TBI and Spinal Cord Injuries Flashcards
Monro-Kellie theory
when the volume of one component of ICP goes up, the others must go down
what is the easiest component of ICP to displace
CSF
second easiest thing to displace in ICP
blood volume
MAP formula
(SBP+2(DBP))/3
CPP
MAP-ICP
approximate cerebral blood flow
50 mL/min/100g
most common cause of cerebral edema
vasogenic
where does vasogenic cerebral edema mostly occur
mainly in white matter
s/s of vasogenic cerebral edema
range from HA to coma
what is cytotoxic edema
disruption of the integrity of the cell membranes
what does cytotoxic edema lead to
inappropriate ADH secreiton
what causes interstitial edema
usually a result of hydrocephaly
where do VS changes in cushing’s triad come from
changes in pressure at the thalamus, hypothalamus, ons and medulle
how to treat increased ICP X3
head midline and elevated 30 degrees
cluster care
low stimulation
care of ICP monitors X6
minimize infection risk
label tubing
keep dressing clean/dry
keep off floor
do not give meds
don’t allow d/c
drugs used in IICP X2
corticosteroids - dexamethasone
hypertonic saline
what is a head injury
any trauma to scalp, skull, brain
what is head trauma
includes an alteration in consciousness - no matter how brief
highest risk of head injury
males 15-24, then little kids, then old people
when is death likely in a head injury
immediately after the injury
within 2 hours after injury
3 weeks after injury
why does death occur immediately after a head injury
catastrophic injury
why does death occur 2 hours after head injury
bleeding out
swelling out of control
why doesdeath occur 3 weeks after a head injury
3 weeks after injury
what is the primary head injury
the actual damage
what is the secondary head injury
what occurs in the coming days
key characteristic in scalp lacs
bleed profusely but heal quickly
how do you know if a skull fracture is open
feel for mushy spots
s/s of basilar skull fractures
ear/nose bleeding
leaking straw colored CSF
CI in basilar fractures
no NG tube
CI in any injury with a CSF leak
do not do anything that would introduce bacteria
concussion s/s X2
brief disruption in the level of consciousness
retrograde amnesia
what happens with repeat concussions
may make future concussions worse
what is a diffuse axonal injury
widespread sheared axonal damage that occurs primarily in the white matter after any brain injury
axonal injury presentation
will arrive unconscious with a blank initial CT
repeat CT shows small bleeds in parenchyma
diffuse axonal injury interventions
head elevated
comfort
midline
clustur care
CI in diffuse axonal injury
no surgery
prognosis for diffuse axonal injury
if they don’t improve within 24 hours they probably wont
x3 focal injuries
brain lacerations
contusions
coup-contrecoup
DAI s/s X4
decreased LOC
IICP
decerebration or decortication
global cerebral edema
what is an epidural hematoma
bleeding between dura and inner surface of the skull
bleeding from middle meningeal artery
hemorrhage in epidural space
s/s of epidural hematoma X4
initial period of unconsciousness
brief lucid interval
decrease in LOC
HA, N/V
epidural hematoma nickanme
walking dead - go straight to OR
acute subdrual hematoma s/s
similar s/s to brain tissue compression in IICP
when do acute SDH’s occur
within 24-48 hours
what is a subacute SDH
the SDH may appear to enlarge overtime after the initial bleeding
when do subacute SDH’s occur
within 2-14 days
what kind of bleed is a acute SDH
arterial bleed
what kind of bleed is a subacute SDH
venous bleed
chronic SDH s/s X4
increased ICP
N/V
vomiting w/o nausea
decreased LOC
peak incidence in chronic SDH
sixth and seventh decades of life
who is most likely to have a chronic SDH
alcoholics d/t chronic falling
are chronic SDH’s emergent
no - probably will not require OR
what is a intracerebral hematoma
occurs from bleeding within the parenchyma usually between the frontal and temporal lobes
what determines outcome in an intracerebral hematoma
size and location
tx of intracerebral hematoma
cannot be removed - must wait to heal
tx s/s
common causes of SAH X3
SA aneurysm, head trauma, HTN
s/s of SAH X3
sudden severe HA often confused with migraine
photophobia
nuchal rigidity
what happens 3-14 days after a SAH
clot lyses and gets reabsorbed
how do you prevent vasospasm in SAH
use Nimodipine (Ca Channel blocker)
where do CN I and II occur
above the medulla and are hard to assess in an unconscious patient
how long does cell death continue after spinal cord injuries
weeks or months
why does permanent injury occur in spinal cord injuries around 24 hours
edema
what is spinal shock
temporary neurologic syndrome
concussion of the spinal cord that resolves as soft tissue swelling goes away
how long does spinal shock last
hours to weeks
spinal shock s/s
flaccid areflexia
warm and dry
neurogenic shock
loss of vasomotor tone - true shock
how does neurogenic shock resolve
usually on its own
when should you assume it’s neurogenic shock
if they don’t respond to fluid - then give pressors
causes of neurogenic shock X4
GB syndrome
spinal anesthesia
ANS toxins
Down’s Kids
s/s of neurogenic shock
loss of sympathetic tone to heart and vascular system
deadly triad
deadly triad in neurogenic shock
hypotension
bradycardia
peripheral vasal dilation
what causes hyperflexion
sudden forward motion
what does starring the windshield mean
hitting the windshield with forehead
most mobile section of spine
C5-6
hyperextension
head accelerates and rapidly decelerates
vertebrae might fracture/subluxate
axial loading
vertical force results in vertebral shatter - diving accident
safest thing to do in combative axial loading pts
medicate and intubate
rotational injury
displacement of the spinal column
skeletal level of injury
at the vertebral level
most damage to vertebral bones and ligaments
neurological level of injury
lowest segment of spinal cord with normal sensory and motor function on both sides of the body
what occurs if the thoracic or lumbar cord is damaged
paraplegia
when are arms rarely damaged in spinal cord injuries
high C damage
what happens in high atlas fractures
death likely - internal decapitation
complete cord involvement
results in total loss of sensory and motor function below level of lesion
incomplete/partial cord involvement
mixed loss of voluntary motor activity and sensation and leaves some tracts intact
central cord syndrome
damage to the scentral spinal cord
where do central cord syndrome injuries commonly occur
commonly in the cervical region in older adults
s/s of central cord syndrom
motor weakness and sensory loss in all limbs but worse in arms than in legs
anterior cord syndrome
caused by damage to anterior spinal artery leading to compromised blood flow
what causes anterior cord syndrome
injuries causing acute compression of anterior portion of spinal cord
brown sequard syndrome
result of damage to one half of the spinal cord
brown sequard syndrome s/s X3
loss of motor function and position and vibration sense on same side of injury
paralysis on same side as injury
opposite side has loss of pain and temp sensation below level of lesion
respiratory complications with a C3 and above injury
near total ventilatory muscle paralysis
artificial airways provide direct access for pathogens
respiratory complications for a C3-C5 injury
loss of phrenic nerve function
respiratory complication for C6-T8
loss of phrenic nerve and intercostals
respiratory complications for T7-T12 injury
loss of abdominal muslces
cardiovascular implications and tx for a T6 and up injury
sympathetic nervous system is reduced
heart rate is slowed
IV fluids
SCD’s, lovenox, TCDB
urinary system implicatoins during spinal cord injuries
urinary retention and hyperirritability common
GI system implicatoins T5+
primary issue is hypomotility
GI issues T12 down
decreased sphincter tone
autonomic dysreflexia X4
HTN
blurred vision
throbbing headache
marked diaphoresis above lesion level
autonomic dysreflexia NI
elevate HOB at 45 degrees+
assess cause (bladder fullness)
notify physician
immediate catheterization
