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GEMC: Traumatic Brain Injury: Resident Training

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This is a lecture by Dr. Mark Rosner from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. 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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GEMC: Traumatic Brain Injury: Resident Training

  1. 1. 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/ We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1
  2. 2. Attribution Key for more information see: http://open.umich.edu/wiki/AttributionPolicy Use + Share + Adapt { Content the copyright holder, author, or law permits you to use, share and adapt. } Public Domain – Government: Works that are produced by the U.S. Government. (17 USC § 105) Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Creative Commons – Zero Waiver Creative Commons – Attribution License Creative Commons – Attribution Share Alike License Creative Commons – Attribution Noncommercial License Creative Commons – Attribution Noncommercial Share Alike License GNU – Free Documentation License Make Your Own Assessment { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (17 USC § 102(b)) *laws in your jurisdiction may differ { Content Open.Michigan has used under a Fair Use determination. } Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (17 USC § 107) *laws in your jurisdiction may differ Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that your use of the content is Fair. To use this content you should do your own independent analysis to determine whether or not your use will be Fair. 2
  3. 3. Traumatic Brain Injury Mark Rosner MD September 15, 2010 3
  4. 4. 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
  5. 5. STRAP UP! Leo Dirac (Flickr) 2007 5
  6. 6. 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
  7. 7. TBI – Demographics 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
  8. 8. TBI – Demographics 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
  9. 9. TBI – Demographics 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
  10. 10. TBI – Demographics Recreational Accidents – Sports Ø  Ice Hockey Ø  Soccer Ø  Boxing Ø  Rugby Ø  Football –  incidence = 10% college 20% high school PER YEAR! 10
  11. 11. TBI – Demographics Combat related Ø  In a 1 year deployment – head injury: –  10% had change in MS –  5% had LOC Ø  due 15% TBI rate to –  Blasts / explosions –  Falls –  MVA –  Penetrating wounds 11
  12. 12. TBI – Demographics 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
  13. 13. TBI – Classification Clinical Severity Scores: GCS: Ø  Severe < 8 Ø  Moderate = 9-12 (13) Ø  Mild = 13 (14) - 15 13
  14. 14. TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component 1 2 3 Eyes open spontaneously 4 No verbal response 1 Incomprehensible sounds 2 Inappropriate words 3 Confused 4 Oriented 5 No motor response 1 Extension to pain 2 Flexion to pain 3 Withdrawal from pain 4 Localizing pain 5 Obeys commands Best motor response No eye opening Eye opening to verbal command Best verbal response Score Eye opening to pain Best eye response Response 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. 14 Source: Reference 2. Source Undetermined
  15. 15. Michael Spencer (Flickr) 2009 15
  16. 16. TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component Best eye response Response Score “Only a Couple” Beers 2 Eye opening to verbal command 3 Eyes open spontaneously 4 XXX No verbal response 1 Incomprehensible sounds 2 Inappropriate words 3 Confused 4 XXX Oriented 5 No motor response 1 Extension to pain 2 Flexion to pain 3 Withdrawal from pain 4 Localizing pain 5 Obeys commands Best motor response 1 Eye opening to pain Best verbal response No eye opening 14 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. 16 Source: Reference 2. Source Undetermined
  17. 17. Gorivero (Wikimedia Commons) 2007 17
  18. 18. TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component Best eye response Response Score “Way Too Many” Beers 2XXX Eye opening to verbal command 3 Eyes open spontaneously 4 No verbal response 1 Incomprehensible sounds 2 Inappropriate words 3XXX Confused 4 Oriented 5 No motor response 1 Extension to pain 2 Flexion to pain 3 Withdrawal from pain 4XXX Localizing pain 5 Obeys commands Best motor response 1 Eye opening to pain Best verbal response No eye opening 9 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. 18 Source: Reference 2. Source Undetermined
  19. 19. TBI – Classification Neuroimaging Scales Ø  Marshall Ø  Rotterdam Not for ED – predicts risk of ICP 19
  20. 20. 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
  21. 21. Pathophysiology - Primary Injury Damage Ø  Hematoma / hemorrhage (extra-axial) Ø  Contusion Ø  Shearing of white matter = diffuse axonal injury (DAI) Ø  Edema / swelling 21
  22. 22. Pathophysiology - Primary Injury Extra-axial Injuries Ø  Epidural hematoma Ø  Subdural hematoma Ø  SAH The deeper the injury, the larger the amount of energy transferred 22
  23. 23. Pathophysiology - Primary Injury 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
  24. 24. 24 Source Undetermined
  25. 25. Pathophysiology - Primary Injury Subdural Hematoma Ø  Bleeding from bridging veins OR from cortical contusion Ø  Crescent shaped Ø  Usually ARE associated with brain injury 25
  26. 26. Source Undetermined 26
  27. 27. Pathophysiology - Primary Injury Ø  SAH –  disruption of small pial vessels Ø  Intraventricular –  tearing of subependymal veins 27
  28. 28. Hawaii.edu Learning Radiology.com SAH 28
  29. 29. Pathophysiology - Primary Injury Ø  Most common injury - Focal cerebral contusions Ø  Occur at basal frontal and basal temporal regions due to striking basal skull surfaces 29
  30. 30. http://mksforum.net/forum/ showthread.php?p=204094 http://www.itriagehealth.com/wl/ disease/cerebral-contusion-(bruiseof-brain) 30
  31. 31. Pathophysiology - Primary Injury Diffuse Axonal Injury Ø  Due to shearing forces Ø  Seen better on MRI Ø  Is present even in concussion / mild TBI 31
  32. 32. Diffuse Axonal Injury Ø  www.learningradiology.com/archives2008/COW%20... 32
  33. 33. 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
  34. 34. Pathophysiology - Secondary Injury Exacerbating factors Ø  HTN (systemic and intracranial) Ø  O2 delivery Ø  Fever Ø  Seizures Ø  glucose 34
  35. 35. TBI Definition TBI GCS LOC P-T CT Amnesia abnl <20 min <24 hrs Moderate 9 - 12 20 min – 7d 24 hrs – 7d Severe >7d >7d (initial in ED at 30 minutes from the injury) Mild 13 - 15 <8 No Yes 35
  36. 36. Mild TBI TBI is oxymoronic (nothing mild about it) Ø  Mild Ø  Is only describing the visible brain injury, not describing functional impairment Ø  Can have severe disability from Mild TBI 36
  37. 37. 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 37
  38. 38. 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
  39. 39. Concussion & Mild TBI Signs of Concussion - CONFUSION –  Inability to focus attention –  Vacant stare –  Memory deficits –  Delayed verbal expression –  Disorientation 39
  40. 40. 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 40
  41. 41. HOW TO REMEMBER THESE SYMPTOMS? 41
  42. 42. Signs of Concussion – CONFUSION HOW DO LECTURES MAKE ME FEEL? • Inability to focus attention • Vacant stare (befuddled facial expression) Victor M. Campos, Jr. (Flickr) 2009 John Morgan (Flickr) 2009 • Disorientation Delayed verbal expression 42 • Memory deficits
  43. 43. Signs of Concussion – SPEECH, COORDINATION, EMOTIONAL HOW DOES DRINKING MAKE ME FEEL? • Slurred or incoherent speech • Gross incoordination • Emotionality out of proportion to circumstances Paukrus (Flickr) 2012 • Any period of LOC (coma, unresponsiveness to stimuli) 43
  44. 44. 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 44
  45. 45. 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
  46. 46. Concussion & Mild TBI: Neurological Sequela Progression of Symptoms Ø  Indicates bleeding and / or progressive edema Ø  Worsening headache, confusion, lethargy, focal neurological signs 46
  47. 47. 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 47
  48. 48. 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: Sensation- examples: Finger-to-Nose/ Rhomberg Coordination- examples: Tandem walk Finger-nose-finger 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 48
  49. 49. 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 49 SAC Total Score /30
  50. 50. Concussion & Mild TBI Revised WPTAS (Westmead Post-Traumatic Amnesia Scale) -1 wrong answer indicates cognitive impairment Ø  Ø  Ø  Ø  Ø  Ø  Ø  Ø  Ø  Ø  What is your name? What is the name of this place? Why are you here? What month are we in? What year are we in? What town are you in? How old are you? What is your date of birth? What time of day is it (morning, afternoon, evening?) Three pictures are presented for subsequent recall Cathy Calamas 2011 (Flickr) Plaisanter 2010 (Flickr) 50 Sassy Bella Melange 2008 (Flickr)
  51. 51. 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
  52. 52. 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
  53. 53. 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 Undetermined 53
  54. 54. Source Undetermined Increase the number of CT’s 54
  55. 55. Source Undetermined Increase the number of admissions 55
  56. 56. 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
  57. 57. Home Observation of Mild TBI Return to ER if: •  Avoid strenuous activity for 24 hours Vision difficulties Worsening headaches •  Awakened q2 hr for 24 hours Won’t wake up Vomiting New somnolence or confusion Restless, unsteady Fever, stiff neck Incontinence bowel or bladder Seizure 57
  58. 58. 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
  59. 59. Second Impact Syndrome - RTP None are evidenced based / prospectively validated Ø  Cantu, Ø  Grade Colorado, AAN 1 Ø  Concussion Grade 2 Grade 3 symptoms, amnesia, LOC 59
  60. 60. Cantu Guideline for Concussion Management Grade 1 Presentation Grade 2 Grade 3 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 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 Management Athlete may return to play if asymptomatic for one week Adapted from: Cantu, RC, J Athl Train 2001; 36:244 60
  61. 61. Colorado Guideline for Concussion Management Grade 1 Grade 2 Grade 3 Presentation 1. Confusion 1. Confusion with amnesia 2. No loss of consciousness 1. Loss of consciousness of any duration Management Evaluate athlete 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. without amnesia 2. No loss of consciousness immediately and every 5 minutes. Athlete may return to play if amnesia or symptoms do not appear for 20 minutes. Colorado Medical Society, Report of the Sports Medicine Committee, 1991. 61
  62. 62. American Academy of Neurology - RTP 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.  Management Athlete may return to play if asymptomatic at 15 minutes. Athlete can return to play if asymptomatic for one week. American Academy of Neurology, Neurology 1997; 48:581 Loss of consciousness of any duration 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). 62
  63. 63. Second Impact Syndrome - RTP None are evidenced based / prospectively validate Grade 1 15 minute Grade 2 Ø  AAN – Ø  Cantu – Ø  Colorado – 20 minute 1 week 1 week 1 week Grade 3 1-2 weeks 2 weeks 4 weeks 2 weeks . 63
  64. 64. Second Impact Syndrome - RTP None are evidenced based / prospectively validate Grade 1 Grade 2 1 week Ø  AAN – 15 min Ø  Cantu – 1 week Ø  Colorado – 20 minute 1 week Grade 3 1-2 weeks 2 weeks 4 weeks 2 weeks Bottom Line: No RTP while symptomatic Go to ER if: LOC > 1 minute OR concussion symptoms > 15-30 mins 64
  65. 65. UpToDate 65
  66. 66. 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  Ø  Most commonly d/t Mild TBI. Less common with whiplash, Mod / Severe TBI LOC not needed for diagnosis 66
  67. 67. 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
  68. 68. Post Concussive Syndrome 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
  69. 69. Post Concussive Syndrome 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
  70. 70. 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
  71. 71. Post Concussive Syndrome 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
  72. 72. 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
  73. 73. Source Undetermined 73
  74. 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 overlapdizziness, headache, anxiety, neck pain, reading difficulty [cognitive, change in personality, behavior, irritability, depression, insomnia] 74
  75. 75. 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
  76. 76. 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  Ø  Ø  Ø  43 TBI patients Symptomatic for 3.5 yrs; fully evaluated and treated prior to intervention Diagnosed w/ VH and treated w/ prismatic lenses 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
  77. 77. TBI and VH Good newsØ  Only treatment so far that addresses so many symptoms HoweverØ  Only partially addresses cognitive and neuropsych issues 77
  78. 78. 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
  79. 79. Management of Severe TBI Ø  GCS Ø  Care <8 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
  80. 80. 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
  81. 81. 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
  82. 82. 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
  83. 83. 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
  84. 84. 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
  85. 85. 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
  86. 86. 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
  87. 87. Source Undetermined 87
  88. 88. Pediatr Crit Care Med 2003 VOL. 4, No. 3 (Suppl.) 88
  89. 89. Source Undetermined 89
  90. 90. Post Traumatic Agitation Witholeary 2009 (Flickr) 90
  91. 91. 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
  92. 92. TABLE 3 Medications with potential to impede TBI recovery* Medications Class 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
  93. 93. Drugs considered safe and effective for TBI neurobehavioral sxs Usual daily dosage* Amantadine 100 to 400 mg Bromocriptine Apathy Drug 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
  94. 94. 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 94
  95. 95. Martin Lopatka 2008 (Flickr) 95
  96. 96. Bibliography Ø  Ø  Ø  Ø  Ø  Ø  Ø  Ø  Phan N, Hemphill, JC. Traumatic brain injury: Epidemiology, classification, and pathophysiology. UpToDate January 2010 Evans R. Concussion and mild traumatic brain injury. UpToDate. January 2010 Evans R. Postconcussion Syndrome. UpToDate. January 2010 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. 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. 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 agitation. Am J Phys Medication Rehabil 2002 Feb. 81(2):90-3 Daniels JP. Traumatic brain injury: choosing drugs to assist recovery. J Fam Prac. 2006 May;5(5) 96
  97. 97. Questions 97

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