Traumatic Brain Injury Flashcards
What is Primary injury
immediate trauma to brain and parenchyma at moment of insult or injury
What is secondary
Result of secondary effects (cascade of events after initial injury that causes damage), hypoxia/ischemia, edema, and increased ICP
What are the MOI for TBI
Contact- Open (skull penetrated) vs closed
Acceleration vs Deceleration
* compresion
* tension
*shearing
Rotation
* angular acceleration
What is the Pathophys of TBI
focal Injury
* Non penetrating (coup-countre coup) vs Penetrating (gunshot)
DAI - diffuse axonal injury
Hypoxic ischemic injury –> ocnstriction or disruption of blood vessel (essentially a stroke)
Increased ICP
Describe Elevated ICP
Normal is 5-20cmH20
- severe raised ICP leads to brain herniation
ICP>20mmH20 = elevated
ICP>25cmH2O = Critical
Why may it take longer in older adults to have increased ICP
SENILE ATROPHY
- due to aging the size of the brain decreases, therefore there is more room in the skull
- therefore even though the ICP is rising it will take longer to reach >25cmH2O
What are Signs of Elevated (10)
-1. Decreased consciousness (stupor (almost unresponsive) and coma (complete unresponsive)
- altered vital signs
- Widened pulse pressure (difference between systolic and diastolic)
- Irregular brething (Cheyne-Stokes) –> breath depth increases then decreases and then stops
- Vommiting
- Headache
- Non-reacting pupils (CN3)
- Papilledema (optic disc or nerve swelling)
- progressive imapirment of motor fucntion
- Seizure activity
What is the Treatment for elevated ICP (4)
- Elevate head of bed 30 degrees (LOWERING BED IS CONTRAINDICATED)
* promotes venous drainage
*immediate relief - Intubate and hyperventilate: results cerebral vasoconstriction
- IV mannitol - promotes cerebral drainage while maintaining perfusion to brain
- Ventricular draiange - CSF drainage decreases ICP
What happens if the primary treatments for elevated ICP fails
- Barbiturate-induced coma: results in cerebral VC and decreased metabolic demand
- Surgical decompression (hemicraniectomy)
- Steroids
What are possible impairments seen in TBI
- Neuromuscular (abnormal tone)
- Cognitive
- Neurobehavioral
- Communication
- Swallowing
- Dysautonomia
- Visio-perceptual
- Post-traumatic seizure
- Secondary impairments and complications
What are some Neuromsucular impairments
- Paresis
- Abnromal tone
- Coordination
- Motor fucniton
- Postural control
- Abnormal gait
- Somatosensory function
What are cognitive impairments seen in TBI
- arousal level (coma, vegetative state, min concious)
- Attentoin
- ocncentration
- Memory
- Learning
- Executive function
Decribe the 3 levels of arousal state
- coma
- vegetative state
- Minimally concious state
Define Coma and S+S
- Arousal system not functioning
- eyes closed
- Sleep/wake cycles ABSENT**
- ventilator dependent**
- No auditory, visual, cognitive, or communicative function
- Abnormal motor and postural reflexes may be present (Decorticate)
Define Vegetative state and S+S
- eyes OPEN, but awareness is ABSENT
- brainstem is able to manage basic cardiac, respiratory, and other functions (patient can be weaned off ventilator)
- sleep/wake cycles are present **
- may startle to visual or auditory stimuli**
- MEANINGFUL motor, cognitive, or communicative function ABSENT (maybe reflexive movement but awareness is absent)
Define Minimally Conscious state
- minimal evidence of AWARENESS
- cognitively mediated behavior occur inconsistently (this is how we know there is awareness)
- Sleep/wake cycles are present
- will localize to NOXIOUS stimuli and may inconsistently reach for objects
- May localize to sound location and demonstrate visual fixation and pursuit (follow with eye and respond to sound - so some awareness) **
What is Stupor and obtunded
Stupor: Almost unresposnive state - can be aroused briefley with VIGOROUS (shake), repeated stimulation
Obtunded: Decreased alertness. Sleeps often
Describe the 4 types of Memory impairments in TBI
- Anomia: difficulty remembering names, proper nouns, or other abstract nouns
- Anterograde amnesia: Not remembering anything from the injury forward
- Likely remember info prior to injury (recognize family and friends) - Retrograde amnesia: Not remembering events PRIOR to injury
- may initially be very long, but can partially resolve
- may never remember events leading up to injury - Post-traumatic amnesia: the time between the injury and when patient is able to recall recent events
What are neurobehavioral impairments
- agitation, apathy, emotional liability, mental inflexibility (can’t change their idea), disinhibiton (lack of resentment), anxiety, aggression, impulsiveness, irritable, lack of inhibition (can’t initiate), psychotic ideation (imagine things that happened that never did), Egocentricity (can’t put themselves in other’s shoes - eveything baout tem), poor self-image, sexual apathy or disinhibiton
What are some communication impairments
Aphasia, auditory processing deficits, or subtle language processing deficits
Disorganized communication, imprecise language, difficulty with word retrieval, socially inappropriate, difficulty communicating in distracting environments, no social cues or adjusting to situation
What is Dysautonomia
Increased SNS activity following TBI (paroxymal sympathetic hyperactivity)
- Results in increased HR, inc. RR, Inc BP, diaphoresis and hyperthermia
what are visuo-perceptual impairments
Damage to occipital lobe can result in visual impairments
Perceptual impairments: apraxia, spatial neglect, somatognosia
What are key areas to examine for TBI
- Arousal, attention and cogntion**
- integumentary integrity - skin (pressure sores)
- Sensory integrity
- Motor fucntion
- ROM
- Reflexes
- Ventilation and respiration
Describe the Glasgow Coma scale
- Measures level of conciousness
- Helps classify severity of injury (mild, moderate, severe)
- Help track progress
3 scores
* eyes opening, motor, verbal
Total score between 3 and 15
Severe <8
Moderate 9-12
Mild>13