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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 [email protected] 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. 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To use this content you should do your own independent analysis to determine whether or not your use will be Fair. 2 Traumatic Brain Injury Mark Rosner MD September 15, 2010 3 Goals and Objectives Demographics of TBI Pathophysiology of TBI – Primary & Secondary Injury Assessment & Treatment of Mild TBI / Concussion Second Impact Syndrome and Return to Play guidelines Post Concussive Syndrome TBI & Binocular Vision Dysfunction (VH) Management of Severe TBI Management of Post Traumatic Agitation 4 STRAP UP! Leo Dirac (Flickr) 2007 5 TBI – Demographics 1.5 million new cases per year in the US Could be 15-20% higher due to underreporting of mild TBI / concussions Leading cause of death in US for ages 145 6 TBI – Demographics Risk factors: Sex: males 2.5:1 females Lower socioeconomic status Age – 0-4 – 15-24 (1/2 of all injuries) – >65 7 TBI – Demographics Mortality = 2% ER & Go Home (mild TBI) = 65% ER & Admit (mod / severe) = 16% Never came to the ER (mild TBI / concussion) = approximately 17% 8 TBI – Demographics Leading causes of TBI: Falls (older) = 30% MVC (young adults) = 45% Violence (lower socioeconomic class)= 5% Work accidents = 10% Recreational accidents = 10% 9 TBI – Demographics Recreational Accidents – Sports Ice Hockey Soccer Boxing Rugby Football – incidence = 10% college 20% high school PER YEAR! 10 TBI – Demographics Combat related In a 1 year deployment – head injury: – 10% had change in MS – 5% had LOC due – – – – 15% TBI rate to Blasts / explosions Falls MVA Penetrating wounds 11 TBI – Demographics Disability 1-2% US population (3-5 million) has LTD (neurologic and functional impairment) due to mod / severe TBI What about mild TBI!! Under-recognized as cause of disability Military has not been considering soldiers w/ mild TBI for Purple Heart 12 TBI – Classification Clinical Severity Scores: GCS: Severe < 8 Moderate = 9-12 (13) Mild = 13 (14) - 15 13 TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component Best eye response Best verbal response Best motor response Response Score No eye opening 1 Eye opening to pain 2 Eye opening to verbal command 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 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 Michael Spencer (Flickr) 2009 15 TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component Best eye response Best verbal response Best motor response Response Score “Only a Couple” Beers No eye opening 1 Eye opening to pain 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 6 XXX 14 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 Gorivero (Wikimedia Commons) 2007 17 TABLE 1 Using Glasgow Coma Scale scores to evaluate brain injury severity Component Best eye response Best verbal response Best motor response Response Score “Way Too Many” Beers No eye opening 1 Eye opening to pain 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 6 9 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 TBI – Classification Neuroimaging Scales Marshall Rotterdam Not for ED – predicts risk of ICP 19 Pathophysiology - Primary Injury Occurs at the time of trauma 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 Pathophysiology - Primary Injury Damage Hematoma / hemorrhage (extra-axial) Contusion Shearing of white matter = diffuse axonal injury (DAI) Edema / swelling 21 Pathophysiology - Primary Injury Extra-axial Injuries Epidural hematoma Subdural hematoma SAH The deeper the injury, the larger the amount of energy transferred 22 Pathophysiology - Primary Injury Epidural Hematomas Torn dural vessels (middle meningeal artery Lenticular Almost always associated with skull fracture Tend NOT to be associated with brain damage 23 24 Source Undetermined Pathophysiology - Primary Injury Subdural Hematoma Bleeding from bridging veins OR from cortical contusion Crescent shaped Usually ARE associated with brain injury 25 Source Undetermined 26 Pathophysiology - Primary Injury SAH – disruption of small pial vessels Intraventricular – tearing of subependymal veins 27 Hawaii.edu Learning Radiology.com SAH 28 Pathophysiology - Primary Injury Most common injury - Focal cerebral contusions Occur at basal frontal and basal temporal regions due to striking basal skull surfaces 29 http://mksforum.net/forum/showthread.p hp?p=204094 http://www.itriagehealth.com/wl/dis ease/cerebral-contusion-(bruise-ofbrain) 30 Pathophysiology - Primary Injury Diffuse Axonal Injury Due to shearing forces Seen better on MRI Is present even in concussion / mild TBI 31 Diffuse Axonal Injury 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 Accelerated release of excitatory neurotransmitters Ach, glutamate and aspartate, – generates free radicals - injure cell membranes Mitochondrial dysfunction Inflammatory responses Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury All cause cell death, cerebral edema and ICP 33 Pathophysiology - Secondary Injury Exacerbating factors HTN (systemic and intracranial) O2 delivery Fever Seizures glucose 34 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 Mild TBI Mild TBI is oxymoronic (nothing mild about it) Is only describing the visible brain injury, not describing functional impairment Can have severe disability from Mild TBI 36 Concussion - ?Definition? Concussion is less severe than Mild TBI, but…terms difficult to differentiate ---consider all concussions to be Mild TBI’s Reflects functional disturbance rather than major structural injury 37 The American Academy of Neurology (AAN) definition of Concussion: Trauma-induced alteration in mental status Confusion and amnesia - hallmarks of concussion Occurs w/i 5 minutes of the head trauma May or may not involve loss of consciousness This definition recognizes three concussion grades: Grade 1: concussion sxs lasts <15 minutes, w/o LOC Grade 2: concussion sxs lasts >15 minutes, w/o LOC Grade 3: LOC. 38 Concussion & Mild TBI Signs of Concussion - CONFUSION – Inability to focus attention – Vacant stare – Memory deficits – Delayed verbal expression – Disorientation 39 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 HOW TO REMEMBER THESE SYMPTOMS? 41 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 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 Concussion & Mild TBI Other Symptoms Occurs within mins to hours: Headache, dizziness / vertigo / imbalance Occurs within mins – days: Mood & cognitive disturbances, sensitivity to light & noise, sleep disturbances 44 Concussion & Mild TBI: Neurological Sequela Seizures Considered 2/2 TBI if it onsets within 7d NOT epilepsy Occurs in < 5% of mild / mod TBI Increased occurrence with severe TBI – 25% occur within 1 hr – 50% occur within 1 day The risk of epilepsy: – 6% (s/p TBI) – 25% (s/p TBI with seizure) 80% of post-traumatic epilepsy onsets w/i 2 yrs 45 Concussion & Mild TBI: Neurological Sequela Progression of Symptoms Indicates bleeding and / or progressive edema Worsening headache, confusion, lethargy, focal neurological signs 46 Concussion & Mild TBI Evaluation and Management: Cognitive assessment Simple orientation questions inadequately sensitive SAC –Standardizes Assessment of Concussion Tool for sideline assessment of athletes – change in 1 point signifies concussion 47 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 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 71-9, 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 Concussion & Mild TBI Revised WPTAS (Westmead Post-Traumatic Amnesia Scale) -1 wrong answer indicates cognitive impairment 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) Neuroimaging CT is the preferred modality for acute evaluation of TBI GCS of 15 = 5% abnormal scans GCS of 13 = 30% abnormal scans Only 1% of abnormal scan need to go to the OR MRI – sees more (contusions, DAI, small bleeds), but doesn’t change clinical management 51 Neuroimaging Canadian CT Head Rule for mild TBI GCS < 15 two hours after injury Suspected open or depressed skull fracture Any sign of basilar skull fracture (hemotympanum, raccoons, Battles, CSF leak) >2 episodes of vomiting >65 years old Amnesia before impact > 30 minutes Dangerous mechanism (pedestrian / MVA, ejected, fall from > 3 feet or > 5 stairs) 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 Source Undetermined 53 Source Undetermined Increase the number of CT’s 54 Source Undetermined Increase the number of admissions 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 Worsening headaches New somnolence or confusion Restless, unsteady Vision difficulties Vomiting Fever, stiff neck Incontinence bowel or bladder Seizure 57 Second Impact Syndrome Diffuse 2nd cerebral edema occuring after a concussion while the patient is still symptomatic from the 1st concussion Rare Controversial Doesn’t occur frequently in boxers (shouldn’t it?) But just in case it’s real….RTP 58 Second Impact Syndrome - RTP None are evidenced based / prospectively validated Cantu, Grade Colorado, AAN 1 Concussion Grade 2 Grade 3 symptoms, amnesia, LOC 59 Cantu Guideline for Concussion Management Presentation Grade 1 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 Colorado Guideline for Concussion Management Grade 1 Presentation 1. Confusion without amnesia 2. No loss of consciousness Management Evaluate athlete immediately and every 5 minutes. Athlete may return to play if amnesia or symptoms do not appear for 20 minutes. Grade 2 Grade 3 1. Confusion with amnesia 2. No loss of consciousness 1. Loss of consciousness of any duration 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 Medical Society, Report of the Sports Medicine Committee, 1991. 61 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 Second Impact Syndrome - RTP None are evidenced based / prospectively validate Grade 1 15 minute Grade 2 AAN – Cantu – Colorado – 20 minute 1 week 1 week 1 week Grade 3 1-2 weeks 2 weeks 4 weeks 2 weeks . 63 Second Impact Syndrome - RTP None are evidenced based / prospectively validate Grade 1 Grade 2 1 week AAN – 15 min Cantu – 1 week 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 UpToDate 65 Post Concussive Syndrome Symptoms Headache Dizziness / vertigo Fatigue Noise sensitivity, light sensitivity Cognitive impairment (decreased ability to remember, to process info, to concentrate) Neurobehavioral & Neuropsychiatric symptoms (change in personality, behavior, irritability, anxiety, depression, insomnia) Most commonly d/t Mild TBI. Less common with whiplash, Mod / Severe TBI LOC not needed for diagnosis 66 Post Concussive Syndrome CONTROVERSIAL Symptoms are vague, subjective, common with many other conditions, difficult to measure / test Doesn’t correlate to severity of TBI, GCS, length of LOC, length of amnesia, CT / MRI abnormalities Underlying pathophysiology is unknown 67 Post Concussive Syndrome 30-80% of mild – mod TBI will have some symptoms of PCS Many are better at 1 month, most are better at 3 months 10-15% are still symptomatic at 1 year – headache, dizziness, anxiety, cognitive – The Miserable Minority Physiologic / functional neuroimaging has same changes as does migraine, depression 68 Post Concussive Syndrome Psychogenic? symptoms similar to anxiety / PTSD, depression – headache, dizziness, sleep impairment Cognitive impairments are seen in anxiety / depression PTSD is the strongly associated with PCS 69 Post Concussive Syndrome 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) Be very careful about diagnosing malingering Litigation? – Many who sue aren’t severe – Many that are severe don’t sue No correlation 70 Post Concussive Syndrome Treatment of symptoms No magic bullet that addresses all symptoms (maybe VH?) Treat Headache, dizziness, psych per SOP – no special tx d/t TBI etiol 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? 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 Vertical Hetero Phoria: – Line of sight of one eye is higher than the other eye when not attempting to fuse an image 72 Source Undetermined 73 TBI and Vertical Heterophoria As compared to Heterotropia (strabismus), patients with Heterophoria are still able to maintain a single image but at great expense Brain avoids diplopia at all costs - overexert EOM’s – elevators and depressors Overuse and fatigue of EOM’s causes symptoms: – dizziness, 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] 74 TBI and Vertical Heterophoria As compared to Heterotropia (strabismus), patients with Heterophoria are still able to maintain a single image but at great expense Brain avoids diplopia at all costs - overexert EOM’s – elevators and depressors Overuse and fatigue of EOM’s causes symptoms: – dizziness, dizziness, anxiety, neck pain, reading difficulties 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 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 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: TBI seems to be precipitating / exacerbating VH Treatment w/ prismatic lenses improves both VH and PCS symptoms 76 TBI and VH Good news Only treatment so far that addresses so many symptoms However Only partially addresses cognitive and neuropsych issues 77 Chronic TBI Cumulative neuropsychological impairment – Cognitive impairment / dementia Football, soccer Dementia pugilistica – boxing – 20% of prof boxers w/ >20 fights Helmets – good or bad? – Decreases TBI in baseball, ice hockey, downhill skiing, snowboarding, bicycles, motorcycles – Encourages risky behavior 78 Management of Severe TBI GCS < 8 Care should be obtained at the most appropriate facility – Level 1 trauma center Secondary brain injury caused by: – Hypoxemia - keep oxygenated – intubate early – Hypotension – fluid resuscitate – Seizures – consider prophylactic antiepileptics Shock is almost never due to head injury alone – look for other sources (spinal cord, internal bleeding) Don’t withhold fluids d/t concerns of exacerbating cerebral edema 79 Management of Severe TBI ICP monitoring indicated for GCS < 8 These patients are at high risk for intracranial hypertension (IC HTN), which requires aggressive tx Open fontanels – can still get ICP For GCS > 8 if exam can’t be followed (sedation, paralysis) IC HTN predicted by 2/3: – Systolic HTN – motor posturing – age > 40 80 Management of Severe TBI Tx IC HTN when ICP > 20 Rate of complications from ICP monitors is low cerebral perfusion pressure (CPP) = MAP ICP Maintain CPP >70 81 Treatment of IC HTN 1. Analgesia and sedation are initial treatments 2. If euvolemic, elevate HOB 30 degrees 3. Paralysis 4. Can drain CSF to lower ICP through ventriculostomy catheter (preferred) or via LP 82 Treatment of IC HTN 5. Osmotic Agents 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 Mannitol also decreases blood viscosity for approximately 75 minutes 3% saline – continuous infusion 83 Treatment of IC HTN 6. Hyperventilation to decrease ICP Keep PaCO2 between 30-35 PaCO2 < 30 second tier option – can cause decreased CBF 2 / 2 vasoconstriction, causing iatrogenic ischemia Aggressive hyperventilation if herniation or rapid decline of neuro status 84 Treatment of IC HTN 7. High dose Barbiturates Reduces ICP and has neuroprotective properties – decreases cerebral metabolism / need for O2 by 50% 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: < 48 hours from injury No episode of ICP > 40 GCS > 3 Secondary clinical deterioration Evolving herniation 86 Source Undetermined 87 Pediatr Crit Care Med 2003 VOL. 4, No. 3 (Suppl.) 88 Source Undetermined 89 Post Traumatic Agitation Witholeary 2009 (Flickr) 90 Post Traumatic Agitation 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 olanzapine (Zyprexa), ziprasidone (Geodon) considered safer Acute management of agitation in ED (my choices): Benzodiazepines Narcs Haldol Don’t have experience yet w/ olanzapine & ziprasidone 91 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 Drugs considered safe and effective for TBI neurobehavioral sxs Apathy Drug Usual daily dosage* 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 Demographics of TBI Pathophysiology of TBI – Primary & Secondary Injury Assessment & Treatment of Mild TBI / Concussion Second Impact Syndrome and Return to Play guidelines Post Concussive Syndrome TBI & Vertical Heterophoria Management of Severe TBI Management of Post Traumatic Agitation 94 Martin Lopatka 2008 (Flickr) 95 Bibliography 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 Questions 97