gemc: traumatic brain injury: resident training

Project: Ghana Emergency Medicine Collaborative Document Title: Traumatic Brain Injury Author(s): Mark Rosner MD, 2012 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/

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Traumatic Brain Injury

Mark Rosner MD September 15, 2010

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Goals and Objectives Ø  Demographics of TBI Ø  Pathophysiology of TBI – Primary & Secondary

Injury Ø  Assessment & Treatment of Mild TBI /

Concussion Ø  Second Impact Syndrome and Return to Play

guidelines Ø  Post Concussive Syndrome Ø  TBI & Binocular Vision Dysfunction (VH) Ø  Management of Severe TBI Ø  Management of Post Traumatic Agitation

4

STRAP UP!

Leo Dirac (Flickr) 2007

5

TBI – Demographics

Ø 1.5 million new cases per year in the US Ø Could be 15-20% higher due to

underreporting of mild TBI / concussions Ø Leading cause of death in US for ages

1-45

6


Risk factors: Ø Sex: males 2.5:1 females Ø Lower socioeconomic status Ø Age

–  0-4 –  15-24 (1/2 of all injuries) – >65

7


Ø Mortality = 2% Ø ER & Go Home (mild TBI) = 65% Ø ER & Admit (mod / severe) = 16% Ø Never came to the ER (mild TBI /

concussion) = approximately 17%

8


Leading causes of TBI: Ø Falls (older) = 30% Ø MVC (young adults) = 45% Ø Violence (lower socioeconomic class)= 5% Ø Work accidents = 10% Ø Recreational accidents = 10%

9


Recreational Accidents – Sports Ø Ice Hockey Ø Soccer Ø Boxing Ø Rugby Ø Football

–  incidence = 10% college 20% high school

PER YEAR!

10


Combat related Ø In a 1 year deployment – head injury:

–  10% had change in MS –  5% had LOC

Ø due to – Blasts / explosions –  Falls – MVA – Penetrating wounds

15% TBI rate

11


Disability Ø 1-2% US population (3-5 million) has LTD

(neurologic and functional impairment) due to mod / severe TBI

Ø What about mild TBI!! Under-recognized as cause of disability

Ø Military has not been considering soldiers w/ mild TBI for Purple Heart

12

TBI – Classification

Clinical Severity Scores: GCS: Ø Severe < 8 Ø Moderate = 9-12 (13) Ø Mild = 13 (14) - 15

13

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 14

Michael Spencer (Flickr) 2009

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TABLE 1


Component

Response Score


Eye opening to pain 2


Eyes open spontaneously 4 XXX


Incomprehensible sounds 2

Inappropriate words 3

Confused 4 XXX Oriented 5


Extension to pain 2

Flexion to pain 3

Withdrawal from pain 4

Localizing pain 5

Obeys commands 6 XXX


Source: Reference 2.

14 “Only a Couple” Beers

Source Undetermined 16

Gorivero (Wikimedia Commons) 2007 17

TABLE 1


Component

Response Score


Eye opening to pain 2XXX


Eyes open spontaneously 4


Incomprehensible sounds 2 Inappropriate words 3XXX Confused 4

Oriented 5


Extension to pain 2

Flexion to pain 3

Withdrawal from pain 4XXX Localizing pain 5 Obeys commands 6


Source: Reference 2.

9 “Way Too Many” Beers


TBI – Classification

Neuroimaging Scales Ø Marshall Ø Rotterdam

Not for ED – predicts risk of ICP

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Pathophysiology - Primary Injury

Ø Occurs at the time of trauma Ø Due to transfer of external mechanical

forces to intracranial contents – Direct impact to skull / brain – Rapid accel / rapid decel without external

skull impact (whiplash - coup / contra coup) – Penetrating injury – Blast wave

20


Damage Ø Hematoma / hemorrhage (extra-axial) Ø Contusion Ø Shearing of white matter = diffuse axonal

injury (DAI) Ø Edema / swelling

21


Extra-axial Injuries Ø Epidural hematoma Ø Subdural hematoma Ø SAH

The deeper the injury, the larger the amount of energy transferred

22


Epidural Hematomas Ø Torn dural vessels (middle meningeal

artery Ø Lenticular Ø Almost always associated with skull

fracture Ø Tend NOT to be associated with brain

damage

23


Subdural Hematoma Ø Bleeding from bridging veins OR from

cortical contusion Ø Crescent shaped Ø Usually ARE associated with brain injury

25


Ø SAH – disruption of small pial vessels

Ø Intraventricular –  tearing of subependymal veins

27

Learning Radiology.com

SAH

Hawaii.edu

28


Ø Most common injury - Focal cerebral contusions

Ø Occur at basal frontal and basal temporal regions due to striking basal skull surfaces

29

http://mksforum.net/forum/showthread.php?p=204094

http://www.itriagehealth.com/wl/disease/cerebral-contusion-(bruise-of-brain)

30


Diffuse Axonal Injury Ø Due to shearing forces Ø Seen better on MRI Ø Is present even in concussion / mild TBI

31

Diffuse Axonal Injury

Ø  www.learningradiology.com/archives2008/COW%20... 32

Pathophysiology - Secondary Injury A cascade of molecular injury mechanisms

that are initiated at the time of the TBI & continue for hours – days

Ø  Accelerated release of excitatory

neurotransmitters Ach, glutamate and aspartate, – generates free radicals - injure cell membranes

Ø  Mitochondrial dysfunction Ø  Inflammatory responses Ø  Secondary ischemia from vasospasm, focal

microvascular occlusion, vascular injury All cause cell death, cerebral edema and ICP 33

Pathophysiology - Secondary Injury

Exacerbating factors Ø HTN (systemic and intracranial) Ø  O2 delivery Ø Fever Ø Seizures Ø  glucose

34

TBI 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 No

Moderate 9 - 12 20 min – 7d 24 hrs – 7d

Severe < 8 >7d >7d Yes

35

Mild TBI

Ø Mild TBI is oxymoronic (nothing mild about it)

Ø Is only describing the visible brain injury, not describing functional impairment

Ø Can have severe disability from Mild TBI

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Concussion - ?Definition?

Ø Concussion is less severe than Mild TBI, but…terms difficult to differentiate - ---consider all concussions to be Mild TBI’s

Ø Reflects functional disturbance rather than major structural injury

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The American Academy of Neurology (AAN) definition of Concussion:

Ø  Trauma-induced alteration in mental status Ø  Confusion and amnesia - hallmarks of concussion Ø  Occurs w/i 5 minutes of the head trauma Ø  May or may not involve loss of consciousness

This definition recognizes three concussion grades: Ø  Grade 1: concussion sxs lasts <15 minutes, w/o LOC Ø  Grade 2: concussion sxs lasts >15 minutes, w/o LOC Ø  Grade 3: LOC.

38

Concussion & Mild TBI Signs of Concussion - CONFUSION

–  Inability to focus attention – Vacant stare – Memory deficits – Delayed verbal expression – Disorientation

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Concussion & Mild TBI

Signs of Concussion – SPEECH, COORDINATION, EMOTIONAL – Slurred or incoherent speech – Gross observable incoordination – Emotionality out of proportion to

circumstances – Any period of LOC

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HOW TO REMEMBER THESE SYMPTOMS?

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Signs of Concussion – CONFUSION HOW DO LECTURES MAKE ME FEEL?

• Disorientation Delayed verbal expression • Memory deficits

• Inability to focus attention • Vacant stare (befuddled facial expression)

Victor M. Campos, Jr. (Flickr) 2009

John Morgan (Flickr) 2009

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Signs of Concussion – SPEECH, COORDINATION, EMOTIONAL

HOW DOES DRINKING MAKE ME FEEL?

• Slurred or incoherent speech • Gross incoordination • Emotionality out of proportion to circumstances

• Any period of LOC (coma, unresponsiveness to stimuli)

Paukrus (Flickr) 2012

43

Concussion & Mild TBI Other Symptoms

Occurs within mins to hours: Ø Headache, dizziness / vertigo / imbalance Occurs within mins – days: Ø Mood & cognitive disturbances, sensitivity

to light & noise, sleep disturbances

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Concussion & Mild TBI: Neurological Sequela

Seizures Ø  Considered 2/2 TBI if it onsets within 7d Ø  NOT epilepsy Ø  Occurs in < 5% of mild / mod TBI Ø  Increased occurrence with severe TBI

–  25% occur within 1 hr –  50% occur within 1 day

Ø  The risk of epilepsy: –  6% (s/p TBI) –  25% (s/p TBI with seizure)

Ø  80% of post-traumatic epilepsy onsets w/i 2 yrs

45

Concussion & Mild TBI: Neurological Sequela

Progression of Symptoms Ø Indicates bleeding and / or progressive

edema Ø Worsening headache, confusion, lethargy,

focal neurological signs

46

Concussion & Mild TBI

Evaluation and Management: Cognitive assessment Ø Simple orientation questions inadequately

sensitive Ø SAC –Standardizes Assessment of

Concussion Ø Tool for sideline assessment of athletes –

change in 1 point signifies concussion

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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

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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 49

Concussion & Mild TBI Revised WPTAS (Westmead Post-Traumatic Amnesia Scale) -1 wrong answer indicates cognitive impairment

Ø  What is your name? Ø  What is the name of this place? Ø  Why are you here? Ø  What month are we in? Ø  What year are we in? Ø  What town are you in? Ø  How old are you? Ø  What is your date of birth? Ø  What time of day is it (morning, afternoon, evening?) Ø  Three pictures are presented for subsequent recall

Cathy Calamas 2011 (Flickr) Plaisanter 2010 (Flickr) Sassy Bella Melange 2008 (Flickr) 50

Neuroimaging

Ø CT is the preferred modality for acute evaluation of TBI

Ø GCS of 15 = 5% abnormal scans Ø GCS of 13 = 30% abnormal scans Ø Only 1% of abnormal scan need to go

to the OR Ø MRI – sees more (contusions, DAI, small

bleeds), but doesn’t change clinical management

51

Neuroimaging

Canadian CT Head Rule for mild TBI Ø  GCS < 15 two hours after injury Ø  Suspected open or depressed skull fracture Ø  Any sign of basilar skull fracture

(hemotympanum, raccoons, Battles, CSF leak) Ø  >2 episodes of vomiting Ø  >65 years old Ø  Amnesia before impact > 30 minutes Ø  Dangerous mechanism (pedestrian / MVA,

ejected, fall from > 3 feet or > 5 stairs) Ø  Neuro deficit, seizure, coagulopathy

52

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


Increase the number of CT’s

Source Undetermined

54

Increase the number of admissions

Source Undetermined

55

If the HCT and Neuro Exam are 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?

56

Home Observation of Mild TBI Return to ER if:

•  Awakened q2 hr for 24 hours

•  Avoid strenuous activity for 24 hours

Won’t wake up

Vision difficulties

Worsening headaches

Vomiting

New somnolence or

confusion

Fever, stiff neck

Restless, unsteady

Incontinence bowel or bladder

Seizure

57

Second Impact Syndrome

Ø Diffuse cerebral edema occuring after a 2nd concussion while the patient is still symptomatic from the 1st concussion

Ø Rare Ø Controversial Ø Doesn’t occur frequently in boxers

(shouldn’t it?) Ø But just in case it’s real….RTP

58

Second Impact Syndrome - RTP

None are evidenced based / prospectively validated

Ø Cantu, Colorado, AAN

Ø Grade 1 Grade 2 Grade 3

Ø Concussion symptoms, amnesia, LOC

59

Grade 1 Grade 2 Grade 3

Presentation

1. No loss of consciousness 2. Post-traumatic amnesia or other signs lasting less than 30 minutes

1. Loss of consciousness for less than 1 minute OR 2. Post-traumatic amnesia or other symptoms for more than 30 minutes, less than 24 hours

1. Loss of consciousness for longer than 1 minute OR 2. 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 Management

Adapted from: Cantu, RC, J Athl Train 2001; 36:244 60

Grade 1 Grade 2 Grade 3

Presentation

1. Confusion without amnesia 2. No loss of consciousness

1. Confusion with amnesia 2. 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 Concussion Management

Colorado Medical Society, Report of the Sports Medicine Committee, 1991. 61

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 - RTP

American Academy of Neurology, Neurology 1997; 48:581 62

Second Impact Syndrome - RTP

None are evidenced based / prospectively validate Grade 1 Grade 2 Grade 3

Ø  AAN – 15 minute 1 week 1-2 weeks

Ø  Cantu – 1 week 2 weeks 4 weeks

Ø  Colorado – 20 minute 1 week 2 weeks

. 63

Second Impact Syndrome - RTP None are evidenced based / prospectively validate Grade 1 Grade 2 Grade 3

Ø  AAN – 15 min 1 week 1-2 weeks

Ø  Cantu – 1 week 2 weeks 4 weeks

Ø  Colorado – 20 minute 1 week 2 weeks

Bottom Line: No RTP while symptomatic

Go to ER if: LOC > 1 minute OR concussion symptoms > 15-30 mins

64

UpToDate 65

Post Concussive Syndrome Symptoms Ø  Headache Ø  Dizziness / vertigo Ø  Fatigue Ø  Noise sensitivity, light sensitivity Ø  Cognitive impairment (decreased ability to remember, to

process info, to concentrate) Ø  Neurobehavioral & Neuropsychiatric symptoms (change

in personality, behavior, irritability, anxiety, depression, insomnia)

Ø  Most commonly d/t Mild TBI. Less common with

whiplash, Mod / Severe TBI Ø  LOC not needed for diagnosis 66

Post Concussive Syndrome

CONTROVERSIAL Ø Symptoms are vague, subjective, common

with many other conditions, difficult to measure / test

Ø Doesn’t correlate to severity of TBI, GCS, length of LOC, length of amnesia, CT / MRI abnormalities

Ø Underlying pathophysiology is unknown

67


Ø  30-80% of mild – mod TBI will have some symptoms of PCS

Ø  Many are better at 1 month, most are better at 3 months

Ø  10-15% are still symptomatic at 1 year – headache, dizziness, anxiety, cognitive –  The Miserable Minority

Ø  Physiologic / functional neuroimaging has same changes as does migraine, depression

68


Psychogenic? Ø symptoms similar to anxiety / PTSD,

depression – headache, dizziness, sleep impairment

Ø Cognitive impairments are seen in anxiety / depression

Ø PTSD is the strongly associated with PCS

69

Post Concussive Syndrome Ø  Bottom line: association of psych disease w/ PCS

is not established –  Maybe psych patients more likely to get TBI? –  Maybe psych patients more likely to get PCS after

TBI? –  Maybe TBI is causing the psych symptoms? (TBI can

cause VH, which can cause psych) Ø  Be very careful about diagnosing malingering Ø  Litigation?

–  Many who sue aren’t severe –  Many that are severe don’t sue

§  No correlation 70


Treatment of symptoms Ø No magic bullet that addresses all

symptoms (maybe VH?) Ø Treat Headache, dizziness, psych per SOP

– no special tx d/t TBI etiol Ø Each patient has their own unique

symptom set –  “When you know 1 TBI, you know 1 TBI” –  “Snowflakes”

71

TBI and Vertical Heterophoria

What is VH? Ø Phoria – the position an eye points (line of

sight) when it is not attempting to fuse an image / fusion is disrupted with a red lens –  eg – exo phoria, eso phoria

Ø Vertical Hetero Phoria: –  Line of sight of one eye is higher than the

other eye when not attempting to fuse an image

72

TBI and Vertical Heterophoria Ø  As compared to Heterotropia (strabismus), patients with

Heterophoria are still able to maintain a single image but at great expense

Ø  Brain avoids diplopia at all costs - overexert EOM’s – elevators and depressors

Ø  Overuse and fatigue of EOM’s causes symptoms: –  dizziness, dizziness, anxiety, neck pain, reading difficulties

Ø  Postconcussive symptoms and VH symptoms overlapdizziness, headache, anxiety, neck pain, reading difficulty [cognitive, change in personality, behavior, irritability, depression, insomnia]

74

TBI and Vertical Heterophoria Ø  As compared to Heterotropia (strabismus), patients with

Heterophoria are still able to maintain a single image but at great expense

Ø  Brain avoids diplopia at all costs - overexert EOM’s – elevators and depressors

Ø  Overuse and fatigue of EOM’s causes symptoms: –  dizziness, dizziness, anxiety, neck pain, reading difficulties

Ø  Postconcussive symptoms and VH symptoms overlap –  dizziness, headache, anxiety, neck pain, reading difficulties –  [cognitive, change in personality, behavior, irritability,

depression, insomnia]

75

TBI and Vertical Heterophoria Ø  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

Ø  43 TBI patients Ø  Symptomatic for 3.5 yrs; fully evaluated and treated prior to intervention Ø  Diagnosed w/ VH and treated w/ prismatic lenses Ø  72% subjective improvement in 3.5 months Conclusion: Ø  TBI seems to be precipitating / exacerbating VH Ø  Treatment w/ prismatic lenses improves both VH and PCS

symptoms 76

TBI and VH

Good news- Ø Only treatment so far that addresses so

many symptoms

However- Ø Only partially addresses cognitive and

neuropsych issues

77

Chronic TBI -

Ø  Cumulative neuropsychological impairment –  Cognitive impairment / dementia

Ø  Football, soccer Ø  Dementia pugilistica – boxing

–  20% of prof boxers w/ >20 fights

Ø  Helmets – good or bad? –  Decreases TBI in baseball, ice hockey, downhill skiing,

snowboarding, bicycles, motorcycles –  Encourages risky behavior

78

Management of Severe TBI Ø  GCS < 8 Ø  Care should be obtained at the most appropriate

facility – Level 1 trauma center Ø  Secondary brain injury caused by:

–  Hypoxemia - keep oxygenated – intubate early –  Hypotension – fluid resuscitate –  Seizures – consider prophylactic antiepileptics

Ø  Shock is almost never due to head injury alone – look for other sources (spinal cord, internal bleeding)

Ø  Don’t withhold fluids d/t concerns of exacerbating cerebral edema

79

Management of Severe TBI Ø  ICP monitoring indicated for GCS < 8 Ø  These patients are at high risk for intracranial

hypertension (IC HTN), which requires aggressive tx

Ø  Open fontanels – can still get ICP Ø  For GCS > 8 if exam can’t be followed

(sedation, paralysis) Ø  IC HTN predicted by 2/3:

–  Systolic HTN –  motor posturing –  age > 40

80

Management of Severe TBI

Ø Tx IC HTN when ICP > 20 Ø Rate of complications from ICP monitors is

low Ø cerebral perfusion pressure (CPP) = MAP -

ICP Ø Maintain CPP >70

81

Treatment of IC HTN

Ø 1. Analgesia and sedation are initial treatments

Ø 2. If euvolemic, elevate HOB 30 degrees Ø 3. Paralysis Ø 4. Can drain CSF to lower ICP through

ventriculostomy catheter (preferred) or via LP

82

Treatment of IC HTN

5. Osmotic Agents Ø Mannitol can be used to decrease ICP –

osmolar agents / dehydrate the brain. Requires intact BBB – may accumulate in injured areas of brain – best to use as boluses

Ø Mannitol also decreases blood viscosity for approximately 75 minutes

Ø 3% saline – continuous infusion

83

Treatment of IC HTN

6. Hyperventilation to decrease ICP Ø Keep PaCO2 between 30-35 Ø PaCO2 < 30 second tier option – can

cause decreased CBF 2 / 2 vasoconstriction, causing iatrogenic ischemia

Ø Aggressive hyperventilation if herniation or rapid decline of neuro status

84

Treatment of IC HTN

7. High dose Barbiturates Ø Reduces ICP and has neuroprotective

properties – decreases cerebral metabolism / need for O2 by 50%

Ø Causes myocardial depression and hypotension – may need fluids, inotropes

8. Consider therapeutic hypothermia for refractory IC HTN

85

Treatment of IC HTN

9. Decompressive craniotomy – consider if: Ø < 48 hours from injury Ø No episode of ICP > 40 Ø GCS > 3 Ø Secondary clinical deterioration Ø Evolving herniation

86

Pediatr Crit Care Med 2003 VOL. 4, No. 3 (Suppl.) 88

Post Traumatic Agitation

Witholeary 2009 (Flickr)

90

Post Traumatic Agitation Ø  Haldol - reports of affecting cognitive function; NMS w/

high parenteral doses; longer periods of post traumatic amnesia –  Also reports of multiple doses w/o problems

Ø  olanzapine (Zyprexa), ziprasidone (Geodon) considered safer

Acute management of agitation in ED (my choices): Ø  Benzodiazepines Ø  Narcs Ø  Haldol Ø  Don’t have experience yet w/ olanzapine & ziprasidone

91

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

92

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. 93

Goals and Objectives Ø  Demographics of TBI Ø  Pathophysiology of TBI – Primary & Secondary

Injury Ø  Assessment & Treatment of Mild TBI /

Concussion Ø  Second Impact Syndrome and Return to Play

guidelines Ø  Post Concussive Syndrome Ø  TBI & Vertical Heterophoria Ø  Management of Severe TBI Ø  Management of Post Traumatic Agitation

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Martin Lopatka 2008 (Flickr) 95

Bibliography Ø  Phan N, Hemphill, JC. Traumatic brain injury: Epidemiology, classification,

and pathophysiology. UpToDate January 2010 Ø  Evans R. Concussion and mild traumatic brain injury. UpToDate. January

2010 Ø  Evans R. Postconcussion Syndrome. UpToDate. January 2010 Ø  Carney N, Chestnut R, Kochanek P. Guidelines for acute medical

management of severe traumatic brain injury in infants, children and adolescents. Pediatr Crit Care Medication 2003. 4(3): Supplement S1-S71.

Ø  Bellamy CJ, Kane-Gill SL, Falcione BA, Seybert AL. Neuroleptic malignant syndrome in traumatic brain injury patients treated with haloperidol. J Trauma. 2009 Mar;66(3):954-8.

Ø  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

Ø  Rosati DL. Early polypharmocological intervention in brain injury agitation. Am J Phys Medication Rehabil 2002 Feb. 81(2):90-3

Ø  Daniels JP. Traumatic brain injury: choosing drugs to assist recovery. J Fam Prac. 2006 May;5(5)

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Questions

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gemc: traumatic brain injury: resident training

Education

binocular vision dysfunction

achieve serum level

secondaryinjury assessment

overexert eoms elevators

tbi primary

reading difficultiespostconcussive symptoms

traumatic brain injury

severe tbi management