Presentation on theme: "Epidemiology and Pathophysiology of Traumatic Brain Injury in Sports"— Presentation transcript:
1 Epidemiology and Pathophysiology of Traumatic Brain Injury in Sports The incidence of TBI exceeds the annual rates of more well established neurological diagnosis of Multiple Sclerosis, Parkinson disease and Alzheimer disease combined.Over 1 million new cases of TBI occur each year in the USDavid W. Wright, M.D.
2 CaseYou are volunteering as a team physician at your local community league hockey game.JR approaches the net for a score when two opposing team players hit him from behind and slam him into the boards.
3 Case continuedHe was slightly off balance when his head hit the brick stepwall.As he hit the ice his body stiffened. His arms stretched outward for a moment before he roused.Finally, he pulled himself up, shook his head and returned to the bench.
4 Case continuedThe next period, JR gets slammed into the corner post of the goal along with the goalie.When he gets up and skates to the bench, he is dazed.You notice a glassy stare as the coach yells at him to pay attention.
5 Case continuedYou convince the coach to sit the player out for the period.Immediately after the incident, he is dazed and has minimal recollection of the last period.His physical and basic neurological evaluations are normal except for the mini-mental status exam.He is slow to answer, cannot calculate serial sevens, and remembers only 1 word of the five you asked him to remember.
6 Case continuedFifteen minutes later the coach is screaming to get him back into play. The player adamantly argues to you that he is fine and feels normal.You decide to reexamine his mini-mental status. He improves his score and is able to remember four out of five words, but still cannot do more than 3 serial sevens and still does not recall any details immediately surrounded the “ding”.
7 Thoughts to PonderWhat is the significance of JR’s blank stare when he first comes of the ice? What should you do?How will you determine if JR has a head injury?What are the key findings on the sideline physical exam to look for?How significant is the fact that he did not seem to lose consciousness?Can a mild concussion be life threatening?Should JR return to play and when?If he gets another concussion, could the damage be cumulative?
8 Sports Head Injuries 300,000 sports related concussions per year 1 out of 20 athletes will get a concussion10% of college and 20% of high school athletes will have a concussionYounger athletes are at higher riskEffects of concussions are cumulativeHead injuries account for 65%-85% of all sport related fatalitiesCosts to society of sports head injury unknown, but overall head injury costs are estimated at $56 billion annually.
11 Winter Sports – Head Injuries Ice Hockey – one of highest incidence of any sport0.27 – 2.24 per 1000 athlete-exposures1,2,3Skiing1.27 per 1000 visitor-exposure12,700 per year in US3Leading cause of death in Skiing injuriesHead injuries account for 14% of all injuries in adults and 22% in children (<16 yo) 3SnowboardingUnknown rate, but head injury increasing from 1000 in 1993 to 5,200 in 19973Beginners have higher incidence of head injury1Cantu, et al; 2CIUAU; NCAA; 3U.S. Consumer Product Safety Commission
12 Winter Sports – Head Injuries Tobogganing, acrobatic freestyle skiing and tubing also account for high incidence of head injury – rate unknownNumber of concussions that do not seek medical attention under-reported and therefore unknown.Ellison, et al; Clancy et al; Johnson et al; Murray et al; Scharplatz et al.
13 Do helmets make a difference? 44% of head injures in adult skiers (7,700 annually) could be prevented with helmets.53% of head injures in childen skiers (2,600 annually) could be prevented with helmets.U.S. Consumer Product Safety Commission
14 Winter Sports - Helmets Underutilized 19/26 ski resorts had helmets for rent1None included in standard package1Only 1% - 8.6% rented helmets1In one study of ER visits for skiing related head injuries, 1/350 was wearing helmet21Hennessay et al; 2Levy et al.
15 HEAD AND CERVICAL SPINE FATALITIES FOR COLLEGIATE FOOTBALLHelmets Save BrainFootball – dramatic reduction in head injuries after new rules about spearing (1976) and helmet use (1978). [Mueller et al.]Head InjuryCervical SpineYearFrequencyPercent8717.23227.311522.82319.716232.14235.96913.71412.0336.554.3 397.7 10.8TOTALS505100.0117
16 Are there permanent and long-term sequellae of mild concussions? Bogdanoff et al. - structural changes in brains of boxers after concussions.Casson et al. Atrophy and chronic encephalopathy after repeat concussions in boxers.Lampert et al. - morphological changes in the brains of boxers.Seroni et al. signs of early dementia in young boxers
17 Are there permanent and long-term sequellae of mild concussions? Erlanger et al – long-term cognitive deficits after concussion.Cantu et al. - second impact syndrome from mild concussion
18 Neuropsychological Deficits Warden et al, 200114 concussions during boxing out of 483 military cadetsPersistant slowing of Simple Reaction Time at 4 daysLovell et al, 2003Some Grade 1 concussions or “Dings” have cognitive deficits for at least 6 daysPERSITENT DEFICITSRT– subjects react asap to stimulusCPT- is letter same as immediate preceding letterMathematical processing- 3 step digital arithmetic problemsSternberg procedure, matching to sample, codes substitution,NEUROPSYCH TESTINGWarden et al, 2001
19 Long lasting? Permanent? Post Concussion Syndrome Symptoms at 3 months in 20-75%Rutherford et al.145 patients with mTBI51% with persistent symptoms 6 weeks after their injury
20 Post Concussion Syndrome Can last weeks to monthsSymptomsFatigueHeadachesEquilibrium disturbancesDifficulty with concentrationNauseaMemory complaintsBlurred visionLight sensitivityDepressionSleep disturbancesLoss of appetiteAnxietyHallucinations3 symptoms lasting > 3 moMALINGERINGKurt Warner
21 Diagnosis Deficits Neuropsychological testing, Neuroimaging Clinical exam and impressionOften not sensitiveNeuropsychological testing,Best testNot available on sidelinesNeuroimagingCurrently not sensitive and/or not availableCT, MRI, fMRI, SPECT, PETReaction time could lead to non- brain sports injuries or impaired performance
22 Are Concussions Cumulative? In addition to the structural changes listed previously, each concussion can take its toll on cognition.[Freidman et al.; Jordan et al; Erlanger et al; Collins et al; Kelly et al; Cantu et al: Drew et al; Gaetz et al; Mrazik et al; Gronwall et al; Bailes et al.]Athletes with > 3 concussions suffer worse after symptoms with subsequent. [Collins et al.]There is a six times risk for repeat concussion if had one previously. [Kelly et al.]
23 Can Mild Head Injury Be Lethal? Second impact syndrome (SIS)First described in 1973 by SchneiderOnset usually causes rapid neurological demise, brain swelling, and death.Inciting factor is second impact prior to recovery of initial mild concussion.Cantu, et al.
24 Second Impact Syndrome Incidence in Football35 probable cases17 “confirmed”10 others “likely”An athlete who has sustained an initial head injury, most often a concussion, sustains a second head injury before symptoms Associated with the first head injury have fully cleared.Cerebral vascular congestion from loss of autoregulation, cerebral swelling, inc ICP. Death results from transtentorial brainstem herniation. Time course 2-5 minutesCantu, et al.
25 Second Impact Syndrome - facts Young athletes more susceptible.Second impact may be very mild and not even to the head.Over 35 reported in football alone.Not limited to football, documented in ice hockey, skiing, etc.Cantu, et al.
26 Second Impact Syndrome - etiology Malignant brain swelling and marked increased intracranial pressures.Due to cerebrovascular congestion, or loss of cerebrovascular auto-regulationRapid onset – high mortality >50%, morbidity nearly 100%Cantu, et al.
27 Definition: Concussion Concussion is atrauma-induced alteration in mental statusNotice - no mention of LOCConfusion and amnesia are key
28 Diagnosing Recognition difficult Variety of signs and symptoms Signs can be subtleAthletes reluctant to reportAwareness of problem limited among health professionalsNo specific diagnostic tool
29 Clinical Signs of Concussion Vacant stareDelayed verbal and motor responseInability to focus attentionDisorientationSlurred or incoherent speechGross observable incoordinationEmotional disturbancesMemory deficitsAny Loss of Consciousness
30 Clinical Symptoms of Concussion EarlyHeadacheDizziness or vertigoLack of awareness of surroundingsNausea and VomitingLatePersistent headacheLightheadednessPoor attention and memory dysfunctionEmotional, irritable and frustratedIntolerance to bright lights or sounds, blurred vision, ringing in earAnxiety and depressed moodSleep disturbances
31 Mental Status Testing in the Field OrientationTime, place, situationConcentrationDigits backwards (3-1-7)( )( )Months of the year in reverse orderMemoryRecall of 3 words and objects at 0 & 5 minutesRecent news events, details of the contestNeuro examStrength, sensation, coordination and agilityExertional Provocation Tests5 push-ups, 5 sit-ups, 5 knee bends, 40 yard sprint
32 General Overview of TBI Classification of TBIMild (GCS 13-15)Moderate (GCS 9-12)Severe (GCS 3-8)Severe TBI or GCS less than 8 considered to be comatose. Implications for airway control and ICP monitoring.
33 Primary & Secondary Injury The first event occurs on impact. Dr. K delivered a superb discussion on the principles and mechanics of injury.Remember the primary, secondary and tertiary impact phenomena. The primary insult occurs from the second and third impact by transmitting the forces through the gelatine like substance of the brain.Imagine having a circuit board where the board was made up of gelatin and the connections were microscopic hairs. Now apply a force to this tissue. Millions of connections are now misaligned. This is the shearing force of the initial impact. For many, the shearing and axonal tearing is too much.Even more complicated - running through the circuit board are large water pipes that burst open and begin to leak. Water wreaks havoc on electric circuit boards shorting out existing circuits and causing a mass effect.Some shearing occurs even with minor TBI. These are the primary insults of TBI.Most common locations of brain contusions after trauma
34 Lacerations Contusions Fracture Coup Contrecoup Herniation Gliding IntermediaryLaceration – injury to the brain parenchyma with a disruption of the pia-arachnoid lining.Contusion – injury to the brain parenchyma (bruise) without disruption of the covering.Coup – a brilliant sudden stroke of stratagem – deathblow: a sudden violent event– a final decisive stroke or event
35 Extra cellular k inc from 4-5 to 20-50, inhibition of action potentials and LOC. Could take several secondsK release can lead to release of glutamate, calcium mediated neurotoxicity.,
38 Secondary Insults at the Neuronal Level Excitatotoxic aminoacidsGlutamateGlycineReceptorsNMDAAMPA/KAOtherMassive calcium influx starts a cascade of deleterious events within the cell subsequently leading to cell necrosis or apoptosis.
39 Structural and Physiological Changes in Response to Brain Injury Events Immediately Following TraumaDisruption of the integrity of the tissueDisruption of the blood-brain barrierIncrease in neurotransmitter levelsDevelopment of edemaInitiation of inflammationRelease of free radicalsEvents Hours to Days Following TraumaAll of the aboveDevelopment of secondary edemaHyperplasia and hypertrophy of glial cellsActivation of inflammatory cellsRelease of neurotrophic factorsExpression of receptors for neuropeptidesAccumulation of free radicals and lipid peroxidationApoptosis and trans-neuronal degenerationStein, et al.
40 Secondary Insults at the Macroscopic Level Brain IschemiaHypotensionHypoxemiaAnemiaIntracranial hemorrhagesEdemaElevated ICPMetabolic insultsWhen the force is transmitted to the brain, a variety of insults occur. Even though these insults are initiated at the point of injury “primary injury”, they are significant contributors of ongoing “secondary” injury
41 Subdural Hematoma Epidural Hematoma First is epidural, caused principally by middle meningial tear, epidural on top of dura matter.Second is subdural, caused principally by bridging veins and clot under duraSubdural HematomaEpidural Hematoma
42 Edema Recognize Dilated pupil Posturing Worsening neurological status CTTreatmentABC’sMannitolHypertonic SalineTwo/three etiologies and two main types of edema.
43 Intracerebral Hypertension RecognizeDilated pupilPosturingWorsening neurological statusCTICP monitorTreatment in Emergency DepartmentABC’sMannitolHypertonic salineModerate hyperventilation (pCO )Rapid neurosurgical consultOne of the most important Concepts is the Cerebral Perfusion Pressure.
44 Future Better tools for Sideline Assessment Serum Markers of NeuroinjuryBetter diagnostic tools for PCSPharmacological interventionsImproved understanding of the mechanisms and who is at risk.
45 Case Follow-upJR’s memory deficits seemed to resolve. Under the pressure of the coach, he returned to the game despite your vigorous discouragement. You had no authority to demand he stay out. During the last period, JR was checked from behind. The impact was hard but he did not lose his balance. He continued to play for approximately 5 minutes when suddenly he collapsed on the ice. You found him unresponsive. His pupils were initially responsive to light and equal in size. His vital signs were O2 sat 99%, BP 130/palp, HR 76, RR 24. When you called for the ambulance to transport him to the ER, you noticed his respirations became slower and more labored, and he seemed to extend his arms. A recheck of his pupils found the left one 4 mm and the right 2 mm. A recheck of the vital signs in the ambulance were O2 sat 98%, BP 160/palp, HR 55, RR 8.
46 Case Follow-up continued Because you appropriately suspected secondary impact syndrome and Cushing’s response (due to increased intracranial pressure), you intubated JR using the rapid sequence technique and hyperventilated him. Normal saline was started at KVO though a large bore IV. No other drugs were available in the ambulance. JR was rushed to the emergency department. In transport he began having seizure activity and was given 5 mg of diazepam. Evaluation in the ER included proper placement of the airway, oxygenation at 95%, and repeat exam and vitals signs. The repeat VS were: O2 sat 99%, BP 210/70, HR 45, RR 16 (ventilated). JR was still extending his arms and had a GCS of 3t (E1VtM2).
47 Case Follow-up continued Mannitol was initiated and Neurosurgery was consulted immediately. JR was whisked to the CT scanner where diffuse cerebral edema, slit-like ventricles, and mild uncal herniation were seen on the CT monitor. He was transferred to the neuro intensive care unit and an intracranial pressure monitor was inserted. The monitor consistently displayed ICP’s in the 40-50’s despite mannitol, sedation, and barbiturates. JR subsequently died later that evening.