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Sports-Associated Traumatic Brain Injury

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As he hit the ice his body stiffened. His arms stretched outward for a moment before he roused. ... When he gets up and skates to the bench, he is dazed. ... – PowerPoint PPT presentation

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Title: Sports-Associated Traumatic Brain Injury


1
Sports-AssociatedTraumatic Brain Injury
  • 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 surrounding the ding.

7
Sports Head Injuries
  • 300,000 sports related concussions per year
  • Head injuries account for 65-85 of all sport
    related fatalities
  • 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
  • Costs to society of sports head injury unknown,
    but overall head injury costs are estimated at
    56 billion annually.

8
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9
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.)

10
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 (lt16 yo) 3

1Cantu, et al 2CIUAU NCAA 3U.S. Consumer
Product Safety Commission
11
Sports head injuries
  • Snowboarding
  • Unknown rate, but head injury increasing from
    1000 in 1993 to 5,200 in 19973
  • Beginners have higher incidence of head injury
  • 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. U.S. Consumer
Product Safety Commission
12
Are there permanent and long-term sequelae 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

13
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

14
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

Warden et al, 2001
15
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

16
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

17
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 gt 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.

18
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.
19
Second Impact Syndrome
  • Incidence in Football
  • 1980-1993
  • 35 probable cases
  • 17 confirmed
  • 10 others likely

Cantu, et al.
20
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.
21
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 gt50, morbidity
    nearly 100

Cantu, et al.
22
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
23
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.
24
Helmets Save Brain
HEAD AND CERVICAL SPINE FATALITIES FOR
COLLEGIATE FOOTBALL17
  • Football dramatic reduction in head injuries
    after new rules about spearing (1976) and helmet
    use (1978). Mueller et al.

25
Definition Concussion
  • Concussion is a
  • trauma-induced alteration in mental status

Confusion and amnesia are key
26
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

27
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

28
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

29
Mental Status Testing in the Field
  • Orientation
  • Time, place, situation
  • Concentration
  • Digits backwards (3-1-7)(4-6-8-2)(5-3-0-7-4)
  • 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

30
Classification of TBI
General Overview of TBI
  • Mild (GCS 13-15)
  • Moderate (GCS 9-12)
  • Severe (GCS 3-8)

31
Primary Secondary Injury
Most common locations of brain contusions after
trauma
32
  • Lacerations
  • Contusions
  • Fracture
  • Coup
  • Contrecoup
  • Herniation
  • Gliding
  • Intermediary

33
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34
Secondary Insults
35
Neuron Destiny
Injured
36
Secondary Insults at the Neuronal Level
  • Excitatotoxic amino acids
  • Glutamate
  • Glycine
  • Receptors
  • NMDA
  • AMPA/KA
  • Othera

Massive calcium influx starts a cascade of
deleterious events within the cell subsequently
leading to cell necrosis or apoptosis.
37
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

David W. Wright, M.D.
Stein, et al.
38
Secondary Insults at the Macroscopic Level
  • Brain Ischemia
  • Hypotension
  • Hypoxemia
  • Anemia
  • Intracranial hemorrhages
  • Edema
  • Elevated ICP
  • Metabolic insults

39
Subdural Hematoma
Epidural Hematoma
40
Edema
  • Recognize
  • Dilated pupil
  • Posturing
  • Worsening neurological status
  • CT
  • Treatment
  • ABCs
  • Mannitol
  • Hypertonic Saline

41
Intracerebral Hypertension
  • Recognize
  • Dilated pupil
  • Posturing
  • Worsening neurological status
  • CT
  • ICP monitor
  • Treatment in Emergency Department
  • ABCs
  • Mannitol
  • Hypertonic saline
  • Moderate hyperventilation (pCO2 30-40)
  • Rapid neurosurgical consult

42
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.

43
Case Follow-Up
  • JRs 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.

44
Case Follow-Up Continued
  • Because you appropriately suspected secondary
    impact syndrome and Cushings 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).

45
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 ICPs in the 40-50s
    despite mannitol, sedation, and barbiturates. JR
    subsequently died later that evening.

46
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