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Clin Med III Unit 3 > Concussions > Flashcards

Concussions Flashcards

1
Q

What is the definition of a concussion?

A

A traumatically induced alteration in mental status that may or may not involve loss of consciousness

Also considered a mild TBI

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2
Q

Concussions are considered to be a _______ injury rather than a ______ injury.

A

Functional

Structural

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3
Q

The term concussion is interchangeable with _____

A

Mild TBI

People just don’t like being told they have a brain injury

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4
Q

What is the gender ratio for concussions?

A

M:F ratio ~ 2:1

Mostly b/c boys are stupid and do dumb shit

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5
Q

Examples of common precipitating events for mild TBIs

A

MVAs, contact sports, accidental falls, occupational hazards

75-95% of these injuries are considered “mild”

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6
Q

What are the requirements for a head injury to be considered a “mild” TBI?

A

GCS > 13

No acute cranial or intracranial pathology (NO STRUCTURAL INJURY)

Non-focal neurological exam

No post-traumatic seizures

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7
Q

Which patients must be closely managed for TBIs?

A

Those on anticoagulants - at higher risk for acute and delayed bleeding

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8
Q

Things you DON’T WANT TO MISS when working up a mild TBI

A

Intracranial hemorrhages (need neurosurg consult, surgical intervention, ICP lowering tx)

Focal neuro findings (intracranial, spinal, or occult peripheral injuries)

Anticoagulated patients (higher risk for acute/delayed bleeding)

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9
Q

What is the key to diagnosing a mild TBI?

A

Keeping the DDx broad

Act immediately on ABC issues and call for help

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10
Q

What is the mechanism of injury in mild TBIs?

A

Direct contact, acceleration/deceleration or “coup countrecoup”

Trauma causes cortical contusion, atonal inflammation, neurotransmitter signal disruption (basically a “brain bruise”)

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11
Q

Do you need imaging studies for mild TBIs?

A

Not usually

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12
Q

Presentation/Sx of Mild TBI

A

Hx of witnessed or suspected head trauma

Acute Sx:
\+/- TRANSIENT LOC
Retrograde/anterograde amnesia
Slow speech
Confusion
Repetitive questions
H/A
Dizziness
Decreased focus and attention
Emotional volatility
Sleep disturbance
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13
Q

W/o history, it is easy to mistake sx of mild TBI for other conditions such as…

A

EtOH intoxication

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14
Q

What are some signs of clinical deterioration in a patient with a TBI?

A

Decreasing mental status, seizures, vitals

“Lucid phase” followed by decreased mental status (associated with ICH, specifically epidural hematoma)

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15
Q

Precipitating sx of worsening condition following TBI

A

Chest pain, dyspepsia, syncopal episode, seizure like sx, severe sudden onset H/A, pleuritic chest pain

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16
Q

Concerning PMH items when working up a TBI

A 
Anticoagulation
DM
Syncopal or cardiac Dx
Seizure hx
Bleeding or platelet disorders
Elderly pt
Young pt
Osteoporosis
Dementia
New meds

Prior Hx of TBI

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17
Q

Concerning answers in SH when working up a TBI

A

Lives alone***
Homeless
Hx of or concurrent substance abuse

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18
Q

To constitute a mild TBI, physical exam findings should be…

A

Generally benign

Improving memory and psych deficits over time
Non-focal neuro exam
No SSx of basilar skull fracture or palpable cranial defect
“Cleared” C-spine

Do head to toe exam to r/o other injury

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19
Q

Concerning PE findings following TBI

A 
Battle sign
Raccoon eyes
CSF leaking from nose
Hemanotympani
Unequal pupils
Cervical spinal injury
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20
Q

How is a mild TBI diagnosed?

A

CLINICALLY

No specific test or imaging

Several scoring scales but have limited utility/not validated
• Sport Concussion Assessment Tool 5th ed. (SCAT5)
•Standardized Assessment of Concussion (SAC)

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21
Q

Any diagnostic tests you order for TBI are to…

A

R/o other illness, complicating factors, or to facilitate management of the patient’s condition

Ex:
Labs prior to hospital admission
CT to rule out structural injury

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22
Q

In general, mild TBI patients need close monitoring for ______

A

24 hours

To make sure their condition doesn’t deteriorate

23
Q

Outpatient treatment of a mild TBI requires…

A

Reliable adult to monitor patient

Discharge with careful, well-explained return precautions

24
Q

Factors that favor inpatient admission of a mild TBI patient

A 
Unstable home situation 
No reliable caregiver
Significant comorbidities
GCS <15
\+ CT findings
\+ post-traumatic seizure
Intractable vomiting
Focal neuro findings
Anticoagulant use
25
Q

How long should a mild TBI patient be on cognitive rest?

A

Generally 2-5 days rest and light activity at home

Gradual return to cognitive activity, school, or work

If patient can tolerate 30-45 min of focus (ie homework) w/o Sx they can trial return to school/work

Implement more rest, reduce activity intensity if return of Sx

26
Q

When should a patient with a mild TBI return to physical activity?sports

A

Can be difficult to implement b/c of non-compliant patient population

Return should be graduated

May use standardized protocol such as Return to Play

27
Q

What are the steps in Return to Play protocol

A
  1. No activity (Recovery)
  2. Light Aerobic Exercise (Increase HR)
  3. Sport Specific Exercise (Add movement)
  4. Non-Contact Training Drills (Inc Exercise, Coordination, Attention)
  5. Full Contact Practice

For each step, if Sx free for 24 hours, step up to next step; if not, step down to previous step until Sx free

28
Q

Pharmaceutical treatment for Mild TBI

A

Symptomatic: APAP, ibuprofen, melatonin

29
Q

What do you do to follow up with a mild TBI

A

Patients should follow up with PCP w/in 7 days

Regular f/u until asymptomatic important for athletes and peds

30
Q

Indications for further f/u or specialty referral following mild TBI

A

Minimal improvement after 10 days

Multiple TBIs, particularly with cumulative neuropsychiatric SSx

Clinical deterioration

31
Q

What is the prognosis for mild TBIs?

A

With full recovery, mild TBI typically benign

May be associated with short and long term sequelae (inc M&M with recurrent TBI, associations with epilepsy, sleep disturbance, mood/behavior disorders, vertiginous disorders)

Secondary and chronic syndromes:
• Postconcussive Syndrome (PCS)
• Second Impact Syndrome
• Chronic Traumatic Encephalopathy

32
Q

Common sequelae of mild TBI that includes HA, dizziness, mental fog, mild cognitive impairment, neurobehavioral changes, usually worst in first 7-10 days but can last up to 30-90

A

Post concussive syndrome (PCS)

33
Q

More severe sx of PCS are correlated with…

A

Repeat injuries w/o full recovery

Increased age

F>M

34
Q

What is the treatment for PCS?

A

Generally supportive
• Tailored to address pt’s specific sx
• Rx: analgesics, sleep aids, anti-depressants
• Non-Rx: Patient Ed!, modified work/school schedule, psychiatric counseling

MRI sometimes considered to r/o missed injury or etiology

35
Q

Rare but potentially catastrophic consequence of suffereing a second concussion prior to full recovery from a prior TBI

A

Second Impact Syndrome

36
Q

Pathophysiology of second impact syndrome

A

Cerebral autoregulation from initial injury leads to uncontrolled increase in ICP —> cerebral edema in context of second injury —> ischemic changes

37
Q

Why is removal from play so important if there is any suspicion of TBI?

A

Risk of second impact syndrome (—> death)

38
Q

Treatment for second impact syndrome

A

Non-specific
Recognize signs of and treat elevated ICP
Neurology, neurosurg consult

39
Q

Constellation of symptoms and pathology findings seen with repeated head trauma (subconcussive blows and TBIs)

A

Chronic Traumatic Encephalopathy

Hallmark is cumulative but often delayed and/or poorly recognized

40
Q

SSx of CTE

A

Cognitive impairment, aggression, psychotic disorders, SI, HI, anxiety, depression, Parkinsonism, ALS, dementia, speech and gait disorders

41
Q

110 of 111 brains of deceased NFL players had signs of …

A

CTE (chronic traumatic encephalopathy)

NFL plays estimated to have 3x the risk of neurodegenerative disease vs general pop

42
Q

Pathophysiology of CTE

A

Pathologically distinct dysregulation of tau proteins (structural CNS proteins)

Damaged, dysfunctional, immunoreactive proteins —> inflammation and further dysregulation of CNS

43
Q

How is CTE diagnosed?

A

Can only be definitively diagnosed POST MORTEM

(+) MRI findings but not sensitive/specific

May be expected clinically based on Hx/presentation

44
Q

Treatment for CTE

A

B/c definitive Dx not practically possible, current tx are symptomatic and non-specific

Current research is all about PREVENTION

45
Q

Anticoagulation with oral meds (Warfarin, others) increases the risk of ______ after head trauma

A

Intracranial bleed

46
Q

All patients with head trauma who are on an oral anticoagulant should have…

A

A stat head CT regardless of LOC or other red flags

47
Q

Intracranial bleed following TBI in patients on oral anticoagulants typically presents ________ after the initial injury

A

6-24 hours (but really, pretty quickly)

That’s why we would observe an old man who hit his head and is on warfarin for 6 hours in the ED before considering D/C

48
Q

Who else can you talk to besides the patient/family to get a better Hx?

A

EMS and nursing staff - they know what’s up

49
Q

What is Cushing Reflex

A

Triad of HYPERtension, BRADYcardia, and IRRegular breathing

Occurs due to increased ICP —> brainstem herniation/compression

50
Q

When is the Cushing reflex most often seen?

A

In terminal phases of acute head injury

Indicates very poor prognosis with death often occurring within minutes

51
Q

How do you deal with Cushing Reflex?

A

Emergency ICP lowering interventions

Emergent neurosurg consult

52
Q

What is a main cause of AMS that can quickly lead to demise and you DON’T WANT TO MISS

A

Hypoglycemia

ALWAYS do a finger stick blood glucose (seriously, it takes like 30 sec)

53
Q

Why are c-collars controversial?

A

Takes patient out of position of comfort
Can’t examine neck
Can interfere with important interventions (ie intubation)
Little data to show they prevent injury

But we use them anyway 🤷‍♀️

Clin Med III Unit 3 (5 decks)

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