Please enable JavaScript.
Coggle requires JavaScript to display documents.
CNSLF Path - Traumatic Brain + Spinal Injury (i) (Intro (primary damage…
CNSLF Path - Traumatic Brain + Spinal Injury (i)
Intro
50% of us will have a traumatic brain injury in our lifetime
leading cause of death in young people (<45)
long term sequelae are significant + costly
M>F (x3)
falls are responsible for nearly 2/3
alcohol in 25% (higher in certain subgroups - e.g. assaults)
50% of motorists not wearing a seatbelt, 50% of cyclists/motorcyclists not wearing a helmet
increasing incidence
many events are preventable
blunt force trauma a/w acceleration/decceleration forces to head that cause brain movement within skull
open injury - increased infection risk
primary damage (immediate)
scalp laceration
skull fracture
cerebral contusions
cerebral lacerations
intracranial haemorrhage
diffuse axonal injury
secondary damage (delayed)
ischaemia
hypoxia
cerebral swelling
infection
collusum marginal art supplies ant cingulate gyrus
Management
pre-hosp emergency care
inpatient care in appropriate units (with access to neurosurg)
post-host care (rehab)
Skull fractures
indicate head has been subjected to localised trauma of considerable force
Contact with a flat surface tends to produced closed tissue fractures, which often extend into base of skull
contact with angled or pointed objects tends to produce localised fractures, which are often open + depressed
contrecoup fractures occur principally in the roofs of the orbits + cribriform plates following falls of other blunt impact involving back of skull
skull base fractures (often hinge fractures) often not seen on CT, so look for clues...
racoon eyes (periorbital bruising)
Battle's sign (post-auricular haemorrhage)
CSF ottorhea
CSF rhinorrhoea
haemotympanum (blood in tympanic cavity of middle ear)
Contusions
bruising of surface of brain
can be a/w overlying fractures (esp depressed skull fractures)
typically involves crests of gyri + often superficial, involving grey matter only
may extend into white matter + form a haematoma
coup + contrecoup contusions
dynamic lesions that evolve with time, chronic changes incl plaque jaune - golden/yellow discolouration due to residual haemosiderin due to macrophage influx
Lacerations
when the severity of trauma has been sufficient to cause tearing of pia
"burst lobe"
ICH will typically evolve within 48hrs
potential mechanisms
post-traumatic coagulopathy (45%)
mannitol (increases cerebral blood flow + lowers ICP)
ICH
within brain parenchyma, doesn't extend through cortical surface into subarachnoid space
deep (basal ganglia)
the outcome for patients with traumatic basal ganglia haemorrhages is poor, with 59% dying + only 16% making a favourable recovery
lobar
some cases can be difficult to distinguish if haemorrhage is primary or secondary
underlying co-morbidities can make vessels more prone to bleed
cerebral amyloid angiopathy (CAA)
atherosclerotic disease
Hernation
subfalcine of singulate gyrus
transtentorial of median temporal lobe
transforaminal herniation of cerebellar tonsil - coming through foramen magnum (resp arrest + death)
Spinal cord injuries
major cause of disability after motor vehicle, horse riding, diving accidents, other sport-related injuries, falls, knife + firearms assaults
cervical cord + cervicomedually injuries are also a feature of non-accidental whiplash injuries that can result from shaking infants
age @ time of injury, neuro status @ time of injury + extent of injury = predictors of survival
closed SCIs are the most common traumatic SCIs in clinical practice, a/w fracture or dislocation of spine due to
hyperflexion/hyperextension movements
compressive forces, such as fall from height landing on top of skull (direct compression)
rotational movements causing fracture dislocations, most typically a/w thoracolumbar lesions
central haemorrhagic infarct can occur after contusional SCI
GCS
eye opening: 1-4 (nil - to pain - to speech - spontaneous)
best motor response: 1-6 (nil - extensor - flexor - withdraws to pain - localises pain - obeys)
best verbal response: 1-5 (nil - incomprehensible sounds - inappropriate words - confused conversation - orientated)
scores: 3-15
13-15 = mild TBI
9-12 = moderate TBI
3-8 = severe TBI
Concussion
some say it's a separate entity (no structural damage), some say it's part of spectrum of TBI (Mayo clinic TBI classification)
headache, dizziness, sleep disturbance, cognitive impairment, fatigue, irritability, anxiety, depression
clinical syndrome of biochemically induced alteration of brain function, typically affecting memory + orientation, which may involve LOC