CNS injury 1-2 Flashcards
peak age groups with head injuries
24-35 y/o male urban from violence and car acidens
small peak at 0-4 for child abuse
peak over 65 from falls
2/3 before hospitalization
mechanisms of head injuries
20-50% transport injuries
20-40% gunshot
falls and nonpentrating assults rest
contact injury (low velocity/blunt) causes
injury to structures protecting brain –> scalp lac, skull fracture, epidural hematoma, cerebral contusion
contact injury (low velocity/blunt)
linear skull fracture
define
outcome
line fracture
good outcome if no underlying
contact injury (low velocity/blunt) depressed skull fracture
comminuted bone fragments may or may not drive into brain
contact injury (low velocity/blunt) basilar fracture
skull base from high velocity blunt injurys
may extend thru cribiform plate or petrous bone –> CSF leak causing meningitis
signs of basilar fracture
meningitis CSF rhinorrhoea or otorrrhea bilateral periorb hematoma (raccoon eyes) Battle sign facial nerve palsy subconjunctival hemorrhage
contact injury (low velocity/blunt) diastatic skull fracture
traumatic separation at suture lines
contact injury (low velocity/blunt) growing fracture
dural tear and herniation of arachnoid into fracture site–> CSF pulsations cause bone loss over month require surg correction
contact injury (low velocity/blunt) epidural hematoma
intracranial extradural ARTERIAL hemorrhage from skull fracture rupture middle meningeal artery
contact injury (low velocity/blunt) epidural hematoma symptoms
shape on mri
can lead to
lucid interval then progressive obtundation and coma as expands
lens shape
can lead to uncal herniation
contact injury (low velocity/blunt)
epidural hematoma
survival rate
treatment
low mortality due to damage from bleeding
treat with removal of mass lesion
acceleration/deceleration
describe translation vs rotational forces
translation = head move after impact
rotation = head move in more than one plane (MVC, rollover)
acceleration/deceleration
translational mechanism of injury
stretch and tear bridging veins causing subdural or cerebral contusions
acceleration/deceleration
subdural hematoma mechanism
assoc with
treatment
rupture of bridging veins in subdura
assoc with brain contusions
treat with remove clot, control ICP, restore cerebral blood flow
acceleration/deceleration
cerebral contusion
location
result in
treatment
frontal (anterior fossa) and temporal lobe (sharp edge of sphenoid wing)
result in swelling, brain shift, incr ICP, herniation
same tx as subdural
rotational injury
mechanism of injury
microscopic tear of nerve cells in brain –> not seen on microscope
rotational injury
diffuse axonal injury
pathology
location
symptom
shear injuries and retraction balls
axonal spheroids
in corpus callosum and brainstem not seen until 24 hr
vegetative with significant recover
monroe kellie doctrine
volume of CSF + cranial blood volume must be constant
so any incr in intracranial volume decr CSF or CBV for constant ICP
mechanism of brain compensation for incr intracranil volume
displace CSF but beyond certain point, ICP causes herniation
equation for CPP
CPP = MAP - ICP
so ICP incr, CPP incr
cellular mechanism of injury causing cytotoxic vs vasogenic edema
1) injury
2) masive depol and excess K+ extracellular
3) rverses glutamate transport so glutamate incr extracell
4) excess K+ taken up by astrocytes –> swell–> cytotoxic edema
5) excess glutamate –> incr Ca2+ –> activates enzymes for leak BBB –> vasogenic edema
after edema happens how does injury occur
1) ICP rises
2) herniation of brain
3) can’t clear glutamate and K+ due to lack of blood supply –> more edema, ischemia, damage
common symptoms of herniation
1) lethargy
2) poor response (obtunded) = hallmark
define subfalcine herniation
cingulate gyrus herniates beneath falx
can kink anterior cerebral –> stroke
define uncal herniation
effects of herniation
aka transtenotrial
uncus herniates across tentorial edge into posterior fossa compressing midbrain and ipsil cerebral peduncle
–> ipsil CN 3 palsy and contralateral hemiparesis or hemiplegia
describe duret hemorrhage
due to uncal herniation if affect ascending reticular activating system
describe cerebral herniation
with downward pressure –> bilateral uncal herniation
describe tonsillar herniation
tonsil herniate down to foramen from mass in post fossa –> compress medulla –> Cushing’s reflex (bradycardia and HTN)
complication from incr CBF at cell level
disrupt autoregulation
can’t constrict vessels so incr vessel diameter –> hyperemia and ischemia
goal of treatment of head injury
decr ICP by maximize O2 and metab delivery
1) intubation
2) control ventilation
3) osmotic diuretic
4) ventricular catheters
5) drug induced coma
reason for control ICP
after brain volume rise beyond compressible compartment space, small change in volume = big change in ICP
this incr MAP, blood vessel compressed –> ischemia
symptoms of incr ICP
lucid interval with HA, n,v, lethargy, LOC
glasgow coma scael
13-15
9-12
3-8
13-15 = mild 9-12 = mod 3-8 = severe
reflexes, which CN pupillary corneal blink cold caloric testing, doll's eyes gag
pupillary = 2, 3, midbrain
corneal blink = 5, 7, pons
cold caloric testing, doll’s eyes = 3, 6, 8, pons–> midbrain)
gag (9, 10, medulla)
