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Traumatic Brain Injury Goals : pressure or metabolic ?

Ike Sri Redjeki Bandung

Objectives
What is Traumatic Brain Injury Management of TBI Specific target in the management of TBI Should ICP or Metabolic parameter as target ?

Traumatic Brain Injury


Represents growing health issue around the world The main priority in the initial treatment of TBI is to maintain oxygenation and perfusion in 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

Definition
Traumatic brain injury an acquired injury to the brain caused by an external physical force resulting in total or partial functional disability or psychosocial impairment, or both

Categorization of Brain Injury


Traumatic Brain Injury
isolated multi-system injuries

Hypoxic-ischemic injury Toxic/metabolic injury

Mechanisms of injury
Primary brain injury

At the time of impact : hematoma contusion axonal injury

Mechanisms of injury Secondary brain injury


The consequence of ischemic insults to the brain that occur following the primary injury Pathologic process :
alteration in the balance between CBF and metabolism Disruption of cerebral autoregulation Loss of cerebral vascular reactivity to CO2 Vasogenic fluid accumulation leading to brain swelling

SECONDARY injury TRAUMATIC BRAIN INJURY

BBB disruption edema formation

inflammation

diffuse axonal injury

apoptosis
necrosis

Brain trauma

ischemia energy failure

cytokines
Eicosanoids endocannabinoids

Acetyl Choline

ROS

polyamines

Calcium

Initial Goal in treating TBI


Avoid and correct hypoxemia ( SpO2 < 90%) Avoid hypotension syst < 90 mmHg to maintain CPP(> 70 mmHg) ICP targeted therapy by : reducing intra cranial volume and pressure ICP monitoring and monitor brain tissue oxygenation can be done simultaneously along with CSF drainage Treatment to lower ICP if ICP > 20 25 mmHg Modalities to lower ICP : manitol ( 0.25 1g/kgBB)

Initial Goal in treating TBI


CPP targeted Therapy Lund approach CPP < 50 mmHg is acceptable Microdialysis : CPP < 50 mmHg lactate level was elevated CPP 50 mmHg threshold for insufficient brain injury Bedside monitoring of biochemical variable Maintain CPP can be achieved with fluids and vasopressor

Initial Goal in treating TBI


Maintain brain tissue oxygenation Maintain brain tissue metabolism

CPP the cerebral perfusion deliver O2 and nutrient to brain tissue

Physiology : CPP
CPP = MAP ICP (CPP<70mmHg : poor outcome following HI) MAP>90mmHg and ICP<20~25mmHg

To provide Optimal CPP MAP and ICP balance is important

ICP
ICP control/ management initial treatment become important to maintain sufficient CPP to deliver O2 and nutrient to brain cells

Intracranial hypertension only independent variable predicting cerebral infarction ( OR 13.27 ; CI 2.8- 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

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 and carbohydrates and intra cellular transport molecule Those process depends on conservation of energy Neuronal threshold on compensation for inadequate substrate supply is low

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
Adrenal medula Epinephrn norepinephr Cortison, aldostr, G.H

Hypothalamus

Kidney
Renin, angiotens

Ant pituitary Post pituitary Adr cortex

Pancr islets

ADH
Aldostrn

Glukagon Insulin

Metabolic monitoring in TBI


Jugular Bulb Venous Oxygen Saturation SjPO2 can be measured continuously ( using fiberoptic catheter A-V Jugular Bulb saturation can be related to CBF AjVDO2 = CMRO2/CBF AjVDO2 normally = 1.8 3.9 mol/ml It is hypothesized that variations of AjVDO2 reflect changes in CBF
decrease hypoperfusion or Increase hyperemia

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 CPP prediction

Metabolic parameter
PaO2, PaCO2, pH Cerebral lactate concentration AjVDO2 ( arterial venous jugular bulb oxygen saturation) SjO2

Important metabolic parameter indicate outcome in TBI

Robertson et al
That is not always true in patient with ischemia His study revealed that changes in AjVDO2 were poorly correlated with changes in CBF However if a correction is made for the presence of ischemia, based on low CBF or increase venous lactate concentration the correlation between CBF and 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

Robertson et al
Changes in SjO2 reflect dynamic CBF SjO2 < 40% associated with development of EEG abnormalities, neurologic deterioration, unconsciousness, and depletion of cerebral energy stores indicating cerebral ischemia This result confirm that monitoring SjO2 indicates critical cerebral perfusion - and cerebral consumption

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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