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