SCI - TBI 1
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2 mill cases annually
% that are severe? % w mild disability?
- severe: 15%
- mild disability: 30-50%
av age for TBI, highest incidence ages?
- av: 30
- high: 15-24(risk seeking behavior), and 5 (abuse)
TBI can be this or that...
- it's a process, not an event, soo...
- primary or secondary
- open or closed
- focal or diffuse
4 main mechanisms for TBI (mind you, they don't happen in a vacuum - one leads to another)
- brain contusion
- increased intracranial pressure
- diffuse axonal injury (sheering)
- stroke (ischemic a/o hemorrhagic - happens 2/2 injury -- not same as an embolic stroke)
define brain contusion
- cell death w hemorrhage (blood leak)
- affects the soft brain tissue
- can occur at site of impact or distal sites (coup contre-coup)
what does he mean by "closed (non penetrating) injury?" - how does this kind of event hurt the brain?
- no skull fracture
- this injury results in diffuse deficits bc the sharp edges of dura matter cut into brain as the brain bounces around
- can have coup contre-coup
- accel/decel of brain --> sheering forces on brain
open-skull fracture - correlates w what? 2 types?
- intracranial hematomas
- displaced: depressed
- non-displaced: linear
who gets a "lucid interval"
- someone with primary brain damage due to an epideral hematoma - the bleed pushes the dura into the brain
- seen in a skull fracture that's associated w superficial vessel laceration
what's a lucid interval?
- loc, conscious, loc
- can be dangerously misleading
what's hppening in subdural hematoma in primary brain damage?
- bleeding from vessels btwn the dura and the brain (blood gets into brain)
- leads to compression syndromes
- seen w accel/decel injuries
- high mortality rate
3 intracranial contents, their %s, why each might increase
- brain: 80% - swelling/edema
- CSF: 10% - accumulation if the roads out get blocked
- blood: 10% - hemorrhage
if the intracranial contents increase, where does the brain go?
- down the foramen magnum
- bad bad bad: brainstem gets compressed in there, breathing stops, living stops.
does axonal injury happen in open or closed injuries?
yes. either. can happen w/wo skull fracture
name one major cause of persistent vegetative state
diffuse axonal injury
what's the most common structural abnormality in TBI?
- diffuse axonal injury -- this is a sheering, stretching force to the axons, it alters their transmission
- can cause mild to fatal deficits
why might a TBI pt have an ischemic stroke?
swelling compresses nearby arteries --> decreased O2 delivered to brain
why might a TBI pt have a hemorrhagic stroke?
- decreased O2 delivery bc blood is leaking into brain tissue, not entering capillary network
- can be a primary or a secondary injury
what kind of damage in "secondary brain damage"
systemic, not focal damage
causes for secondary brain damage - I'm not sure if these are 3 different issues or a stream of events
- airway obstruction or trauma --> arterial hypoxemia
- brain loses ability to autoregulate vasodilation/constriction
- cerebral hyper/hypoperfusion
the cytotoxic edema in secondary brain damage - what is it? how fast does it happen?
- swelling of all cellular elements of the brain
- if there's acute cerebral ischemia, within minutes there'l be swelling of neurons, glia, and endothelial cells
sodium and ATP role in secondary brain damage's cytotoxic edema?
ATP-dependant ion transport fails ----> rapid accumulation of sodium within cell --> water follows to maintain equilibrium
what's the story with vasogenic edema as seen in secondary brain damage?
- w massive injury there can be increased permiability of brain capillary endothelial cells, leading to increased extracellular fluid volume
- ... can lead to a downward brain herniation
which edema comes first?
acute hypoxia --> cytotoic edema ... hours to days later vasogenic edema as infarctin develops
how much of an increase in ICP is ok?
- this slide is confusing, but I think if it goes up 5-10 mmHg, needs surg/med help
- norm is 7-15 mmHg, says wikipedia
2 ways to deal w hihg ICP
- decompressive craniotomy
- steroids to reduce swelling
coma - a general term meaning unresponsive to stimuli. Define the more specific terms -- "normal consciousness," "stupor," "obtundity," "delirium"
- nc: arousal and cognition are fine
- stupor: arousable only by vigorous stim
- obtundity: slow/delayed response to stim
- delirium: misinterpretation of stim, can't understand what a stim means
when is a glasgow comma scale used
in field and at 24 hrs
glasgow coma scale - 3 fields it looks at?
(it is "predictive but not localizing")
glasgow coma scale scoring?
- get a 1 in each arena for having no response, and then more points the more responsive
- 8 or less is a coma and needs long term care
scoring fr the motor response in the glasgow coma scale (and what #2 and 3 mean)
- 6 - obeys command
- 5 - localizes - can id stim and push it away
- 4 - withdraws from noxious stim
- 3 - decortiate posturing - ext except flexed elbows
- 2 - decerebrate posturing - ext
- 1 - no response
decerebrate vs decorticate posuring
- both: extended legs, IR, PF, arms add, wrists pronated and fingers flexed
- decorticate: elbows flexed (3 on CGS) (hands by the core)
- decerebrate: elbows ext (2 on GCS) ("re" - so repeat the extension, do it in yr elbows too)
glasgow coma scale verbal scoring
- 5 - oriented
- 4 - responsive-disoriented -- knows she's disoriented
- 3 - inappropriate - speaks intelligibly, but nonsens
- 2 - moans - beware tho- could be dysarthria
- 1 - no response
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