Traumatic Brain Injury (TBI) Flashcards
Causes of TBI
Object striking head
-Head striking non moving object
-Acceleration/Deceleration of brain without external impact
-Foreign body penetrating brain
-Force from blast or explosion
Its what you think it is, anything causing trauma to brain
Most common cause of TBI
Falls
Motor vehicle accidents are number 2
Closed head trauma
Acceleration and rapid deceleration or collision with a blunt force causing dmg to brain tissue
-Your brain is rattling around in your skull
Open head trauma
Your head is opened, and the object that causes the trauma damages brain tissue and/or dura matter
Concussion
Mild TBI that can affect brain function
-Usually temp, but can lead to headaches and problems with concentration memory, balance and coordination
-Happens in sports
Contusion
Brain bruise as a result of the brain bouncing off the inside of the skull
-Can be coup or contrecoup sites
Diffuse axonal injury
-Shearing of brain’s long connecting nerve fibers (Axons) when the brain shifts and rotates within the bony skull from the primary injury
-Essentially grey matter rubs on the skull causing friction, tearing away from the white matter tearing those nerve fibers
Intracranial hemorrhage
Bleed in the skull
Epidural hemorrhage: Skull and dura matter
Subdural hemorrhage: Below dura matter
Subarachnoid hemorrhage: In subarachnoid space
Intraparenchymal hemorrhage: Brain bleed
Primary brain injury
Occurs at time of injury
-Directly as a result of force against the skull
-Shearing of tissue, tears, and bruising of brain tissue
-Local or diffuse
-Goal is to prevent secondary injury
Secondary Injury
-Comes after the initial injury
-Results from inadequate nutrients and oxygen to brain cells
-Hematoma formation (Epidural, subdural, Intraventricular, intracerebral)
-Cerebral edema (Swelling of brain tissue)
-Increased ICP
-Infection (Open head injury)
-Elevated temp (Increased metabolism and cerebral perfusion pressure)
Normal ICP
0-15 mmHg max upper limit is 15
Coup
Primary impact
Contrecoup
Brain slamming to opposite side after the primary impact
Basal skull fracture
-Occurs in the floor of the skull, areas around eyes, ears, nose or at the top of the neck near the spine
-Raccoon eyes
-Battle sign
-Caused by bleeding out of the skull,CSF can leak out of these areas too
Raccoon eyes
Bruising around the eyes indicating bleeding from the skull
Battle sign
Bruising of the mastoid process, (Behind the ear) indicative of bleed
Patho of TBI
TBI occurs
-Brain swelling or bleeding increasing intracranial volume
-Rigid cranium allows no room for expansion increasing ICP
-Increased ICP puts pressure on the blood vessels slowing flow to the brain
-Cerebral hypoxia and ischemia occur
-ICP continues to rise, brain may herniate
-Cerebral blood flow ceases
Intracranial pressure (ICP)
Pressure inside the skull from brain, tissue and CSF
Normal is 0-15
Cerebral spinal fluid (CSF)
FLuid that is in the brain, ventricles and spine
Cerebral perfusion pressure (CPP)
Pressure gradient that drives o2 delivery to cerebral tissue
-Normal is 60-80 mmHg
-Calculated by (CPP= MAP-ICP )
Mean arterial pressure (MAP)
Average pressure in a patients arteries in one cardiac cycle
MAP= (SBP+ 2(DBP))/3
Monro-Kellie doctrine
-3 parts to a cranial vault
-Blood
-Brain
-CSF
If there is an increase in one there is has to be a decrease in the others (Hopefully not the brain). And if there isnt a compensation with the blood or CSF the brain herniates
First sign of increasing ICP
Cushings triad
Cushings triad
-Increase in SYSTOLIC BP
-Decrease in pulse
-Decrease in respiration
Glasgow coma scale
-Determine level of consciousness, gauging severity of TBI, and can correlate with outcome of TBI
-Gauged on 3 categories
Eye opening
Verbal responses
Motor response
Min is 3
Max is 15
Glasgow coma scale: Totally fine
15
Glasgow coma scale: Comatose
8 and below
Glasgow coma scale: Totally unresponsive
3
Glasgow coma scale: Eye opening response
4 Spontaneously opens eyes
3 To speech
2 To pain
1. No response
Glasgow coma scale: Verbal response
5 Orientated times 3
4 Confused speech
3 Inappropriate words (Dont fit the context)
2 Incomprehensible sounds
1 No response
Glasgow coma scale: Motor response
6 Obeys commands
5 Moves to localized pain (Guarding and such)
4 Flexion withdrawal to from pain
3 Abnormal flexion (decorticate)
2 Abnormal extension (Decerebrate)
1 No response
Decorticate
Abnormal flexion, inwards to core
3 on the Glasgow coma for motor
Decerebrate
Abnormal extension which you move away from the core
2 on Glasgow coma for motor
Other changes with TBI
Damage to thebrain which may lead to changes in mental, physical, and emotional behavior.
These changes may last for a short time or may last forever.
Trouble with memory, learning, or judgment
Loss of motor function
Problems in communicating that could lead to frustrations, conflicts, and moreinjuries. Impulsivity—decreased executive function.
Changes in actions and feelings that cause anger or moodiness
Problems with senses–hearing, smelling, or eyesight
Seizures
Higher chance for otherbraindiseases, such as Alzheimer’s & Parkinson, if they live that long
Mild concussion or contusion
-Manifested by LOC change or loss of memory
-No abnormal imaging studies
-No neurological changes
-Recovery is weeks to months without specific treatment
Mild concussion or contusion: Symptoms
H/A
Dizzyness
Poor memory
Difficulty concentrating
Fatigue
Irritability
Tinnitus
Chronic Traumatic Encephalopathy (CTE)
People that have repeated blows to the heads and repeat concussions
-The idea of mini concussions stacking up
-Diagnosis is made after death
-Symptoms include
-Memory issues
-Confusion
-Personality changes
-Erratic behavior including aggression, depression and suicide
-People may not develop symptoms until decades after injuries occur
Moderate TBI
-Secondary injury occurs
-Loss of consciousness over 20 min
-Glasgow of 9-12
-Cerebral edema occurs
-Multiple small hemorrhages
-Pt exhibits neuro deficits (Hemiparesis)
-May exhibit long term neuro deficits
-Needs extensive rehab, to return to pre-injury lifestyle
Severe TBI
-Loss of consciousness over 8 hours
-Glasgow 3-8 (Comatose)
-Sustains diffuse axonal injury*
-Bleeding due to tearing of brain tissue
-Requires extensive rehab
-Can have long term neuro defects
-High risk of brain herniation, due to cerebral edema, increasing ICP –> which can lead to brain death
TBI medical treatment
-Goal is stabilization of patient
-Prevent secondary injury
-Hematoma formation
-Meds to decrease ICP
-Diagnostic test, CT MRI, EEG, MRA
Acute SEVERE TBI assessment /mgmt
-Assess LOC/Coma
-Surgery for skull fractures, debridement if open injury, placement of ICP monitor or drain
-mgmt in ICU with monitoring of EKG. CV status and mechanical vent
-Barbiturate coma
-Nutrition, NG tube, PEG tube
-Immobility
-Seizure mgmt (Check drug levels and all that)
-Family education and support
Barbiturate coma
-Those with severe TBI are induced into a coma to decrease ICP
-Can cause issues with electrolyte balances
-Decreases metabolic rate to decrease ICP
Mgmt of TBI in acute phase
-ICP monitoring
-See for alterations in LOC and orientation
-Glasgow coma scores and changes
-Vitals, pressures, EKG, thermoregulation
-Seizure precautions and safety
-I+O and fluids and electrolytes
Nutrition
Infection
-Environment, calm low lights
-Family, freinds
-All the issues that occur with immobility
-NOTIFY PROVIDER IF ANY CHANGES OCCUR
Why monitor I+O, and fluid and electrolytes for those with a TBI in the acute phase
They have a chance of developing diabetes insipidus and SIADH
Mgmt of increased ICP
-Hyperventilating them for increased CO2
-Treat hyperthermia (keep temp normal or hypothermic)
-Drainage of CSF
-Open skull, gives brain somewhere to go
-Barb coma
-HOB 30 degrees (Dont flex neck)
-Cerebral perfusion pressure
-Fluid mgmt
Why does hyperventilation decrease ICPW
Hyperventilation decreases CO2 in the blood which causes vasoconstriction, decreasing cerebral blood flow (Monro-kellie)
Why do we allow for permissive hypothermia with TBI
-Decreases metabolism, reduces swelling
-Decreases cerebral blood flow
Fluid Mgmt with increased ICP
-Dieresis (Mannitol)
-Fluid restriction
-Decrease IV fluids
-Electrolyte replacement
-Decreasing amount of fluid, decreases amount of blood, which decreases ICP
Mannitol
Powerful diuretic used to decrease fluids
TBI prognosis
Ability to recover is based on severity of injury and extent of brain dmg (GCS, and time spent in coma)
-65% survive
-35% are moderately disabled, remainder is severely disabled or vegetive state (this sounds wrong)
-Brain death for organ donation
3 Cardinal signs of brain death
-No brainstem reflexes
-Apnea
-Coma
-Other ones include, cerebral blood flow testing , EEG, transcranial doppler, auditory evoked, dolls eyes
Dolls eyes reflex (oculocephalic reflex)
Essentially you fix their eyes open, and shake their head left and right. The normal response is if the eyes move opposite direction the head is moving, a negative sign (Brain death) is when they move with the head or stay fixed midline
Cheyne -strokes respirations
-Apnea and hyperventilation cyclically at regular intervals.
-Hyperventilation occurs from increased CO2 in the blood (From the apnea)
-After the CO2 levels are down, Apnea occurs, leading to increased CO2 again
-This continues
-During the apnea phase ICP increases due to increasing CO2 in the blood, when this CO2 is blown out during the hyperventilation phase, ICP decreases
Other causes of Cheyne-strokes
-Brain tumor, CHF, Metabolic encephalopathy
-Meds: MORPHINE,
-Carbon monoxide
Osmotic diuretics
Diamox, Mannitol
-Decrease volume for elevated ICP
Loop diuretics
Lasix
-Decreases volume
Anticonvulsants
-Phenytoin, carbamazepine, benzos
-Prevents seizures
Steroids
-Sou-medrol, Dexamethasone
-Decreases inflamation
Barbituates
-Phenobarbital
-Sedates for that coma, decreasing ICP
Antibiotics
Used if there is an open head injury, ventricular drain or sensor to prevent infection
Post TBI clinical manifestations: Alterations in cognition
-Difficulty processing info
-Short attention span
-Decreased ability to concentrate
Post TBI clinical manifestations: Perceptive symptoms
-Changes in vision, hearing , touch, balance, pain and sensation
Post TBI clinical manifestations: Physical symptoms
-Persistent Headache
-Extreme physical and mental fatigue
-Impaired speech
-Gait disturbances
-Seizures
Post TBI clinical manifestations: Behavioral and emotional symptoms
-Apathy, irritability, impatience, impulsivity, lack of inhibition, emotional lability
-Think: Phineas Gage
Discharge plan from acute rehab
Differs for every patient
-Home rehab
-Home outpatient rehab services
-Residential TBI
-Discharge to long term facility
Rancho Los Amigos Scale (RLAS)
-Cognitive and behavioral patterns found in brain injury patients as they recover from injury
-Goes from levels 1-10 with 9-10 being deemed superior functioning
Rancho Los Amigos Scale (RLAS) Level 1
-No response, Total assistance needed
-No response to external stimuli
Rancho Los Amigos Scale (RLAS): Level 2
Generalized response: Total assistance
-Responds inconsistently and non purposefully to external stimuli
-Responses are the same regardless to stimulus
-You sternal rub and they kick their leg, you press their nail bed and they kick their leg
Rancho Los Amigos Scale (RLAS): Level 3
-Localized response: Total assistance
-Responds inconsistently and specifically to external stimuli
-Responds are directly related to stimulus
-Example: screams with a sternal rub
-Responds more to people they know
Rancho Los Amigos Scale (RLAS): Level 4
Confused and agitated: Maximal assistance
-Person is in a hyperactive state with bizarre and non purposeful behavior
-Demonstrates agitated behavior that originates more from internal confusion than external
-No short term memory
Rancho Los Amigos Scale (RLAS): Level 5
Confused, Inappropriate, non-agitated, maximal assistance
-Shows increase in consistency with following and responding to simple commands
-Responses are non-purposeful and random to more complex commands
-Behavior and verbalization is often inappropriate and individual appears confused and often confabulates
-If action or tasks is demonstrated, individual can perform but does not initiate tasks on own
-Memory is severely impaired and learning new info is difficult
-Differs from 4 in that the individual does not demonstrate agitation to INTERNAL stimuli but my become agitated from external stimuli
Rancho Los Amigos Scale (RLAS): Level 6
-Confused, appropriate, moderate assistance
-Follows simple commands well
-Retain learning for familiar tasks performed pre- injury (Brushing teeth, washing face)
-CANNOT retain learning for new tasks however
_Increased awareness of self, situation and environment
-Not aware of specific impairments and safety concern
-Responses may be incorrect secondary to memory impairments but appropriate to situation
Rancho Los Amigos Scale (RLAS): Level 7
-Automatic, appropriate; minimal assistance for daily living skills
-Orientated in familiar settings
-Able to perform
-Daily routine automatically with minimal confusion
-Demonstrates carry over for new tasks as well as pre-injury tasks
-Superficially aware of ones diagnosis but unaware of specifics
-Demonstrates lack of insight, decreased judgment and safety awareness
-Show interest in social and recreational activities in structured settings
-Needs minimal supervision
Rancho Los Amigos Scale (RLAS) Level 8
-Purposeful, Appropriate, stand by assistance
-Orientated times 3
-Carries out familiar tasks in a non-distracting environment independently
-starts to show awareness for specific impairments and how they interfere with tasks
-Able to use assistive memory devices to recall daily schedule
-Acknowledges others emotions and requires minimal assistance to respond appropriately
-Improved memory of events and able to consolidate past and future events
-Often depressed, irritable with low frustration threshold
Rancho Los Amigos Scale (RLAS) Level 9
-Purposeful, Appropriate, Stand by assistance on request
-Can shift between different tasks and complete them independently
-Aware and acknowledges impairments when they interfere with tasks and able to use compensatory strategies to cope
-Unable to independently anticipate obstacles that may arise secondary to impairment
-With assistance, able to think about consequences of actions and decisions
-Acknowledges the emotional needs of others with stand by assistance
-Continues to demonstrate depression and low frustration threshold
Rancho Los Amigos Scale (RLAS) Level 10
Purposeful, appropriate: Modified independent
-Able to multitask in many different environments with extra time or devices to assist
-Able to create own methods and tools for memory retention
-Independently anticipates obstacles that may occur as a result of impairments and take corrective actions
-Demonstrates intermittent periods of depression and low frustration threshold, while under stress
-Able to appropriately interact with others in social situations
Education for home discharge: Call for
-Decreased LOC
-Headache which is not resolving, especially if accompanies by other neuro symptoms
-Persistent nausea or vomiting, especially with other neuro symptoms
-New onset weakness, paralysis
-Bleeding from any orifice, nose, ears especially
-Fever 38c
-Seizures, new and not new may need to adjust meds
-Trouble walking or talking
Education for home discharge:
Medications: what, why, how, not to stop unless instructed by provider
Diet: PEG tube vs regular diet vs thickened liquids/soft solids
Activity: ambulation +/- walker, quad cane, assistance, hoyer
Trach Care: cleaning site, suctioning, mechanical ventilation, Oxygen
Skin Care: Change position frequently in wheelchair, turn every 2 hours when in bed if unable to do unassisted, monitor for pressure sores
Safety in the home/Falls precautions—Lifeline
Confusion management
Follow up: Keep follow-up appointments
