9/28 Concussion - Womack Flashcards
concussion
complex pathophys process induced by trauma and affecting brain
- caused by direct blow to head/face/neck/elsewhere with IMPULSIVE FORCE transmitted to head
- rapid onset of short-lived impairment of neuro fx which resolves spontaneously
- might see neuropatho changes BUT acute clinical sx reflect fx disturbance rather than structural injury
- graded set of clinical syndromes that may or may not involve loss of consciousness
- typical neuroanatomical imaging shows no abnormality
concussions will gradually get better if you leave alone! shouldnt see better-worse-better-etc cycles → thats prob something else
concussion as mild traumatic brain injury
diffuse or acute?
what’s the root cause?
- diffuse brain injury without structural change
- due to rotational, shearing, counter-coup forces
pathophysiology of concussion
1. concussed brain is in hypermetabolic state
- fuel use : fuel delivery ratio is out of balance (glucose utilization : cerebral blood flow)
- dramatic incr in glucose metabolism in first minutes to days
- increased Ca influx → decreased cerebral blood flow
- decr blood flow puts cells in a state of vulnerability
- cells not dead, but trying to recover! low flow → cell death and worse prognosis
clinical presentation of concussion
+/- loss of consciousness
retro/anterograde amnesia (not remembering plays)
inappropriate activity
emotional lability
confusion, dazed-ness
headache, dizziness, blurry vision
signs that should make you suspect concussion
symptoms
- somatic: headache
- cognitive: feeling “in a fog”
- emotional: lability
physical signs
- loss of consciousness
- amnesia
behavioral changes (ex. irritability)
cognitive impairment (slowed rxn time)
sleep disturbance (ex. drowsiness)
concussion: after the fact
symptoms seen after concussion
- confusion
- difficulty concentrating
- recurrent headache
- slowed speech/comprehension
- sleep disturbance
- emotional lability
- photo/phonophobia
- dizziness
***vomiting
***worsening sx
***changes in consciousness
acute physical exam
ABC (airway, breathing, circulation)
cervical exam
neuro exam
SCAT3 test (sport concussion assessment tool)
link between concussion sx and severity
confusion
antergrade amnesia
retrograde amnesia
LOC
confusion +/-
antergrade amnesia +
retrograde amnesia ++
LOC +/-
imaging choices?
- CT scan should be 1st choice if worried about more severe traumatic brain injury
- MRI if prolonged sx and not improving
Nexus 2 mnemonic
BEAN BASH
Behavior (abnormal)
Emesis (intractable)
Age > 65
Neuro deficit
Bleeding
Altered mental status
Skull fracture
Hematoma on scalp
treatment for concussion
conrnerstone of tx right now: complete cognitive and physical rest
provocative tests
use only when asymptomatic (normally done on sideline if unsure of concussion)
- shake head, tap head
- run 40yd
- 5 situps/pushups
- 5 kneebends
testing coordination, multiple limbs
cutting edge of concussion testing
- balance testing (tends to get better with fitness…older more exp athletes have better balance than younger/less exp)
- ocular examination
- tablet based testing
rules for return to play
no return unless asymptomatic at rest and exertion
- NOTE: 20-30% of nonconcussed athletes have headache
any LOC or amnesia = out for the day
repeated assessment is the standard
continuing/worsening sx? ED!
second impact syndrome
occurrence of a catastrophic (often fatal) brain injury following relatively minor initial injury
- can occur when athlete returns to play while still symptomatic from initial injury
- in this period, brain’s ability to regulate blood flow is affected → disordered cerebral vascular regulation
- rapid cerebral edema and brainstem herniation can occur (under 5min)
- 50% mortality, 100% morbidity
- happens in high school and younger
- best treatment: PREVENTION
many guidelines/protocols established based upon this risk
