B7.055 Prework: Traumatic Brain Injury Flashcards
types of TBI
penetrating: gunshots and severe blunt trauma, severe damage and a high incidence of infection
nonpenetrating: blunt trauma
primary injury
at the time of trauma
secondary injury
complications subsequent to trauma (why patients get worse)
types of primary brain injury
concussion CNS axonal injury cranial nerve injury contusion laceration
causes of concussion
freely moving head struck
OR
rapid acceleration of head without impact
damage done in concussion
partly tethered brain rotates
rotational motion > shearing stresses
worst in high brainstem
shear may also affect gray white junction
torque to RAS causes loss of consciousness
severity of shearing lesions
- torque causes transient stretching without transection with rapid recovery of consciousness (concussion)
- torque tears axons with slow recovery and permanent disability (diffuse axonal injury)
- torque lacerates upper brainstem with no recovery
concussion definition
reversible traumatic paralysis of nervous function defined by: -LOC -amnesia OR -other brain dysfunction (headache) effects immediate can have long term sequelae
clinical manifestations of concussion
unconsciousness loss of body tone (fall) transient arrest of resp bradycardia and hypotension sometimes convulsions anterograde amnesia
post concussion syndrome
recovery from concussion may be followed by recurrent headache, impaired ability to concentrate, and other minor neurologic symptoms
symptoms are usually transient but in some cases may persist for months or years
diffuse axonal injury
predominant abnormalities in severe head injury occur in: -midbrain/ diencephalon -corona radiata -gray white junction
cranial nerve injury in head trauma
often associated with basilar skull fractures
any nerve can be affected
CN I, VII, and VIII most susceptible
olfactory nerve injury
anterior skull
common without a fracture
CN 7 injury
transverse petrous
CN 8 injury
petrous pyramid
CN 12 injury
hypoglossal canal
CN 4 injury
most common extraocular muscle nerve damaged
cerebral contusion
more severe trauma
loss of consciousness longer than with concussion
may lead to death or severe residual neurologic deficit
findings associated with cerebral contusion
edema
hemorrhage
necrosis
subarachnoid bleeding
mechanism of contusion
blunt trauma to specific portions of the brain
underlying brain tissue crushed
coup-contrecoup
coup injury- under the site of impact with an object contrecoup injury- on the side opposite the area that was hit
what portions of the brain are selectively vulnerable to contusions
areas near rough, bony prominences -anterior temporal -subfrontal -corpus callosum falx
cognitive symptoms of contusion
apathy and short term memory deficits
laceration
grossly visible tear in brain
blunt or penetrating trauma
brainstem avulsion
types of secondary injuries
edema bleeding herniation CSF derangements seizures infection
mechanism of edema
vasogenic and cytotoxic
cytotoxic cascade
increases during the first 24-72 hrs
may be massive and lead to herniation
types of brain bleeds
epidural
subdural
intracerebral
subarachnoid
cause of acute epidural hemorrhage
tear in meningeal artery, vein, or dural sinus
symptoms and signs of epidural hemorrhage
headache, confusion, somnolence, seizures, and focal deficits
can lead to coma, resp depression, and death unless evacuated
location of epidural hematoma
lateral cerebral convexities
presentation of epidural hematoma
classically lucid interval then coma
age at risk of epidural hematoma
children
young adults
radiologic features of epidural hematoma
acute bulging epidural clot
bounded by cranial sutures
lenticular in shape
treatment of epidural hematoma
urgent evacuation
cause of acute subdural hemorrhage
tearing of bridging pial veins and arteries
location of acute subdural hemorrhage
lateral cerebral convexities
evolution of acute subdural hemorrhage
many hours
symptoms of acute subdural hematoma
similar to epidural
interval before onset of symptoms is longer
age at risk of acute subdural hematoma
all
radiologic findings of acute subdural hematoma
acute blood rimming broad region of cerebral convexity
treatment of acute subdural hematoma
urgent evacuation if large enough to cause symptoms
cause of chronic subdural hematoma
trauma
can expand over time as large proteins in blood break down into smaller ones, increase osmolality and draw more fluid
risk factors for chronic subdural
coagulopathy
severe brain atrophy
evolution of chronic subdural
days to weeks
signs and symptoms of chronic subdural
headache, progressive alteration in mental status +/- focal neuro signs
age at risk of chronic subdural
elderly
radiologic findings of chronic subdural
hyper- or isodense
unilateral or bilateral
treatment of chronic subdural
evacuation in some circumstances
etiology of intracerebral hemorrhage
develops immediately after injury
often evolves from contusion
clinically resembles hypertensive hemorrhage
cause of intracerebral hemorrhage
shearing of parenchymal vessels
risk factors for intracerebral hemorrhage
coagulopathy
amyloid vasculopathy
location of intracerebral hemorrhage
inferior frontal and temporal lobes
evolution of intracerebral hemorrhage
expand over 12-48 hours
age at risk of intracerebral hemorrhage
any
radiologic findings in intracerebral hemorrhage
multiple, confluent regions of edema intermixed with focal, acute blood
treatment of intracerebral hemorrhage
evacuate if large
cause of traumatic subarachnoid hemorrhage
bleeding of pial vessels
location of subarachnoid hemorrhage
typical basilar cisterns
evolution of subarachnoid hemorrhage
minutes to hours
symptoms and signs of subarachnoid hemorrhage
headache, meningismus, delayed manifestations, vasospasm
age at risk of subarachnoid hemorrhage
any
radiologic findings in subarachnoid hemorrhage
acute blood lining cortex in subarachnoid space
treatment for subarachnoid hemorrhage
generally supportive
what is herniation
mass effect of edematous brain or hematoma
compression of diencephalon, midbrain, pons, medulla
rostral caudal deterioration of function
syndrome of central herniation
bilateral midsize, nonreactive pupils
diffuse edema or midline lesion
para and sym affected
syndrome of lateral herniation
unilateral dilated, nonreactive pupil
CN III affected (para)
traumatic hydrocephalus
flow of CSF disrupted by subarachnoid and intraventricular blood
communicating hydrocephalus
obstruction outside of brain
non-communicating hydrocephalus
obstruction within brain
CSF leak
tear of dura and arachnoid leads to extracranial CSF leakage and CSF hypotension (headache)
results of CSF leak
increased risk of infection
tension pneumocephalus
post traumatic seizures
common
do not increase risk of subsequent seizures
may increase ICP
prevent with acute prophylactic anti-seizure meds
post traumatic infection
penetrating injuries and CSF leak increase risk of post traumatic infection
meningitis
abscess
empyema
glascow coma scale
3= worst 15= best
treatment of TBI
ICU care
prevent infection
treat seizures
control ICP
what is ICP
intracranial pressure proportional to volume of: -blood -CSF -brain
how to decrease ICP
decrease
- blood
- CSF
- brain
CPP
cerebral perfusion pressure
must be maintained
CPP = MAP - ICP
ways to decrease blood volume
evacuate hematoma hyperventilation -decreased CO2 -vasoconstriction -decreased cerebral perfusion
ways to decrease CSF volume
external ventricular drainage
ways to decrease brain volume
decreased fluid
hyperosmolar therapy (mannitol, hypertonic saline)
steroids
give swollen brain more room?
craniectomy
chronic sequelae of TBI
post concussion syndrome post traumatic encephalopathy post traumatic epilepsy permanent vegetative state dementia pugilistica
