management of traumatic brain injury · falx cerebri tentorium cerebelli falx cerebelli ventricular...
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Management of
Traumatic Brain Injury
What happens, why & what
can we do…
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Levels of Injury
MILD
MODERATE
SEVERE
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The Extent of the Problem
1,000,000
150,000
12,000
17,000
5,000
120,0003
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Who is Most at Risk?
� The risk of TBI in men is twice that of women.
� The risk is higher in adolescents, young adults and people over 75years.
� More than 50% of persons with brain injury were intoxicated at the time of injury.
� Most TBI’s occur mid afternoon to early evening
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Phases of Injury
� First/Primary
�at time of incident
�closed, open or crushing
�not treatable
� Second
�events or injuries worsen original injury
� Third
�occurs days to weeks following first injury
�causes extreme pressure and can be fatal5
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What causes brain damage?
Region at risk
Blood flow reducedby brain swelling
Injured Brain
Lesion core
“Primary Injury”
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Effects of Injury
� Impaired airway reflexes.
� Abnormal respiratory pattern.
� Neurogenic pulmonary oedema.
� Hypertension.
� Cardiac dysrhythmias & ECG
abnormalities.
� Coagulation disturbances.
� Endocrine & electrolyte disturbances
� Stress response
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Key Concepts
� Monro-Kellie Hypothesis
� Brain compliance
� Managing intracranial pressure
� Cerebral Blood Flow & Autoregulation
� Cerebral Metabolism
� Prevention of secondary brain injury
SRP20048
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Cranial compartments
� Dural folds divide up the
cranium into
compartments:
� Falx cerebri
� Tentorium cerebelli
� Falx cerebelli
� Ventricular system
distributes pressure
evenly
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Monro-Kellie Doctrine
“The skull is a rigid
compartment, filled to
capacity with non-
compressible material.
Any increase in the
volume of one component
must be matched by a
corresponding decrease
in one or both of the
others, or intracranial
pressure will rise”
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Monro-Kellie Doctrine
SRP201511
� 3 components in a
rigid compartment.
� Need to measure
pressure effects of
expanding intracranial
mass seen after TBI.
� ICP monitoring first
described in 1951 by
Guillaume & Janny.
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Pressure & Volume
Compensation mechanisms protect the brain from increases in ICP
Decompensation –Small increases in volume result in progressively larger increases in ICP
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Compensation
� Decrease in CSF volume:
� Displacement to lumbar theca
� Decrease in cerebral blood volume:
� Compression of the venous sinuses
� Decrease in CSF production
� Decrease in arterial blood supply
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Compliance� Change in pressure resulting from a change in
volume
Compliance = change in volume
change in pressure
Low compliance – (stiff brain)
High compliance –
(slack brain)
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Factors Increasing ICP
Hypercapnoea
Decreased Venous Drainage
Hypo-osmolar States
Hypertension
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Traditional Therapies
Hyperventilation
Head Elevation
Dehydration
Barbiturates
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Physiology of Cerebral Blood Flow
� Cerebral blood flow (CBF) main determinant of
oxygen and energy supply.
� Normal CBF = 50ml/100g/min.
� CBF <30ml/100g/min leads to symptoms of
failing oxygen supply.
� Ischaemic threshold <20ml/100g/min.
� Effects time dependent and may be reversible.
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The Ischaemic Penumbra
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CBF Following Head Injury
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Manipulating CBF
100
50
0
Cerebral Blood Flow (ml/100g/min)
Cerebral Blood Flow (ml/100g/min)
6 12 18 24
Arterial PO2 (kpa) Arterial PCO2 (kpa)
Response to Oxygen Response to CO2
3 6 9 12
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Autoregulation� Cerebral blood flow: 50ml/100g/min
� Grey matter: 100ml/100g/min
� White matter: 20ml/100g/min
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Autoregulation
50mmHg 150mmHg
C.P.P
CBF
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Blood Pressure Autoregulation
� CBF maintained constant when MABP remains within range.
� CBF heterogenic.
� Autoregulation due to the myogenic response of smooth muscle.
� With a drop in MABP, CBF decreases and oxygen extraction increases.
� Impaired autoregulation can increase regional CBF leading to BBB damage and cerebral oedema.
Mean arterial pressure (mmHg)
C
B
F
Autoregulation
C
B
F
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Cerebral Metabolism
� Need to control metabolism
�high dose barbiturates
�neuromuscular blockade
�Hypothermia
� Need to understand relationship between metabolism and cerebral blood flow
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Therapeutic Hypothermia
� Slows certain secondary processes, e.g. ischaemic rises & brain acidosis
� No definitive level of hypothermia determined
� Mild to moderate reduces release of excitatory amino acids
� Therapy has major implications for nursing care
SRP201525
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CBFMET CBFMETCBFMET
CBFMETCBFMETCBFMET
CBFMET
Increased Cerebral
Blood Flow
Decreased Cerebral
Blood Flow
ISCHAEMIAAPPROPRIATE
CEREBRALPERFUSION
HYPERAEMIA
OXYGEN
EXTRACTION
NORMAL
Fig 1. Relationship of cerebral blood flow and metabolism in the presence of ischaemia and hyperaemia.
Modified from Menon 2000.
Changes in Cerebral Blood Flow
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Primary Injury
Inflammatory Response
Increased vascular permeability& vasodilatation
Vasogenic Oedema
Cerebral Ischaemia &Impaired Autoregulation
Cytotoxic Oedema Decreased ATP Production
Increased Lactic Acidosis
Increased Intracellular Influx
of Sodium, Chloride, Calcium & Water
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Physiological Insults Following Head Injury-Relation to Outcome
Mortality GOS
Duration of hypotension yes yes
(SBP < 90 mmHg )
Duration of hypoxia yes no
(SpO2 < 90%)
Duration of pyrexia yes no
(Tcore > 38oC)
Intracranial hypertension yes no
(ICP > 30 mmHg)
Cerebral perfusion pressure yes no
(CPP < 50 mmHg)
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Initial Management
� Be aware of the effects of a severe brain injury-
�GCS <8 will need airway protection for
transfer
� Maintain effective ventilation-
�Hyperoxygenate
�Mild hyperventilation only for first 24 hours
� Ensure adequate resuscitation-
�Assume ICP of around 30mmHg.29
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Cerebral OedemaVasogenic - Protein rich fluid passes
through damaged blood vessel walls.
Cytotoxic – Fluid accumulates
within the cells.
Interstitial – CSF forced under
pressure into the extracellular space.
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Jugular Bulb
CommonFacial Vein Jugular venous
cannula
InternalJugular Vein
Jugular Bulb Monitoring
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Tissue Oxygen Measurement
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Principles of Microdialysis
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Clinical ApplicationMarkers of Ischaemia
� Fall in brain glucose
� Increase in lactate
� Fall in pyruvate
� Increase in LP ratio
� Increase in glutamate
� Increase in gylcerol