Second Impact Syndrome
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Transcript of Second Impact Syndrome
Second Impact Syndrome
Tanvir Choudhri, MDAssistant Professor of Neurosurgery
Ichan School of Medcine at Mount Sinai
Department of Neurosurgery
When repeat injury is sustained before symptoms of previous head injury have been resolved
Rare, often fatal,
SIS: What is it?
Department of Neurosurgery
traumatic brain injury occurs(Weinstein et al., 2013)
Saunders RL, Harbaugh RE The second impact in
catastrophic contact-sports head trauma
JAMA 252:538-539, 1984
SIS: What is it?
Department of Neurosurgery
Exact incidence unknown Less than 20 documented SIS cases
in world literature (Randolph et al., 2009, Arch Clin Neuropsychol)
1 possible SIS for every 205,000 player seasons
Annual participation rate: 1.8 million high school/collegiate subjects
(McCrory, et al., 2012, Current sports medicine reports)
SIS: How often does it occur?
Department of Neurosurgery
Males 16-23 years old (Mori et al., 2006, Acta Neurochirugica Supplementum)
Most brain fatalities occurred during games (Boden et al., 2013. Am J Sports Med)
Fatal injury sustained most frequently either tackling or being tackled (Cantu & Mueller, 2003, Neurosurgery)
SIS: What are the risk factors?
Department of Neurosurgery
History of 3+ concussions 3x more likely to sustain incident concussion
(Guskiewicz et al., 2003, JAMA)
Within vulnerable period from previous injury (Weinstein et al., 2013, J Neurosurg)
Impairment of cellular energetic metabolism Loss of autoregulation of cerebral blood flow
Subsequent vascular engorgement Increased intracranial pressure Eventual herniation
Subdural hematoma
Brain Swelling
SIS: How does it occur?
Department of Neurosurgery
Loss of autoregulation Rapid onset massive cerebral edema Transtentorial brain herniation Raised intracranial pressure Death can be as early as 2-5 min (Zollman,
2011, Demos Medical Publishing)
SIS: Effects of 2nd Impact
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Functional injury Reinjury to neuronal cells within vulnerable
period from previous injury (Weinstein et al., 2013, J Neurosurg Pediatrics)
Dysautoregulation hyperemic brain swelling Increased intracranial pressure Herniation Brainstem compression
SIS: Pathophysiology
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Neurometabolic cascade (Marshall, 2012, J Can Chiropr Assoc)
Mechanical stretching/shearing of neurons
Disrupts ion channels Excitation phase Neuronal suppression
Net result = neuronal ion imbalance, cellular dysfunction, cerebral energy deficit
Requires max function of Na+/K+ pump to restore homeostasis
Concussion: Pathophysiology
Department of Neurosurgery
▶ http://www.youtube.com/watch?v=KrvC2UUEJ8Y
▶ http://www.youtube.com/watch?v=uEGXcNNyzpY
Mount Sinai / Presentation Slide / December 5, 2012 10
Concussion: Pathophysiology
2nd injury generally not severe Remains standing - appears dazed Sec-min after 2nd blow collapses to
ground Semicomatose, dilating pupils, loss of
eye movement, respiratory failure (Cantu & Gean, 2010, Journal of neurotrauma)
Death can be as early as 2-5 min of 2nd impact (Zollman, 2011, Demos Medical Publishing)
SIS: How to recognize it?
Department of Neurosurgery
Headache most commonly reported Dizziness Neck painNausea and vomitting Light/Noise sensitivity Sleep pattern changes Memory/Concentration problems Fatigue Respiratory arrest Aniscoria Coma
SIS: Symptoms
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Hyperemic swelling Brain Herniation Post-herniation ischemia CT (Cantu & Gean, 2010, Journal of Neurotrauma)
Engorged cerebral hemisphere Abnormal mass effect Midline shift
MRI (McCrory et al., 2012, Current sports medicine reports)
Metabolic change up to 15 d after concussive injury
SIS: Evaluation and Management
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Neurosurgical consult in case of anatomic abnormality (Bey & Ostick, 2009, Western Journal of Emergency Medicine)
Attention for potential c-spine injury Patient immediately stabilized Airway management Rapid intubation Mannitol to minimize morbidity Surgery generally not effective for treatment
of impaired autoregulation
SIS: Neurosurgeon’s role
Department of Neurosurgery
- Previously healthy 17 yo M
- Helmet to helmet hit
- Felt dizzy, played immediately after-Reported H/A after game from hit-Resumed typical activities-c/o fatigue and persistent H/A
Case (Weinstein et al., 2013, J Neurosurg Pediatrics)
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- Normal evaluation/neurological exam with PCP 4d after game- Head CT: WNL
Case (Weinstein et al., 2013, J Neurosurg Pediatrics)
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- Persistent H/A, difficulty with concentration
- 5 days after initial injury participated in practic (including hitting drills)
- After a hit on fourth drill: slow to get up “OK” but H/A
- Several plays later down on one knee dizziness and headache couldn't feel legs unresponsive generalized seizure activity
- Local ER: intubated, treated with lidocaine, mannitol, fosphenytoin, fentanyl, midazolam
- Air transport to trauma/NS center
- 143/79, HR 93, GCS 7T, 3mm sluggish pupils, ICP 25-30
- Coagulation studies normal, Utox neg
Case (Weinstein et al., 2013, J Neurosurg Pediatrics)
Department of Neurosurgery
- Brain/cervical spine MRI:
mild downward transtentorial herniation,
bilateral subdural hematomas,
abnormal T2 signal
restricted diffusion in medial left thalamus
- Midline structures displaced caudally (thalamus hypothalamus)
Case (Con’t)
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Hospital course:
Episode of hypotension, severe metabolic acidosis and renal failure, Sepsis, ventilator-assoc. pneumonia with empyema, disseminated intravascular coagulation, cardiac arrest
Later resolution of subdural hematomas and areas of encephalomalacia
At time of discharge (day 98) nonverbal and nonambulatory
Case (Con’t)
Department of Neurosurgery
3+ years after injury living at home
regained limited verbal, motor, cognitive skills
Case (Con’t)
Department of Neurosurgery
http://www.youtube.com/watch?v=V12Zqmd3Btc
SIS
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Bleeding into the space between the dura mater and the brain
From venous hemorrhage 12-30% of patients with severe head injury 36-79% mortality Often requires surgical
intervention
Traumatic Subdural Hematoma
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Bleeding into the space between the dura mater and the skull
From arterial laceration Typically from disruption of middle
meningeal artery Arterial bleeding
increased intracranial pressure cell lesion & brain damage
~20% mortality
Traumatic Epidural Hematoma
Department of Neurosurgery
Persistent post-concussion symptoms 3+ months Increased risk of depressionWorking memory and Info processing speed impairments in mild TBI and persistent PCS (Dean & Sterr, 2013, Frontiers in Human Neuroscience)
Post Concussion Syndrome
Department of Neurosurgery
Repetitive brain trauma necessary for development of CTE
Progressive neurodegenerative disease Symptoms present years after trauma (Stern et al., 2011,
American Academy of Physical Medicine and Rehabilitation) Decline of memory/cognition Depression Suicidal behavior Poor impulse control Aggressiveness Parkinsonism Dementia Generalized atrophy
Chronic Traumatic Encephalopathy
Department of Neurosurgery
Vulnerable window following TBI Second impact before resolution of symptoms can result in catastrophic brain injury/ fatality Highlights importance of return-to-play decisions PCS and CTE represent long-term consequences of repetitive head impacts
Conclusions
Department of Neurosurgery
Better identification of concussions
X2 Helmet
Better protocols (sideline, ER, etc)Increased awareness
Future Directions
Department of Neurosurgery
Alexa Dessy, BAJonathan Rasouli, MDMount Sinai PLAYSAFE teamAlex Gometz, DPT, CIC (Concussion Management of New York)
Acknowledgements
Department of Neurosurgery