W3: Traumatic Brain Injury Flashcards
Cerebral Blood Flow (CBF)
maintained to meet metabolic needs of brain
3-4x more to gray matter>white matter due to metabolic activity
Cerebreal Perfusion Pressure (CPP) range
70-90mm Hg
CPP
pressure required to perfuse cells of the brain
pressure it takes for the heart ro provide the brain with blood
Cerebral Blood Volume (CBV)
amt of blood in intracranial vault at a given time
any imbalance displaces CSF in the brain
Cerebral blood oxygenation
measured by oxygen saturation in internal jugular vein
Blood pressure should always be higher than the ____
CPP (cerebral perfusion pressure)
Features of cerebral hemodynamic injury
alterations in:
cerebral blood flow
ICP
oxygen delivery
Goals of hemodynamics
balance ICP with IJV oxygen saturation
alterations in cerebral hemodynamics =
increased ICP
cerebral edema (fluid infusing brain cells= swelling)
Normal ICP range?
5-15mm Hg
Increased ICP is caused by?
edema, excessive ICP, hemorrhage
when the contents of the brain vault (brain tissue, CSF, blood) increase in volume. b/c the vault is rigid and cannot accomadate the change.
Increased ICP: Stage 1
vasoconstruction and external compression (try to maintain normal BP and CPP)
no changes in ICP due to compensation (only pain at site)
Increased ICP: Stage 2
neuronal oxygen compromised, systemic arterial vasconstriction
body is trying to maintain perfusion
Increased ICP, Stage 2: S/S
drowsy
confusion
restlessness
light pupillary changes (constriction)
breathing changes
Increased ICP: Stage 3
brain hypoxia and hypercapnia, autoregulation lost
Increased ICP: Stage 3 S/S
difficulty arrousing
panting like dog (hyperventilation, irregular respiration)
widened pulse
bradycardia
pupil constriction and sluggish
Increased ICP: Stage 4
brain herniates, several herniation syndromes
most structures in brain shift to fill the brain cavity and will not return to original state
Therapeutic Mgt Goals: CPP
> 70 mmHg
Therapeutic Mgt Goals: ICP
<15 mmHg
Therapeutic Mgt Goals: CO2 pressure
35 mmHg
Therapeutic Mgt Goals: mean and arterial pressure
90 mmHg
Therapeutic Mgt Goals: Temperature
34C-36C
Therapeutic Mgt Goals: pulmonary capilalry wedge pressure
10-15 mmHg
What is TBI?
alteration in brain function/pathology d/t external force
Common causes of TBI for children & OA?
falls
blunt trauma
motor vehicle
accidents
Types of TBI’s
Open (penetrating) trauma
Closed (blunt) trauma
Open Trauma
injury breaks dura and exposes cranial contents to environment
causes primarily focal injuries
Closed Trauma
head –> hard surface OR object –> head
dura remains intact, brain tissues not exposed
causes focal OR diffuse injuries
more common than open injuries
Terms: supratentorial
above tentorium cerebelli
Terms: infratentorial
subtentorial, below tentorium cerebelli
Terms: Subdural
below dura matter
Terms: extracerebral
outside brain tissue
Terms: intracerebral
inside brain tissue
Metabolic Alterations d/t TBI
In delivery of energy substrates
neuronal excitbility from drugs or toxins
Primary Brain Injury
caused by direct impact/injury
can be focal or diffused
Focal Brain Injury
affects one area of the brain
Focal brain Injury: examples
coup
countercoup
contusions
subdural hematoma
epidural hematoma
intracerebral hematoma
Diffuse brain injury
involves more than one area of the brain
Secondary Brain Injuries
indirect result of primary brain injury (trauma, strokes)
-brain hypoperfusion
-ischemia
d/t systemic, cerebral, intracerebral processes
brain damage develops hours-days later
Secondary Brain Injury Mgt
prevent hypoxia and maintain CPP
-removal of hematoma (surgey)
-treat hypotension, hypoxemia, anemia, cerebral edema, ICP (anemia will kill cells)
-manage fluid and electrolyte imbalance, temperature, ventilation, nutrition
nutrition is important for survival of brain injury (initate within 24 hrs)
Systemic complications (pneumonia, fever, infection, immobility)
Focal brain Injury: Coup & Counter-Coup Injury
Coup: injury at the site of impact
countercoup: injury from brain rebounding and hitting the opposite side of the skull
Focal Brain Injury: Contusion
blood leaks from an injured vessel (bruising of brain)
smaller the area of impact, greater the severity
Contusions: Manifestations
loss of conciousness <5mins
loss ofr reflexes
transient loss of respiration
brief bradycardia
decrease in BP (few secs-mins)
Contusions can cause ___
epidural hematoma
subdural hematoma
intracerebral hematoma
Epidural Hematoma
bleeding between the dura mater and the skull
usually arterial + skull fracture (red!)
side of the skull
Subdural hematoma
blood between the dura matter and the brain
venous (burgundy, black)
top of the head
Intracerebral Hematoma
bleeding within the brain
difficult to extract and treat
Epidural Hematoma: Causes
motor accidents
sports
falls
Epidural Hematoma: common site of injury
temporal fossa (middle meningeal artery/vein)
Epidural Hematoma: Clinical Manifestations
Loss of conciousness –> lucid period (hours-days)
increasingly severe headaches
vomiting
drowsiness
confusion
seizure
hemiparesis
Epidural Hematoma: Tx
Medical emergency, surgical evacuation of hematoma
Subdural Hematoma: Physiology
caused by teating of the veins
expanding clots compress brain
Subdural Hematoma: Onset
within hours
Subdural Hematom: CM
headache
drowsiness
restlessness
Aagitation
slowed cognition
confusion
symptoms get worse overtime
LOC, respiration, pupillary (dysconjugate gaze, gaze palsies)
Subdural Hematoma: Tx
burr hole to remove clot
craniotomy (remove gelatnous blood)
percutanous drainage
Subacute Subdural Hematoma: Onset
48 hrs- 2weeks
Chronic Subdural Hematoma: Onset
weeks to months
subdural space gradually fills with blood
Chronic Subdural Hematoma: CM
chronic headaches
tenderness at site of injury
Intracerebral Hematoma: physiology
expanding mass, increased ICP & compression = ischemia and edema
Intracerebral Hematoma: Onset
3-10 data after injury
Intracerebral Hematoma: CM
decreasing levels of conciousness
Intracerebral Hematoma: Tx
reduce ICP (allow hematoma to reabsorb-mannitol)
surgery
Diffused Brain injury: Mechanisms
severity corresponds to amount of shearing force applied to brain
rotational & twisting movements
acceration and deceleration forces
axonal damage
Diffuse Brain Injury: Categories
Mild concussion
mild TBI
moderate TBI
severe TBI
Diffuse Brain Injury: DAI
AKA traumatic axonal injury OR multifocal axonal injury
occurs with all severties of brain injury
DAI: physiology
high levels of aceleration/deceleration injury
whiplash/rotational forces cause shearing/stretch of delicate axonal fibres and white matter tracts from cerebral cortex
severity depends on shearing force
DAI: effects
ability of nerce cells to communicate is lost/impaired
behavioural, cognitive, phyiscal changes (decreased LOC)
severe disabilities
longterm neurodegenrative processes (changes may continue years after)
- CTE, alzhiemers
Is DAI visible on CT scan?
No, too small to be seen. may be seen as diffude hemorrhades where axons and vessels are torn
can be seen post-mortem w/ electron microscope
Diffuse Brain Injury: suburachnoid hemorrhage
when vessel tears, blood pumped into subrachnoid space. blood coats nerve roots, clogs, impairs CSF resabsorption and obstructs passages. impairing CSF circulation
blood also = inflammatory response
Subrachnoid Hemorrhage: physiology
vasospasm with microthrombosis causes decreased cerebral perfusion ischemic injury
- delayed cerebral ischemia occurs in 3-14 days after hemorrhage in 50% , causes mortality and morbidity.
Subrachnoic Hemorrhage: CM
leaking vessels: episodic HA, changes in mental status/LOC, N/V, visual/speech disturbances
ruptured vessels: explosive headaches, N/V, visual disturbances, motor deficits, LOC
meningeal irritation= neck stiffness, photophobia, blurred vision, irritability, restlessness, low grade fever
poitive ekernig sign & brudzinski sign
hunt and hess scale used
Subrachanoid Hemorrhage: Tx
control: BP, ICP, vasospasm, fluid volume (fluids,diuretics)
improve: CPP
prevent: ischemia, hypoxia
avoid: rebleeding episode (mortality)
surgery (meds given for bleeding can = stroke/clots)
Diffuse Brain Injury: Concussion
mildest form of TBI
head injury causes sudden change in mental status
Concussion: CM
LOC <30mins
alteration in conciousness
post-traumatic amnesia <24h
GCS 13-15
none/transient focal neurological signs
CT/MRI negative
axonal twsiting/stretch = secondary disconnection
TBI Categories
mild
mod
severe
Mild TBI
imemdiate but transitory cm
temporary axonal disturbance = attention/memory defecits
no LOC / <30 mins
confusional state = 1-couple mins
retrograde amnesia
Mild TBI: S/S
ha
n/v
inability to concentrate
difficulty sleeping
Mild TBI: GCS
13-15
Moderate TBI
basak skull fracture, no brain stem injury
transitory decebreation/ decortication w/ unconciousness for days-weeks
moderate TBI: CM
LOC 30mins-6hrs
confusion
post-trauamtic anterograde amnesia (>24hrs)
selective attention, vigilanve, detection, working memory, data processing, vision, perception, language, mood/affect
brain imaging abnormal
Moderate TBI: GCS
9-12
Severe TBI: CM
6+ hrs of LOC
brainstem damange (pupilalry reaction, cardiac/resp symptoms, decorticate, decerebrate postur, abnormal reflex)
increased ICP, pulmonary complications, sensorimotor/cognitive defecits
compromised coordination, verbal writeen communication
inability to learn and reason
inability to modulate behaviour
brain imaging abnormal
Severe TBI: GCS
3-8
Cerebral Edema Types
Vasogenic
Cytotoxic
Interstitial
Vasogenic Cerebral Edema: Cause
increased permeability of capillaries (blood brain barrier) that form BBB
Cytotoxic Cerebral Edema: Cause
ischemia/hypoxia leading to faliure of active transportation systems
Interstitial Cerebral Edema: Cause
increased CSF colume and transependymal movement of CSF from ventirlces into extracellular spaces of brain tissues
Brain Herniation Syndrom
shifting of brain tissue, disrupts blood flow and damages brain tissue
Brain Herniation Syndrome: Types
Supratentorial herniation
- uncal
- central
- cingulate gyrus
- transcalavarial
Infratentorial herniation
- upward herniation of the cerrebellum
- cerebellar tonsil moves down through foramen magnum
Postconcussion Syndrome
occurs with mild TBI
Postconcussion Syndrome: CM
weeks-months
h/a
dizzy
fatigue
nervous,anxiety, irritability
insomnia
depression
inability to concentrate, forgetfullness
Postconcussion Syndrome: Tx
reassurance and symptomatic relief
close observation for 24 hrs
Post-traumatic Seizure
associated with focal & diffuse injury that creates epileptogenic foci
can occin within days OR 2-5 yrs + after trauma
Postconcussion Syndrome Tx
phenytoin
neuromodulation
CTE
progresive dementing disease that develops with repeated brain injury
tau neurofibrillary tangles present in brain
sports, blast injuries, work-related head trauma
CTE CM
violent behaviour
loss of control
depresison/suicide
memory loss
cognitive changes (min 12 mo)
CTE Dx
hx
clinical eval
autopsy
Determining Extent of Brain Injury
LOC
Breathing
Pupillary Reaction
Oculomotor response
motor response
LOC Changes
critical indec
indicate improvement/deterioration
abnormal = confusion –> coma
Term: loss of ability to think rapidly and clearly. impaired judgement and decison making
confusion
beginning loss of conciousness. disoirneted to time and place. impaire memory. recognition to self lost last.
disorientation
limited spontaneous movement/speech. easy arousal with normal speech/touch. may not be oriented to time, place, person.
lethargy
mild-mod reduction in arousal with limited response to environment. falls asleep unless stimulated. minimum responses.
obtundation
condition of deep sleep or unresponsiveness. may be aroused or caused to open eyes only by vigorous and repeated stimulation. response is withdrawal or grabbing stimulus.
stupor
associated with purposeful movement on stimulation.
light coma
no verbal response to environment or stimuli. noxious stimuli yields motor movement.
coma
associated with unresponsiveness or no response to any stimulus
deep coma
Abnormal Respiration Patterns
Cheyne-Strokes Respirations
Central neurgenic hyperventilation
apneustic respiration
cluster respiration
ataxic respirations
Cheyne-Strokes Respirations
alternating periods of hyperventilating and apnea
injury and lesions in forebrain and diencephalon
Central Neurogenic Hyperventilation
sustained hyperventilation
lesions of midbrain, pons, or medulla
Cluster Respirations
periods or clusters of rapid respirations of near equal depth
trauma or compression to medulla
Apneustic Respirations
prolonged inspiratory and expiratory phases
injury to pons or upper medulla
Ataxic Respirations
irregular respirations with prolonged periods of apnea
damage to medulla
Doll’s Eyes Phenomenon
A positive doll’s eye reflex (eyes move in opposite direction of head movement) indicates an intact brainstem.
Caloric Ice-Water test
stimulates your acoustic nerve by delivering cold or warm water or air into your ear canal. When cold water or air enters your ear and the inner ear changes temperature, it should cause fast, side-to-side eye movements called nystagmus
Pattern of Response can be
purposeful
innapropriate or not purposeful
not present
What symptom points to a neurological problem –> Direct involvement of central neural mechanism.
Vomiting without nausea.
Decorticate
rabbit (hands tucked inwards towards chest).
Decerebrate
hands on the sides, moving outwards
Mild GCS
13-15
associated with mild concussion
Moderate GCS
9-12
associated with structural injury such as hemorrhage or contusion
Severe GCS
3-8
associated with cognitive/physical disability or death
Brain Death
brain has no potential for recovery, can no longer maintain body’s internal homeostasis.
entire brain, brainstem, cerebellum stops functioning.
brain is autolyzing (self-digesting) or has already autolyzed on post-mortem examination.
Cerebral Death
irrerversible coma
death of cerebral hemisphere is exlcusive of brain stem and cerebellum
brainstem may continue to maintain internal homeostasis (activity present)
no behavioural or environmental responses
normal respiratory and CV function, temperature control, GI function.
not advised to remove life support
Brain Death
body cannot maintain internal homeostasis
irreversible cessation of entire brain (includes brainstem and cerebellum)
Brain Death Criteria
completion of all appropriate therapeutic precedures (no possibility of recovery)
unresponsive coma (absence of reflexes)
no spontaneous respirations (apnea)
no brainstem function
isoelectric (flat) EEG for 6-12 hours
persistence of these signs for an apprpriate observation period
Survivors of Cerebral Death
remain in a coma
1.emerge into a vegetative state/minimally concious
- eyes closed with no eye opening
- inability to follow commands, speak, or have voluntary movement
- exhibit kinetic mutism
- eye opening with visual tracking
- little/no spontaneous speech/following commands - minimal concious state
- exhibits minimal but defined behavioural evidence of self or environment awareness - cannot communicate either through speech/body movement but is fully concious with intact cognitive function
Pharmacotherapy for TBI
osmotic diuretic: mannitol
Mannitol: Indications of use
reduced ICP (after trauma)
precents/treats AKI
lowers intraocular pressure in acute glaucoma
Mannitol: MOA
increases osmolality of plasma –> draws fluid into vascular space
filtered by glomerulus but cannot be reabsorbed from renal tubules
- causes osmotic gradient in glomerular filtrate (pulls water into nephron and causes decreased H2O and Na reabsorption –> rapid diuresis)
Mannitol: DE
pulls fluid out of extravascular spaces
- draws water out of brain into intravascular compartment
- decreases cerebral edema and decreases ICP
Mannitol: AE
fluid and electrolyte imbalances (Na, K, Cl)
HF
pulmonary edema
hypovolemia
dehydration
tachycardia
fatigue
dizziness
convulsions
