Ensure that airway is clear (mouthpiece, tongue, etc.)
B – Breathing
Look, listen and feel
C – Circulation
Evaluate for presence carotid pulse
D – Disorientation/Dysfunction
Conscious vs. unconscious
Position and Posture
Position
Ideal circumstances have athlete supine
If prone or side laying, will eventually need to be rolled to supine position
Posture
Decerebrate posture – indicative of brainstem injury
Extension of extremities, retraction of head
Decorticate posture – injury above brainstem
Flexion of elbows/wrists, clenched fists, extension of LEs
Flexion contracture – spinal cord injury at C5-C6 level
Arms flexed across chest
Abnormal Postures
Unconscious Athlete
Activate EMS
Must assume that athlete has head and/or cervical spine injury
If ABCs not intact, must initiate rescue breathing or CPR
If ABCs intact:
Establish and monitor vital signs
Evaluate pupillary response (PEARL)
Palpate skull and c-spine for deformity, swelling, etc.
Equipment Considerations
Consensus that helmet should not be removed during pre-hospital care of head/c-spine injury
Facemask removal allows for access to airway
Shoulder pads should not be removed during pre-hospital care of head/c-spine injury
Straps and laces are cut to expose chest for auscultation and/or chest compressions
Justifiable reasons for removing helmet and shoulder pads
Necessity or likelihood of defibrillation
Inability to remove facemask to access airway
If remove one, must remove other to avoid imbalance
Conscious Athlete – Secondary Survey
Assumes ABCs intact – establish and monitor vital signs
History
Loss of consciousness, mechanism of injury, symptoms (pain, numbness/tingling, etc.)
Orientation x 4 (self, others, place, time)
Inspection
Skull/c-spine alignment
Palpation
For bony deformity, swelling, muscle spasm (guarding)
Neurological screening
Sensory testing (dermatomes) compared bilaterally
Motor testing not performed clinically – if all other symptoms negative, may ask to wiggle fingers and toes to establish distal motor function
Clinical Scenario
Assumes that all field scenario evaluations are benign and it’s determined to be safe to allow the athlete to leave the field for further evaluation on sideline or in clinical environment – continuous monitoring of athlete occurs (vital signs, level of orientation, etc.)
History
Inspection
Palpation
Special Tests
Functional testing
Neurological testing
History
Location of symptoms
Mechanism of injury/etiology
Head vs. cervical spine
Loss of consciousness
Prior history of head injury
Complaints of weakness
Location of Symptoms
Cervical pain or muscle spasm
More concerning if accompanied by numbness, tingling, burning sensations and/or radiating pain
Head pain
If localized, may indicate contusion, skull fracture and/or intracranial bleeding
Most common complaint is headache
Mechanism of Injury
Head injuries
Coup – stationary skull struck by high velocity object, results in trauma at site of impact
Contrecoup – moving skull strikes a non-moving object, brain “floats” and strikes skull opposite impact causing trauma
Rotational or shear forces – sudden acceleration/deceleration forces, can disrupt CNS activity and result in concussive symptoms
Cervical spine injuries
May involve any ROM (flexion, extension, lateral flexion and/or rotation – may be combined)
If flexed ~30 degrees, lordotic curve is lost and cervical spine most susceptible to axial load injury (unable to dissipate forces)
Other Historical Elements
Loss of consciousness
Component of memory evaluation
Can athlete or others establish whether there was or was not momentary loss of consciousness
History of concussion
Recent history of prior concussion increases risk of second impact syndrome
Complaints of weakness
Reports of weakness in extremities may indicate brain, spinal cord and/or nerve root injury
Inspection
Bony structures
Eyes
Nose and ears
Bony Structures
Position of head
Should be centered - if rotated/laterally flexed, may indicate cervical dislocation
Cervical vertebrae
Observe spinous processes for normal alignment - if displaced or rotated, may indicated cervical dislocation
Mastoid processes
Ecchymosis indicative of basilar skull fracture - “Battle’s sign”
Skull and scalp
Evaluate for deformity, swelling and bleeding
Bony Injuries
Eyes
Dazed stare may indicate abnormal function
Nystagmus
Presence of involuntary flutter and/or eye movements
May indicate cranial nerve and/or inner ear injury
Pupil size
Unilaterally dilated pupil indicative of intracranial bleeding
Must be aware of anisocoria – “normal” unequal pupils
Pupils reaction to light
Should be ipsilateral and contralateral constriction with exposure to light
Absence may indicate cranial nerve injury
Pupil Reaction
Nose and Ears
Bleeding from nose may indicate nasal and/or skull fracture
Bleeding from ears may indicate skull fracture
Halo test – gauze placed in ear to absorb leaking fluids, if “halo” forms around sample it indicates leakage of CSF = skull fracture
Ecchymosis around eyes (“raccoon’s eyes”) may indicate nasal and/or skull fracture
Eye Ecchymosis
Palpation of Bony Structures
Skull
Palpate all cranial bones for pain and deformity
Spinous processes
Palpate cervical spinous processes for pain and crepitus associated with fracture
Transverse processes
Can only directly palpate C1, but palpate area over remaining transverse processes for pain and crepitus
Palpation of Soft Tissues
Musculature
Palpate sternomastoid and upper trapezius muscles for spasm secondary to strain, sprain, fracture and/or dislocation
Throat
Palpate thyroid cartilage, cricoid cartilages and hyoid bone to rule out larynx and tracheal injury
Special Tests
Functional testing – evaluates function of CNS
Memory
Cognitive function
Neuropsychological testing (computer based also)
Balance and coordination
Standardized Assessment of Concussion (SAC)
Vital signs
Neurological testing
Cranial nerve function
Nerve root evaluation
Memory
Retrograde amnesia
Difficulty or inability to remember events preceding the injury – more severe if can’t remember events of day before as opposed to more recent events
Some assessed with orientation x 4, pre-game meal?, who played last game?
Anterograde amnesia
Difficulty or inability to remember events after the onset of injury
Athlete given verbal list of items and asked to repeat them serially over time
Cognitive Function
Brain injury can present as abnormal behavior, personality changes, inability to process information accurately
Behavior
May become violent, belligerent, etc. - abnormal
Analytical ability
Typically assessed with serial number repetitions
Information processing
Cannot follow simple instructions
Neuropsychological Testing
Multiple neuropsychological test methods (six in text – not responsible for exam)
Hopkins Verbal Learning Test (HVLT)
Wechsler Digit Span Test (WDST)
Controlled Oral Word Association Test (COWAT)
Used to objectively quantify amount of dysfunction demonstrated by athlete
More and more common to see these tests employed during PPE as baseline upon which to compare results after head injuries and for return to play considerations
Computerized Neuropsychological Testing
Limited applications due to financial constraints and personnel to implement the recommended models (pre- and post-injury testing and comparisons)
Most computerized testing takes 20-30 minutes per athlete – can be done in group format (all at computers at same time) for efficiency
Allows for more precise measurement of subtle deficits associated with concussion including reaction time, cognitive processing speed, and response latency
Essential benefits to research on concussions and return to play criteria
Also allows for easy storage/access of data
Computerized Neuropsychological Testing
HeadMinder Concussion Resolution Index (CRI) - 1999
Internet-based neuropsychological test to compare post-concussion performance to pre-injury baseline
Measures memory, reaction time, speed of decision making and speed of information processing
University of Pittsburgh Medical Center Immediate Post-concussion Assessment and Cognitive Testing (ImPact) – mid-1990’s
Software includes Self-Report Symptom Questionnaire, a Concussion History Form and tests to evaluate the elements listed below
Measures attention span, working memory, sustained attention, selective attention, non-verbal problem solving, reaction time, visual and verbal memory, and response variability
Balance and Coordination
Evaluation for possible cerebellar injury affecting muscle coordination (ataxia)
Romberg test – single leg stance with shoulders abducted 90 degrees, eyes closed and head back
Tandem walking – heel to toe walking forward and backward along straight line
Balance Error Scoring System (BESS)
Double leg, single leg, and tandem leg stance on firm and then foam surfaces with eyes closed and hands on hips
Attempt to hold for 20 seconds, points for errors
Scores can be used as baseline for comparison following head injuries and for return to play considerations
Standardized Assessment of Concussion
Standardized Assessment of Concussion (SAC)
Quick (5 minutes) screening instrument to administer and assess four domains of cognition
Orientation
Immediate Memory
Concentration
Delayed Recall
Composite score is identified to provide index of cognitive impairment and injury severity
Vital Signs
Pulse rate, respiratory rate, blood pressure taken early in evaluation process to establish baseline and repeated serially for comparison
Neurological Testing
Cranial nerve function
Serial evaluations must be performed initially to evaluate for changes
Cranial nerves arise from brain and are susceptible to impairment secondary to intracranial bleeding and resulting pressure
Nerve root evaluation
Sensory (dermatome), motor (myotome) and reflex testing necessary to rule out or identify level of spinal cord injury
Cranial Nerve Evaluation
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducens
Facial
Acoustic/Vestibulocochlear
Glossopharyngeal
Vagus
Accessory (spinal)
Hypoglossal
On
Old
Olympus
Towering
Top
A
Fin
And
German
Viewed
A
Hop
Cranial Nerve Evaluation
I – Olfactory
Sense of smell
II – Optic
Visual acuity
III – Oculomotor
Pupillary size and reaction
Eye adduction and downward rolling
Elevation of upper eyelid (blink)
Cranial Nerve Evaluation
IV – Trochlear
Upward eye rolling
V – Trigeminal
Muscles of mastication (chewing)
Facial sensation
VI – Abducens
Lateral eye movements
Cranial Nerve Evaluation
VII – Facial
Taste
Facial expressions
VIII – Acoustic/Vestibulocochlear
Hearing
Equillibrium/balance
IX – Glossopharyngeal
Taste
Swallowing
Cranial Nerve Evaluation
X – Vagus
Gag reflex
Swallowing
Involved in heart rate, respirations, digestion, etc.
Hallmark symptoms include mental confusion, altered mental status, amnesia and potential loss of consciousness
Multiple occurrences may produce cumulative degenerative effects
Ultimate assessment based upon duration of loss of consciousness (if any) and neuropsychological findings
Concussion
Additional symptoms of concussion may include but are not limited to:
Dizziness
Tinnitus
Nausea/vomiting
Motor impairment
Memory loss
Glasgow coma scale
Allows for objective evaluation of symptoms of brain injury
Normal score is 15 – scores >11 likely to recover
Classification of Concussions
Concussion rating systems
Injury graded at time of injury based upon existing signs/symptoms within 15 minutes of injury
American Academy of Neurology Concussion Grading Scale
Injury graded after all signs/symptoms have resolved
Cantu Evidence-Based Grading Scale
Recommendations from 2001 & 2004 Vienna Conference on Concussion in Sport
Individual’s recovery attended to based upon symptoms, neuropsychological tests and postural stability tests
Concussion Rating Systems
Guidelines for identifying concussion severity and determining return to play timeline – often considered conservative for athletic population
Significant differences between scales – be consistent with scale utilized – more than 16 rating systems have been identified
American Academy of Neurology Concussion Grading Scale
Cantu Evidence-Based Grading Scale
Vienna Conference Recommendations
Simple vs. complex concussions
Simple concussions
Most common concussion but most difficult to recognize
Complex concussions
Involves persistent symptoms and also individuals suffering multiple concussions over time
Simple Concussions
Signs & symptoms
No LOC
Only neurological deficit is brief post-traumatic confusion and/or post-traumatic amnesia
Symptoms typically resolve within 30 minutes – if persist for more than 30 minutes, a more serious (complex) concussion exists
Simple Concussions
Management
Removed from activity with serial evaluations following initial evaluation at ~5 minute intervals until asymptomatic
Once asymptomatic, introduce exertion – if exertion exacerbates symptoms, disqualify from activity
If asymptomatic for 15 minutes at rest and with exertion, can return to activity
Second episode during same activity session disqualifies individual from further activity that day
If symptoms progress – ultimate progression of evaluation for return to activity is; at rest, with exertion, with sport-specific activities, return to full activity
Complex Concussions
Signs & symptoms
Persistent symptoms (with and/or without exertion), specific sequelae (prolonged LOC), or prolonged cognitive impairment
Also includes those with multiple concussions over time
Protracted post-traumatic amnesia is typical, usually lasting 30 minutes – 24 hours
Complex Concussions
Management
Removed from activity that day
Serial evaluations to identify or rule out potential development of intracranial pathology – may require referral to physician for special test evaluation (CT/MRI)
Formal neuropsychological testing should be considered – performance utilized to make decisions regarding return to activity (return to baseline – ideally pre-injury baseline is available)
Return to Play Criteria
Multiple factors to consider include whether or not loss of consciousness occurred, duration of symptoms, total number of concussive episodes, exertional testing
Universal agreement that individual who lost consciousness for any period of time should not be allowed to return to activity on the same day even if all symptoms have resolved
Post-Concussion Syndrome
Individuals may present with concussion symptoms long after “normal” resolution would have occurred
Common symptoms include
Decreased attention span
Difficulty concentrating
Memory impairment
Prolonged headaches
Balance impairments
Decreased cognitive function
Second Impact Syndrome
Defined as symptoms resulting from second concussive episode before symptoms of first concussive episode have resolved
Entirely preventable, return to play considerations
Second trauma typically not as violent as initial injury – thought to affect brain blood supply causing increased intracranial pressure which impacts brainstem function
Quick progression from mild concussive symptoms to comatose state
Even if treated appropriately, has ~50% mortality rate
Intracranial Hemorrhage
Named for location relative to meningeal layers
Caused by injury to blood vessels supplying brain blood supply
Increased pressure from bleeding in confined space compresses neural tissue
Onset of symptoms associated with nature of bleeding – venous vs. arterial (lucid interval)
Epidural hematoma
Subdural hematoma
Epidural Hematoma
Arterial bleeding between skull and dura mater
Initially may present with concussive symptoms
Short lucid interval (typically <48 hours)– individual appears “OK”
Due to arterial nature of bleeding
Subsequently may c/o disorientation, confusion, drowsiness, increasing headache intensity, signs of cranial nerve changes (esp. pupil changes)
If untreated, can be fatal
Epidural Hematoma
Subdural Hematoma
Venous bleeding between brain and dura mater
May not present with symptoms of concussion
Longer lucid interval – may be hours, days or weeks before symptoms present
Due to venous nature of bleeding
Subsequent development of headaches, confusion, changes in cognitive/motor abilities, cranial nerve changes
More likely to cause death due to lack of recognition of nature/source of symptoms and delay in subsequent treatment
Subdural Hematoma
Skull Fractures
Minimal risk with head protection, but may still suffer bony injury
May cause CSF leakage from nose/ear, may have residual/secondary ecchymosis
Linear
Hairline fractures in bone
Comminuted
Multiple fracture fragments
Depressed
Easier to identify on evaluation – gross deformity
Potential for fragments to injure meninges/brain
Skull Fractures
Cervical Spinal Cord Injuries
Risk minimized with rules and coaching emphasis changes
Spinal cord injury caused by
Impingement/laceration from bony displacement
Compression from bleeding, swelling, ischemia to cord
Mechanism of injury is key to decisions on management – must assume worst case scenario until proven otherwise
Trauma at spinal cord level affects function distal to level of injury
At or above C4 level – death is likely due to impact on brainstem and vital functions
Cervical Fracture/Dislocation
Spinal cord injury typically secondary to actual bony injury from swelling, bony fragment displacement, etc.
With dislocation, diameter of canal for spinal cord is impacted and can compress spinal cord
Must differentiate between spinal cord symptoms and brachial plexus injury symptoms (longer duration vs. transient symptoms)
Often treat with steroid injections to limit swelling and subsequent pressure on spinal cord with these injuries
Quadriplegia
Transient quadriplegia often results from cervical hyperextension, hyperflexion and/or axial loading
Several predisposing factors
Cervical stenosis
Cervical spine instability
Posterior arch abnormalities of cervical spine
If truly transient, symptoms often resolve within 48 hours
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