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Traumatic Brain InjuryTraumatic Brain Injury
Galen V. Henderson, M.D.Brigham and Women’s Hospital
Harvard Medical School
Outline
• Epidemiology• Concussion• Types of hemorrhages with TBI• Treatment of intracranial HTN• Penetrating injuries• Surgical decompression• Intracranial monitoring vs. neuro
exam and cerebraling
TBI in the United States
52,000 Deaths
275,000Hospitalizations
1,365,000Emergency Department Visits
??? Receiving Other Medical Care or No Care
At least 1.7 million
TBIs occur in the United States
each year.*
* Average annual numbers, 1995-2001
Causes of Death in US, Causes of Death in US, 20122012
(37/100,000)
Causes of Death in US, Causes of Death in US, 20122012
Age > 65: Accidents are #9 cause of death; rate 94.5/100,000
Classification of Head Classification of Head (Brain) Injury(Brain) Injury MinimalMinimal
GCS 15GCS 15
MildMild GCS 14-15GCS 14-15
ModerateModerate GCS 9-13GCS 9-13
SevereSevere GCS GCS << 8 8
Glasgow Coma ScaleGlasgow Coma ScaleBest Motor Response:Best Motor Response:
ObeysObeys 66Localizes painLocalizes pain 55Flexion withdrawalFlexion withdrawal 44Flexion abnormal (decorticate rigidity)Flexion abnormal (decorticate rigidity) 33Extension (decerebrate rigidity)Extension (decerebrate rigidity) 22No responseNo response 11
Best Verbal Response:Best Verbal Response:Oriented and conversesOriented and converses 55Disoriented and conversesDisoriented and converses 44Inappropriate wordsInappropriate words 33Incomprehensible soundsIncomprehensible sounds 22No responseNo response 11
Eye Opening:Eye Opening:SpontaneouslySpontaneously 44To verbal stimuliTo verbal stimuli 33To painTo pain 22Never Never 11
3-3-1515
ConcussionConcussion Immediate and transient loss of consciousnessImmediate and transient loss of consciousness accompanied by a brief accompanied by a brief
period of amnesia after a blow to theperiod of amnesia after a blow to the head. head.
128/100,000 population in the US128/100,000 population in the US
The clinicalThe clinical status of the momentary sensation of being "starstruck," orstatus of the momentary sensation of being "starstruck," or
dazed, after head injury without a brief period of loss of consciousnessdazed, after head injury without a brief period of loss of consciousness is is uncertain, but it is generally considered the mildest formuncertain, but it is generally considered the mildest form of concussion.of concussion.
Young children have the highest rates.Young children have the highest rates. Sports and bicycle accidents account for the majority of casesSports and bicycle accidents account for the majority of cases
among 5- to 14-year-oldsamong 5- to 14-year-olds
Falls and vehicular accidentsFalls and vehicular accidents are the most common causes of are the most common causes of concussion in adults.concussion in adults.
Mechanism of Concussion
Ropper A, Gorson K. N Engl J Med 2007;356:166-172
Somatic Symptoms
Persistent low grade headache
Dizziness
Vertigo
Fatigability
Insomnia
Nausea/vomiting
Symptoms of post-concussive syndrome
Mood
Anxiety
Depression
Irritability
Cognitive Deficits
Slow thinking
Poor attention and concentration
Impaired memory
fMRI and symptom severityfMRI and symptom severity
Control group
Low PCS group
Moderate PCS group
High PCS group0
0.1
0.2
0.3
0.4
0.5
∆ B
OL
D
(%)
2
0
0.1
0.2
0.3
0.4
**
∆ B
OL
D
(%)
1
Chen JK, Johnston KM, Collie A, McCrory P, Ptito A. J Neurol Neurosurg Psychiatry 2007; 78(11): 1231-1238.
12
Control Low PCS Moderate PCS High PCS
Spectrum of
Pathologic Features
and Outcomes
of Traumatic
Brain Injury
DeKosky ST et al. N Engl J Med 2010;363:1293-1296.
Epidural HemorrhageEpidural Hemorrhage Occurs in about 3% of head injuriesOccurs in about 3% of head injuries
Acute presentation; 40% have lucid interval with Acute presentation; 40% have lucid interval with delayed (hrs) LOCdelayed (hrs) LOC
90% have skull fx; 85% of these are temporal90% have skull fx; 85% of these are temporal
Children get EDHs without fxChildren get EDHs without fx
Elderly rarely get EDHs – dura firmly adherentElderly rarely get EDHs – dura firmly adherent
Amount of blood seen in fatal EDHs is 100-150mlAmount of blood seen in fatal EDHs is 100-150ml
Source of bloodSource of blood Torn meningeal vesselsTorn meningeal vessels Torn dural sinusTorn dural sinus Diploic veinsDiploic veins Marrow sinusoidsMarrow sinusoids
Epidural HemorrhageEpidural Hemorrhage
Hyperdense Bi-ConcaveHyperdense Bi-Concave
Limited by sutures (unless Limited by sutures (unless fracture crossed suture fracture crossed suture line)line)
Subdural HemorrhageSubdural Hemorrhage Acute to subacute presentationAcute to subacute presentation
Associated with severe trauma (except in elderly and Associated with severe trauma (except in elderly and especially those with coagulopathy)especially those with coagulopathy)
Associated with non-traumatic events (hypertensive Associated with non-traumatic events (hypertensive hemorrhage or ruptured AVM with SAH/SDHhemorrhage or ruptured AVM with SAH/SDH
Source of bloodSource of blood Torn bridging veinsTorn bridging veins Laceration of cortical vesselsLaceration of cortical vessels Expanding contusion hematomaExpanding contusion hematoma
Acute SDHAcute SDH
50% associated with a skull fx (not always 50% associated with a skull fx (not always at site of SDH)at site of SDH)
Most lethal form of SDH; 40-60% mortality Most lethal form of SDH; 40-60% mortality raterate
Frequently associated with other forms of Frequently associated with other forms of injury (DAI, contusions etc.)injury (DAI, contusions etc.)
Acute SDHAcute SDH
Amount of blood which is Amount of blood which is ““significantsignificant”” depends on pt age and rate of accumulationdepends on pt age and rate of accumulation
Infants: few mlsInfants: few mls
Toddlers: 30-50 mlToddlers: 30-50 ml
Children and adults: 150-200 mlChildren and adults: 150-200 ml
Subarachnoid HemorrhageSubarachnoid Hemorrhage
TraumaticTraumatic Most common causeMost common cause Seen in almost any significant injury (+/- impact)Seen in almost any significant injury (+/- impact)
In areas of contusions, lacerations, penetrating injuriesIn areas of contusions, lacerations, penetrating injuries Under SDHs where traction on bridging veins tears Under SDHs where traction on bridging veins tears
arachnoid vesselsarachnoid vessels
Non-traumaticNon-traumatic Ruptured aneurysm/vascular malformationRuptured aneurysm/vascular malformation Torn/dissection of vertebral arteryTorn/dissection of vertebral artery
Acceleration/DecelerationAcceleration/Deceleration Brain:Brain:
SDHSDH Diffuse vascular injuryDiffuse vascular injury Traumatic axonal injuryTraumatic axonal injury Contusional TearsContusional Tears
Eye:Eye: Retinal hemorrhages, Optic nerve Retinal hemorrhages, Optic nerve
sheath hemorrhagesheath hemorrhage Spine:Spine:
StretchingStretching
Gunshot WoundsGunshot Wounds
Damage is dependent on energy of Damage is dependent on energy of missile which is dependent on the missile which is dependent on the velocityvelocity
Tissue damageTissue damage Permanent track of bulletPermanent track of bullet Temporary cavity which follows bulletTemporary cavity which follows bullet
Low-velocity bullet: 4-5 x bullet sizeLow-velocity bullet: 4-5 x bullet size Hi-velocity bullet: up to 15 times bullet sizeHi-velocity bullet: up to 15 times bullet size
Secondary missiles (bone fragments)Secondary missiles (bone fragments)
Gunshot WoundsGunshot Wounds
Low Velocity Bullets (most civilian handguns)Low Velocity Bullets (most civilian handguns) Most often do not exit skullMost often do not exit skull Ricochet off inner table to form secondary trackRicochet off inner table to form secondary track Exhaust energy and come to rest in brainExhaust energy and come to rest in brain
High Velocity Bullets or Shotgun at close/contact High Velocity Bullets or Shotgun at close/contact rangerange Most often exit skull producing massive fracturesMost often exit skull producing massive fractures Large temporary cavityLarge temporary cavity Often thrusts much of brain out of headOften thrusts much of brain out of head
DON’T FORGET TO PROTECT THE C-SPINE !!
Hemopericardium
Liver lacerations
FACTORS CAUSING SECONDARY BRAIN INJURY
THE 4 H’s• HYPERCAPNEA
• HYPOXIA ( PaO2 < 60 mmHg; SpO2 < 90%)
• • SYSTEMIC HYPOTENSION ( < 90 mmHg )
• INTRACRANIAL HYPERTENSION
OTHER FACTORS CAUSING SECONDARY BRAIN INJURY
ISCHEMIA
VASOSPASM
SEIZURES
LOSS OF AUTOREGULATION
Intracranial HTN Treatment ModalitiesIntracranial HTN Treatment Modalities
Insert ICP monitorInsert ICP monitor General goals: Maintain ICP < 20 mm Hg and CPP > General goals: Maintain ICP < 20 mm Hg and CPP >
70 mm Hg70 mm Hg For ICP > 20-25 mm Hg for > 5 minutesFor ICP > 20-25 mm Hg for > 5 minutes
Drain CSF via ventriculostomyDrain CSF via ventriculostomy Elevate head of bedElevate head of bed OsmotherapyOsmotherapy Sedation, agitation and fever controlSedation, agitation and fever control HyperventilationHyperventilation Pressor therapy to maintain MAP and ensure CPPPressor therapy to maintain MAP and ensure CPP
For refractory intracranial HTNFor refractory intracranial HTN Phenobarbital/Hypothermia/Decompressive Phenobarbital/Hypothermia/Decompressive
craniotomycraniotomy
Osmolality of IV fluidsOsmolality of IV fluids
Fluid Osmolality (mOsm/kg)
5% Dextrose 252
Lactated ringers 250-260
Plasma 285
5% Albumin 290
Normal Saline 0.9% 308
25% Albumin 310
6% Hetastarch 310
2% Normal Saline 682
3% Normal Saline 1025
25% Mannitol 1375
7.5% Normal Saline
23.4% Normal Saline
2400
8008
Surgical Treatment of Surgical Treatment of Intracranial HTNIntracranial HTN
Original Article Decompressive Craniectomy in Diffuse Traumatic
Brain Injury
D. James Cooper, M.D., Jeffrey V. Rosenfeld, M.D., Lynnette Murray, B.App.Sci., Yaseen M. Arabi, M.D., Andrew R. Davies, M.B., B.S., Paul D'Urso, Ph.D., Thomas
Kossmann, M.D., Jennie Ponsford, Ph.D., Ian Seppelt, M.B., B.S., Peter Reilly, M.D., Rory Wolfe, Ph.D., for the DECRA Trial Investigators and the Australian and New
Zealand Intensive Care Society Clinical Trials Group
N Engl J MedVolume 364(16):1493-1502
April 21, 2011
Study Overview
• Patients with severe traumatic brain Patients with severe traumatic brain injury and refractory intracranial injury and refractory intracranial hypertension were randomly assigned hypertension were randomly assigned to either decompressive craniectomy or to either decompressive craniectomy or standard care.standard care.
• Craniectomy was associated with a Craniectomy was associated with a significant reduction in intracranial significant reduction in intracranial pressure but worse outcomes.pressure but worse outcomes.
.
Cooper DJ et al. N Engl J Med 2011;364:1493-1502
.
Cooper DJ et al. N Engl J Med 2011;364:1493-1502
Original Article A Trial of Intracranial-Pressure Monitoring in
Traumatic Brain Injury
Randall M. Chesnut, M.D., Nancy Temkin, Ph.D., Nancy Carney, Ph.D., Sureyya Dikmen, Ph.D., Carlos Rondina, M.D., Walter Videtta, M.D., Gustavo Petroni, M.D.,
Silvia Lujan, M.D., Jim Pridgeon, M.H.A., Jason Barber, M.S., Joan Machamer, M.A., Kelley Chaddock, B.A., Juanita M. Celix, M.D., Marianna Cherner, Ph.D., and Terence
Hendrix, B.A.
N Engl J MedVolume 367(26):2471-2481
December 27, 2012
Study Overview
• In this randomized trial involving 324 In this randomized trial involving 324 patients with severe traumatic brain patients with severe traumatic brain injury in Bolivia and Ecuador, guideline-injury in Bolivia and Ecuador, guideline-based management with intracranial based management with intracranial pressure monitoring was not superior to pressure monitoring was not superior to management based on imaging and management based on imaging and clinical assessments.clinical assessments.
Cumulative Survival Rate According to Study Group.
Chesnut RM et al. N Engl J Med 2012;367:2471-2481
Cellular Cellular MetabolismMetabolism
ICPICP
ExamExam
EEGEEG
CPPCPP
TCDTCDMAPMAP
Summary
• Epidemiology• Concussion• Types of hemorrhages with TBI• Treatment of intracranial HTN• Penetrating injuries• Surgical decompression• Intracranial monitoring vs. neuro
exam and cerebral imaging
Thank You For Your AttentionThank You For Your Attention