TBI Flashcards
normal parameters of ICP
0-15
normal parameters of CPP
60-150
< 60 = brain is not being perfused
normal parameters of MAP
70-110
Epidemiology TBI
TBI is 2:1 Male:Female
Trimodal distribution (0-4, 15-24, >75)
Mortality rate increases with age
Etiologies of TBI
Motor vehicle collisions are primary cause of blunt head injury to young adults and children
Fall MC in elderly
“Signature injury” of combat veterans in Iraq and Afghanistan
Monro-Kellie Hypothesis
1 or 2 of the 3 components of intracranial content will adjust to small increases in ICP
when mechanisms are used up, increased ICP will decrease CPP
Primary TBI Pathophysiology
Brain injury = unable to autoregulate and adjust CPP to > 60
decrease brain perfusion and cause hypoxia
tx of traumatic HoTN in primary TBI
Aggressive fluid resuscitation req/ to prevent HoTN and secondary brain injury
Maintain a MAP of >80 mmHG
Secondary neurotoxic cascade:
ongoing damage to the brain following initial impact that causes worsen neurologic outcome
Secondary insults
HoTN
Hypoxemia
Hyperglycemia
glutamate and TBI
Prolonged ischemia = glutamate levels increase, activate NMDA receptor channels = increase in Ca = Calcium Cascade
types of cerebral edema
Cytotoxic edema
Vasogenic (extracellular) edema
Cytotoxic edema
via NMDA rec/calcium cascade causing ionic shifts and loss of integrity due to mitochondrial damage
Vasogenic (extracellular) edema
direct damage to or breakdown of BBB (i.e. cancer)
TLDR: glutamate and TBI pahto
TBI ischemia causes increase in glutamate which activates NMDA channels to kick off calcium cascade, leading to worsening damage to brain tissue and cell death. This also causes cerebral edema and potentially herniation.
GCS TBI Scoring:
Mild:
Moderate
Severe
Mild: 14-15
Moderate: 9-13
Severe 3-8
GCS limitations
Unable to asses mild TBI
Not useful as single acute measure of severity, more of a tool to assess progression over time
Imaging TBI
non-contrast CT (helps determine if C Spine injury or any cranial bleeding)
who always gets CT
GCS < 12, pt on anticoagulant, antiplatelet or children
req. to use New Orleans or Canada
GCS >12 + LOC or Amnesia
New Orleans Criteria (15)
HA Vomiting Age > 60 Intoxication Persistent amnesia seizure
Canada (13-15)
GCS <15
suspected skull fracture
> 65
1+ vomiting
Dangerous mechanism
Treatment goals
maintain cerebral perfusion and oxygenation
via optimizing intravascular volume and ventilation
Tx mechanisms/elements (8)
Prevention of secondary insult
Observe for s/s of increased ICP
Airway breathing
Circulation:
Raising head of bed
Glucose control
Temperature control
Seizure tx
Prevention of secondary insult:
correction of hypoxia, hypercapnia, hyperglycemia, hyperthermia, anemia, hypoperfusion
Avoid HoTN and Hypoxemia!!! BP < 90, hypoxemia <60 = 150% increase in mortality
Observe for s/s of increased ICP
will look like on imaging?
decreased visibility and gyri, compressed lateral ventricles
Airway breathing - who is intubated
severe injury GCS <8
Glucose control:
hyperglycemia worsens outcome +/- insulin drips
Temperature control:
increased temp = increased metabolic demand and excessive glutamate release, increased
ICP – goal is normothermia
Seizure tx
seizures worsen outcome (decreased oxygen, blood flow, increased ICP)
when is lorazepam prophylaxis indicated?
GCS <10, abnormal CT, acute seizure
fosphenytoin (Cerebyx)
cerebral herniation management
repeat non contrast CT
mannitol
hypertonic saline (HoTN >)
TBI goal target
Pulse Ox, Systolic BP, MAP
Pulse OX: >90%
Systolic BP: > 90
MAP: >80
TBI goal target
PaCO2, Temp, PbtO2
PaCO2: > 15 mmHg
Temp: 96-100.9
PbtO2: > 15
TBI goal target
CPP, ICP, pH
CPP: > 60
ICP: < 30
pH: 7.35-7.45
TBI goal target
Na, INR, Platelets, HgB
Na: 135-140
INR: <1.4
Platelet: >75k
HgB: >8
CPP management if GCS <8
place drain ASAP to monitor ICP and direct tx
try to keep at 60, but can go to 70
Consider ICP monitoring for (3)
2+ of:
- Age over 40
- unilateral/bilateral motor posturing
- Systolic BP <90 mmHG
Epidermal Hematoma
Indications for conservative tx (3)
Alert with no neuro findings
EDH volume < 15 mm
Midline shift <5 mm
any positive = sx
Epidermal Hematoma surgical options?
Craniectomy and hematoma evacuation
Burr hole trephination
Subdural Hematoma Management
Indications for conservative tx:
Alert with no neurologic findings
EDH volume < 15 mm
Midline shift <5 mm
Subdural Hematoma surgical intervention indicated if?
SDH >10 mm and > 5 mm shift
GCS < 8
Concussion/mTBI
Clinical features:
GCS score of 14/15
Confusion, dazed/foggy, HA, n/v, light/sound sensitivity
Concussion/mTBI
Diagnostics:
Hx: any alteration in consciousness at time or shortly after event
presence of LOC/amnesia supports
SCAT3
Biomarkers
Cognitive screening tool,
psychometrics
Concussion/mTBI
Treatment:
avoid ASA/NSAID
Physical and neuro rest until symptoms abate fully
return to ER if symptoms worsen
Cerebral Contusion/hematoma
Clinical features:
Typically associated with SAH
May occur @ site of injury or on opposite site (contrecoup injury)
Can occur days after inciting event
Cerebral Contusion/hematoma
Diagnostics:
Non-contrast CT
may not have positive findings immediately following
Cerebral Contusion/hematoma
Treatment:
serial CT if change in mental status + coagulopathy until clot is stable
Subdural hematoma
Acceleration and deceleration
Collection of blood between dura mater and arachnoid mater
VENOUS origin = slower development
MC in chronic alcoholics, elderly, children < 2
Subdural hematoma diagnostics
non contrast CT
Acute: subdural hematomas, hyperdense (white) “crescent shaped lesions” cross suture lines +/- swirl sign
Chronic: isodense brain should be reordered initially (dark bc of iron oxidation
Penetrating Head Injury tx
Use GCS score to manage (>8 = 25% death, <5 = 100% chance)
IV vanco + IV ceftriaxone
Leave objects in until surgical removal allowed
features of Cushing’s Reflex
Hypertension
Bradycardia
Respiratory irregularity
Cushing’s reflex patho
- ICP elevation = HTN to maintain pressure
- Baroreceptors decrease HR to decrease HTN
- Bradycardia = reduced perfusion/swelling/herniation to brainstem = abnormal respiration
types of herniation
- cingulate midline shift
- uncle transtenorial
- central transtentorial
- cerebellar tonsilla posterior fossa
Cingulate “Midline Shift” herniation
Displacement of cingulate gyrus and falx cerebri to opposite side of brain
Compresses tissue and blood supply from anterior cerebral artery
clinical features of midline shift
Unilateral leg weakness
Uncal transtentorial
Expanding lesion in temporal lobe
displaced inferiorly thru tentorium and into posterior fossa
Compression of diencephalon + midbrain compressed/ displaced laterally
uncal transtentorial clinical features
compression of parasympathetic fibers running along oculomotor n.
Ipsilateral fixed and dilated pupil
Pyramidal tract compression = contralateral motor paralysis
Central transtentorial
Midline lesions (i.e. frontal or occipital lobes)
Downward displacement of cerebral hemisphere, basal ganglia, diencephalon, midbrain thru tentorial notch
Central transtentorial herniation
BILATERAL
2-3 mm pupils
babinski signs
Decorticate posturing
Cheyne stokes respiration
Cerebellar Tonsillar “Posterior Fossa” + clinical features
Cerebellar tonsils herniate thru foramen magnum
Clinical features: pinpoint pupils, flaccid paralysis, sudden death
TBI pathophys:
Ionic shift that causes momentary disruption in function
Repeat trauma: increased density of ion channels = brain vulnerable to over activation, neuron toxicity, cell death
Mitochondrial dysfunction and depletion of intracellular energy stores
Microscopic histological changes on exam
Second Impact Syndrome
Result in long term deficits and structural damage to brain
If second one occurs during recovery = cerebral edema and death
Theorized to be due to loss of autoregulation and ion imbalance, causing edema
Post Concussive Syndrome
Physical, emotional, cognitive symptoms in days /weeks following TBI
HA, dizziness, decreased concentration, memory/sleep disturbances, fatigue, depression
Unable to predict if this will occur, tx symptomatically
long term risks associated with how many concussions?
3+
CTE
Repeat concussion can cause deficits such as personality changes, depression ,suicide, dementia, speech
Early onset of memory loss and depression
Typically found in athletes
TAU protein deposits