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Epidemiology and Pathophysiology of Traumatic Brain Injury in Sports

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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 US David W. Wright, M.D.

2 Case You 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 continued He 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 continued The 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 continued You 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 continued Fifteen 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 Ponder What 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 concussion 10% of college and 20% of high school athletes will have a concussion Younger athletes are at higher risk Effects of concussions are cumulative Head injuries account for 65%-85% of all sport related fatalities Costs to society of sports head injury unknown, but overall head injury costs are estimated at $56 billion annually.

9 75 % MTBI

10 Consequences of Concussions
Immediate Cognitive impairment (attention, memory, slowed reaction time) Somatic problems: Sensitivity to light, dizziness, headaches, etc. Life Threatening Second Impact Syndrome Long term Post concussive syndrome (cognitive impairment, personality changes, language difficulties, etc.)

11 Winter Sports – Head Injuries
Ice Hockey – one of highest incidence of any sport 0.27 – 2.24 per 1000 athlete-exposures1,2,3 Skiing 1.27 per 1000 visitor-exposure 12,700 per year in US3 Leading cause of death in Skiing injuries Head injuries account for 14% of all injuries in adults and 22% in children (<16 yo) 3 Snowboarding Unknown rate, but head injury increasing from 1000 in 1993 to 5,200 in 19973 Beginners have higher incidence of head injury 1Cantu, 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 unknown Number 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 rent1 None included in standard package1 Only 1% - 8.6% rented helmets1 In one study of ER visits for skiing related head injuries, 1/350 was wearing helmet2 1Hennessay et al; 2Levy et al.

15 HEAD AND CERVICAL SPINE FATALITIES
FOR COLLEGIATE FOOTBALL[17] Helmets Save Brain Football – dramatic reduction in head injuries after new rules about spearing (1976) and helmet use (1978). [Mueller et al.] Head Injury Cervical Spine Year Frequency Percent 87 17.2 32 27.3 115 22.8 23 19.7 162 32.1 42 35.9 69 13.7 14 12.0 33 6.5 5 4.3  39 7.7  1 0.8 TOTALS 505 100.0 117

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, 2001 14 concussions during boxing out of 483 military cadets Persistant slowing of Simple Reaction Time at 4 days Lovell et al, 2003 Some Grade 1 concussions or “Dings” have cognitive deficits for at least 6 days PERSITENT DEFICIT SRT– subjects react asap to stimulus CPT- is letter same as immediate preceding letter Mathematical processing- 3 step digital arithmetic problems Sternberg procedure, matching to sample, codes substitution, NEUROPSYCH TESTING Warden et al, 2001

19 Long lasting? Permanent? Post Concussion Syndrome
Symptoms at 3 months in 20-75% Rutherford et al. 145 patients with mTBI 51% with persistent symptoms 6 weeks after their injury

20 Post Concussion Syndrome
Can last weeks to months Symptoms Fatigue Headaches Equilibrium disturbances Difficulty with concentration Nausea Memory complaints Blurred vision Light sensitivity Depression Sleep disturbances Loss of appetite Anxiety Hallucinations 3 symptoms lasting > 3 mo MALINGERING Kurt Warner

21 Diagnosis Deficits Neuropsychological testing, Neuroimaging
Clinical exam and impression Often not sensitive Neuropsychological testing, Best test Not available on sidelines Neuroimaging Currently not sensitive and/or not available CT, MRI, fMRI, SPECT, PET Reaction 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 Schneider Onset 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 Football 35 probable cases 17 “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 minutes Cantu, 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-regulation Rapid onset – high mortality >50%, morbidity nearly 100% Cantu, et al.

27 Definition: Concussion
Concussion is a trauma-induced alteration in mental status Notice - no mention of LOC Confusion and amnesia are key

28 Diagnosing Recognition difficult Variety of signs and symptoms
Signs can be subtle Athletes reluctant to report Awareness of problem limited among health professionals No specific diagnostic tool

29 Clinical Signs of Concussion
Vacant stare Delayed verbal and motor response Inability to focus attention Disorientation Slurred or incoherent speech Gross observable incoordination Emotional disturbances Memory deficits Any Loss of Consciousness

30 Clinical Symptoms of Concussion
Early Headache Dizziness or vertigo Lack of awareness of surroundings Nausea and Vomiting Late Persistent headache Lightheadedness Poor attention and memory dysfunction Emotional, irritable and frustrated Intolerance to bright lights or sounds, blurred vision, ringing in ear Anxiety and depressed mood Sleep disturbances

31 Mental Status Testing in the Field
Orientation Time, place, situation Concentration Digits backwards (3-1-7)( )( ) Months of the year in reverse order Memory Recall of 3 words and objects at 0 & 5 minutes Recent news events, details of the contest Neuro exam Strength, sensation, coordination and agility Exertional Provocation Tests 5 push-ups, 5 sit-ups, 5 knee bends, 40 yard sprint

32 General Overview of TBI
Classification of TBI Mild (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
Intermediary Laceration – 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 seconds K release can lead to release of glutamate, calcium mediated neurotoxicity. ,

36 Secondary Insults

37 Neuron Destiny Injured

38 Secondary Insults at the Neuronal Level
Excitatotoxic amino acids Glutamate Glycine Receptors NMDA AMPA/KA Other Massive 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 Trauma Disruption of the integrity of the tissue Disruption of the blood-brain barrier Increase in neurotransmitter levels Development of edema Initiation of inflammation Release of free radicals Events Hours to Days Following Trauma All of the above Development of secondary edema Hyperplasia and hypertrophy of glial cells Activation of inflammatory cells Release of neurotrophic factors Expression of receptors for neuropeptides Accumulation of free radicals and lipid peroxidation Apoptosis and trans-neuronal degeneration Stein, et al.

40 Secondary Insults at the Macroscopic Level
Brain Ischemia Hypotension Hypoxemia Anemia Intracranial hemorrhages Edema Elevated ICP Metabolic insults When 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 dura Subdural Hematoma Epidural Hematoma

42 Edema Recognize Dilated pupil Posturing Worsening neurological status
CT Treatment ABC’s Mannitol Hypertonic Saline Two/three etiologies and two main types of edema.

43 Intracerebral Hypertension
Recognize Dilated pupil Posturing Worsening neurological status CT ICP monitor Treatment in Emergency Department ABC’s Mannitol Hypertonic saline Moderate hyperventilation (pCO ) Rapid neurosurgical consult One of the most important Concepts is the Cerebral Perfusion Pressure.

44 Future Better tools for Sideline Assessment
Serum Markers of Neuroinjury Better diagnostic tools for PCS Pharmacological interventions Improved understanding of the mechanisms and who is at risk.

45 Case Follow-up JR’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.


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