TBI Flashcards

1
Q

normal parameters of ICP

A

0-15

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2
Q

normal parameters of CPP

A

60-150

< 60 = brain is not being perfused

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3
Q

normal parameters of MAP

A

70-110

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4
Q

Epidemiology TBI

A

TBI is 2:1 Male:Female
Trimodal distribution (0-4, 15-24, >75)
Mortality rate increases with age

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5
Q

Etiologies of TBI

A

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

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6
Q

Monro-Kellie Hypothesis

A

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

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7
Q

Primary TBI Pathophysiology

A

Brain injury = unable to autoregulate and adjust CPP to > 60

decrease brain perfusion and cause hypoxia

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8
Q

tx of traumatic HoTN in primary TBI

A

Aggressive fluid resuscitation req/ to prevent HoTN and secondary brain injury

Maintain a MAP of >80 mmHG

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9
Q

Secondary neurotoxic cascade:

A

ongoing damage to the brain following initial impact that causes worsen neurologic outcome

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10
Q

Secondary insults

A

HoTN
Hypoxemia
Hyperglycemia

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11
Q

glutamate and TBI

A

Prolonged ischemia = glutamate levels increase, activate NMDA receptor channels = increase in Ca = Calcium Cascade

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12
Q

types of cerebral edema

A

Cytotoxic edema

Vasogenic (extracellular) edema

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13
Q

Cytotoxic edema

A

via NMDA rec/calcium cascade causing ionic shifts and loss of integrity due to mitochondrial damage

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14
Q

Vasogenic (extracellular) edema

A

direct damage to or breakdown of BBB (i.e. cancer)

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15
Q

TLDR: glutamate and TBI pahto

A

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.

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16
Q

GCS TBI Scoring:
Mild:
Moderate
Severe

A

Mild: 14-15
Moderate: 9-13
Severe 3-8

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17
Q

GCS limitations

A

Unable to asses mild TBI

Not useful as single acute measure of severity, more of a tool to assess progression over time

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18
Q

Imaging TBI

A

non-contrast CT (helps determine if C Spine injury or any cranial bleeding)

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19
Q

who always gets CT

A

GCS < 12, pt on anticoagulant, antiplatelet or children

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20
Q

req. to use New Orleans or Canada

A

GCS >12 + LOC or Amnesia

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21
Q

New Orleans Criteria (15)

A
HA 
Vomiting
Age > 60 
Intoxication 
Persistent amnesia 
seizure
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22
Q

Canada (13-15)

A

GCS <15

suspected skull fracture

> 65

1+ vomiting

Dangerous mechanism

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23
Q

Treatment goals

A

maintain cerebral perfusion and oxygenation

via optimizing intravascular volume and ventilation

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24
Q

Tx mechanisms/elements (8)

A

Prevention of secondary insult

Observe for s/s of increased ICP

Airway breathing

Circulation:

Raising head of bed

Glucose control

Temperature control

Seizure tx

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25
Prevention of secondary insult:
correction of hypoxia, hypercapnia, hyperglycemia, hyperthermia, anemia, hypoperfusion Avoid HoTN and Hypoxemia!!! BP < 90, hypoxemia <60 = 150% increase in mortality
26
Observe for s/s of increased ICP | will look like on imaging?
decreased visibility and gyri, compressed lateral ventricles
27
Airway breathing - who is intubated
severe injury GCS <8
28
Glucose control:
hyperglycemia worsens outcome +/- insulin drips
29
Temperature control:
increased temp = increased metabolic demand and excessive glutamate release, increased ICP -- goal is normothermia
30
Seizure tx
seizures worsen outcome (decreased oxygen, blood flow, increased ICP)
31
when is lorazepam prophylaxis indicated?
GCS <10, abnormal CT, acute seizure fosphenytoin (Cerebyx)
32
cerebral herniation management
repeat non contrast CT mannitol hypertonic saline (HoTN >)
33
TBI goal target Pulse Ox, Systolic BP, MAP
Pulse OX: >90% Systolic BP: > 90 MAP: >80
34
TBI goal target PaCO2, Temp, PbtO2
PaCO2: > 15 mmHg Temp: 96-100.9 PbtO2: > 15
35
TBI goal target CPP, ICP, pH
CPP: > 60 ICP: < 30 pH: 7.35-7.45
36
TBI goal target Na, INR, Platelets, HgB
Na: 135-140 INR: <1.4 Platelet: >75k HgB: >8
37
CPP management if GCS <8
place drain ASAP to monitor ICP and direct tx try to keep at 60, but can go to 70
38
Consider ICP monitoring for (3)
2+ of: - Age over 40 - unilateral/bilateral motor posturing - Systolic BP <90 mmHG
39
Epidermal Hematoma | Indications for conservative tx (3)
Alert with no neuro findings EDH volume < 15 mm Midline shift <5 mm any positive = sx
40
Epidermal Hematoma surgical options?
Craniectomy and hematoma evacuation Burr hole trephination
41
Subdural Hematoma Management | Indications for conservative tx:
Alert with no neurologic findings EDH volume < 15 mm Midline shift <5 mm
42
Subdural Hematoma surgical intervention indicated if?
SDH >10 mm and > 5 mm shift GCS < 8
43
Concussion/mTBI | Clinical features:
GCS score of 14/15 Confusion, dazed/foggy, HA, n/v, light/sound sensitivity
44
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
45
Concussion/mTBI | Treatment:
avoid ASA/NSAID Physical and neuro rest until symptoms abate fully return to ER if symptoms worsen
46
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
47
Cerebral Contusion/hematoma | Diagnostics:
Non-contrast CT | may not have positive findings immediately following
48
Cerebral Contusion/hematoma Treatment:
serial CT if change in mental status + coagulopathy until clot is stable
49
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
50
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
51
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
52
features of Cushing’s Reflex
Hypertension Bradycardia Respiratory irregularity
53
Cushing's reflex patho
1. ICP elevation = HTN to maintain pressure 2. Baroreceptors decrease HR to decrease HTN 3. Bradycardia = reduced perfusion/swelling/herniation to brainstem = abnormal respiration
54
types of herniation
1. cingulate midline shift 2. uncle transtenorial 3. central transtentorial 4. cerebellar tonsilla posterior fossa
55
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
56
clinical features of midline shift
Unilateral leg weakness
57
Uncal transtentorial
Expanding lesion in temporal lobe displaced inferiorly thru tentorium and into posterior fossa Compression of diencephalon + midbrain compressed/ displaced laterally
58
uncal transtentorial clinical features
compression of parasympathetic fibers running along oculomotor n. Ipsilateral fixed and dilated pupil Pyramidal tract compression = contralateral motor paralysis
59
Central transtentorial
Midline lesions (i.e. frontal or occipital lobes) Downward displacement of cerebral hemisphere, basal ganglia, diencephalon, midbrain thru tentorial notch
60
Central transtentorial herniation
BILATERAL 2-3 mm pupils babinski signs Decorticate posturing Cheyne stokes respiration
61
Cerebellar Tonsillar “Posterior Fossa” + clinical features
Cerebellar tonsils herniate thru foramen magnum Clinical features: pinpoint pupils, flaccid paralysis, sudden death
62
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
63
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
64
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
65
long term risks associated with how many concussions?
3+
66
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