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48 Cards in this Set
- Front
- Back
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Define TBI |
Blow jolt or penetrating injury to the head that disrupts brain function Severity ranges from mild of brief change in mental status to severe prolonged changes Can cause behavior, emotional, and personality disturbances |
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Epidemiology of TBI |
15-24yr at time of injury Greatest risk <10 or >74 Causes -50% MVA -25% Falls -15% assault -10% Sports |
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What is the MOI of TBI |
External force hitting head hard enough to cause brain movement with and without skull fracture -Brain tissue makes direct contact with an object (Acceleration injuries, penetrating objects, blast injuries) |
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Primary Damage from TBI |
Contusions Hematomas DAI Penetrating objects Blast injuries |
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Describe contusions of the brain |
Bruise or bleeding on the brain - collecting in extracellular matrix from bursting of capillaries Occipital blows are more likely to cause contusions May be associated with lacerations in areas in which the cranial vault is irregular (anterior lobe, under temporal or frontal lobe) |
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What cranial nerves can be damaged in a TBI |
Optic Vestibulocochlear Oculomotor Abducens Facial |
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Describe an epidural hematoma |
Between Duramater and skull Usually seen in adults Skull fracture common I/M lucideness Can result in death |
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Describe a subdural hematoma |
Between Duramater and soft tissue of the brain Acceleration/deceleration injuries -Bridging veins to the superior sagital sinus are torn Weakness, lethargy can become life threatening Symptoms from slow bleed may not be present for weeks |
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What is DAI
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Shearing of the axons -Different areas of the brain have different densities causing unequal acceleration, deceleration and rotation Most common MOI causing mod-severe TBI May cause coma May cause abnormal posturing of extremities and autonomic dyfunction |
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Describe Penetrating injuries (low vs high velocity) |
Low velocity objects damage tissue they directly contact High velocity objects like bullets or shrapnel can cause damage in remote areas of the brain due to shock waves (DAI) |
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What is a primary blast injury |
Direct affect of blast overpressure (shock wave) -Direct transcranial blast wave propagation -Transfer of kinetic energy from the blast wave through the vasculature triggering oscillations in the blood vessels -Elevations in CSF or venous pressure caused by compression of the thorax and abdomen shock wave |
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What are secondary and tertiary blast injuries
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S: Shrapnel and other objects T: Person thrown back against objects |
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What are examples of secondary brain damage? |
–Increasedintracranial pressure –Cerebralhypoxiaor ischemia – torn blood vessels –Intracranialhemorrhage –Electrolyteimbalance and acid-base imbalance –Infectionfrom open wounds –Seizuresfrom pressure or scarring |
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Describe Inc ICP
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Normal: 4-15mmHg Causes -Edema/swelling -Abnormality of brain fluid dynamics -Hematomas Severe ICP can result in herniation of the brain |
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Symptoms of ICP |
-Nausea and vomitting -Headache -Drowsiness -Frontal lobe gait ataxia -Visual and eye movement problems |
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Describe Hypoic Ischemic Injury (HII) |
Occurs when blood vessels are ruptured or compressed --Lack of blood or O2 to the brain Can lead to global damage --Associated with poorer cognitive functioning and lower expected outcomes |
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Associated trauma/Complications with HII |
–Systemichypotension due to massive blood loss –Damageto specific vascular territories –Anoxia –MI –Pericardialeffusion –Arrhythmia –CHF –Pulmonaryembolus –Pneumothorax |
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Describe Intracranial Hemorrhage
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Hypoxia to tissues red by hemorrhaging vessels Adds pressure and distortion to brain tissue Metabolic products damage cells Cell death within minutes due to ischemia and toxicity |
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Electrolyte and acid base imbalance effects on cells |
Secondary Cell death caused by -Swelling and then bursting of the cellullar membrane (necrosis) -Destruction from within the cell through DNA (apoptosis) -Cell death can occur days, weeks, months, after injury |
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Describe infections and seizures |
Infection of brain tissue may cause swelling and cell death Seizures are most common Immediately after injury 6mo-2 years post Seizures can cause additional damage due to high O2 and Glucose requirements |
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Describe Paroxysmal Sympathetic Hyperactivity |
Dysautonomia (8-33% of ICU TBI pts) Elevated sympathetic activity -Inc HR and RR -Hypethermia -Inc BP -Diaphoresis, sialorrhea -Dilated pupils -Vomiting -Dystonic Posturing |
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What motor changes are associated with a TBI |
-Combinations --asymmetricalcerebellarand pyramidal signs --bilateralpyramidal andextrapyramidal signs -Paresis,paralysis -Cranialnerve injury -Poorcoordination -Abnormalreflexes -Abnormalmuscle tone -Lossof selective motor control -Poorbalance, abnormal gait -Lossof bowel and bladder control |
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Sensory changes from TBI |
-Hypersensitivity to light or sound -Loss of hearing or sight -Visual field changes -Numbness and tingling -Loss of somatosensory function -Dizziness -Agnosia -Apraxia |
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Cognitive,Personality and Behavior Impairments from TBI |
-Arousal -Attention -Concentration -Memory -Learning -Exec function -Behavioral |
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Most common problems at one year in relation to Cognitive, Personality and Behavior Impairments |
-Poor memory -Problem solving -Stress management -Emotional upsets -Inability to control temper -Managing money, paying bills |
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Define Concussion |
Short (or no) episode of loss of consciousness </= 20min Can cause DAI resulting in temporary or permanent damage Effects are cumulative - second impact syndrome |
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Symptoms of concussion |
Little or no retrograde amnesia Irritability Headache Fatigue Dizziness Personality/Emotional changes PTSD |
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What is Decorticate posturing |
Flexor posturing -Arms flexed of bent inward, hands clenched, legs extended, feet turned in Damage to cerebral hemispheres, internal capsul and thalamus possible midbrain |
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Describe Decerebrate posturing |
Extensor posturing Arm extension and internal rotation, ehad arched back, legs extended; pt is rigid with teeth clenched Indicates brainstem damage below the level of the red nucleus |
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Decorticate --> Decerebrate posturing |
May indicate uncal herniation. Swelling pushes the brain down thru the foramen magnum. |
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Define Stupor, Obtundity, Delirium, and Clouding of Consciousness |
S: general unresponsiveness - temp arousal to vigorous stimuli O: Very sleepy - reduced alertness, disinterest in environment, slow responsiveness D: Disorientation, fear, misinterpretation of sensory stimuli - may be loud and agitated C: Quiet confusion, distractibility, faulty memory, slow response to stimuli |
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Retrograde Amnesia |
Incident and backward -Partial or total inability to recall events during the period immediately preceding brain injury -May improve over time |
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Post traumatic amnesia (PTA) |
Incident forward Unique to TBI -Time Lapse betweenthe accident and point at which the functions concerned with memory arerestored Unlikely to dc to community, will req behavioral care until condition resolves |
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Constellation of behavioral symptoms associated with PTA |
Poor safety awareness and insight into deficits Dec Attention Loss of impulse control |
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Anterograde memory |
Inability yo form new memories Last function to return after loss of memory |
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How is TBI severity measured |
Mild/Mod/Severe GCS: 13-15 / 9-12 / 3-8 LoC: <30min / 30min - 24hr / > 24hr PTA: 0-1 day / 2-7 days / > 7 days |
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What is a vegetative state? |
Wakefulreduced responsiveness with no evidence of cortical function –Preservationof brain stem function although higher CNS functions are not working |
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What functions may be present in a vegetative state due to brainstem? |
-Weaned off ventilation -Sleep/wake cycles -Eyes may track -May orient to sound or visual stimuli -Spontaneous movement -Reflexive smiling/crying -Withdraw to noxious stimuli |
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How long will a vegetative state last |
May last >1yr following TBI, >3mo following anoxia -Do not apply persistent until the condition has been stable for more than 1 year |
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What is locked in syndrome |
De-efferentedstate; pseudocoma --Damage to the pons Complete loss of voluntary movement except eyes and eyelids Able to communicate through eye movement and blinking |
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What is brain death |
Glasgow coma scale 3 Absence of brainstem reflexes Pupils in a midsize fixed position Absence of ocular movements Absence of corneal reflex Absence of facial muscle movement to noxious stimulus Absence of gag and cough reflex |
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What is a minimally conscious state |
-Minimal awareness of self or environment -Congnitively mediated behaviors are inconsistent but reproducible and sustained well enough to differentiate from reflexive behaviors -Sleep/wake cycles -Localization to noxious stimuli, sound or visual pursuit Inconsistent reach for objects |
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What determines prognosis of a TBI |
Lesion size and area -Frontal/temporal have poorer prognosis -Corpus Calloum and DL brainstem --> persistent veg state Time since lesion Age > 40 - longer PTA and worse outcome // <50 normal sitting and standing balance PTA: -WhenPTA is combined with age, sitting balance, and limb strength at admission,prediction of productive outcome is high Sitting and standing balance –Age< 50 years, GCS at admission, length of PTA, length of coma, acute carelength of stay all related to impaired sitting and standing balance –Pupillaryresponse, respiratory failure, pneumonia, soft tissue infections and UTI hadrelationship with impaired sitting –No relationship between balance ratings and neurological orradiological findings, injury severity, or medical complications Motor disturbances generally have good prognosis |
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Examination of Communication |
-Nonaphasic -Disorganizedand tangential communication -Increaseddifficulty when distracted -Wordretrieval difficulties -Disinhibitedand socially inappropriate behavior -Difficultyreading social cues and adjusting communication to the demands of the situation |
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How to assess cognitive, behavioral and communication deficits? |
MoCA MARS (moss attention rating scale) Community integration Questionaire |
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Testing Nervous system |
Sensory function and incoordination Proprioception, light touch 2pt, stereognosis Visual and visual perception (CN testing) |
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Interventions for TBI |
EBP –Functionaltraining for sit-to-stand, UE use, gait –Highintensity treatment regimens ---Mayneed to use procedural approach if memory impairments persist ---Traditionalstrengthening regimens ---Functionalor body weight exercises ---Incorporatespeed Cardiovascularfitness Flexibility Strengthand Power Dynamicbalance ADL Functionalambulation |
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Secondary impairments and concomitant injuries associated with TBI |
DVT Heterotopicossification Pressureulcers Pneumonia Chronicpain Decreasedendurance Contractures Muscleatrophy |
