Lecture 16 - TBI

Question 1

What is concussion

Answer 1

• TEMPORARY loss of neurologic function with NO APPARENT STRUCTURAL DAMAGE
• CLOSED HEAD
• Seconds to minutes of unconsciousness only

Question 2

What causes LOC in concussion

Answer 2

shock wave goes to core structures in brainstem (RAS), disrupting brain signals, causing loss of consciousness.

Question 3

What are the 3 effects of brain injury

Answer 3

coup - site of impact (primary)

contrecoup - opposite side of impact (secondary)

spiral effect - rotational effect around fixed point

causes diffuse axonal injury

Question 4

what is PTA

Answer 4

posttraumatic amnesia

measure with westmead PTA scale

Question 5

what are the three determinatnts of mild, moderate or severe injury

Answer 5

GCS
PTA
LOC

Question 6

what classifies as a mild TBI

Answer 6

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.

Question 7

what classifies as a moderate TBI

Answer 7

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

Question 8

what classifies as a severe TBI

Answer 8

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

Question 9

when is head CT not indicated

Answer 9

No headache
No vomiting
Age < 60yrs
No intoxication
No short term memory deficit
No seizures
No evidence of trauma above the clavicle

Question 10

When is there low risk?

Answer 10

 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

Question 11

When do we have to be aware of ‘talk and die’

Answer 11

moderate TBI

Question 12

why is alcohol bad for tbi

Answer 12

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

Question 13

what is post concussive syndrome

Answer 13

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

Question 14

what are the mechanisms of injury for TBI

Answer 14

closed:
- explosion
- motor vehicle
- fall

open (dura is breached)

• gunshot
• stab or fragment

Question 15

describe the neuropathology of what happens in a closed TBI

Answer 15

primary injury:

• contusions/haemorrhages
• diffuse axonal injury

secondary:

• blood flow or metabolic changes
• traumatic haematomas
• cerebral oedema
• hydrocephalus
• increased intracranial pressure

Question 16

what are 3 MECHANISMS of a primary injury in tbi

Answer 16

• impact - extra dural, subdural, condusion, intracerebral haemorrhage, skull fracture
• intertial - concussion, diffuse axonal injury
• ischaemic or hypoxic

Question 17

What is DAI

Answer 17

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

Question 18

Describe free radical damage

Answer 18

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.

Question 19

What are some secondary mechanisms of brain damage that are systemic?

Answer 19

• Arterial hypotension
• Hypoxia
• Hyper-/hypokapnia
• Hyper-/hypoglycaemia
• Hyperthermia
• Disturbances of water and electrolyte balance

Question 20

What are some secondary mechanisms of brain damage that are intracranial?

Answer 20

• Mass lesion
• Brain oedema, hyperemia
• ICP ⇑ Cerebral perfusion pressure ⇓
• Vasospasms
• Epileptic seizures
• Inflammation

Question 21

How can ischaemia globally affect the brain as seconday injury?

Answer 21

• Hypoxia and ischaemia of the brain

- Reduced cerebral blood flow can be due to raised intracranial pressure

Question 22

How can ischaemia focally affect the brain as a secondary injury?

Answer 22

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

Question 23

What is one of the fastest mechanisms of secondary injury

Answer 23

free radials, glutamine, calcium and sodium

occurs within 2-8 hrs after injury

Question 24

What is a reperfusion injury

Answer 24

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.

Question 25

What is the monro-kellie doctrine

Answer 25

v.intracranial (constant) = v.brain + v.CSF + v.blood + v.mass lesion

v is volume

Question 26

What are some reasons ICP may increase after a TBI

Answer 26

• Oedema - fluid cavity
• Secondary to physical, ischemic or excitotoxic activity
• Traumatic mass lesions
• Obstruction of CSF flow
• Viscoelastic change (compliance of parenchyma)

Question 27

how does calcium influx affect injury

Answer 27

deranged calcium hypothesis

Question 28

what is hyperglycolysis in tbi

Answer 28

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.

Question 29

What does hyperglycolysis tell us about mitochondria

Answer 29

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

Question 30

stats for gun shot wounds?

Answer 30

 76% of GSW to head die at the scene
 GCS <5 associated with a near 100% mortality
 GSC > than 8 has 75% survival

Question 31

Basilar Skull Fracture?

Answer 31

break of a bone in the base of the skull

 Haemotympanum 
 Rhinorrhea
 Otorrhea
 Battle/raccoon sign 
 Cranial nerve deficits  Dizziness
 Nystagmus