
• DECRA - early decompressive craniectomy if ICP
  gt20 for 20 minutes despite medical therapy

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Cerebral metabolic rate

• CMRO2 - metabolic activity parallels blood flow,
  both regionally and globally.
• Highest cerebral cortex
• Reduced by
• Sleep
• Hypothermia (37?27?C, ?50)
• Sedation (barbituate, propofolgt benzo, narcotic)

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TBI-Barbituates

• Theoretical improvement
• No evidence for improve outcome
• Barbituates, propofol most effective, reduce
  CMRO2, CBF, ICP but
• associated reduction MAP,CPP
• Barb prolonged effect
• Barb assoc immunosuppression VAP

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Stage 2 - Hyperaemia

• Mechanism
• Intra-cranial
• Reperfusion injury
• Hyperglycolysis
• Vasoplegia
• Extra-cranial
• Augment CPP
• Catecholamines ( cross BBB??CMRO2 ??ICP)
• Osmotic agents

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Stage 2 - Hyperaemia

• Diagnosis
• D3 onwards of ICH on Noradr to maintain CPP gt70,
  hyperosmolar, etc..
• ICP continues to rise, increasing NA
• Re-evaluate target ?
• Lower CPP D3,4 55-60 mmHg
• Is ICP correct - drift
• Measure CBF ( SjO2, Doppler)
• Early decompression craniectomy
• Consider medical therapies

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Stage 2 - Hyperaemia

• Medical therapies
• Vasoconstrictor / hypotensive (Lund)
• D1,2
• EVD,SjO2,xenon
• Low dose barbs, modest hyperosmolar, steroids for
  temp
• D3
• Metoprolol, clonidine for MAP 80 mmHg
• ICPs fell
• ie, dont push brain too hard D3.
• Hypothermia
• No studies after D3

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Stage 2 - Hyperaemia

• SjO2
• Not widely used
• Macmillan 2001
• 55-75 OK
• lt50 bad
• gt75 bad - ? hyperaemia

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Stage 3 - Vasospasm

• Measure
• Angio
• Doppler
• Xenon
• AVDO2
• Incidence lt15 _at_ D10-12
• Treat
• Restore MAP
• Nimodipine - no role
• HHH (hypertensive, hypervolaemic, hemodilute) -
  no role

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Outcome
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Conclusion

• Dont get into car with 18-24 yr males
• Dont drive between 10pm-6am
• Find a route to work which involves left turns
  only
• Get airbags