Alteration in brain function, or other evidence of brain pathology caused by an external force
Populations more likely to sustain a TBI
People 75 years and older
Men (adolescents and young adults)
American Indian
Alaska native
Leading causes of TBI
Falls
Motor vehicle accidents
Being hit by or colliding with an object
Assault
Open head injuries
With a skull fracture
Penetrating objects
Dura is open
Meninges are breached
Brain is exposed
Localized focal lesions
Direct cellular and vascular damage
Secondary damage due to injuries to the face and neck
Closed head injuries
Without a skull fracture
Dura and skull intact
Brain forced into contact with the hard, bony outer covering of the skull
Acceleration-deceleration injury
Focal, multifocal, and diffuse lesions
Characteristics of mild traumatic brain injuries
Loss of consciousness: <= 30 min
Alteration of consciousness: brief to 24 hours
Post-traumatic amnesia: < 0 to 1 day
Glasgow Coma Scale: 13 to 15
Neuroimaging: normal
Post concussion syndrome: poor cognitive function, difficulty with concentration and irritability
Chronic traumatic encephalopathy: due to repeated mild TBI's during recovery period after previous injury
Characteristics of moderate traumatic brain injuries
Loss of consciousness: > 30 minutes < 24 hours
Alteration of consciousness: > 24 hours
Post-traumatic amnesia: > 1 to < 7 days
Glasgow Coma Scale: 9 to 12
Neuroimaging: normal or abnormal
Characteristics of severe traumatic brain injuries
Loss of consciousness: > 24 hours
Alteration of consciousness: > 24 hours
Post-traumatic amnesia: > 7 days
Glasgow Coma Scale: < 9
Neuroimaging: normal or abnormal
Primary injury
Due to direct trauma to the parenchyma
Secondary injury
Cascade of biomechanical, cellular and molecular events that evolved over time due to initial injury and injury-related hypoxia, edema, and elevated intracranial pressure
Contusions
Bruising of the brain surface; local area of edema and small capillary hemorrhages
Lacerations
Tearing of the pia or arachnoid matter or brain tissue
Types of intracranial hematomas or hemorrhages
Subdural hematomas
Epidural hematoma
Subarachnoid hemorrhage
Intraventricular hemorrhage
Diffuse axonal injury
Rapid rotational and linear acceleration and deceleration of the brain causing shear, tensile, and compression forces within the brain injuring axons (stretching, tearing) disrupting nerve communication
Excitotoxicity and oxidative stress
Excessive releases of glutamate, dopamine and norepinephrine
Excessive glutamate leads to influx of Na+ and Ca++ into the cell with subsequent cellular edema and contraction of the extracellular space
Stimulates reactive oxygen species production which are detrimental to neurons attacking the cell membrane and degrading other key cellular components leading to cell death
Increased intracranial pressure
TBI alters permeability of the blood-brain barrier
Swelling of the brain or intracranial hematoma & distortion & shift and brain herniations
Acute hydrocephalus caused by accumulation of blood in the ventricular system expanding the ventricles
Lead to changes in Pco2 & nervous tissue death
Cerebral hypoxia or ischemia
Due to ruptured or compressed blood vessels
Lack of blood to the brain: relative reduction in cerebral blood flow
Lack of oxygen in the blood due to airway obstruction or chest injuries
Intracranial hemorrhage
Hypoxia to brain tissues fed by hemorrhaging blood vessels
Increases pressure and distortion to brain tissue
Brain tissues is bathed in metabolic products from the damaged cells and blood
Immediate cell death from ischemia, edema, necrosis and toxic effects of blood on neural tissue
Infections in the brain
Open wounds due to penetrating brain injuries
Prolonged invasive monitoring such as ICP monitoring
Infection in the brain tissue can cause swelling and cell death
Seizures
Due to pressure or scarring
Can cause additional brain damage due to high oxygen and glucose requirements
Electrolyte and acid-base imbalances
Secondary cell death occurs via necrosis (swelling and then bursting of the cellular membrane) and apoptosis (destruction from within the cell through changes in DNA)
Coma
Condition of being unarousable
No response to strong stimuli, including strong pinching of the Achilles tendon
Vegetative state
Complete loss of consciousness, without alternation of vital functions
Spontaneous eye opening
Regular sleep/wake cycles
Normal respiratory patterns
Loss of tissue in subcortical, thalamic, and brainstem regions
Minimally conscious state
Severely altered consciousness with at least one behavioral sign of consciousness
Following simple commands
Gestural or verbal yes/no responses
Intelligible speech
Movements or affective behaviors that are not reflexive
Loss of tissue in subcortical, thalamic, and brainstem regions
Posttraumatic confusion
Person being awake most of the time but is confused, easily distractable with faulty memory, and with slowed but consistent responses to stimuli
Amnesia
Loss of declarative memory and is divided into two aspects, retrograde amnesia and anterograde amnesia
Retrograde amnesia
May prevent patients from knowing their family members, friends and information that defines who they are such as occupation and likes and dislikes
Procedural and semantic memories are typically unaffected or more mildly affected
Anterograde amnesia
Prevents new memory accrual, including memory for those providing the patient's care, the location of care and the ability to verbalize what events or activities occurred previously, earlier in the day or over preceding days
Procedural learning can occur
Post-traumatic amnesia
Persons emerging from coma after moderate to severe TBI progress through vegetive state to a gradual reemergence of responsiveness and severe confusion, memory disruption and abnormal behaviors such as agitation, disinhibition and altered mood
Effects of TBI on consciousness
May be impaired temporarily or for a prolonged period
Often have difficulty directing attention (distractibility) and attending to several things simultaneously
Effects of TBI on personality
Decreased goal-behavior (executive functions) if lateral prefrontal cortex is involved
Impulsiveness and other inappropriate behaviors if ventral prefrontal cortex is damaged
Lower tolerance for frustration
Emotional lability
Effects of TBI on cognition and memory
Slow mental processing
Decreased cognitive flexibility
Delusions
Effects of TBI on communication
Disorganized and tangential oral or written communication
Imprecise language
Word-retrieval difficulties
Disinhibited and socially inappropriate language
Effects of TBI on sensory, motor and visual functions
Sensory may be impaired
Perseveration of movements
Degree of motor impairment depends on severity of injury
Paresis/paralysis, apraxia, spasticity, contracture, lack of coordination, balance, posture, gait, speech, swallowing and eye movement disorders
Decreased acuity, field cuts, visual neglect or inattention
Effects of TBI on autonomic functions
Problems with autonomic regulation secondary to damage to or compression of the brainstem and/or hypothalamus
Paroxysmal sympathetic hyperactivity
Common medical complications after TBI
Post traumatic seizures
Deep vein thrombosis
Heterotopic ossification
Pressure ulcers
Pneumonia
Chronic pain
Contractures
Depression
Glasgow Coma Scale
Performed either at the prehospital stage or in the emergency department to test the function of the brainstem and cerebrum through eye, motor and verbal response
Glasgow Coma Scale scores
13 to 15: mild brain injury
9 to 12: moderate brain injury
8 or less: severe brain injury
Categories assessed in Glasgow Coma Scale
Eye
Motor
Verbal
Decompressive craniotomy
Large portion of the skull is removed to allow the brain to swell
Used when intracranial pressure is elevated for 25 mm Hg for 1 to 12 hours despite other medical interventions