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WI18 Neuro > TBI > Flashcards

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
Q

Prevention of secondary insult:

A

correction of hypoxia, hypercapnia, hyperglycemia, hyperthermia, anemia, hypoperfusion

Avoid HoTN and Hypoxemia!!! BP < 90, hypoxemia <60 = 150% increase in mortality

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26
Q

Observe for s/s of increased ICP

will look like on imaging?

A

decreased visibility and gyri, compressed lateral ventricles

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27
Q

Airway breathing - who is intubated

A

severe injury GCS <8

28
Q

Glucose control:

A

hyperglycemia worsens outcome +/- insulin drips

29
Q

Temperature control:

A

increased temp = increased metabolic demand and excessive glutamate release, increased

ICP – goal is normothermia

30
Q

Seizure tx

A

seizures worsen outcome (decreased oxygen, blood flow, increased ICP)

31
Q

when is lorazepam prophylaxis indicated?

A

GCS <10, abnormal CT, acute seizure

fosphenytoin (Cerebyx)

32
Q

cerebral herniation management

A

repeat non contrast CT

mannitol

hypertonic saline (HoTN >)

33
Q

TBI goal target

Pulse Ox, Systolic BP, MAP

A

Pulse OX: >90%

Systolic BP: > 90

MAP: >80

34
Q

TBI goal target

PaCO2, Temp, PbtO2

A

PaCO2: > 15 mmHg
Temp: 96-100.9
PbtO2: > 15

35
Q

TBI goal target

CPP, ICP, pH

A

CPP: > 60
ICP: < 30
pH: 7.35-7.45

36
Q

TBI goal target

Na, INR, Platelets, HgB

A

Na: 135-140
INR: <1.4
Platelet: >75k
HgB: >8

37
Q

CPP management if GCS <8

A

place drain ASAP to monitor ICP and direct tx

try to keep at 60, but can go to 70

38
Q

Consider ICP monitoring for (3)

A

2+ of:

  • Age over 40
  • unilateral/bilateral motor posturing
  • Systolic BP <90 mmHG
39
Q

Epidermal Hematoma

Indications for conservative tx (3)

A

Alert with no neuro findings

EDH volume < 15 mm

Midline shift <5 mm

any positive = sx

40
Q

Epidermal Hematoma surgical options?

A

Craniectomy and hematoma evacuation

Burr hole trephination

41
Q

Subdural Hematoma Management

Indications for conservative tx:

A

Alert with no neurologic findings

EDH volume < 15 mm

Midline shift <5 mm

42
Q

Subdural Hematoma surgical intervention indicated if?

A

SDH >10 mm and > 5 mm shift

GCS < 8

43
Q

Concussion/mTBI

Clinical features:

A

GCS score of 14/15

Confusion, dazed/foggy, HA, n/v, light/sound sensitivity

44
Q

Concussion/mTBI

Diagnostics:

A

Hx: any alteration in consciousness at time or shortly after event
presence of LOC/amnesia supports

SCAT3

Biomarkers

Cognitive screening tool,

psychometrics

45
Q

Concussion/mTBI

Treatment:

A

avoid ASA/NSAID

Physical and neuro rest until symptoms abate fully

return to ER if symptoms worsen

46
Q

Cerebral Contusion/hematoma

Clinical features:

A

Typically associated with SAH

May occur @ site of injury or on opposite site (contrecoup injury)

Can occur days after inciting event

47
Q

Cerebral Contusion/hematoma

Diagnostics:

A

Non-contrast CT

may not have positive findings immediately following

48
Q

Cerebral Contusion/hematoma

Treatment:

A

serial CT if change in mental status + coagulopathy until clot is stable

49
Q

Subdural hematoma

A

Acceleration and deceleration

Collection of blood between dura mater and arachnoid mater

VENOUS origin = slower development

MC in chronic alcoholics, elderly, children < 2

50
Q

Subdural hematoma diagnostics

A

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
Q

Penetrating Head Injury tx

A

Use GCS score to manage (>8 = 25% death, <5 = 100% chance)

IV vanco + IV ceftriaxone

Leave objects in until surgical removal allowed

52
Q

features of Cushing’s Reflex

A

Hypertension
Bradycardia
Respiratory irregularity

53
Q

Cushing’s reflex patho

A
  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
Q

types of herniation

A
  1. cingulate midline shift
  2. uncle transtenorial
  3. central transtentorial
  4. cerebellar tonsilla posterior fossa
55
Q

Cingulate “Midline Shift” herniation

A

Displacement of cingulate gyrus and falx cerebri to opposite side of brain

Compresses tissue and blood supply from anterior cerebral artery

56
Q

clinical features of midline shift

A

Unilateral leg weakness

57
Q

Uncal transtentorial

A

Expanding lesion in temporal lobe

displaced inferiorly thru tentorium and into posterior fossa

Compression of diencephalon + midbrain compressed/ displaced laterally

58
Q

uncal transtentorial clinical features

A

compression of parasympathetic fibers running along oculomotor n.

Ipsilateral fixed and dilated pupil

Pyramidal tract compression = contralateral motor paralysis

59
Q

Central transtentorial

A

Midline lesions (i.e. frontal or occipital lobes)

Downward displacement of cerebral hemisphere, basal ganglia, diencephalon, midbrain thru tentorial notch

60
Q

Central transtentorial herniation

A

BILATERAL

2-3 mm pupils
babinski signs
Decorticate posturing
Cheyne stokes respiration

61
Q

Cerebellar Tonsillar “Posterior Fossa” + clinical features

A

Cerebellar tonsils herniate thru foramen magnum

Clinical features: pinpoint pupils, flaccid paralysis, sudden death

62
Q

TBI pathophys:

A

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
Q

Second Impact Syndrome

A

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
Q

Post Concussive Syndrome

A

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
Q

long term risks associated with how many concussions?

A

3+

66
Q

CTE

A

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

WI18 Neuro (16 decks)

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