Severe/Moderate Traumatic Brain Injury Flashcards
Medical Definitions for Moderate/Severe Brain Injury:
Acquired Brain Injury
Open and Closed Head Injuries (Blunt Trauma)
Shaken Baby Syndrome Abuse
Medical Definitions for Moderate/Severe Brain Injury:
Non-Traumatic Brain Injury (Stroke)
Coup-Contra Coup Injury (Acceleration and Deceleration)
Diffuse Axonal Injury (DAI)
Medical Definitions for Moderate/Severe Brain Injury:
Anoxic Brain Injury
Complete Occulsion of Oxygen
15 seconds Loss of Consiousness
4 minutes
Medical Definitions for Moderate/Severe Brain Injury:
Hypoxic Brain Injury
Not sufficienct Oxygen Saturation (Altitude)
Suffocation
Leading Causes of TBI
Falls 40.5%
Motor Vehical Accident 14.3%
Traumatic Brain Injury Incidence
Higher incidence in Males at age 14-25
Males and Females increase starting at age 70 due to increased risk of falling
Brain Trauma:
Immediate Primary Damage
Scalp Laceration
Skull Fracture
Cerebral Contusions
Cerebral Lacerations
Intracranial Hemorrhage
Diffuse Axonal Injury
Brain Trauma:
Secondary Damage
Ischemia
Hypoxia
Cerebral Swelling
Infection
Results of a Brain Injury
Brain Injury (trauma)
results in cascade of biochemical, cellular, and molecular events that evolve over time due to the initial injury and injury-related hypoxia, edema, and elevated intracranial pressure (ICP)
Definition Traumatic Brain Injury
An alteration in brain function, or other evidence of brain pathology, caused by an external force
External force is defined by blunt trauma, acceleration and or deceleration or shock wave injury
DON’T HAVE TO LOSE CONSCIOUSNESS TO HAVE A TBI
Primary Damage:
Diffuse Axonal Injury (DAI) = Shearing
Most common type of primary lesion
Unequal deceleration, acceleration, or rotational injuries
Diffuse Axonal Injury
Grade 1
Mildest form of DAI
Microscopic changes in the white matter of the Cerebral Cortex, Corpus Callosum, Brain Stem, and Cerebellum
Diffuse Axonal Injury
Grade 2
Moderate form of DAI
Grossly evident focal lesions isolated to the Corpus Callosum
Diffuse Axonal Injury
Grade 3
Severe from of DAI
Addiitonal and severe focal lesions on the brainstem itself
Diffuse Axonal Injury Outcomes
50% of people have a good recovery
How to take care of a DAI
Treat it like a Muscle Injury
Take a break and get sepcific training for recovery
Diffuse Axonal Injury MRI
Injury to the White Matter
Corpus Callosum, Cerebral Cortex, or Cerebellum
Diffuse = Widespread damage because of the shearing forces
Holes in the brain can heal with proper treatment
Primary Damage TBI:
Dural Hematomal
Penetrating Objects and Epidural Hematoma
- Skull fracture tearing Meningeal Artery Vessels
Subdural Hematoma
- Tears the Bridging veins in Superior Sagittal Sinus
Acute Subdural Hematoma
Midline shift and reduced/irregular shape of the Ventricles
Parimary Damage TBI:
Penetrating Injuries
Getting shot in the head man
Secondary Complications of Severe to Moderate TBI:
Cellular
a lot of things
Cerebral Edema
Cerebral Hypoxia and Ischemia
Cerebral Metabolic Impairment
Cerebral Vasospasm
Increased Intracerebral Pressure
Mitochondiral Dysfunction
Impairment of Glucose Metabolism
Increased Glutamate
Complement activation inflammation
ROS generation
Excitotoxicity
BBB Damage
Cell Death
Secondary Damage of modTBI:
Glutamate
Glutamate: Excitoxicity
Leads to CA++ entry into cells
Cerebral Edema
Cell Death
Secondary Complications of modTBI:
Cellular Excitotoxicity
Leads to Inflammation and Reactive Oxygen Species
Secondary Complications of modTBI:
Blood Brain Barrier
Neutrophils and activated Microglia crossing through the Blood Brain Barrier
Microglia cells are the immune cells of the CNS and play important roles in brain infections and inflammation.
Two types of Microglia M1 and M2
Neuroprotective and Neurotoxic Microglia
Neurotoxic Microglia
Can increase after 10-12 days
Continue to have symptoms, but there is a larger difference between the Pre and Post of the 10-12 day mark
Neuroprotective Microglia
Peak at 1 day post TBI and decrease over the next 7 days
Microglial Activity in a TBI
Even after 30 days, there is a possiblity of increasing damage, from Microglial Activity
Severity of the damage depends on the secondary injury by the fluctuating Microglia
Especially the M1 (Neurotoxic) microglia
Similarities with mTBI and Repetitive injuries and Severe TBI
Mild Repetitive TBI
- Variable chronic cognitive and/or neuropsychiatric impairment, assocaited with PTSD
- Dementia Pugilistica, chronic traumatic encephalopathy, pugilistic parkinsonism
Severe TBI
- Alzheimer Disease
- Total or partial functional recovery, often with variable chornic cognitive and/or neuropsychiatric impairment
Recovery after a Traumatic Brain Injury
Recovery after TBI takes place in the 2 years after the Injury
In some patients, further improvement is seen even as late as 5-10 years after injury
Brain Areas involved in TBI:
Midbrain Structures
- Prefrontal Cortex (Decreased)
- Working Memory
- Self-Control
- Decision Making - Amygdala (Increased)
- Emotional regulation
- Fear response - Hippocampus (Decreased)
- Learning Memory
Motor Areas Affected in TBI
Brainstem, Mid Brain
Cerebellum, Cortex, Basal Ganglia
Neuro-Cognitive Effects in TBI
Memory (STM & LTM)
Judgement (Safety)
Language (Aphasia)
Sleep-Wake Cycle/Arousal (Mid-Brain)
Behavioral Effects of TBI
Impulsive, Irrational
Behaviors out of context
Personality Changes
Outcomes of Moderate to Severe TBI:
Motor Outcomes
- Hemiparesis
- Synergistic versus primary weakness - Ataxia
- Cerebellar - Signs of Hypertonia
- Clonus, Spasticity, Rigidity
- Contractures - Syndergistic Movement
- Tremors
Outcomes of Moderate to Severe TBI:
Arousal/Attention
- Attentional
- Arousal
- Coma Status
Outcomes of Moderate to Severe TBI:
Autonomic Nervous System
- Sleep Wake Cycle
Reticular Activating System:
3 Systems of Control
- Waking
- Increasing Thalamic input (Sensory) - Arousal
- Attention and activation of appropriate responses - Sleeping
- Reduction in Sensory Information
- Atonia (not activating movement) - Fight or Flight
- Autonomic Nervous System
- Hypothalamus
- Circadian Rhythm
Reticular Formation
The reticular formation functions as an integration, relay, and coordination center
Due to the expansive network of tracts and the interconnected structure
Other Functions of the Reticular Formation
Circadiain Rhythm
Sleep-Wake Cycles
Coordination of Somatic Movement
CV and Respiratory Control
Pain Modulation
Habituation
Reticular Formation:
Associations
Associated with the Cranial Nerve Motor Nuclei of the Trigeminal, Facial, Glossopharyngeal, Vagus, and Hypoglossal nerves to coordinate the complex task of Respiration
Reticular Formation:
Brainstem
Brainstem is a complex area of neurons and nuclei that are necessary for survival
Forms a network of brain systems that govern many essential functions of the CNS and PNS
Ascending brainstem sensory systems to the reticular foramtion influence the entire cortex
Sleep Dysfunction Melatonin in TBI
Sleep Dysfunction Melatonin is reduced in TBI
Pathophysiology of Post-TBI Sleep Dysfunction
- Primary Injury
- Sheer Force
- Stretching - Secondary Injury
- Oxidative Stress
- Neuroinflammation
- Excitotoxicity - Apoptosis
- Neurodegeneration
What lobe is vulnerable to TBI?
TBI vulnerability is in the Frontal Temporal Lobe
How is nighttime Melatonin affected by TBI?
REDUCED (41% of TBIs)
What assists with sleep in Post-TBI Sleep Dysfunction?
The Hypothalamus
Suprchiasmistic Nucleus (SCN) produces hormones that regulate rhythm
Disruption of Melatonin in a TBI
Long pathways are susceptible in TBI
Disrupts these long pathways and it is thought to disrupt to melatonin
Memory Disruptions in TBI
Short Term in Moderate and Mild TBI
In severe TBI, LTM is disrupted.
Connections involved hippocampus and cortex (Prefrontal)
What does Memory Involve?
Memory not only involves persons/events
- Identification of Objects
- Use of Objects (Apraxia)
- Finding their way back to their room or rehab (spatial cognition)
Relearning of Mobility, Transfers, Assistive Devices
Memory Loss in TBI
Loss of Synaptic Signaling
The Hippocampus retrieves, stores, and recalls memory and interacts with the Pre-frontal cortex
Both the Hippocampus and Cortex work together for Spatial Info (Naviation) and Non-Spatial (Identification)
Memories in Moderate to Severe TBI
Memories become harder to retrieve or store
Rehabilitation works with Physical Activity to assist in Memory Formation
Parts of the Brain involved in Memory:
TBI
- Prefrontal Cortex
- Working Memory - Amygdala
- Emotional Memory - Hippocampus
- Episodic Memory - Cerebellum
- Procedural Memory
Exercise and BDNF
BDNF helps increase Long Term Potentiation, Synaptic Plasticity, and Neurogenesis
Injury and Repairs: BDNF and Orexin-A
Primary Injury
Shearing and Tesnile Effects -> Traumatic Axonal Injury and Neuronal Disconnection
Injury and Repairs: BDNF and Orexin-A
Secondary Injury
Neuronal and Vascular Damage -> Proteolytic pathways, Excitotoxicity, Oxygen-free radicals, Apoptosis, Inflammatory processes, and ischemia
Injury and Repairs: BDNF and Orexin-A
Repair
Increases in BDNF and Neurotrophic Factors -> Reconnection through fiber sprouting and synaptogenesis
Exercise and the Reduction of Inflammatory Cytokines
Exercise leads to:
Decreased Proinflammatory Cytokines
Increased Antinflammatory Cytokines
Decreased Neurotoxic activation of Microglia
Increased Neuroprotective activation of Microglia
TBI Pathology:
Primary Injury
Focal brain ontusion
Vascular and Blood-Brain Barrier Rupture
Hemorrhage
Neuronal and Axonal Injury
Release of Cytokines, Chemokines, and damage associated molecular patterns
TBI Pathology:
Secondary Injury
Excitotoxicity
Oxidative Stress
Inflammation
Programmed Cell Death
Demyelination
Autoimmunity
Neurodegeneration
TBI Pathology:
Neurological Deficits
Loss of Neurological Function
Cognitive Decline
Psychological Alterations
Chronic Disability
TBI Combination of Primary & Secondary Injury
Secondary injury can continue for years
Microglial and Astrocyte activation contribute to Pro-inflammatory elements and Neuronal Death
What kind of Issues are seen in a
Moderate to Severe TBI
Physical, Cognitive, Neurocognitive, and Behavioral Issues
2 Stages of Moderate to Severe TBI
Initial Trauma
Hematoma, Hemorrhage, Diffuse Axonal Injury
Cellular Response
Can last for weeks, months, years
Cranial Pressure after Severe TBI
Increased Cranial Pressure can lead to Edema, Hemorrhage or Hematoma
This can lead to brain herniation and requires monitoring
What is Increased Cranial Pressure after Severe TBI correlated with?
ICP is correlated with lower outcomes and higher mortality
Linked to Acute Hydrocephalus
Increased Cranial Pressure after Severe TBI:
Acute Hydrocephalus
Blood begins to accumlate in the Ventricles and requires External Ventricular Drain
Increased Cranial Pressure after Severe TBI:
Normal Pressure Ranges
Normal Pressure: 7-15 mm Hg
Increased Cranial Pressure after Severe TBI:
When to be concerned
LOSS OF CONSCIOUSNESS
Pupillary Changes
HEADACHE
“GET-UP Trial” - Post TBI:
The Focus
Focus on Early Mobilization
Assess whether a patient is allowed to mobilize early after a burr hole craniotomy for cSDH would lead to better outcomes
“GET-UP Trial” - Post TBI:
Significance
Provided evidence that early mobilization after a craniotomy can be a safe and beneficial practice
Hydrocephalus with TBI
Ventricular Catheter
Intracerebral Monitor pressure from Hydrocephalus
Brain Bolt
Monitor Brain Oxygenation
TBI - Epidueral Hematoma
TBI often leads to Epidural Hematomal skull flap with Burr Hole or Hydrocephalus - External Ventricular Drain
Medical Considerations for Epidural Hematoma
Ventilation
Constant ICP monitoring
Nasogastric Tube
Compression Leggings
Foley Catheter
Central Line
IV Catheter for Meds & Drawing Blood
Pulse Oximeter and BP/HR monitors
PT with EVD
While in bed, the elevation of bed and patient position must not change
Before mobilizing, EVD must be clamped with Nurse
Monitor CPP, ICP, HR, BP, and O2 saturation
Importance of Cerebral Perfusion Pressure
Amont of pressure for blood perfusion for overall brain function >60
Intracranial Pressure <20
Medical Defintion of Consciousness:
Loss of Consciousness
Duration: Several minutes to hours to days
Medical Defintion of Consciousness:
Coma
Complete paralysis of cerebral function: state of unresponsiveness
Eyes closed, no resopnse to painful, auditory or tactile stimulation
Medical Defintion of Consciousness:
Persistent Vegetative State
Reduced responsiveness with no evidence cerebral cortical function
Diffuse hypoxia, axonal white matter impact
Symptoms of TBI:
Physical
LOC unable to arouse
Convulsions or seizures
Dilation of Pupils
Inability to awaken
Weakness, Ataxia, Tremors
Symptoms of TBI:
Cognition
Attention
Memory
Orientation
Judgment/Safety
Awareness
Symptoms of TBI:
Behavioral
Profound Confusion
Agitation
Combativeness
Personality Change
Amnesia (Loss of Memory)
TBI Assessments:
ICU
Glasgow or LOC
- Neuro
- CN
- Movement
TBI Assessments:
Acute
Glasgow or LOC
- Physiological
- Neuro
- Movement
- Function
- Amnesia
- Rancho Levels
TBI Assessments:
Rehab
Rancho Levels
- Neuro
- Movement
- Function: FGA
- Memory
- Safety/Judgement
- Spatial Oreintation
- Disability Rating Scale
Attention and Orientation - TBI:
Arousability
Tactile
Sound
Pain
Attention and Orientation - TBI:
Attention
Visual Attention
Auditory Attention
Follows Commands
Attention and Orientation - TBI:
Orientation
Self, Place, and time
Orientation in Room
Severity of TBI:
Glasgow Coma Scale
GOLD STANDARD
Mild: 13-15
Moderate: 9-12
Severe: <9
Severity of TBI:
Post Traumatic Amnesia
Mild: <1 day
Moderate: >1 to <7 days
Severe: > 7 days
Severity of TBI:
Loss of Consciousness
Mild: 0-30 min
Moderate: >30 min to <24 hours
Severe >24 hours
Glasgow Coma Scale
Areas of Examination
Eye Opening
Verbal Response
Motor Response
Severe Brain Injury
What GCS Score?
GCS below 8
Severe Brain Injury
Prolonged unconsious state or coma lasts days, weeks, months
Subgroups of Severe Brian Injury
Coma
Vegetative State
Persistent Vegetative State
Minimal Responsive State
Locked-In Syndrome
Rancho Cognitive Functioning
Levels 1-5
Level 1
No reponse, deep sleep
Level 2
Generalized reponse, inconsistent reaction not direct
Level 3
Localized response, inconsisent reaction direct
Level 4
Confused/Agitated, confused
Level 5
Confused-Inappropriate, innacurate response
Rancho Cognitive Functioning
Levels 6-10
Level 6:
Confused-Appropriate, confused
Level 7:
Automatic-Approriate, minimal confusion
Level 8:
Purposeful-Appropriate, functioning memory
Level 9:
Purposeful-Appropriate, stand-by assistance
Level 10:
Purposeful-Appropriate, requries more time
Motoric Issues in TBI
Motor Planning and Execution Affected
(Pre-Frontal Lobe)
Weakness and Possible contractures
Spasticity/Hypertonia
Coordination (Cerebellar and Basal Ganglia)
Balance Disorders
Syndergistic Patterns
Postural Malalignment
Cognitive Assessment in Mod to Severe TBI
Arousability: Coming in room, sound
Alertness: Eyes open, orient to sound, Visual
Orientation: Self, Place, Time (Cues?)
Verbal Direction: 1 step, 2 step, Complex
Memory: Recent / Past events, Spatial, ID, Procedural
Judgement: Functional judgement - Transfers, Gait
Agitated Behavior Scale (ABS)
Common items from the ABS that occur in the Acute Phase in persons with Moderate to Severe TBI
Agitated Behavior Scale (ABS)
Early Issues
Violent or Explosive Anger
Resistant to care
Pulling at tubes
Sudden changes in mood
Impulsivity and lack of judgement
Considerations for Functional Assessment
Bed Mobility: Memory, safety, impulsiveness, procedure
Transfers: Motor loss, visual capability, impulsivity
Upright Stability: Postural alignment, dizziness, orientation, fatigue
Gait: Assistive device, fatigue, ocular disturabances, environmental stimulation
Environmental Consideration for TBI
Light Source
Background Noise
People in Room
Extraneous Movement
