Traumatic Brain Injury (TBI) Test 2 Flashcards
Traumatic brain injuries can occur
prior to birth, during birth or anytime after
-also called transient brain ischemia
Incidence of TBI ( in US)
- Every 5 min an individual dies from a head injury and another is permanently disabled
- 2 million head injuries/year
- 500,000 require hospitalization
- 90,000 left with life long permanent disabilty
- 3:1 male to female ( risktakers)
- majority ages 15-24 y/o
- in peds bimodal peaks:
Healthy people 2020 goal
decrease TBI due to accidents and violence
-car seats/seat belts
-legislation
The greatest cure is prevention
Prevalence of TBI
- 5 million Americans are living with TBI related disablities
- Mechanisms of injury
- MVA-50%
- Falls
- Violence (firearms ~10% -leading cause of TBI related death , has been increasing)
- Overall mortality due to TBI has decreased 20% since 1980 ( due to decline in MVA)
Risk Factors for TBI >65 y/o
- female
- poor vision
- history of previous falls (increased risk in elderly due to falls)
- dementia
- polypharmacy (overlapping meds for the same thing ie Tylenol & Motrin, increase # of meds taken-> increase risk of falls)
Closed Head injury( CHI)
- non penetrating head injury
- accelerating or decelerating blow
- minor-severe and irreversible brain damage
- may see brainstem damage,contusions,diffuse white matter lesions, injury to blood vessels,damage to cranial nerves or CSF rhinorrhea
ie. concussion, blow to the head
Edema due to a closed head injury
- increased protein and NT in brain tissue (toxic) leads to 2ndary damage
- increased intracranial pressure (max threshold~ impair/stop circulation)
- mass effect; swelling -> shift in midline
Open Head Injury (OHI)
-meninges have been breached
-penetrating head injuries
-may be caused by accelerating or decelerating forces
-amount of damage due to areas affected
-increased likelihood of CNS infection
ie gunshot wound ( may leave lines of force in brain tissue on image), knife, golf club
Fractures associated with head injury
-skull fx - can just be depressed
Primary injury
occurs at time of impact
ie shear or tension on brain tissue, laceration, depression etc
Secondary injury
occurs after the impact secondary to the bodys response to injury
-due to cascade of cellular events (dumping of NT into interstitial space, dead neurons-> increased proteins-> increased fluid vol & swelling-> further damage
Primary damage
Local Brian Damage or Diffuse Brain injury
Local Brain damage
localized to area of brain under site if impact on skull
- primary damage
- likely MOI: direct contact
- coup-contrecoup
- polar brain damage( brain moves forward inside skull, suddenly stops due to impact with skull- ant& post type of coup contrecoup)
Coup contrecoup
Intial injury and force causes brain to shift in opposite direction or any direction and leads to damage in both areas
-Ant/Post region: polar brain damage
Diffuse brain damage
diffuse axonal injury -primary damage -likely MOI: non-contact -acceleration or deceleration or rotational forces (shear is placed on brain w/great force-> axonal injury) ie MVA or amusmant ride
Secondary Injury
- Hypoxic-ischemic injury(may be due to insult to specific vascular territory due to brain shift or diffuse injury caused by arterial hypoxemia
- intracranial hematoma
- mass effect (shift in brain caused by edema)
- increased intracranial pressure (ICP) (rises above 40mgHg it can stop circulation to other areas of brain- heart can’t fight against it-> further damage)
- hydrocephalus
Causes of secondary injury
- neurochemical and cellular changes
- hypotnesion->
- hypoxia
- increased ICP which leads to decreased CPP(cerebral perfusion pressure)
- electrolyte imbalances
- ischemia
Dx of head injury
-xray and CT
Intracranial hemorrhage
- bleed in brain parenchyma
- due to accelerating/decelerating forces
Pathogenesis of head injuries
- Vasoparalysis: arrest in circulation w/ instaneous rise in ICP( > 40 mmHg)
- shearing forces :due to blow to cranium causing rotation of the brain within the skull
- contusions:lead to hemorrhage and an increase in ICP
- lacerations cause direct damage to neural tissue (ie gunshot/knife)
Shear injury
- commonly seen in acute injuries due to the differences between white and gray matter
- when you stop quickly these layers will separate
- typically separate at corticomedullary junctions and they typically have blood in them
- Poor prognosis
Immediate complications of head injuries
Edema
- Vasogenic edema: occurs in regions bordering those damage during ischemia. Increased permeability-> increased vol of extracellular fluid; most common edema
- Cerebrospinal fluid: in steady state with extracellular fluid
- Cytotoxic edmea: follows cerebral ischemia or hypoxia; caused by swelling of endothelial cells, neurons, and glia
Diffuse Cerebral Edema leads to
other immediate problems:
-Herniation
-infection
(shear injury, swelling throughout brain)
Dx imaging of head injury
- X-rays ( gives idea of stability/ instability of structures- need for immobilization/fx)
- CT scan( integrity of brain tissue)
- MRI ( useful but not done in emergency room)
- Cerebral bloodflow mapping( Pet or SPECT- look at brain function)
- EEG ( mild-severe head injury - brain dead or vegetative state
Glasgow Coma Scale (GCS)
- nuerosurgical defintion of coma is ; no eye opening, no recognizable speech, no following of motor commands.
- commonly used to assess level of consciousness of pts in the early stages or minimal response phase after suspected brain injury
- gives info on motor/ sensory / cognitive function
Eye opening on Glasgow Coma Scale (GCS)
graded on 4 pt scale 1-none 2-to pain 3-to speech 4- spontaneous
Motor response on Glasgow Coma Scale (GCS)
movements graded on a 6 pt scale 1-none 2-extension 3-abnormal flexion 4-withdrawl 5-localizes pain 6- obeys commands
Verbal response on Glasgow Coma Scale (GCS)
talking graded on 5 pt scale 1-none 2-incomprehemsible sounds 3- inappropriate words 4-confused conversation 5-oreinted
Glasgow Coma Scale (GCS)
- scored on a scale of 3-15pts
- equal to the total of the three categories of response; eye opening, motor (movement), and verbal response
- max score is 15 and min score is 3
- scores from 13-15 represent mild injury
- scores from 9-12 represent moderate brain injury
- scores of 8 or less represent severe brain injury
- can tract over time to see improvements or deterioration
Degrees of head injury
- minor head injury (better prognosis, multiple casues)
- moderate head injury
- severe head injury ( may be brain dead or in consistent veg. state)
Minor head injury
-uncomplicated course
-observation of patent at home by family
-minor signs and symptoms may progress to more serious pathology
-common complaints: “see stars”, stunned, nervous, poor memory of events just prior to or just following event
(microscopic damage- not visible on CT, likely doesn’t get imaging, ie fall or concussion in sports, may lose consciousness but not likely)
Concussion
-violent jarring or shaking that results in a disturbance
of brain function
-momentary interruption of brain function w/ or w/out loss of consciousness
-considered a mild form of diffuse axonal injury
-microscopic changes in neurons and glia within hours of injury
(obsevre; behavior/cognitive/nausea/vomiting/ consciousness )
-dx based on subjective pr report( not objective tests)
Return to play guidlines
- depends on sport/league
- Cantu
- NATA ( national AT association)
- how to manage results post
- return to sports based on some objective test taken before and after concussion-impact test, reaction time
Post Concussive Syndrome
-Persistence of mild symptoms such as headache, irritability, insomnia, poor concentration and memory (sensitivity to light/noise, drowsy/diff to stay awake,)-not prescribed to take pain meds for headches bc cant monitor symptoms and meds may impact blood flow
-can be persistent for weeks-months
-organic basis for post concussive syndrome is suspected
-some controversy due to psychological/subjective complaints
-may limit ability to complete ADLs or employment ( esp. if repeated concussion)
-may need cognitive retraining or pyschological support (esp. if repeated concussion)
( 2 concussions in 1 game -> accelerated injury/rate of damage -> serous problems)
Moderate Head injury
- acute epidural hemorrhage
- acute subdural hemorrhage
- chronic subdural hemorrhage
- cerebral hemorrhage
- subarchnoid hemorrhage
Acute Epidual Hemorrhage
- moderate head injury
- no initial coma but deterioration in neuro status if left unresolved
- resolved w/surgical intervention
Acute Subdural Hemorrhage
- results quickly in coma
- arterial bleed
- bleed arrested by increased ICP (pressure increases to a point that it stops bleeding from getting worse)
- requires surgical intervention (craniotomy; may go into brain tissue-evacuate blood accumulation-risky surgery may create damage)
Chronic Subdural Hematoma
-slow venous leak
-neuro deterioration over period of weeks
-CT scan-encapsulated mass often mistaken as tumor
-surgical intervention(evacuate bleed/seal vessel)
ie elderly person falls and mental status deteriorates
Cerebral Hemorhage
- disruption of intrinsic cerebral circulation (due to acceleration or deceleration or blow to brain)
- managed similar to hypertensive stroke
- surgery may be necessary
Subarchnoid hemorrhage
-managed similar to epidural hemorrhage
Severe Head injuries
-present with immediate LOC(loss of conciousness)
-complete paralysis of cerebral function (coma)
may see immediate cerebral lacerations, SAH (subarchnoid hemorrhage), subdural hemorrhage, coup-countrecoup sites, damage along the lines of the force of injury
-multiple system involvement
-permanent deficits will persist
ie MVA, ejected from vechile
Severe Head injury-incompatible with life
-deep coma
-initially may be flaccid, become spastic or rigid with posturing (decerebrate or decorebate)
-unresponsive to pain and all stimuli( 3 on coma scale)
-ventilator required to maintain breathing
-deregulation of body temperature and BP
-poor EEG
(may result in death, brain dead(lack of electrical activity), or persistent vegetative state)
-autonomic / brainstem affected
