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Project: Ghana Emergency Medicine Collaborative
Document Title: Traumatic Brain Injury
Author(s): Mark Rosner MD, 2012
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22
Traumatic Brain InjuryTraumatic Brain Injury
Mark Rosner MDMark Rosner MD
September 15, 2010September 15, 2010
33
Goals and ObjectivesGoals and Objectives Demographics of TBIDemographics of TBI Pathophysiology of TBI – Primary & Pathophysiology of TBI – Primary &
Secondary InjurySecondary Injury Assessment & Treatment of Mild TBI / Assessment & Treatment of Mild TBI /
Concussion Concussion Second Impact Syndrome and Return to Second Impact Syndrome and Return to
Play guidelinesPlay guidelines Post Concussive SyndromePost Concussive Syndrome TBI & Binocular Vision Dysfunction (VH)TBI & Binocular Vision Dysfunction (VH) Management of Severe TBIManagement of Severe TBI Management of Post Traumatic AgitationManagement of Post Traumatic Agitation
44
STRAP UP! STRAP UP!
Leo Dirac (Flickr) 2007
55
TBI – Demographics TBI – Demographics
1.5 million new cases per year in the 1.5 million new cases per year in the USUS
Could be 15-20% higher due to Could be 15-20% higher due to underreporting of mild TBI / underreporting of mild TBI / concussionsconcussions
Leading cause of death in US for Leading cause of death in US for ages 1-45 ages 1-45
66
TBI – DemographicsTBI – Demographics
Risk factors:Risk factors: Sex: males 2.5:1 femalesSex: males 2.5:1 females Lower socioeconomic statusLower socioeconomic status AgeAge
– 0-40-4– 15-24 (1/2 of all injuries)15-24 (1/2 of all injuries)– >65>65
77
TBI – DemographicsTBI – Demographics
Mortality = 2%Mortality = 2% ER & Go Home (mild TBI) = 65%ER & Go Home (mild TBI) = 65% ER & Admit (mod / severe) = 16%ER & Admit (mod / severe) = 16% Never came to the ER (mild TBI / Never came to the ER (mild TBI /
concussion) = approximately 17%concussion) = approximately 17%
88
TBI – DemographicsTBI – Demographics
Leading causes of TBI:Leading causes of TBI: Falls (older) = 30%Falls (older) = 30% MVC (young adults) = 45%MVC (young adults) = 45% Violence (lower socioeconomic Violence (lower socioeconomic
class)= 5%class)= 5% Work accidents = 10%Work accidents = 10% Recreational accidents = 10%Recreational accidents = 10%
99
TBI – DemographicsTBI – Demographics
Recreational Accidents – SportsRecreational Accidents – Sports Ice HockeyIce Hockey SoccerSoccer BoxingBoxing RugbyRugby Football Football
– incidence = 10% college incidence = 10% college 20% high school20% high school
PER YEAR!PER YEAR!
1010
TBI – DemographicsTBI – Demographics
Combat relatedCombat related In a 1 year deployment – head injury:In a 1 year deployment – head injury:
– 10% had change in MS10% had change in MS– 5% had LOC 5% had LOC
due to due to – Blasts / explosionsBlasts / explosions– FallsFalls– MVAMVA– Penetrating woundsPenetrating wounds
15% TBI rate
1111
TBI – DemographicsTBI – Demographics
DisabilityDisability 1-2% US population (3-5 million) has 1-2% US population (3-5 million) has
LTD (neurologic and functional LTD (neurologic and functional impairment) due to mod / severe TBI impairment) due to mod / severe TBI
What about mild TBI!! Under-What about mild TBI!! Under-recognized as cause of disabilityrecognized as cause of disability
Military has not been considering Military has not been considering soldiers w/ mild TBI for Purple Heartsoldiers w/ mild TBI for Purple Heart
1212
TBI – ClassificationTBI – Classification
Clinical Severity Scores:Clinical Severity Scores:
GCS:GCS: Severe Severe << 8 8 Moderate = 9-12 (13)Moderate = 9-12 (13) Mild = 13 (14) - 15Mild = 13 (14) - 15
1313
TABLE 1 Using Glasgow Coma Scale
scores to evaluate brain injury severity
Component
Response Score
Best eye response No eye opening 1
Eye opening to pain 2
Eye opening to verbal command 3
Eyes open spontaneously 4
Best verbal response No verbal response 1
Incomprehensible sounds 2
Inappropriate words 3
Confused 4
Oriented 5
Best motor response No motor response 1
Extension to pain 2
Flexion to pain 3
Withdrawal from pain 4
Localizing pain 5
Obeys commands 6
GCS total score ≥12 is mild injury, 9 to 11 is moderate, and ≤8 is severe (90% of patients with scores ≤8 are in a coma). Coma is defined as not opening eyes, not obeying commands, and not saying understandable words. Composite scores with eye, verbal, and motor responses (such as E3V3M5) are clinically more useful than totals.
Source: Reference 2. Source Undetermined
1414
Michael Spencer (Flickr) 2009
1515
TABLE 1 Using Glasgow Coma Scale
scores to evaluate brain injury severity
Component
Response Score
Best eye response No eye opening 1
Eye opening to pain 2
Eye opening to verbal command 3
Eyes open spontaneously 4 XXX
Best verbal response No verbal response 1
Incomprehensible sounds 2
Inappropriate words 3
Confused 4 XXX
Oriented 5
Best motor response No motor response 1
Extension to pain 2
Flexion to pain 3
Withdrawal from pain 4
Localizing pain 5
Obeys commands 6 XXX
GCS total score ≥12 is mild injury, 9 to 11 is moderate, and ≤8 is severe (90% of patients with scores ≤8 are in a coma). Coma is defined as not opening eyes, not obeying commands, and not saying understandable words. Composite scores with eye, verbal, and motor responses (such as E3V3M5) are clinically more useful than totals.
Source: Reference 2.
14“Only a Couple” Beers
Source Undetermined1616
Gorivero (Wikimedia Commons) 20071717
TABLE 1 Using Glasgow Coma Scale
scores to evaluate brain injury severity
Component
Response Score
Best eye response No eye opening 1
Eye opening to pain 2XXX
Eye opening to verbal command 3
Eyes open spontaneously 4
Best verbal response No verbal response 1
Incomprehensible sounds 2
Inappropriate words 3XXX
Confused 4
Oriented 5
Best motor response No motor response 1
Extension to pain 2
Flexion to pain 3
Withdrawal from pain 4XXX
Localizing pain 5
Obeys commands 6
GCS total score ≥12 is mild injury, 9 to 11 is moderate, and ≤8 is severe (90% of patients with scores ≤8 are in a coma). Coma is defined as not opening eyes, not obeying commands, and not saying understandable words. Composite scores with eye, verbal, and motor responses (such as E3V3M5) are clinically more useful than totals.
Source: Reference 2.
9“Way Too Many” Beers
Source Undetermined1818
TBI – ClassificationTBI – Classification
Neuroimaging ScalesNeuroimaging Scales MarshallMarshall RotterdamRotterdam
Not for ED – predicts risk of ICPNot for ED – predicts risk of ICP
1919
Pathophysiology - Primary Pathophysiology - Primary Injury Injury
Occurs at the time of trauma Occurs at the time of trauma Due to transfer of external mechanical Due to transfer of external mechanical
forces to intracranial contentsforces to intracranial contents– Direct impact to skull / brainDirect impact to skull / brain– Rapid accel / rapid decel without external Rapid accel / rapid decel without external
skull impact (whiplash - coup / contra coup)skull impact (whiplash - coup / contra coup)– Penetrating injuryPenetrating injury– Blast waveBlast wave
2020
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
DamageDamage Hematoma / hemorrhage (extra-Hematoma / hemorrhage (extra-
axial)axial) ContusionContusion Shearing of white matter = diffuse Shearing of white matter = diffuse
axonal injury (DAI)axonal injury (DAI) Edema / swellingEdema / swelling
2121
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
Extra-axial InjuriesExtra-axial Injuries
Epidural hematomaEpidural hematoma Subdural hematomaSubdural hematoma SAHSAH
The deeper the injury, the larger the The deeper the injury, the larger the amount of energy transferredamount of energy transferred
2222
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
Epidural HematomasEpidural Hematomas Torn dural vessels (middle meningeal Torn dural vessels (middle meningeal
arteryartery Lenticular Lenticular Almost always associated with skull Almost always associated with skull
fracturefracture Tend Tend NOTNOT to be associated with brain to be associated with brain
damagedamage
2323
Source Undetermined2424
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
Subdural HematomaSubdural Hematoma Bleeding from bridging veins OR from Bleeding from bridging veins OR from
cortical contusioncortical contusion Crescent shapedCrescent shaped Usually Usually AREARE associated with brain associated with brain
injuryinjury
2525
Source Undetermined2626
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
SAHSAH– disruption of small pial vesselsdisruption of small pial vessels
IntraventricularIntraventricular– tearing of subependymal veinstearing of subependymal veins
2727
Learning Radiology.com
SAH
Hawaii.edu
2828
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
Most common injury - Focal cerebral Most common injury - Focal cerebral contusions contusions
Occur at basal frontal and basal Occur at basal frontal and basal temporal regions due to striking temporal regions due to striking basal skull surfacesbasal skull surfaces
2929
http://mksforum.net/forum/showthread.php?p=204094
http://www.itriagehealth.com/wl/disease/cerebral-contusion-(bruise-of-brain)
3030
Pathophysiology - Primary Pathophysiology - Primary InjuryInjury
Diffuse Axonal InjuryDiffuse Axonal Injury Due to shearing forcesDue to shearing forces Seen better on MRISeen better on MRI Is present even in concussion / mild Is present even in concussion / mild
TBITBI
3131
Diffuse Axonal InjuryDiffuse Axonal Injury
www.learningradiology.com/archives2008/COW%20... www.learningradiology.com/archives2008/COW%20... 3232
Pathophysiology - Secondary Pathophysiology - Secondary InjuryInjury
A cascade of molecular injury mechanisms A cascade of molecular injury mechanisms that are initiated at the time of the TBI & that are initiated at the time of the TBI & continue for hours – dayscontinue for hours – days
Accelerated release of excitatory Accelerated release of excitatory neurotransmitters Ach, glutamate and neurotransmitters Ach, glutamate and aspartate, aspartate, – generates free radicals - injure cell generates free radicals - injure cell
membranesmembranes Mitochondrial dysfunctionMitochondrial dysfunction Inflammatory responsesInflammatory responses Secondary ischemia from vasospasm, focal Secondary ischemia from vasospasm, focal
microvascular occlusion, vascular injurymicrovascular occlusion, vascular injuryAll cause cell death, cerebral edema All cause cell death, cerebral edema and ICPand ICP
3333
Pathophysiology - Secondary Pathophysiology - Secondary InjuryInjury
Exacerbating factorsExacerbating factors HTN (systemic and intracranial)HTN (systemic and intracranial) O2 deliveryO2 delivery FeverFever SeizuresSeizures glucoseglucose
3434
TBI DefinitionTBI Definition
TBI GCS(initial in ED at 30
minutes from the injury)
LOC P-T Amnesia
CT abnl
Mild 13 - 15 <20 min <24 hrs NoNo
Moderate 9 - 12 20 min – 7d 24 hrs – 7d
Severe < 8 >7d >7d YesYes
3535
Mild TBIMild TBI
Mild TBI is oxymoronic (Mild TBI is oxymoronic (nothing mild nothing mild about it)about it)
Is only describing the visible brain Is only describing the visible brain injury, not describing functional injury, not describing functional impairmentimpairment
Can have severe disability from Mild Can have severe disability from Mild TBITBI
3636
Concussion - ?Definition?Concussion - ?Definition?
Concussion is less severe than Mild Concussion is less severe than Mild TBI, but…terms difficult to TBI, but…terms difficult to differentiate - ---consider all differentiate - ---consider all concussions to be Mild TBIconcussions to be Mild TBI’’ss
Reflects functional disturbance Reflects functional disturbance rather than major structural injuryrather than major structural injury
3737
The American Academy of The American Academy of Neurology (AAN) definition of Neurology (AAN) definition of
Concussion:Concussion: Trauma-induced alteration in mental statusTrauma-induced alteration in mental status Confusion and amnesia - hallmarks of concussion Confusion and amnesia - hallmarks of concussion Occurs w/i 5 minutes of the head trauma Occurs w/i 5 minutes of the head trauma May or may not involve loss of consciousnessMay or may not involve loss of consciousness
This definition recognizes three concussion grades:This definition recognizes three concussion grades: Grade 1: concussion sxs lasts <15 minutes, w/o Grade 1: concussion sxs lasts <15 minutes, w/o
LOCLOC Grade 2: concussion sxs lasts >15 minutes, w/o Grade 2: concussion sxs lasts >15 minutes, w/o
LOCLOC Grade 3: LOC. Grade 3: LOC.
3838
Concussion & Mild TBIConcussion & Mild TBISigns of Concussion - CONFUSIONSigns of Concussion - CONFUSION
– Inability to focus attentionInability to focus attention– Vacant stareVacant stare– Memory deficits Memory deficits – Delayed verbal expression Delayed verbal expression – DisorientationDisorientation
3939
Concussion & Mild TBIConcussion & Mild TBI
Signs of Concussion – SPEECH, Signs of Concussion – SPEECH, COORDINATION, EMOTIONALCOORDINATION, EMOTIONAL– Slurred or incoherent speech Slurred or incoherent speech – Gross observable incoordination Gross observable incoordination – Emotionality out of proportion to Emotionality out of proportion to
circumstances circumstances – Any period of LOCAny period of LOC
4040
HOW TO REMEMBER THESE HOW TO REMEMBER THESE SYMPTOMS?SYMPTOMS?
4141
Signs of ConcussionSigns of Concussion – CONFUSION – CONFUSION
HOW DO LECTURES MAKE ME FEEL?HOW DO LECTURES MAKE ME FEEL?
•DisorientationDisorientation Delayed verbal Delayed verbal expressionexpression•Memory deficitsMemory deficits
•Inability to focus Inability to focus attentionattention •Vacant stareVacant stare (befuddled facial (befuddled facial expression)expression)
Victor M. Campos, Jr. (Flickr) 2009
John Morgan (Flickr) 2009
4242
Signs of ConcussionSigns of Concussion – – SPEECH, SPEECH, COORDINATION, EMOTIONALCOORDINATION, EMOTIONAL
HOW DOES DRINKING MAKE ME FEEL?HOW DOES DRINKING MAKE ME FEEL?
•Slurred or incoherent speechSlurred or incoherent speech •Gross incoordinationGross incoordination •Emotionality out of proportion Emotionality out of proportion to circumstancesto circumstances
•Any period of LOCAny period of LOC (coma, unresponsiveness to (coma, unresponsiveness to stimuli)stimuli)
Paukrus (Flickr) 2012
4343
Concussion & Mild TBI Concussion & Mild TBI Other SymptomsOther Symptoms
Occurs within mins to hours:Occurs within mins to hours: Headache, dizziness / vertigo / Headache, dizziness / vertigo /
imbalance imbalance
Occurs within mins – daysOccurs within mins – days:: Mood & cognitive disturbances, Mood & cognitive disturbances,
sensitivity to light & noise, sleep sensitivity to light & noise, sleep disturbancesdisturbances
4444
Concussion & Mild TBI:Concussion & Mild TBI: Neurological SequelaNeurological Sequela
SeizuresSeizures Considered 2/2 TBI if it onsets within 7dConsidered 2/2 TBI if it onsets within 7d NOT epilepsyNOT epilepsy Occurs in < 5% of mild / mod TBIOccurs in < 5% of mild / mod TBI Increased occurrence with severe TBIIncreased occurrence with severe TBI
– 25% occur within 1 hr25% occur within 1 hr– 50% occur within 1 day50% occur within 1 day
The risk of epilepsy:The risk of epilepsy:– 6% (s/p TBI)6% (s/p TBI)– 25% (s/p TBI with seizure)25% (s/p TBI with seizure)
80% of post-traumatic epilepsy onsets w/i 2 80% of post-traumatic epilepsy onsets w/i 2 yrsyrs
4545
Concussion & Mild TBI:Concussion & Mild TBI: Neurological SequelaNeurological Sequela
Progression of SymptomsProgression of Symptoms Indicates bleeding and / or Indicates bleeding and / or
progressive edemaprogressive edema Worsening headache, confusion, Worsening headache, confusion,
lethargy, focal neurological signslethargy, focal neurological signs
4646
Concussion & Mild TBIConcussion & Mild TBI
Evaluation and Management:Evaluation and Management:
Cognitive assessmentCognitive assessment Simple orientation questions Simple orientation questions
inadequately sensitiveinadequately sensitive SAC –Standardizes Assessment of SAC –Standardizes Assessment of
ConcussionConcussion Tool for sideline assessment of athletes Tool for sideline assessment of athletes
– change in 1 point signifies concussion– change in 1 point signifies concussion
4747
Figure 1: Standard Assessment of Concussion –SAC Name:____________________________________
Team:_________________Examiner:__________ Date of Exam:__________Time:______________ Exam(Circle One): Bline Injury Post-Px/Game Day1 Day2 Day3 Day5 Day7 Day90
Neurologic Screening: Loss of Consciousness/ No Yes Witnessed Unresponsiveness Length: Post-Traumatic Amnesia? No Yes Poor recall of events after injury Length: Retrograde Amnesia? No Yes Poor recall of events before injury Length:
Introduction: I am going to ask you some questions. Please listen carefully and give your best effort.
Strength Normal Abnormal Right Upper Extremity Left Upper Extremity Right Lower Extremity Left Lower Extremity
Orientation: What month is it? 0 1 What’s the date today? 0 1 What’s the day of the week? 0 1 What year is it? 0 1 What time is it right now? (within1 hr)0 1 Award 1 point for each correct answer. Orientation Total Score
Sensation- examples: Finger-to-Nose/ Rhomberg Coordination- examples: Tandem walk Finger-nose-finger
4848
Immediate Memory: I am going to test your memory. I will read you a list of words and when I am done, repeat back as many words as you can remember, in any order. List Trial 1 Trial 2 Trial 3 Elbow 0 1 0 1 0 1 Apple 0 1 0 1 0 1 Carpet 0 1 0 1 0 1 Saddle 0 1 0 1 0 1 Bubble 0 1 0 1 0 1 Total Trials 2&3: I am going to repeat that list again. Repeat back as many words as you can remember in any order, even if I said the word before. Complete all 3 trials regardless of score on trial 1&2. Score 1pt. for each correct response. Total score equals sum across all 3 trails. Do not inform the subject that delayed recall will be tested.
Concentration Digits Backward: I am going to read you a string of numbers and when I am done, you repeat them back to me backwards, in reverse order of how I read them to you. For example, if I say 7-1-9, you would say 9-1-7. If correct, go to next string length, if incorrect, read trial 2. Score 1 pt. for each string length. Stop after incorrect on both trials. 4-9-3 6-2-9 0 1 3-8-1-4 3-2-7-9 0 1 6-2-9-7-1 1-5-2-8-6 0 1 7-1-8-4-6-2 5-3-9-1-4-8 0 1 Months in Reverse Order: Now tell me the months of the year in reverse order. Start with the last month and go backward. So you’ll start with December, November…Go ahead. 1 pt. for entire sequence correct. Dec-Nov-Oct-Sept-Aug-Jul-Jun-May-Apr-Mar-Feb-Jan 0 1
Immediate Memory Total Score Concentration Total Score
Exertional Maneuvers: If subject is not displaying or reporting symptoms, conduct the following maneuvers to create conditions under which symptoms are likely to be elicited and detected. These measures need not be conducted if a subject is already displaying or reporting any symptoms. If not conducted allow 2 minutes to keep time delay constant before testing Delayed Recall. These methods should be administered for baseline testing of normal subjects. 5 Jumping Jacks 5 Push-Ups 5 Sit ups 5 Knee Bends
Delayed Recall: Do you remember that list of words I read a few times earlier? Tell me as many words from the list as you can remember in any order. Circle each word correctly recalled. Total score equals number of words recalled. Elbow Apple Carpet Saddle Bubble Delayed Recall Total Score SAC Scoring Summary: Exertional Maneuvers & Neurologic Screening are important for examination, but are not incorporated into SAC Total Score. Orientation /5 Immediate Memory /15 Concentration /5 Delayed Recall /5 SAC Total Score /30 4949
Concussion & Mild TBIConcussion & Mild TBIRevised WPTAS (Westmead Post-Traumatic Amnesia Revised WPTAS (Westmead Post-Traumatic Amnesia
Scale)Scale)-1 wrong answer indicates cognitive impairment-1 wrong answer indicates cognitive impairment
What is your name?What is your name? What is the name of this place?What is the name of this place? Why are you here?Why are you here? What month are we in?What month are we in? What year are we in?What year are we in? What town are you in?What town are you in? How old are you?How old are you? What is your date of birth?What is your date of birth? What time of day is it (morning, afternoon, evening?)What time of day is it (morning, afternoon, evening?) Three pictures are presented for subsequent recallThree pictures are presented for subsequent recall
Cathy Calamas 2011 (Flickr) Plaisanter 2010 (Flickr) Sassy Bella Melange 2008 (Flickr)5050
NeuroimagingNeuroimaging
CT is the preferred modality for acute CT is the preferred modality for acute evaluation of TBIevaluation of TBI
GCS of 15 = 5% abnormal scansGCS of 15 = 5% abnormal scans GCS of 13 = 30% abnormal scansGCS of 13 = 30% abnormal scans Only 1% of abnormal scan need Only 1% of abnormal scan need
to go to the ORto go to the OR MRI – sees more (contusions, DAI, MRI – sees more (contusions, DAI,
small bleeds), but doesnsmall bleeds), but doesn’’t change t change clinical managementclinical management
5151
NeuroimagingNeuroimaging
Canadian CT Head Rule for mild TBICanadian CT Head Rule for mild TBI GCS < 15 two hours after injuryGCS < 15 two hours after injury Suspected open or depressed skull fracture Suspected open or depressed skull fracture Any sign of basilar skull fracture Any sign of basilar skull fracture
(hemotympanum, raccoons, Battles, CSF (hemotympanum, raccoons, Battles, CSF leak)leak)
>>2 episodes of vomiting2 episodes of vomiting >>65 years old65 years old Amnesia before impact Amnesia before impact >> 30 minutes 30 minutes Dangerous mechanism (pedestrian / MVA, Dangerous mechanism (pedestrian / MVA,
ejected, fall from ejected, fall from >> 3 feet or 3 feet or >> 5 stairs) 5 stairs) Neuro deficit, seizure, coagulopathyNeuro deficit, seizure, coagulopathy 5252
Acute evaluation and disposition of patients with
mild TBI
Data from: Vos, PE. Eur J Neurol 2002; 9:207 and Borg, J. J Rehabil Med 2004; S43:61.
Normal exam and normal HCT (and no CI’s) = home observation
Source Undetermined5353
Increase the number of CT’s
Source Undetermined
5454
Increase the number of admissions
Source Undetermined
5555
If the HCT and Neuro Exam are If the HCT and Neuro Exam are Normal, then why Observe?Normal, then why Observe?
• None of 542 “mild” TBI’s admitted to the hospital overnight deteriorated
• GCS = 15, normal Neuro exam and normal HCT and no coagulopathy DO NOT deteriorate
• - so, why home observation?just in case?
CYA?
5656
Home Observation of Mild Home Observation of Mild TBITBI
Return to ER if:Return to ER if:
• Awakened q2 hr for Awakened q2 hr for 24 hours 24 hours
• Avoid strenuous Avoid strenuous activity for 24 hoursactivity for 24 hours
WonWon’’t t wake upwake up
Vision Vision difficultiesdifficulties
Worsening Worsening headacheheadache
ss
VomitingVomiting
New New somnolence somnolence or confusionor confusion
Fever, stiff Fever, stiff neckneck
Restless, Restless, unsteadyunsteady
Incontinence Incontinence bowel or bowel or bladderbladder
SeizureSeizure
5757
Second Impact SyndromeSecond Impact Syndrome
Diffuse cerebral edema occuring after Diffuse cerebral edema occuring after a 2a 2ndnd concussion concussion while the patient is while the patient is still symptomatic from the 1still symptomatic from the 1stst concussionconcussion
RareRare ControversialControversial DoesnDoesn’’t occur frequently in boxers t occur frequently in boxers
(shouldn(shouldn’’t it?)t it?) But just in case itBut just in case it ’’s real….RTPs real….RTP
5858
Second Impact Syndrome - Second Impact Syndrome - RTPRTP
None are evidenced based / None are evidenced based / prospectively validatedprospectively validated
Cantu, Colorado, AANCantu, Colorado, AAN
Grade 1 Grade 2 Grade 3Grade 1 Grade 2 Grade 3
Concussion symptoms, amnesia, LOC Concussion symptoms, amnesia, LOC
5959
Grade 1 Grade 2 Grade 3
Presentation1. No loss of consciousness2. Post-traumatic amnesia or other signs lasting less than 30 minutes
1. Loss of consciousness for less than 1 minuteOR2. Post-traumatic amnesia or other symptoms for more than 30 minutes, less than 24 hours
1. Loss of consciousness for longer than 1 minuteOR2. Post-traumatic amnesia or other symptoms for longer than 24 hours
Management Athlete may return to play if asymptomatic for one week
Athlete may return to play in 2 weeks if asymptomatic at rest and on exertion for 7 days
Athlete may return to play in one month if asymptomatic at rest and on exertion for 7 days
Cantu Guideline for Concussion Cantu Guideline for Concussion ManagementManagement
Adapted from: Cantu, RC, J Athl Train 2001; 36:244 6060
Grade 1 Grade 2 Grade 3
Presentation 1. Confusion without amnesia2. No loss of consciousness
1. Confusion with amnesia2. No loss of consciousness
1. Loss of consciousness of any duration
Management Evaluate athlete immediately and every 5 minutes. Athlete may return to play if amnesia or symptoms do not appear for 20 minutes.
Examine the athlete the next day. Athlete may return to play after one week if asymptomatic during that time.
Transport athlete to the emergency department; athlete may return to play if asymptomatic for 2 weeks and cleared by neurologist or neurosurgeon.
Colorado Guideline for Colorado Guideline for Concussion ManagementConcussion Management
Colorado Medical Society, Report of the Sports Medicine Committee, 1991.6161
Grade 1 Grade 2 Grade 3
Presentation 1. Transient confusion
2. No loss of consciousness
3. Concussion symptoms for less than 15 minutes
1. Transient confusion
2. No loss of consciousness
3. Concussion symptoms for more than 15 minutes
1. Loss of consciousness of any duration
Management Athlete may return to play if asymptomatic at 15 minutes.
Athlete can return to play if asymptomatic for one week.
Transport to the hospital and observe overnight. Athlete may return to play when symptomatic for one week (if loss of consciousness was brief, i.e., seconds) or for two weeks (if loss of consciousness was prolonged).
American Academy of Neurology - RTPAmerican Academy of Neurology - RTP
American Academy of Neurology, Neurology 1997; 48:581 6262
Second Impact Syndrome - Second Impact Syndrome - RTPRTP
None are evidenced based / prospectively validateNone are evidenced based / prospectively validate Grade 1 Grade 2 Grade 3Grade 1 Grade 2 Grade 3
AAN – 15 minute 1 week 1-2 weeksAAN – 15 minute 1 week 1-2 weeks
Cantu – 1 week 2 weeks 4 weeksCantu – 1 week 2 weeks 4 weeks
Colorado – 20 minute 1 week 2 weeksColorado – 20 minute 1 week 2 weeks
..6363
Second Impact Syndrome - Second Impact Syndrome - RTPRTP
None are evidenced based / prospectively validateNone are evidenced based / prospectively validate Grade 1 Grade 2 Grade 3Grade 1 Grade 2 Grade 3
AAN – 15 min 1 week 1-2 weeksAAN – 15 min 1 week 1-2 weeks
Cantu – 1 week 2 weeks 4 weeksCantu – 1 week 2 weeks 4 weeks
Colorado – 20 minute 1 week 2 weeks Colorado – 20 minute 1 week 2 weeks
Bottom Line:Bottom Line:No RTP while symptomaticNo RTP while symptomatic
Go to ER if:Go to ER if:LOC > 1 minute OR concussion symptoms > 15-30 LOC > 1 minute OR concussion symptoms > 15-30
minsmins6464
UpToDate6565
Post Concussive SyndromePost Concussive Syndrome
SymptomsSymptoms HeadacheHeadache Dizziness / vertigoDizziness / vertigo FatigueFatigue Noise sensitivity, light sensitivityNoise sensitivity, light sensitivity Cognitive impairment (decreased ability to Cognitive impairment (decreased ability to
remember, to process info, to concentrate)remember, to process info, to concentrate) Neurobehavioral & Neuropsychiatric symptoms Neurobehavioral & Neuropsychiatric symptoms
(change in personality, behavior, irritability, (change in personality, behavior, irritability, anxiety, depression, insomnia)anxiety, depression, insomnia)
Most commonly d/t Mild TBI. Less common with Most commonly d/t Mild TBI. Less common with whiplash, Mod / Severe TBIwhiplash, Mod / Severe TBI
LOC not needed for diagnosisLOC not needed for diagnosis6666
Post Concussive SyndromePost Concussive Syndrome
CONTROVERSIALCONTROVERSIAL Symptoms are vague, subjective, Symptoms are vague, subjective,
common with many other conditions, common with many other conditions, difficult to measure / testdifficult to measure / test
DoesnDoesn’’t correlate to severity of TBI, t correlate to severity of TBI, GCS, length of LOC, length of amnesia, GCS, length of LOC, length of amnesia, CT / MRI abnormalitiesCT / MRI abnormalities
Underlying pathophysiology is Underlying pathophysiology is unknownunknown
6767
Post Concussive SyndromePost Concussive Syndrome
30-80% of mild – mod TBI will have some 30-80% of mild – mod TBI will have some symptoms of PCSsymptoms of PCS
Many are better at 1 month, most are Many are better at 1 month, most are better at 3 monthsbetter at 3 months
10-15% are still symptomatic at 1 year – 10-15% are still symptomatic at 1 year – headache, dizziness, anxiety, cognitiveheadache, dizziness, anxiety, cognitive– The Miserable MinorityThe Miserable Minority
Physiologic / functional neuroimaging has Physiologic / functional neuroimaging has same changes as does migraine, same changes as does migraine, depressiondepression
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Post Concussive SyndromePost Concussive Syndrome
Psychogenic?Psychogenic? symptoms similar to anxiety / PTSD, symptoms similar to anxiety / PTSD,
depression – headache, dizziness, depression – headache, dizziness, sleep impairmentsleep impairment
Cognitive impairments are seen in Cognitive impairments are seen in anxiety / depressionanxiety / depression
PTSD is the strongly associated with PTSD is the strongly associated with PCSPCS
6969
Post Concussive SyndromePost Concussive Syndrome Bottom line: Bottom line: association of psych disease association of psych disease
w/ PCS is not establishedw/ PCS is not established– Maybe psych patients more likely to get TBI?Maybe psych patients more likely to get TBI?– Maybe psych patients more likely to get PCS Maybe psych patients more likely to get PCS
after TBI?after TBI?– Maybe TBI is causing the psych symptoms? Maybe TBI is causing the psych symptoms?
(TBI can cause VH, which can cause psych)(TBI can cause VH, which can cause psych) Be very careful about diagnosing Be very careful about diagnosing
malingeringmalingering
Litigation?Litigation?– Many who sue arenMany who sue aren’’t severet severe– Many that are severe donMany that are severe don’’t suet sue
No correlationNo correlation 7070
Post Concussive SyndromePost Concussive Syndrome
Treatment of symptomsTreatment of symptoms No magic bullet that addresses all No magic bullet that addresses all
symptoms (maybe VH?)symptoms (maybe VH?) Treat Headache, dizziness, psych per Treat Headache, dizziness, psych per
SOP – no special tx d/t TBI etiolSOP – no special tx d/t TBI etiol Each patient has their own unique Each patient has their own unique
symptom setsymptom set– ““When you know 1 TBI, you know 1 TBIWhen you know 1 TBI, you know 1 TBI””– ““SnowflakesSnowflakes””
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TBI and Vertical TBI and Vertical HeterophoriaHeterophoria
What is VHWhat is VH?? Phoria – the position an eye points Phoria – the position an eye points
(line of sight) when it is not (line of sight) when it is not attempting to fuse an image / fusion attempting to fuse an image / fusion is disrupted with a red lens is disrupted with a red lens – eg – exo phoria, eso phoriaeg – exo phoria, eso phoria
Vertical Hetero Phoria:Vertical Hetero Phoria:– Line of sight of one eye is higher than the Line of sight of one eye is higher than the
other eye when not attempting to fuse an other eye when not attempting to fuse an imageimage
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Source Undetermined7373
TBI and Vertical TBI and Vertical HeterophoriaHeterophoria
As compared to Heterotropia (strabismus), patients As compared to Heterotropia (strabismus), patients with Heterophoria are still able to maintain a single with Heterophoria are still able to maintain a single image but at great expenseimage but at great expense
Brain avoids diplopia at all costs - overexert EOMBrain avoids diplopia at all costs - overexert EOM’’s s – elevators and depressors– elevators and depressors
Overuse and fatigue of EOMOveruse and fatigue of EOM’’s causes symptoms:s causes symptoms:– dizziness, dizziness, anxiety, neck pain, reading difficultiesdizziness, dizziness, anxiety, neck pain, reading difficulties
Postconcussive symptoms and VH symptoms overlapdizziness, headache, anxiety, neck pain, reading difficulty [cognitive, change in personality, behavior, irritability, depression, insomnia]
7474
TBI and Vertical TBI and Vertical HeterophoriaHeterophoria
As compared to Heterotropia (strabismus), As compared to Heterotropia (strabismus), patients with Heterophoria are still able to patients with Heterophoria are still able to maintain a single image but at great expensemaintain a single image but at great expense
Brain avoids diplopia at all costs - overexert EOMBrain avoids diplopia at all costs - overexert EOM ’’s s – elevators and depressors– elevators and depressors
Overuse and fatigue of EOMOveruse and fatigue of EOM’’s causes symptoms:s causes symptoms:– dizziness, dizziness, anxiety, neck pain, reading difficultiesdizziness, dizziness, anxiety, neck pain, reading difficulties
Postconcussive symptoms and VH symptoms Postconcussive symptoms and VH symptoms overlapoverlap– dizziness, headache, anxiety, neck pain, reading dizziness, headache, anxiety, neck pain, reading
difficultiesdifficulties – [cognitive, change in personality, behavior, irritability, [cognitive, change in personality, behavior, irritability,
depression, insomnia]depression, insomnia]
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TBI and Vertical TBI and Vertical HeterophoriaHeterophoria
Retrospective study Retrospective study PM R 2010;2:244-253
Identification of Binocular Vision Dysfunction (Vertical Heterophoria) in Traumatic Brain Injury Patients and Effects of Individualized Prismatic Spectacle Lenses in the Treatment of Postconcussive Symptoms: A Retrospective Analysis
Jennifer E. Doble, MD, Debby L. Feinberg, OD, Mark S. Rosner, MD, Arthur J. Rosner, MD
43 TBI patients 43 TBI patients Symptomatic for 3.5 yrs; fully evaluated and treated prior to Symptomatic for 3.5 yrs; fully evaluated and treated prior to
interventionintervention Diagnosed w/ VH and treated w/ prismatic lensesDiagnosed w/ VH and treated w/ prismatic lenses 72% subjective improvement in 3.5 months72% subjective improvement in 3.5 months
Conclusion:Conclusion: TBI seems to be precipitating / exacerbating VH TBI seems to be precipitating / exacerbating VH Treatment w/ prismatic lenses improves both VH and Treatment w/ prismatic lenses improves both VH and
PCS symptoms PCS symptoms 7676
TBI and VHTBI and VH
Good news-Good news- Only treatment so far that addresses Only treatment so far that addresses
so many symptoms so many symptoms
However-However- Only partially addresses cognitive Only partially addresses cognitive
and neuropsych issuesand neuropsych issues
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Chronic TBI -Chronic TBI - Cumulative neuropsychological impairmentCumulative neuropsychological impairment
– Cognitive impairment / dementiaCognitive impairment / dementia Football, soccer Football, soccer Dementia pugilistica – boxing Dementia pugilistica – boxing
– 20% of prof boxers w/ >20 fights20% of prof boxers w/ >20 fights
Helmets – good or bad? Helmets – good or bad? – Decreases TBI in baseball, ice hockey, downhill Decreases TBI in baseball, ice hockey, downhill
skiing, snowboarding, bicycles, motorcyclesskiing, snowboarding, bicycles, motorcycles– Encourages risky behaviorEncourages risky behavior
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Management of Severe TBIManagement of Severe TBI GCS GCS << 8 8 Care should be obtained at the most Care should be obtained at the most
appropriate facility – Level 1 trauma centerappropriate facility – Level 1 trauma center Secondary brain injury caused by:Secondary brain injury caused by:
– Hypoxemia - keep oxygenated – intubate earlyHypoxemia - keep oxygenated – intubate early– Hypotension – fluid resuscitateHypotension – fluid resuscitate– Seizures – consider prophylactic antiepilepticsSeizures – consider prophylactic antiepileptics
Shock is almost never due to head injury Shock is almost never due to head injury alone – look for other sources (spinal cord, alone – look for other sources (spinal cord, internal bleeding)internal bleeding)
DonDon’’t withhold fluids d/t concerns of t withhold fluids d/t concerns of exacerbating cerebral edemaexacerbating cerebral edema
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Management of Severe TBIManagement of Severe TBI ICP monitoring indicated for GCS ICP monitoring indicated for GCS << 8 8 These patients are at high risk for These patients are at high risk for
intracranial hypertension (IC HTN), which intracranial hypertension (IC HTN), which requires aggressive txrequires aggressive tx
Open fontanels – can still get ICPOpen fontanels – can still get ICP For GCS > 8 if exam canFor GCS > 8 if exam can’’t be followed t be followed
(sedation, paralysis)(sedation, paralysis) IC HTN predicted by 2/3:IC HTN predicted by 2/3:
– Systolic HTNSystolic HTN– motor posturingmotor posturing– age > 40age > 40
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Management of Severe TBIManagement of Severe TBI
Tx IC HTN when ICP Tx IC HTN when ICP >> 20 20 Rate of complications from ICP Rate of complications from ICP
monitors is lowmonitors is low cerebral perfusion pressure (CPP) = cerebral perfusion pressure (CPP) =
MAP - ICPMAP - ICP Maintain CPP >70Maintain CPP >70
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Treatment of IC HTNTreatment of IC HTN
1. Analgesia and sedation are initial 1. Analgesia and sedation are initial treatments treatments
2. If euvolemic, elevate HOB 30 2. If euvolemic, elevate HOB 30 degreesdegrees
3. Paralysis3. Paralysis 4. Can drain CSF to lower ICP through 4. Can drain CSF to lower ICP through
ventriculostomy catheter (preferred) ventriculostomy catheter (preferred) or via LPor via LP
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Treatment of IC HTNTreatment of IC HTN
5. Osmotic Agents5. Osmotic Agents Mannitol can be used to decrease ICP Mannitol can be used to decrease ICP
– osmolar agents / dehydrate the – osmolar agents / dehydrate the brain. Requires intact BBB – may brain. Requires intact BBB – may accumulate in injured areas of brain – accumulate in injured areas of brain – best to use as bolusesbest to use as boluses
Mannitol also decreases blood Mannitol also decreases blood viscosity for approximately 75 minutesviscosity for approximately 75 minutes
3% saline – continuous infusion3% saline – continuous infusion
8383
Treatment of IC HTNTreatment of IC HTN
6. Hyperventilation to decrease ICP6. Hyperventilation to decrease ICP Keep PaCO2 between 30-35Keep PaCO2 between 30-35 PaCO2 < 30 second tier option – can PaCO2 < 30 second tier option – can
cause decreased CBF 2 / 2 cause decreased CBF 2 / 2 vasoconstriction, causing iatrogenic vasoconstriction, causing iatrogenic ischemiaischemia
Aggressive hyperventilation if Aggressive hyperventilation if herniation or rapid decline of neuro herniation or rapid decline of neuro statusstatus
8484
Treatment of IC HTNTreatment of IC HTN
7. High dose Barbiturates7. High dose Barbiturates Reduces ICP and has neuroprotective Reduces ICP and has neuroprotective
properties – decreases cerebral properties – decreases cerebral metabolism / need for O2 by 50%metabolism / need for O2 by 50%
Causes myocardial depression and Causes myocardial depression and hypotension – may need fluids, hypotension – may need fluids, inotropesinotropes
8. Consider therapeutic hypothermia for 8. Consider therapeutic hypothermia for refractory IC HTNrefractory IC HTN
8585
Treatment of IC HTNTreatment of IC HTN
9. Decompressive craniotomy – 9. Decompressive craniotomy – consider if:consider if:
< 48 hours from injury < 48 hours from injury No episode of ICP > 40No episode of ICP > 40 GCS > 3GCS > 3 Secondary clinical deteriorationSecondary clinical deterioration Evolving herniationEvolving herniation
8686
Source Undetermined8787
Pediatr Crit Care Med 2003 VOL. 4, No. 3 (Suppl.)8888
Source Undetermined8989
Post Traumatic AgitationPost Traumatic Agitation
Witholeary 2009 (Flickr)
9090
Post Traumatic AgitationPost Traumatic Agitation Haldol - reports of affecting cognitive function; Haldol - reports of affecting cognitive function;
NMS w/ high parenteral doses; longer periods of NMS w/ high parenteral doses; longer periods of post traumatic amnesiapost traumatic amnesia– Also reports of multiple doses w/o problemsAlso reports of multiple doses w/o problems
olanzapine (Zyprexa), ziprasidone (Geodon) considered safer
Acute management of agitation in ED (my choices):Acute management of agitation in ED (my choices): BenzodiazepinesBenzodiazepines NarcsNarcs HaldolHaldol DonDon’’t have experience yet w/ olanzapine & t have experience yet w/ olanzapine &
ziprasidoneziprasidone9191
TABLE 3
Medications with potential to impede TBI recovery*
Class
Medications
Alpha-2 agonist Clonidine
Antidepressant Trazodone
Antiepileptic Phenytoin, phenobarbital
Benzodiazepine – impairs memory – not for long term use
Diazepam
Neuroleptic – causes decline in cognitive performance; NMS; amnesia
Haloperidol, thioridazine
*Suggested by animal or clinical studies
Source: References 11-20
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Drugs considered safe and effective for TBI neurobehavioral sxs
Drug Usual daily dosage*
Apathy Amantadine 100 to 400 mg
Bromocriptine 1.25 to 100 mg
Cognition Donepezil
Inattention Dextroamphetamine 5 to 60 mg
Methylphenidate 10 to 60 mg
Depression, PTSD symptoms Fluoxetine 20 to 80 mg
Agitation, mood stabilization
Anticonvulsants
Lamotrigine 25 to 200 mg
Divalproex sodium 10 to 15 mg/kg/day†
Carbamazepine 400 to 1,600 mg‡
Atypical antipsychotics
Olanzapine (Zyprexa) 2.5 to 20 mg 2.5-10 mg IM
Quetiapine 50 to 800 mg
Risperidone 0.5 to 6 mg
Ziprasidone (Geodon) 20 to 160 mg 10-20 mg IM
Beta blocker
Propranolol 20 to 480 mg
PTSD: posttraumatic stress disorder
* Dosage may be divided; see full prescribing information.
† Adjust dosage to achieve serum level of 50 to 100 mcg/mL.
‡ Adjust dosage to achieve serum level of 4 to 12 mcg/mL.
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Goals and ObjectivesGoals and Objectives Demographics of TBIDemographics of TBI Pathophysiology of TBI – Primary & Pathophysiology of TBI – Primary &
Secondary InjurySecondary Injury Assessment & Treatment of Mild TBI / Assessment & Treatment of Mild TBI /
Concussion Concussion Second Impact Syndrome and Return to Second Impact Syndrome and Return to
Play guidelinesPlay guidelines Post Concussive SyndromePost Concussive Syndrome TBI & Vertical HeterophoriaTBI & Vertical Heterophoria Management of Severe TBIManagement of Severe TBI Management of Post Traumatic AgitationManagement of Post Traumatic Agitation
9494
Martin Lopatka 2008 (Flickr)9595
BibliographyBibliography Phan N, Hemphill, JC. Traumatic brain injury: Epidemiology, Phan N, Hemphill, JC. Traumatic brain injury: Epidemiology,
classification, and pathophysiology. UpToDate January 2010classification, and pathophysiology. UpToDate January 2010 Evans R. Concussion and mild traumatic brain injury. UpToDate. Evans R. Concussion and mild traumatic brain injury. UpToDate.
January 2010January 2010 Evans R. Postconcussion Syndrome. UpToDate. January 2010Evans R. Postconcussion Syndrome. UpToDate. January 2010 Carney N, Chestnut R, Kochanek P. Guidelines for acute medical Carney N, Chestnut R, Kochanek P. Guidelines for acute medical
management of severe traumatic brain injury in infants, children management of severe traumatic brain injury in infants, children and adolescents. Pediatr Crit Care Medication 2003. 4(3): and adolescents. Pediatr Crit Care Medication 2003. 4(3): Supplement S1-S71.Supplement S1-S71.
Bellamy CJ, Kane-Gill SL, Falcione BA, Seybert AL. Neuroleptic Bellamy CJ, Kane-Gill SL, Falcione BA, Seybert AL. Neuroleptic malignant syndrome in traumatic brain injury patients treated with malignant syndrome in traumatic brain injury patients treated with haloperidol. J Trauma. 2009 Mar;66(3):954-8.haloperidol. J Trauma. 2009 Mar;66(3):954-8.
Doble JE, Feinberg DL, Rosner MS, Rosner AJ. Identification of binocular vision dysfunction (vertical heterophoria) in traumatic brain injury patients and effects of individualized prismatic spectacle lenses in the treatment of postconcussive symptoms: a retrospective analysis. PM R 2010 April.2(4):244-253
Rosati DL. Early polypharmocological intervention in brain injury Rosati DL. Early polypharmocological intervention in brain injury agitation. Am J Phys Medication Rehabil 2002 Feb. 81(2):90-3agitation. Am J Phys Medication Rehabil 2002 Feb. 81(2):90-3
Daniels JP. Traumatic brain injury: choosing drugs to assist Daniels JP. Traumatic brain injury: choosing drugs to assist recovery. J Fam Prac. 2006 May;5(5)recovery. J Fam Prac. 2006 May;5(5)
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Questions
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