UNDERSTANDING
TRAUMATIC BRAIN INJURY
Rachel Garvin, MD
Assistant Professor, Department of Neurosurgery, Neurocritical Care
Assistant Professor, Department of Emergency Medicine
OUTLINE
• Statistics
• Defining TBI
• Secondary injury
• Management strategies
TBI STATS
• 2 million TBI’s treated each year in US, one every 15
seconds
• Up to 2% of US population living with TBI
• Leading cause of M&M in ages 1-44
• Single severe TBI victim can generate 4 million dollars in
lifetime costs
• Adults ages >75 have highest rates of TBI related
hospitalization and death
• 70-90% of TBI worldwide are considered “mild,” 1% of
those require a surgical intervention
http://www.cdc.gov/traumaticbraininjury/data/rates.html
http://www.cdc.gov/traumaticbraininjury/data/dist_ed.html
CLASSIFICATION OF TBI
• Pathoanatomic
• Physical Mechanism
• Pathophysiologic
• Injury Severity
Pathoanatomic
Epidural
Subdural
Subarachnoid
Contusion
Axonal injury
KNOWING ANATOMY IS IMPORTANT
PHYSICAL MECHANISM
•
Impact vs Inertial loading
INJURY SEVERITY
• GCS
• 13-15  Mild TBI
• 9-12  Moderate TBI
• <8  Severe TBI
PATHOPHYSIOLOGIC
• Primary Injury
• Immediate damage done
• Secondary Injury
• Excitotoxic cascade
• Potentially avoidable factors
• Hypoxia, hypotension, hypercarbia,
hyponatremia, seizures
SECONDARY INJURY
GLUTAMATE’S TOXIC EFFECTS
TIME MATTERS
GOALS OF TBI MANAGEMENT
• Preventing secondary injury
• ICP
• CPP
• Neuroprotection
• Good neurologic recovery
PREVENTING SECONDARY INJURY
• Keeping things “normal”
• Avoid processes that increase CMRO2
• Avoiding processes that increase ICP
• Maintain CPP
CEREBRAL METABOLISM
• CMRO2 rate 3.5ml/100g/min
• Accounts for 20% of O2 consumption at rest
• Average blood flow of 50ml/100g/min
• CBF <20ml/100g/min = risk for permanent neurologic damage
• CBF <10ml/100g/min = neuronal death
• Uses glucose as primary substrate
• >90% glucose consumption is oxidative
• <5% metabolized to lactate
• <1% ketones and others
FICK EQUATION
• CMRO2 = CBF x AVDO2
• AVDO2 = CaO2 – CjvO2
•
CBF = CPP/CVR
•
CMRO2 = cerebral metabolic rate of oxygen
•
AVDO2 = arterio-venous difference in oxygen
CEREBRAL AUTOREGULATION
BRAIN COMPLIANCE
CAUSES OF INCREASED ICP
• Intracranial
• Extracranial
• Hematomas/Contusi
ons
• Hypoxia
• Ischemia
• Hyper/Hypotension
• Hydrocephalus
• Increased CBF
• Hypercarbia
• Head rotation
• Fever
• Seizure
• Increased
intraabdominal pressure
DO WE NEED TO MONITOR ICP
DOES MONITORING ICP IMPROVE OUTCOMES
• Multicenter, randomized, parallel-group trial
• ICP monitor vs imaging and clinical exam
• Inclusion: >13, GCS 3-8
• Groups stratified up by age and severity of injury
• Baseline CT, 48 hours and 5-7 days
• 6 month outcomes with 21 components
MANAGEMENT OF TBI
• ABC’s
• Preventing secondary injury
• ICP management
• Emergent therapies
ABC’S
• Airway
• Avoiding hypoxia
• RSI
• Post-intubation sedation
• Breathing
• Normocarbia
• Circulation
• Avoiding hypotension
TIERED APPROACH TO ICP MANAGEMENT
• Positioning
• Sedation
• Fentanyl, Propofol, Ketamine
• HTS vs Mannitol
• Pentobarbital
• Surgery
• Literature review
• Primary outcome: ICP post-ketamine
• Secondary outcome: CPP, MABP, patient outcome,
AE
• Level of evidence assessment (Oxford and GRADE)
• 371 articles  7 articles
• 4 studies with continuous infusion
RESULTS
• Continuous Infusion:
• ICP: no clinically significant difference
• CPP and MABP: 2 studies no difference; 2 studies
increase
• Bolus Dosing:
• ICP: no increase; trend towards decrease
• CPP and MABP: 2 no effect documented; 3 rd
increase CPP and decrease MABP
LEVELS OF EVIDENCE
• GRADE level of evidence:
• 2 studies GRADE B
• 4 studies GRADE C
• 1 study GRADE D
• Oxford level of evidence:
• 6 studies level 2b
• 1 level 4
Recommendations: Oxford 2b, GRADE C level of
evidence to support that ketamine does not increase ICP
ICP MONITORS
Most often placed within ventricle or brain
parenchyma
•
Waveforms P1-P3
• P1: percussion wave
• Reflects arterial pressure
transmitted through choroid
• P2: tidal wave
• Represents cerebral compliance
• P3: dicrotic wave
• Represents venous pressure
MULTI-MODAL MONITORING
• PBtO2
• Microdialysis
• Brain Temperature
Monitoring
• SjvO2
• CBV
EMERGENT TREATMENT
• Hyperventilation
• Decompressive Hemicraniectomy
HYPERVENTILATION
• Decreased PaCO2 alkalinizing CSF  cerebral
vasoconstriction
• Decreased CBV  decreased ICP
• Effects last around 15 hours until CSF pH equilibrates
• Then there is re-dilation of cerebral arteries  rebound
ICP
MANNITOL VS HYPERTONIC SALINE
• Mannitol
• HTS
• Rheologic and
osmotic effects
• Rheologic and
Osmotic effect
• Osmotic effects
• Can be used in
hypovolemic pts
• Crosses BBB
• Contraindicated in
hypovolemic pts
• Can cause
hyperchloremic
acidosis
HYPEROSMOLAR THERAPY
DECOMPRESSIVE HEMICRANI
• For expanding lesions
associated with
declining neuro status
• Prophylactic
• Need cranioplasty later
on
DECOMPRESSIVE HEMICRANI
• Used since the 1970’s
• Mostly salvage technique
• DECRA trial 2011
DECOMPRESSIVE HEMICRANI
OTHER THERAPIES
• Hypothermia
• Progesterone
• ProTECT III -> results now showed no improvement
• Statins
• Citicoline
• Cyclosporine A
PREDICTING OUTCOMES
• Clinical predictors:
• Age, post-resuscitation GCS, hypotension, hypoxia,
pupils, multi-system injury
• Radiologic Predictors:
• Absent basal cisterns, midline shift, SAH, brainstem
injury
• CRASH and IMPACT prognostic scoring
SUMMARY
• TBI is common and severe TBI can have devastating
consequences
• Controlling secondary injury and the excitotoxic cascade are
imperative
• ICP, CPP and multi-modality monitoring helpful but data limited
• Hypertonic saline for hyperosmolar therapy
• Surgery is an option
• Prognosis is challenging
QUESTIONS?
REFERENCES
•
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•
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•
Le Roux et al. Consensus Summary Statement of the International Multidisciplinary Consensus Conference on Multimodality Moni toring in
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