TBI Flashcards
What is the most common cause of TBI in children?
falls and abuse
What is the most common cause of TBI in adolescents and young adults?
Falls, assault, and MVA
What is the most common cause of TBI in older adults?
FALLS
What is the difference between opened and closed injuries? Is one more serious than another?
open - penetrating type of wound (knife, gunshot, sharp object)
- skull fractured or displaced
closed - impact to head but skull is not fractured
- only cortical neuronal tissue is damaged
Open is worse b/c of infection risk plus debris
What happens to the meninges during open TBI? Closed TBI?
open - meninges are compromised and at risk for infection, bleeding, impaired CSF circulation
closed - meninges remain intact
What is meant by primary brain damage? What types of primary brain damage exist?
direct injury that results from mechanical issue at the time of trauma
focal and diffuse injury
Focal injury
localized to area under site of impact or site opposite of impact
- coup-contracoup injury
Diffuse injury
more widespread injury
hematoma
pool of clotted or partial clotted blood that congregates and settles in whatever space it is confined in
- due to rupture or damage to meningeal structures when in skull
Epidural hematomas
- location
- characteristics
- intervention
location - between the dura mater and skull
characteristics - involve brief loss of consciousness followed by period of awareness and then crash
- unconsciousness (bad) - alert (better) - deteriorate (way worse)
intervention - craniotomies and hematoma evacuation
subdural hematomas
- location
- characteristics
- intervention
location - rupture to the cortical bridging veins between dura and arachnoid
characteristics - blood slowly leaks over several hours or weeks and symptoms similar to CVA
intervention - small clots reabsorbed and larger ones require surgical removal
Which type of focal injury is seen in elderly after falls w/ blow to the head?
subdural hematomas
- they think they are fine and family member will start to notice something is off and then go to ER to find bleed
subarachnoid hemorrhage
- location
- sequela
location - between arachnoid and brain tissue
sequela - vasospasm
intracerebral hemorrhage
- location and cause
- sequela
location and cause - within the brain itself from significant brain injury
sequela - seizures, stroke-like presentation
What type of hemorrhage is the most life-threatening?
subarachnoid hemorrhage
What is a brain contusion? How does it present?
bruising on the surface of the brain is sustained at time of impact
presents on side of impact or opposite side of impact
coup lesion
contusion on the same side of the brian as the impact
contrecoup lesion
surface hemorrhages on the opposite side of the brain trauma as a result of deceleration
- whiplash of the brain
Which is typically worse in damage, coup or contrecoup injuries? Why?
contrecoup injuries are worse because of momentum of brian towards the impact side is little than picks up speed (there is more room) and slams into opposite sides
- PHYSICS!
What areas are most commonly involved in coup contrecoup injuries?
anterior poles and underside of temporal and frontal lobes
What is a diffuse axonal injury (DAI)? What typically causes it?
widespread shearing and retraction of damaged axons that results in traumatic “micro bleeds”
- significant neurological involvement and poor prognosis
caused from HUGE acceleration, deceleration, and rotational forces (MVA most common)
What areas are most suspectable to damage from a DAI?
corpus callosum
basal ganglia
brainstem
cerebellum
What occurs with secondary brain damage?
global reduction of O2 in the body so brain starts to die
- can further lead to reduction in CO and/or ischemic event
What occurs with secondary brain damage caused from a TBI?
electrolyte imbalance and mass release of damaging neurotransmitters
- causes apoptosis
What occurs with secondary brain damage not caused from a TBI?
hypoxic/ischemic injury
swelling/edema - increased ICP
anoxic vs hypoxic brain injury
anoxic - no O2 to brain
hypoxic - little O2 to brain
What causes anoxic/hypoxic brain injuries?
Lack of O2 blood to brain
- cardiac arrest, CO2 toxicity, near drowning, internal bleeding
- anything that causes systemic hypotension
What are anoxic/hypoxic brain injuries associated with?
poor prognosis for cognitive function
- lower expected functional outcomes
What areas of the CNS are more vulnerable to oxygen depletion?
hippocampus
cerebellum
basal ganglia
tertiary blast injury
blast causes you to fall and hit head like TBI
secondary blast injury
result of shrapnel
- cause multifocal injuries because of multiple shrapnel pieces
- HIGHER risk of infection
primary blast injury
direct effect of blast overpressure on organs
- blast causes brain to move
What type of brain damage usually occurs with primary blast injuries?
diffuse brain damage
What happens to CSF or venous pressure after primary blast injury?
increase
What type of diagnostic imaging is usually included in TBI workup?
- MRI
- CT - better than MRI
- PET - shows brain function
- EEG - used if concerns for seizures
What are the major goals of medication management for acute TBIs?
- decrease BP and ICP
- decrease intracranial bleeding
- anti-seizure
- decrease body temp
- decrease infection rate
When is ICP elevation a risk post TBI?
highest risk during acute phase but can occur several months later
Why is an increase in ICP problematic?
- compress brain tissue
- decrease perfusion to brain tissue
- possible herniation
What is normal ICP and what is abnormal ICP?
normal - 5-10 mmHG
abnormal - > or = 20 mmHg
- use caution when > or = 15 mmHg
T/F - you cannot treat a patient with ICP 20 mmHg or above
true
What activities have the potential to increase ICP?
- full supine or Trendelenburg
- cervical flexion
- percussion and vibration
- Valsalva (coughing, sneezing, holding breath)
- exertional activities
- quick elevating head of bead
- supine to sit
What are the signs and symptoms of elevated ICP?
- decreased responsiveness, irritability
- impaired consciousness
- severe HA, seizures - impaired sensory and motor function
- vomiting
- papilledema, pupillary changes, impaired eye movement
- change in vitals - increased BP, decreased HR, irregular RR
- posturing - decerebrate, decorticate, flaccid
- changes in speech
What are the signs and symptoms of elevated ICP in infants?
- bulging fontanels
- increased head circumference
- high pitched cry
How is elevated ICP managed?
medication and ventricular peritoneal shunting if needed for permanent correction
What is abnormal ICP?
> or = to 20 mmHg
- Do not treat patients w/ elevated ICP 20 mmHg or above
Increased pressure can _______ brain tissue, _________ perfusion to brain tissues or possible herniation
compress, decrease
How are TBIs and seizures related?
increased risk of seizure after TBI
What are some examples of events that could trigger a seizure post-TBI?
- stress
- poor nutrition
- electrolyte imbalances
- missed medications or drug use
- flickering lights
- infection
- fever
- anxiety
common S & S of seizures
- focal or diffuse twitching, jerking; stiffening
- or - loss of consciousness
- absent staring
Can you treat a patient who is on medication to lower body temperature after a TBI?
No - they are too medically unstable
How are seizures managed post-TBI?
medications and continuous electroencephalogram (cEEG)
When is it safe to mobilize a patient after a seizure?
more than 24 hours after being seizure-free
What is PAID? What are characteristics?
Paroxysmal Autonomic Instability and Dystonia
- sympathetic (fight or flight) system goes into overdrive
What type of TBI is PAID seen with?
- severe TBI
- glascow coma score 3-8
clinical S & S of PAID
- tachypnea
- tachycardia
- HTN
- Diaphoresis
- Decorticate/Decerebrate Posturing
- agitation
How is PAID diagnosed? How is it managed?
diagnosed through clinical obeservation
managed w/ medication that suppresses sympathetic nervous system
What do you do if a patient is suffering from PAID?
No treatment if patient is having active issues (storming)
Describe the relationship between heterotopic ossificans (HO) and TBI. What increases risk?
10-20% of TBI and increased risk if TBI polytrauma results in fracture near joint line
- common in large joints
When does heterotopic ossification occur after TBI?
~ 4-12 weeks after brain injury
What is Heterotopic Ossification clinical presentation?
- loss of ROM w/ hard end feel and pain
- local erythema, pain w/ movement, swelling, warm to touch (like DVT)
- severe HO may result in vascular and/or nerve compression
What is difference between HO and DVT when it comes to ROM?
DVT ROM will not have hard end feel
How is HO managed?
- maintain ROM and prevent further complications
- medications
- surgical excision after it has stopped growing
What is didronel used for?
prevents calcium from being deposited in bony matrix to prevent HO
What is used for symptom management for HO?
anti-inflammatories
What is the most common and debilitating cognitive deficit following TBI?
attention deficits
What are the 5 categories of attention?
- focused
- sustained
- selective
- alternating
- divided
S & S of impaired attention
- unable to engage on relevant info
- unable to sustain attention to task
- unable to switch to new task
- unable to resist distraction
- unable to multitask
- unable to manipulate mental info while maintaining overarching goal in mind
What dysfunction is most common when there is damage to prefrontal cortex?
executive function deficits
general characteristics of executive function deficits seen post-TBI
impairment to:
- volition/planning
- problem solving
- insight (impulsive)
- social pragmatics
- self-regulation
general characteristics of memory deficits seen post-TBI
- retrograde (unable to recall) and/or anterograde (unable to create new memories) amnesia
- posttraumatic amnesia
- short term > long-term
- Declarative (dates, time, history) and procedural (skills) memory often impaired
T/F- TBI patients have more issues with long term memory over short term memory.
false - short term > long term memory
If TBI patient is having issue with speech, it is more likely due to _______ impairment instead of ______
cognitive impairment instead of aphasia
general characteristics of language deficits seen post-TBI
- non-aphasic and more cognitive impairment
- disorganized and tangential oral and written communication
- imprecise language
- word-retrieval difficulties
- disinhibited language
What is the most enduring and socially disabling of impairments after TBI?
behavioral issues
- usually temporary and can be managed
What types of behavioral issues can be seen post-TBI?
- sexual disinhibition
- apathy
- aggressive disinhibition
- agitation
- hyperactive, restless
- low frustration tolerance
- depression
- EASILY OVER-STIMULATED
What are the 2 common syndromes after frontal lobe damage from TBI?
orbitofrontal lobe syndrome - disinhibited
- lack of restraint manifested in disregard of social conventions, impulsivity, and poor risk assessment
frontal convexity syndrome - apathetic
- showing or feeling no interest, enthusiasm, or concern
Signs of orbitofrontal lobe syndrome
- impulsive behavior
- inappropriate jocular affect, euphoria
- emotional liability
- poor judgement and insight
- distractibility
Signs of Frontal Convexity Syndrome
- apathy (lack of interest, enthusiasm, concern)
- indifference
- motor preservation and impersistence
- stimulus-bound behavior
- motor programming deficits
- poor word list generation
Diffuse injuries more so characterized by ________ and ________ deficits over true strength deficits
motor control and coordination
What types of tone abnormalities can be seen post-TBI
- flaccidity, rigidity, or hypertonicity
- decorticate and decerebrate rigidity
- primitive and tonic reflexes
Decorticate Rigidity
LE extension and UE flexion
Decerebrate Rigidity
LE and UE extension
What sensory deficits are most common post-TBI?
proprioceptive and kinesthetic deficits
What cranial nerves are commonly found to be damaged post-TBI?
- CN 1 - olfactory
- CN 2 (optic), 3 (oculomotor), 4 (trochlear), 6 (abducens)
- CN 5 - trigeminal
- CN 7 - facial
What CN is commonly affected by concussion?
CN 1 olfactory
conjugate gaze palsy is injury to what?
CNS
unilateral gaze palsy is injury to what?
PNS
tonic (constant) downward gaze is injury to what?
severe injury to thalamus, midbrain or pons
tonic (constant) upward gaze is injury to what?
severe injury to both hemispheres
What is an indication of seizure activity when it comes to the eyes?
rapid horizontal eye movement
What is the common culprit of PNS gaze abnormalities? How will the patient present?
abducens nerve - patient will have unilateral gaze towards adduction
What structure is damaged if the patient has monocular blindness and absent pupillary response?
optic nerve
Why is oculomotor and trochlear nerve damage less common?
damage occurs to the muscle bellies and tendons vs the nerve
What CN are commonly damaged due to their superficial proximity?
trigeminal and facial nerve
Where is trigeminal nerve damage common and what are the presentations?
- Peripheral injury to where divisions leave orbit common
- Results in loss of sensation to the nose, eyebrow and forehead
Where is facial nerve damage common and what are the presentations?
- Peripheral injury when temporal bone damaged
- Muscle weakness, loss of tear production, decreased saliva secretion, and taste
Vestibular rehabilitation may take up to ______ as long than those without TBI compared to other vestibular patients
3x
Where is the damage if a patient is unable to perform sensory integration for balance?
brainstem or cortex involving vestibular pathways
common ANS symptoms seen with TBI
- HR variability
- RR variability
- BP changes
- elevated body temp.
- excessive sweating, salivation, tearing
- dilated pupils
- vomiting
- anxiety, panic disorder, PTSD
What predicative capabilities does the GCS have as it relates to TBI mortality?
lower the score the higher the mortality rate
- GCS of 3 at initial presentation results in 65-100% TBI mortality rate
T/F - A mild TBI is a concussion
true
Mild TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging
- GCS - 13-15
- LOC - 0-30 minutes
- brief (<24 hours) alteration of consciousness
- post-traumatic amnesia < 1 day
- normal imaging
Moderate TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging
- GCS - 9-12
- LOC - > 30 min but < 24 hours
- alteration of consciousness > 24 hours
- post traumatic amnesia > 1 day but < 7 days
- normal or abnormal imaging
Severe TBI: GCS, LOC, alteration of consciousness, post-traumatic amnesia, imaging
- GCS - 3-8
- LOC - > 24 hours
- alteration of consciousness > 24 hours
- post-traumatic amnesia > 7 days
- normal or abnormal imaging
What does Disability Rating Scale measure?
impairment, function, and participation
Looks at 4 major categories
- consciousness
- cognitive ability
- independence
- employability
What is scoring for Disability Rating Scale and what can it predict?
30 point scale and higher scores represent high level of disability
- can predict return to work potentional
What is the Glasgow Outcome Scale mainly used for?
used more for research vs clinical
- classifies global outcomes for TBI patients
How can patients generally be described when falling under severe, moderate, and good recovery categories for Glascow Outcome Scale?
Severe - dependent
Moderate - independent but participation in community is limited
Good - can return to work, school, etc but may need some accommodations
Negative prognostic indicators for TBI (10)
- Older age
- Female (worst recovery compared to men)
- GCS score
- Length of PTA
- Acquired injury (vs Traumatic)
- Lower education level/pre-injury IQ
- Delayed or inability to use neurostimulants
- Presence of pre-injury psychological issues or substance abuse
- GOS: Level 1-3
- Initial GCS: 3-8
Severe TBI negative prognostic factors (5)
- older age
- absence of light reflex
- presence of extensive subarachnoid hemorrhage
- sustained elevated ICP
- midline shift
