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?

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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?

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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?

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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?

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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?

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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

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- 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)

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- 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)

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3+ years after injury living at home

regained limited verbal, motor, cognitive skills

Case (Con’t)

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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

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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

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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

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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

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Better identification of concussions

X2 Helmet

Better protocols (sideline, ER, etc)Increased awareness

Future Directions

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Alexa Dessy, BAJonathan Rasouli, MDMount Sinai PLAYSAFE teamAlex Gometz, DPT, CIC (Concussion Management of New York)

Acknowledgements

Department of Neurosurgery