Rachel Garvin, MD

Assistant Professor, Department of Neurosurgery, Neurocritical Care

Assistant Professor, Department of Emergency Medicine

UNDERSTANDING TRAUMATIC BRAIN INJURY

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

• Intracranial

• Hematomas/Contusions

• Ischemia

• Hydrocephalus

• Increased CBF

• Extracranial• Hypoxia

• Hypercarbia

• Hyper/Hypotension

• Head rotation

• Fever

• Seizure

• Increased intraabdominal pressure

CAUSES OF INCREASED ICP

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; 3rd 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

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

ICP MONITORS

• PBtO2

• Microdialysis

• Brain Temperature Monitoring

• SjvO2

• CBV

MULTI-MODAL MONITORING

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

• Rheologic and osmotic effects

• Osmotic effects

• Crosses BBB

• Contraindicated in hypovolemic pts

• HTS

• Rheologic and Osmotic effect

• Can be used in hypovolemic pts

• Can cause hyperchloremic acidosis

MANNITOL VS HYPERTONIC SALINE

HYPEROSMOLAR THERAPY

• For expanding lesions associated with declining neuro status

• Prophylactic

• Need cranioplasty later on

DECOMPRESSIVE HEMICRANI

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• Bazarian JJ, McClung J, Cheng YT, Flesher W, Schneider SM. Emergency department management of mild traumatic brain injury in the USA.

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• Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury. Journal of Neurotrauma 2007; 24

• Chestnut RM et al. A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury. N Engl J Med 2012; 367: 2471-81.

• Le Roux et al. Consensus Summary Statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care. Neurocrit Care. Published online 11 September 2014.

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• Roberts et al. Sedation for critically ill adults with severe traumatic brain injury: A systematic review of randomized controlled trials. Crit Care Med 2011; 39(12): 2743-2751

• Roozenbeek et al. Prediction of Outcome after Moderate and Severe Traumatic Brain Injury: External Validation of the IMPACT and CRASH Prognostic Models. Crit Care Med 2012; 40(5): 1609-1617

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• Sterr A, Herron K, Hayward C, Montaldi D. Are mild head injuries as mild as we think? Neurobehavioral concomittants of chronic post-concussion syndrome. BMC Neurology 2006: 1471-2377

• Spiotta AM, Stiefel MF, Gracias VH, Garuffe AM, Kofke WA, Maloney-Wilensky E, Troxel AB, Levine JM, Le Roux PD. Brain tissue oxygen-directed management and outcome in patients with severe traumatic brain injury. J Neurosurg 2010: 113: 571-580

• Thompson HJ, McCormick WC, Kagan SH. Traumatic brain injury in older adults: Epidemiology, outcomes, and future implications.

• Torre-Healy A, Marko NF, Weil RJ. Hyperosmolar Therapy for Intracranial Hypertension. Neurocrit Care 2012; 17: 117-130.