traumatic brain injury 2/18

moderate to severe TBI

injury to the brain by a mechanical force that leads to altered brain function

#1 leading cause of death and disability in children and young adults in the US

risk factors

age (major cause of morbidity and mortality in YA and elderly)

males

alcohol use

previous brain injury

etiology

falls (most common in children and OAs)

MVAs

assaults/violence

sports injuries

workplace accidents

types

diffuse and focal; open and closed

diffuse TBIs

concussion

axonal injury

blast injury

abusive head trauma

focal TBIs

contusion

penetrating

hematoma→epidural, subarachnoid, subdural, intraventricular, intracerebral

open (penetrating) TBI

skull fractured, breaches meninges, brain tissue exposed

focal, penetrating

ex. GSW

closed TBI

external force, skull remains intact, but brain is injured

soft tissue forced into contact with skull

diffuse (concussion) or focal (contusion)

impact (coup/bounce against skull)→counter coup (rebound bounce): severe neck injury, symptoms worse w/ rotational component

primary injury pathogenesis

direct mechanical injury to brain tissue

contusion, cerebral laceration, intracerebral hemorrhage or hematoma, diffuse axonal injury

cerebral laceration

tearing

diffuse axonal injury (DAI)

widespread damage to axons due to rotational forces

acceleration/deceleration disrupts axons through shearing neurofilaments within axon

types of brain hemorrhage

A: epidural

B: subdural/subarachnoid

C: intracerebral—seen most commonly in strokes

A and B most common

subdural hematomas

typically occur in older population

more severe initial presentation

greater midline shifts

higher incidence of death

secondary injury pathogenesis

indirect sequalae/cascading events—after pry injury, secondary processes exacerbate neuronal damage/death and cause worse outcomes hours to days after injury

processes include: inflammatory response, vascular changes, edema, parenchyma changes, cellular & metabolic components

secondary TBI vascular changes

ischemia/hypoxia

impaired cerebral perfusion

secondary TBI edema

brain swelling/compressive damage

increased intracranial pressure (ICP)

brain stem herniation

secondary TBI parenchymal changes

cognitive and consciousness fluctuations

imaging

structural damage can be seen with CT or MRI

CT

1st line imaging for surgical decision making and repeated for progression

indication considerations: vomiting, headaches, altered mentation, loss of consciousness, intoxication, post-traumatic seizures, post traumatic amnesia, signs of basal skull fracture, facial injury, multiple traumatic injuries

MRI

used more often after stabilization of injury for better visualization

good prognostic factors

intact brainstem reflexes 24 hours post injury

eye opening

pupillary activity

spontaneous

movements with localized motor responses

poor prognostic factors

non-reactive pupils

absent motor responses

prognosis complications

trauma to other areas (ex. internal organ trauma, ortho injuries, etc.)

prognosis 2 years after injury

93% live in private residence

34% require some level of supervision

34% living w/ spouse or s/o, 29% parents

33% employed

glosgow coma scale

assesses consciousness via response to stimulus via eyes, voice, and motor reactions

total score out of 15

greater than or equal to 13=mild brain injury

9-12=moderate

8 or less=severe

alert

awake, looks around, responds in a meaningful manner to verbal instructions or gestures

coma

unarousable and unresponsive, does not open eyes to deep pain

secondary TBI cellular & metabolic components

cell autonomous death pathways

neuroinflammation

mitochondrial dysfunction

functional impairment

toxic proteinopathies

excitotoxicity and calcium flux

structural axonal injury

other processes

stupor

unresponsive except to vigorous stimuli, may attempt to verbalize to vigorous stimuli, opens eyes to pain

confused

disoriented to time, place, or person, memory difficulty, difficulty w/ commands, exhibits alteration in perception of stimuli, may be agitated

delirium

confusion of circumstances, may hallucinate or act as if in dream-like state, conversation may not make sense; often acute ICU setting, emergence from coma

lethargic

drowsy, oriented when awake but if left alone will sleep, loud voice needed to keep awake and engaged

physical clinical manifestations

loss of or altered levels of consciousness

seizures

hemiparesis (contralateral)

ataxia

impaired coordination

cranial nerve deficits

abnormal posturing (decerebrate and decorticate)

abnormal reflexes (ex. babinski)

cognitive/behavioral clinical manifestations

memory deficits (processes & amnesia)

difficulty with attention, reasoning, concentration

personality changes

impulsivity, irritability, aggression

depression, anxiety

rancho levels of cognitive functioning

describes levels of cognitive recovery

speed of progression through levels predicts fullness of recovery

no response: total assist

generalized response: total assists

localized response: total assist

confused, agitated: max assist

confused, inappropriate non-agitated: max assist

confused, appropriate: mod assist

automatic, appropriate: min assist

purposeful, appropriate: standby

assistance

purposeful, appropriate: standby assistance on request

purposeful, appropriate: modified independent

frontal lobe clinical manifestations

CL hemiparesis, difficulty in higher-level executive functions; personality changes; behavior and mod changes

temporal lobe clinical manifestations

CL hemiparesis, visual field deficits, memory deficits, speech & language deficits, seizures

parietal lobe clinical manifestations

CL sensory deficits & neglect, difficulty with right-left discrimination

occipital lobe clinical manifestations

visual deficits, homonymous hemianopsia

cerebellum clinical manifestations

ataxia, nystagmus, nausea

brainstem clinical manifestations

cranial nerve deficits, motor and sensory deficits, ataxia, nystagmus, nausea

early acute medical management goals

prevent hypotension, keep BP >90

prevent hypoxemia, O2 sat >90%

prevent elevated ICP, keep <20 mmHg (CPP 60-70 mmHg)

assess GCS

early acute medical management

cervical stabilization

may require ventilation—benefit of early tracheostomy unclear, may reduce ventilator days but not risk of pneumonia

early acute medical management—not recommended

steroid use

prophylactic hyperventilation

prophylactic hypothermia

look at o’sullivan table

indications for intracranial pressure monitoring

GCS 3-8

unilateral or bilateral motor posturing

abnormal CT

>40 y/o

SBP >90 mmHg

external ventricular catheter drain (EVD)

allows accurate measurements and drainage of CSF for treatment and culture

intraparenchymal devices (IPD)

inserted into cortical-subcortical brain region

allow reliable ICP monitoring especially with collapsed ventricles

neurosurgery

evacuation of hematoma to prevent secondary injury and central herniation

decompression with craniotomy and craniectomy (delayed bone replacement, considered for diffuse TBI)

early, larger craniotomy, removal of bone flap may improve outcomes

neurosurgery indications for epidural hemorrhage

surgery indicated if volume >30 cc (>15mm thickness) on CT

often non-surgical if volume <30 cc on CT or <5mm midline shift and GCS >8

neurosurgery indications for subdural hemorrhage

indicated if thickness >10mm & midline shift >5mm on CT, GCS drops by 2+, ICP >20mmHg, abnormal pupillary response

monitor ICP all people with TBI with GCS <9 & repeat CT

post-surgical precautions for craniotomy/craniectomy

head of bed =/>30 degrees (aspiration and perfusion)

if craniectomy, MUST wear helmet at all times when out of bed

avoid bending over with head in dependent position

may have lifting and exercise restrictions until cleared by MD

avoid activities which increase ICP (sneezing, blowing nose, valsalva, no straws)

pharmacologic management

analgesics & anticonvulsants

neuroprotective drugs

sedatives and anxiolytics

analgesics and anticonvulsants

decrease pain, prevent seizures

neuroprotective drugs

reduce secondary injury

ex. Ca channel blockers

sedatives and anxiolytics

manage pain, agitation, anxiety

common medication side effects

sedation, confusion, dizziness, hypotension

risk of dependency with prolonged use (ex. narcotics)

complications

post-traumatic epilepsy: seizures occurring post injury, requires meds

hydrocephalus

autonomic dysfunction (HR, BP, temp)

hydrocephalus

abnormal accumulation of CSF→incr ICP→brain herniation (life threatening emergency)

ethical considerations

informed consent: consider cognitive impairment

autonomy: consider extent of cognitive decline and role of family/guardians to make decisions as appropriate

ICF

body structure and function: neurologic impairments (motor dysfunction and sensory disturbance)

activities: impaired walking, transfers, dressing, eating, other ADLs

participation: limitations in social roles, work, community involvement

environmental factors: accessibility (home setup, community access) social support

PT contraindications

elevated ICP or severe brain edema

acute/unstable fractures (ex. c-spine)

severe/uncontrolled seizures

red flag for PT

ICP >15 mmHg →headache, nausea/vomiting, elevated BP, decline in mental status, double vision, shallow breathing, non-reactive pupils, seizures, alteration in consciousness/coma

MD may treat with meds, shunt, decompression craniectomy

ensure head of bed elevated 30 deg

PT considerations

dysautonomia

executive functions

judgment deficits

communication deficits

behavioral deficits

perceptual deficits

dysautonomia (paroxysmal sympathetic hyperactivity)

overactive elevated sympathetic nervous system activity

increased HR, BP, RR; diaphoresis; hyperthermia; hypertonic

10-33% of ppl with TBI

develops in early stages, lasting days to months

longer duration=poorer outcome

executive functions

problem solving deficits—big impact on function

includes capacity to plan, start and stop activities, recognize errors, problem solve, think abstractly

may require more time for planning, need simple and concrete directions and feedback, not be able to detect or know how to correct errors, may need cues to remain on task or remember directions, need cues and plans for maintaining safety

judgment deficits

limited insight into disability

inappropriate, socially unacceptable behavior, impulsiveness

dress, communication, sexual drive, food drives, substance abuse

communication deficits

aphasia: receptive and expressive

anemia

alexia

alexia with agraphia

deafness

dysarthria

verbal apraxia

echolalia

behavioral deficits

agitation

poor emotional control

apathy

lack of insight & denial of disability

self-centered, egocentrism

impulsive, lack of inhibition

secondary depression & withdrawal

perceptual deficits

neglect (parietal lobe)

lateropulsion/postural vertical deficit

apraxia—motor agnosia (frontal lobe)

other processes (selecting, integrating, interpreting stimuli from body and environment)