Unit 10b - Spinal and Head Injuries Flashcards
frontal lobe
problem solving
judgement
planning
personality
emotions
organization
Attention
concentration
smell
movement
temporal lobe
memory
hearing
understanding language
Organization
sequencing
parietal lobe
sense of touch
spatial perception
visual perception
sensation
occipital lobe
vision
speech (L side)
abstract concepts (R side)
cerebellum
balance
coordination
Skilled motor activity
brain stem
breathing
heart rate
arousal, consciousness
sleep and wake cycles
attention, concentration
sport related concussion (SRC)
“traumatic brain injury induced by biomechanical forces”
- force cause shaking of brain in skull resulting in the brain swelling, bleeding, shear/tear nerve fibers
crushing’s reflex
body’s natural response to an increase in intracranial pressure and often indicates severe head injury
- respiration changes (deep, irregular)
- increase BP (bigger gap btwn SBP and DBP)
- bradycardia (slower heart rate)
s/s of brain injury
- change in LOR
- paralysis or flaccidity of muscles (usually one side)
- unequal facial mvmnts or disturbance of vision/pupils
- ringing in ears or hearing disturbances
- limb rigidity
- lose balance
- rapid, weak pulse
- high BP and slow pulse
- breathing problems
- vomiting
- incontinence
5 SRC defining features
- direct blow to head/face/neck or elsewhere w impulsive force transmitted to the head
- result in rapid onset of short lived neurological impairments that resolve spontaneously
- neuropathological changes but acute clinical s/s reflect functional disturbance, not structural
- may not have gone unconscious; resolve in sequential course
-cannot be explained by intoxications, other injuries or comorbidities
concussion resolution
80-90% of concussions resolve on their own with in 7-10 days.
- they are no longer graded as minor/mild/severe
- recovery time longer in kids and teens
- not RTP
- not left alone
- assess, monitor constantly for change/deterioration
- evaluated by medical doctor
- follow RTP process and listen to doctor
coup effect
force causes direct damage to the brain
- where brain hits the skull
- ex: hit forehead on wall
countercoup effect
external force cause brain to accelerate and hit skull (coupe) and decelerate and hit opposite side of skull (countercoup) –> 2 points of contact of brain on skull
- ex: whiplash
result of coupe and countercoup
- edema of brain (swelling)
- decrease blood flow to brain
- changes in cerebral metabolism
- loss of brain’s ability to autoregulate
- changes in EEG activity
- changes in higher cortical function
clinical domains
- symptoms (somatic, cognitive, emotional)
- physical signs(ex: lose conc, amnesia, neurological deficit)
- balance impairment (ex: gait unsteady)
- behavior changes (ex: irritable)
- cognitive impairment (ex: slowed rxn times)
- sleep disturbances (ex: drowsy, wide awake)
concussion s/s
- lose consciousness
- seizure or convulsion
- headache
- pain in neck
- “foggy” feeling
- “not feel right”
- dizzy
- blurred speech
- tinnitus
- sensitive to light, noise
- hard to remember or concentrate
- fatigue, low energy
- confusion
- sad, anger, irritable, nervous
- nystagmus (involuntary eye mvnmnt)
- retrograde amnesia (events prior)
- anterograde amnesia (events after)
on field assessment
- MOI, CC
- use or rule out SMR
- primary assessment
- EMS if needed
- assess injury/illness per MOI
- history (SAMPLE)
- physical assessment
- vitals (GCS baseline)
- concussion present (somatic, cognitive, behavioral, emotional changes)
- cranial nerve assessment
cranial nerve assessment
- optic (II): visual acuity
- oculomotor (III): pupil reaction
- trochlear (IV): eye movement
- facial (VII): facial movements
concussion suspected
not urgent: progressively stand and walk of field for further treatment; no SMR needed, GCS and vitals normal
urgent: EMS and spine board
SRC off field
- standardized concussion test (SCAT 5) 10 min after
- monitor athlete for 30 min and reassess unless EMS arrives
- assess GCS: time 0, 2-3hrs, 24 hrs, 48, 72 hrs post
concussion in sport
the real danger is the s/s of internal bleed can be delayed for hours, even days.
- delayed intracranial bleeds cause pressure resulting in severe damage and/or death
home instructions
call clinic/EMS if these occur at home: change in behaviour, vomit (more than 3 for kid, more than 1 for adult), dizzy, worse headache, double vision, excessively drowsy
-rest, avoid physical/mental activity for 24 hours
- no alcohol or sleeping pills
- paracetamol or codeine for headaches (no aspirin or anti-inflammatories)
- no driving, playing/training until medically cleared
sleep and cognitive rest
- do not wake athlete unless they are in too deep of sleep or exhibit irregular sleep behaviour
- no screen time or reading; dim lights
- monitor after sleep
- if in doubt, wake them up
physician referral
all concussions are referred to a physician. remain in contact for 48-72
- urgent: assess for intracranial bleed (see s/s)
- same day referral
- post concussion referral: s/s not go away or need to return to work/play
post concussion syndrome
Symptoms not dissipating after 7-10 days:
- persistant headaches
- anxiety, irritable, fatigue
- depression
-unable to concentrate
- impaired memory
- visual disturbances
catastrophic brain injury
SIS and intercranial bleeds
second impact syndrome (SIS)
Rare and fatal condition of a seemingly mild blow to previously concussed brain leads to massive brain swelling (“concussion missed and allowed to carry on”)
brain cannot regulate flow > blood vessel engorgement > cerebral edema > intracranial pressure > rapid respiratory failure > coma > neurological death > DEATH (AED not work)
risk for s/s
people under 18 are greatest risk for SIS
- brain not fully developed
- blood vessels in brain tear more easily
- skull is thinner
head injury red flags
scalp wound
facial fracture
swelling, bruising
lose consciousness
nasal discharge
stiff neck
intracranial bleeding injuries
epidural hematoma
subdural hematoma
subarachnoid hematoma
intracerebral hematoma
cerebral hematoma
(intracranial bleed)
- skull fit tight to brain
- any bleeding = increase intracranial pressure, lead to permanent neurological death or injury
- worse s/s
- unequal or unreactive pupils
- disorientation
- mental status deteriorate
- lose consciousness
- seizures
- cranial nerve deficits
- increase BP gradually
- decrease RR or HR
- s/s present after initial lucid period
epidural hematoma
Skull fracture leading to laceration of meningeal arteries ; rapid blood accumulation btwn skull and dura. Quicker than subdural hematoma
-asymptomatic lucid period, headache, nausea, dizzy, ipsilateral pupil dilation (dilate same side as injured), LOR change, drowsy, decrease HR, periorbital/auricular ecchymosis
- lose, regain, lose consciousness
- sluggish, non reactive pupils
subdural hematoma
low pressure venous bleeding btwn dura and brain
- skull fracture is less common
- acute or chronic
- instant or delayed s/s (headache, visual disturbances, personality changes, difficulty speaking, deficit motor functions)
acute subdural hematoma
48-72 hours post trauma
- alert w no focal neurological deficits
- slip into coma (look into sleep patterns)
- sizable hematoma»_space; neurological deficits (n/t, motor skills, LOR)»_space; altered LOR»_space; coma
chronic subdural hematoma
“hematoma present 3+ weeks after injury”
- small venous bleed not stop/coagulate»_space; intracranial bleed pressure
- take up to 30 days to appear
- personality change, neurological deficits, progressive/severe headache
subarachnoid hematoma
arterial bleed in subarachnoid space (btwn arachnoid and pia mater path wher ecnf circulates) due to spontaneous rupture of cerebral aneurysm/head injury
- severe, rapid headache; vomit; seizure; decrease LOR, confusion; CSF exit via nose/ears
intracerebral hematoma
bleeding with in cerebrum
- life threatening bleed, cerebral infarction, necrosis, edema
- most common traumatic head injuries
- present normal»_space; neurological deficits and coma
Cushing reflex
increase Systolic BP in response to low blood supply to brain while attempt to lower heart rate; also have irregular breathing
cushing’s triad: respiration changes, increase BP, bradycardia
Chronic Traumatic Encephalopathy (CTE)
form of dementia caused by repeated head trauma such as concussions
- atrophy of cerebral hemispheres
- abnormal protein deposit in brain
- only diagnosed post mortem
- often die from suicide
Gradual + progressive neurological deterioration, memory disturbances, Dementia, Behavioural + personality changes, Parkinsonism, Speech + gait abnormalities
