2.dr.ike traumatic brain injury

7/30/2019 2.Dr.ike Traumatic Brain Injury

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Traumatic Brain InjuryGoals : pressure or metabolic ?

Ike Sri Redjeki

Bandung


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Objectives

What is Traumatic Brain Injury

Management of TBI

Specific target in the management of TBI Should ICP or Metabolic parameter as target ?


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Traumatic Brain Injury

Represents growing health issue around theworld

The main priority in the initial treatment of

TBI is to maintain oxygenation and perfusionin order to avoid aggravating secondary injury

No definitive drug or strategy that can be

utilized to provide neuroprotection in TBI Phase III trial unable to demonstrate clinical

efficacy


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Categorization of Brain Injury

Traumatic Brain Injury

isolated

multi-system injuries

Hypoxic-ischemic injury

Toxic/metabolic injury


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Mechanisms of injuryPrimary brain injury

At the time of impact :

hematoma

contusion

axonal injury


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Mechanisms of injury

Secondary brain injury

The consequence of ischemic insults to thebrain that occur following the primary injury

Pathologic process :

alteration in the balance between CBF andmetabolism

Disruption of cerebral autoregulation

Loss of cerebral vascular reactivity to CO2 Vasogenic fluid accumulation leading to brain

swelling


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Brain trauma

BBBdisruption

diffuse axonal

injury

edema

formation

Eicosanoids

endocannabinoids

necrosis

energy failure

cytokines

SECONDARY injury TRAUMATIC BRAIN INJURY

apoptosisinflammation

ROS polyaminesCalciumAcetyl

Choline

ischemia


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Initial Goal in treating TBI

Avoid and correct hypoxemia ( SpO2 < 90%)

Avoid hypotension syst < 90 mmHg to maintainCPP(> 70 mmHg)

ICP targeted therapy by : reducing intra cranialvolume and pressure

ICP monitoring and monitor brain tissue oxygenationcan be done simultaneouslyalong with CSF

drainage Treatment to lower ICP if ICP > 20 25 mmHg

Modalities to lower ICP : manitol ( 0.25 1g/kgBB)


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CPP targeted Therapy

Lund approach CPP < 50 mmHg is acceptable

Microdialysis : CPP < 50 mmHg lactate level

was elevated CPP 50 mmHg threshold forinsufficient brain injury

Bedside monitoring of biochemical variable

Maintain CPP can be achieved with fluids andvasopressor


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Maintain brain tissue oxygenation

Maintain brain tissue metabolism

CPP the cerebral perfusion

deliver O2 and nutrient to brain tissue



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CPP = MAP ICP (CPP90mmHg and ICP


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ICP

ICP control/ management initial

treatment become important tomaintain sufficient CPP to deliver O2 and

nutrient to brain cells


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Intracranial hypertension only independent

variable predicting cerebral infarction ( OR 13.27 ; CI2.8- 62.6 )

ICU mortality was significantly higher in patients

with cerebral infarction ( OR 3.87 ; CI 1.1-14.2 )

3 patients cerebral infarction developed after

operative decompression ( total patients 89 )

Neurology 67 October 2006


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Brain Cell Metabolism

Complex function of CNS are based on generation of

membrane potentials and their synaptic transmission

Require effective ion pumps within cellular

membranes, metabolism of protein, lipids andcarbohydrates and intra cellular transport molecule

Those process depends on conservation of energy

Neuronal threshold on compensation forinadequate substrate supply is low


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Stress Response ( neuroendocrine response )

A. Afferent stimuli

(Hypovolemia, trauma, hypoxemia,pain, anesthesia, MODS, sepsis,toxins &bacteria )

B. Transmitters

( Blood and lymphatics, peripheral nerves, CNS)

C. Effector site

Sympathetic nerv syst Hypothalamus Kidney Pancr

isletsAdrenal medula Ant pituitary Post pituitary

Epinephrn

norepinephr

Adr cortex

Cortison, aldostr,

G.H

ADH

Renin,

angiotens

Glukagon

InsulinAldostrn


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Metabolic monitoring in TBI

Jugular Bulb Venous Oxygen Saturation

SjPO2 can be measured continuously ( usingfiberoptic catheter

A-V Jugular Bulb saturation can be related toCBF

AjVDO2 = CMRO2/CBF

AjVDO2 normally = 1.8 3.9 mol/ml

It is hypothesized that variations of AjVDO2 reflectchanges in CBF decrease hypoperfusion or

Increase hyperemia


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Metabolic monitoring in TBI

Microdialysis : CPP < 50 mmHg lactate level

was elevated CPP 50 mmHg threshold for

insufficient brain injury

Correlation between lactate concentration and CPPprediction


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Metabolic parameter

PaO2, PaCO2, pH

Cerebral lactate concentration

AjVDO2 ( arterial venous jugular bulb oxygen

saturation) SjO2

Important metabolic parameter indicate outcome in

TBI


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Robertson et al

That is not always true in patient with ischemia

His study revealed that changes in AjVDO2 werepoorly correlated with changes in CBF

However if a correction is made for the presence ofischemia, based on low CBF or increase venouslactate concentration the correlation between CBFand AjVDO2 improved to r = 0.74

They suggest that a cerebral lactate oxygen index

less than 0.08 serve as a reliable indicator of ischemia And this index provides a significant indicator of

outcome

Neurosurg 1998- 70 ;22


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Robertson et al

Changes in SjO2 reflect dynamic CBF

SjO2 < 40% associated with developmentof EEG abnormalities, neurologic

deterioration, unconsciousness, and depletionof cerebral energy stores indicating cerebralischemia

This result confirm that monitoring SjO2indicates critical cerebral perfusion - andcerebral consumption


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Conclusions

For a better patient outcome use

Pressure targeted and cerebral metabolic

parameter !!!

Example : hyperventilation ICP decrease

but it was confirmed by SjO2 associated

with worsened CBF


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