Lecture 16 - TBI Flashcards
What is concussion
- TEMPORARY loss of neurologic function with NO APPARENT STRUCTURAL DAMAGE
- CLOSED HEAD
- Seconds to minutes of unconsciousness only
What causes LOC in concussion
shock wave goes to core structures in brainstem (RAS), disrupting brain signals, causing loss of consciousness.
What are the 3 effects of brain injury
coup - site of impact (primary)
contrecoup - opposite side of impact (secondary)
spiral effect - rotational effect around fixed point
causes diffuse axonal injury
what is PTA
posttraumatic amnesia
measure with westmead PTA scale
what are the three determinatnts of mild, moderate or severe injury
GCS
PTA
LOC
what classifies as a mild TBI
13-15 GCS (not below 13 at 30 mins)
LOC <30 mins
PTA <24hrs
80% of all head injury patients
3% with MTBI will deteriorate
All patients do not require a non-contrast head CT but much controversy exists as to who does require a CT.
Must differentiate high risk vs. low risk patients.
what classifies as a moderate TBI
GCS 9-12
LOC 30min-24hR
PTA >24 hr
10% of all head injury patients
40% abnormal CT
8% lapse into coma (beware of PT that talks and deteriorates)
70% unable to work at 3mo
50% permanent disability
90% persistent HA and memory deficit
All require CT scan and ICU observation at a minimum
what classifies as a severe TBI
GCS 3-8
LOC >24hr
PTA >7 days
10% of TBI who reach ED alive
Up to 25% will require surgery
Mortality 40%
Only 7% have moderate disability or good outcome.
All require CT, neurosurgery consultation and transfer to intensive neurosurgical facility
when is head CT not indicated
No headache No vomiting Age < 60yrs No intoxication No short term memory deficit No seizures No evidence of trauma above the clavicle
When is there low risk?
Initial GCS 13-15 No change in consciousness Currently asymptomatic No other injuries No focal exam findings Normal pupils Intact orientation and memory Accurate history Trivial mechanism Injury > 24hrs ago Reliable home observer
When do we have to be aware of ‘talk and die’
moderate TBI
why is alcohol bad for tbi
no intoxication because makes symptoms worse
and makes the body’s ability to deal with the effects of injury (coping mechanisms) less effective
oxy period - need to be out for 5 mins at least to have long term residual brain effects
what is post concussive syndrome
A constellation of largely subjective somatic, cognitive, and affective symptoms that persist following mild TBI
diagnosed >3months post injury!
often diagnosed by neuropsychs… diffuse wm deficits, EF deficits
but… if you do blind tests, the level of compromise that psychiatric stress, chronic pain, sleep disturbance etc.. can cause the same symptoms…
WAS IN DSM IV BUT NOT DSM V
symptoms are nOT unique to concussion
what are the mechanisms of injury for TBI
closed:
- explosion
- motor vehicle
- fall
open (dura is breached)
- gunshot
- stab or fragment
describe the neuropathology of what happens in a closed TBI
primary injury:
- contusions/haemorrhages
- diffuse axonal injury
secondary:
- blood flow or metabolic changes
- traumatic haematomas
- cerebral oedema
- hydrocephalus
- increased intracranial pressure
what are 3 MECHANISMS of a primary injury in tbi
- impact - extra dural, subdural, condusion, intracerebral haemorrhage, skull fracture
- intertial - concussion, diffuse axonal injury
- ischaemic or hypoxic
What is DAI
diffuse axonal injury
-stretching or tearing of axons or even breaking
Impairment of axoplasmic transport,
focal swelling of the axon, progression to axonal separation; axon retraction balls
Describe free radical damage
Chemically unstable molecules known as free radicals are produced simultaneously when the body burns oxygen to produce energy. Free radicals cause damage to brain cells by taking electrons from the body’s healthy molecules to balance themselves.
What are some secondary mechanisms of brain damage that are systemic?
- Arterial hypotension
- Hypoxia
- Hyper-/hypokapnia
- Hyper-/hypoglycaemia
- Hyperthermia
- Disturbances of water and electrolyte balance
What are some secondary mechanisms of brain damage that are intracranial?
- Mass lesion
- Brain oedema, hyperemia
- ICP ⇑ Cerebral perfusion pressure ⇓
- Vasospasms
- Epileptic seizures
- Inflammation
How can ischaemia globally affect the brain as seconday injury?
- Hypoxia and ischaemia of the brain
- Reduced cerebral blood flow can be due to raised intracranial pressure
How can ischaemia focally affect the brain as a secondary injury?
Impaired cerebral blood flow or change in the extra-
cellular environment due to altered/ damaged tissue
While passive damage is instantaneous, secondary brain insults occur from hours to several days after TBI and signicantly alters the prognosis
What is one of the fastest mechanisms of secondary injury
free radials, glutamine, calcium and sodium
occurs within 2-8 hrs after injury
What is a reperfusion injury
Reperfusion injury is the tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of oxygen (anoxia or hypoxia).
The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function.
What is the monro-kellie doctrine
v.intracranial (constant) = v.brain + v.CSF + v.blood + v.mass lesion
v is volume
What are some reasons ICP may increase after a TBI
- Oedema - fluid cavity
- Secondary to physical, ischemic or excitotoxic activity
- Traumatic mass lesions
- Obstruction of CSF flow
- Viscoelastic change (compliance of parenchyma)
how does calcium influx affect injury
deranged calcium hypothesis
what is hyperglycolysis in tbi
within the initial 30 mins of tbi, there is an increase in glucose usage (hyperglycolysis
), and then a chronic low rate for the following 5-10 days.
due to disrupted ionic gradients across neuronal cell membranes and activation of energy-dependent ionic pumps
thought that due to lack of blood flow, anarobic respiration takes place, causing lack of ATP, increase of lactate in levels in extracellular space, acidosis, which contributes to cell damage.
What does hyperglycolysis tell us about mitochondria
it’s thought anarobix respiration only occured bc of lack of blood
not true thoguh, when there is no occlusion of blood supply, brain still does this after trauma.
suggests trauma causes dysfunction to mitochondrial phosphorylation, leading to anarobic shift
stats for gun shot wounds?
76% of GSW to head die at the scene
GCS <5 associated with a near 100% mortality
GSC > than 8 has 75% survival
Basilar Skull Fracture?
break of a bone in the base of the skull
Haemotympanum Rhinorrhea Otorrhea Battle/raccoon sign Cranial nerve deficits Dizziness Nystagmus
