Traumatic Brain Injury (TBI)
polar brain damage
(A→P) brain moves forward inside the skull, suddly stops due to impact with skull one type of coup contre coup
Care of patient/ Return to play guidelines
(usually go home and observe if significant change in cognitive state, consciousness, nausea, vomiting increased ICP) depends on sport CANTU and NATA
Severe Head Injury: how does this present?
*immediate Loss of consciousness (LOC) *complete paralysis of cerebral function *may see immediate cerebral lacerations, subarachnoid hemorrhage (SAH), subdural hemorrhage, cou-contre-coup sites, damage along the line of force of injury *multiple system involvement (MVA thrown out of car, brain frx, spinal cord, internal bleeding) *permanent deficits will persist (eg gun shot wound)
Post concussive syndrome: what is it? how long does it last? limitations?
*persistence of mild symptoms such as headache, irritability, insomnia, poor concentration and memory (sensitive to light/ noise, drowsy, difficulty staying awake : headache is typical but don't take meds) *can persists for weeks to months *organic basis *may limit ability to complete ADL's or employment * may need cognitive retraining or psychological support
Diffuse Brain Damage
-diffuse axonal injury likely moi: no-contact acceleration/ deceleration or rotational forces
Prevalence of TBI
5 million ind. in the US are living with TBI related disabilities MOI MVA (50%) falls , violence (firearms ~10% leading cause of TBI related death has been ↑)
Moderate Head Injury: types
Acute Epidural Hemorrhage Acute subdural Hemorrhage Chronic Subdural Hematoma Cerebral Hemorrhage Subarachnoid Hemorrhage
Severe Head injury: brain death incompatbility
Brain Death- criteria to be present for 30 minutes at least 6 hours after onset of coma and apnea *coma with cerebral unresponsivity *apnea- absence of spontaneous respiration *absent cephalic reflexes-pupillary, corneal, snout, pharyngeal, cough and swallowing *electrocerebral silence- EEG with absence of electrical potentials of cerebral origins over 2 microvolts
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 interacranial hematoma→ bleed accumulates mass effect→shift of brain caused by edema (↑ICP →swelling) hydrocephalus
Causes of Secondary brain injury
Neurochemical and cellular changes hypotension hypoxia increased ICP which leads to decreased CPP ( cerebral perfusion pressure) electrolyte imbalances Ischemia
pathogenesis of Head injury
Vasoparalysis- arrest in circulation with instantaneous rise in ICP ( >40 mmHg) [loss of circulation to the brain] shearing forces due to blow to cranium causing rotation of the brain inside the skull constitutions: lead to hemorrhage and an increase in ICP lacerations cause direct damage to neural tissue
Persistent Vegitative State (PVS)
Wakeful, reduced responsiveness with no evident cerebral cortical function life expectancy--weeks, months, years if in PVS> 3 months then poor prognosis usually see posturing, some movement, no communication, feeding tube, uses reflexes for movement
Diagnostic imaging Of head injury
X ray ( 1st likely issues stability/ instability➡ immobilize fx) CT (2nd integrity of brain tissue ) MRI (not in ER too long) Cerebral blood flow mapping *** PET or SPECT*** (brain function coming back) EEG ( MILD MOD, SEVERE brain injury➡ brain dead?)
Concussion: define
a violent jarring or shaking that results in a disturbance of brain function temporary/ momentary interruption/disruption of brain function with or without loss of consciousness considered a mild form of diffuse axonal injury microscopic changes in neurons and glia within houses of injury
healthy people 2010 recommendations regarding head injury
by far the greatest "cure" is "prevention"
Types of head injury
closed head injury and open head injury
Shear injury
commonly seen in acute injuries due to the differences in grey and white matter. when you top quickly these layers will separate typically at the cortico-medually junctions and they typically have blood in them. prognosis is poor
Glasgow Coma Scale: define
commonly used to assess the level of consciousness of patients in the early and/ or minimal response phases after suspected brain injury used when get to hospital rapid infor motor/sensory/cognition continue to monitor
Coup Contre Coup
coup-injury on side of impac
Cerebral Hemorrhage
disruption of intrinsic cerebral circulation managed similar to hypersensitive stroke
Incidence of TBI
every 5 minutes an individual dies from a head injury and another is permanently disabled 3:1 male to female majority of ages 15-24 years <5 years old (abuse;falls) [ shaken, struck in the head, thrown down,] [bike, simple thing] mid-late adolescence (mva)
Risk factors for TBI > 65 yo
female, poor vision, history of previous falls, dementia, polypharmacy (related to falling and hitting their head) (medication ↑ likelihood of fall)
Cytotoxic Edema
follows cerebral ischemia or hypoxia; caused by swelling of endothelial cells, neurons and glia
Severe Head injury: compatibility with life
incompatible with life *** deep coma, initially may be flaccid become spastic or rigid with posturing, unresponsive to pain and all stimuli, ventilator required, to maintain breathing, deregulation of body temperature and BP, poor EEG*** may not survive, vegitiative state or brain dead low Glasgow coma scale
EDEMA: what happens when this is in the brain
increased edema to a fixed space increases the pressure and will impact circulation to parts of the brain mass effect= midline shift
skull fracture risks
increased risk of infection, TBI, meningitis, encephalitis, abscess
Primary Damage
local damage & diffuse brain injury
Local damage
located to area of brain under site of impact on skull likely MOI: direct contact Coup- contre coup
Subarachnoid Hemorrhage
managed similar to epidural hemorrhage
Open Head Injury (OHI)
meninges have been breached penetrating head injuries may be caused by accelerating or decelerating force amount of damage due to areas affected more likely to be infected
Degree of Head injury
minor head injury (better prognosis) moderate head injury severe head injury (WORSE PROGNOSIS) (possible vegetative state or brain dead)
Neurosurgical definition of coma
no eye opening, no recognizable speech, no following of motor commands
Acute Epidural Hemorrhage
no initial coma but deterioration in neuro status if left unresolved resolved with surgical intervention
Closed Head Injury (CHI)
non-penetrating head injuries accelerating or decelerating blow minor or severe and irreversible brain damage may see brainstem damage, contusions, diffuse white matter lesions, injury to blood vessels, damage to cranial nerves or CSF rhinorreha (CSF leak out the nose)
Vasogenic Edema
occurs in regions bordering those damaged during ischemia. increased permeability➡increased volume of extracellular fluid; most common edema CSF in steady state with extracellular fluid
Primary vs Secondary injury
primary occurs at the time of impact primary damage→ will lead to cellular response ↑inflammation and lead to secondary injury secondary-→occurs after the impact secondary to the body's response to injury proteins will produce more fluid into area→fixed space→edema→further damage
Acute Subdural Hemorrhage
results quickly in coma bleed arrested by increased ICP (like a cut put pressure on it, it will stop) requires Surgical Intervention
Characteristics of the Glasgow coma scale
scored on a scale of 3-15 points eaul to the total of the three categories of response: eye opening, motor (movement) and verbal response. Max score is 15 minimum is 3 13-15 mild 9-12 moderate 8 or less represent severe brain injury
Chronic Subdural Hematoma:
slow venous leak (change over weeks) neuro deterioration over peroid of weeks CT scan- encapsulated mass often mistaken as tumor surgical intervention
Minor Head Injury
uncomplicated course observation of patient 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**
types of edema
vasogenic edema cytotoxic edema
whats the difference between OHI and CHI
whether the meninges are in tact or not