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PAT401 > W3: Traumatic Brain Injury > Flashcards

W3: Traumatic Brain Injury Flashcards

1
Q

Cerebral Blood Flow (CBF)

A

maintained to meet metabolic needs of brain
3-4x more to gray matter>white matter due to metabolic activity

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2
Q

Cerebreal Perfusion Pressure (CPP) range

A

70-90mm Hg

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3
Q

CPP

A

pressure required to perfuse cells of the brain
pressure it takes for the heart ro provide the brain with blood

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4
Q

Cerebral Blood Volume (CBV)

A

amt of blood in intracranial vault at a given time

any imbalance displaces CSF in the brain

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5
Q

Cerebral blood oxygenation

A

measured by oxygen saturation in internal jugular vein

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6
Q

Blood pressure should always be higher than the ____

A

CPP (cerebral perfusion pressure)

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7
Q

Features of cerebral hemodynamic injury

A

alterations in:
cerebral blood flow
ICP
oxygen delivery

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8
Q

Goals of hemodynamics

A

balance ICP with IJV oxygen saturation

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9
Q

alterations in cerebral hemodynamics =

A

increased ICP
cerebral edema (fluid infusing brain cells= swelling)

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10
Q

Normal ICP range?

A

5-15mm Hg

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11
Q

Increased ICP is caused by?

A

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.

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12
Q

Increased ICP: Stage 1

A

vasoconstruction and external compression (try to maintain normal BP and CPP)

no changes in ICP due to compensation (only pain at site)

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13
Q

Increased ICP: Stage 2

A

neuronal oxygen compromised, systemic arterial vasconstriction

body is trying to maintain perfusion

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14
Q

Increased ICP, Stage 2: S/S

A

drowsy
confusion
restlessness
light pupillary changes (constriction)
breathing changes

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15
Q

Increased ICP: Stage 3

A

brain hypoxia and hypercapnia, autoregulation lost

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16
Q

Increased ICP: Stage 3 S/S

A

difficulty arrousing
panting like dog (hyperventilation, irregular respiration)
widened pulse
bradycardia
pupil constriction and sluggish

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17
Q

Increased ICP: Stage 4

A

brain herniates, several herniation syndromes

most structures in brain shift to fill the brain cavity and will not return to original state

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18
Q

Therapeutic Mgt Goals: CPP

A

> 70 mmHg

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19
Q

Therapeutic Mgt Goals: ICP

A

<15 mmHg

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20
Q

Therapeutic Mgt Goals: CO2 pressure

A

35 mmHg

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21
Q

Therapeutic Mgt Goals: mean and arterial pressure

A

90 mmHg

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22
Q

Therapeutic Mgt Goals: Temperature

A

34C-36C

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23
Q

Therapeutic Mgt Goals: pulmonary capilalry wedge pressure

A

10-15 mmHg

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24
Q

What is TBI?

A

alteration in brain function/pathology d/t external force

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25
Q

Common causes of TBI for children & OA?

A

falls

blunt trauma
motor vehicle
accidents

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26
Q

Types of TBI’s

A

Open (penetrating) trauma
Closed (blunt) trauma

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27
Q

Open Trauma

A

injury breaks dura and exposes cranial contents to environment
causes primarily focal injuries

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28
Q

Closed Trauma

A

head –> hard surface OR object –> head
dura remains intact, brain tissues not exposed
causes focal OR diffuse injuries
more common than open injuries

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29
Q

Terms: supratentorial

A

above tentorium cerebelli

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30
Q

Terms: infratentorial

A

subtentorial, below tentorium cerebelli

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31
Q

Terms: Subdural

A

below dura matter

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32
Q

Terms: extracerebral

A

outside brain tissue

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33
Q

Terms: intracerebral

A

inside brain tissue

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34
Q

Metabolic Alterations d/t TBI

A

In delivery of energy substrates
neuronal excitbility from drugs or toxins

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35
Q

Primary Brain Injury

A

caused by direct impact/injury
can be focal or diffused

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36
Q

Focal Brain Injury

A

affects one area of the brain

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37
Q

Focal brain Injury: examples

A

coup
countercoup
contusions
subdural hematoma
epidural hematoma
intracerebral hematoma

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38
Q

Diffuse brain injury

A

involves more than one area of the brain

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39
Q

Secondary Brain Injuries

A

indirect result of primary brain injury (trauma, strokes)
-brain hypoperfusion
-ischemia

d/t systemic, cerebral, intracerebral processes

brain damage develops hours-days later

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40
Q

Secondary Brain Injury Mgt

A

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)

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41
Q

Focal brain Injury: Coup & Counter-Coup Injury

A

Coup: injury at the site of impact

countercoup: injury from brain rebounding and hitting the opposite side of the skull

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42
Q

Focal Brain Injury: Contusion

A

blood leaks from an injured vessel (bruising of brain)

smaller the area of impact, greater the severity

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43
Q

Contusions: Manifestations

A

loss of conciousness <5mins
loss ofr reflexes
transient loss of respiration
brief bradycardia
decrease in BP (few secs-mins)

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44
Q

Contusions can cause ___

A

epidural hematoma
subdural hematoma
intracerebral hematoma

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45
Q

Epidural Hematoma

A

bleeding between the dura mater and the skull

usually arterial + skull fracture (red!)

side of the skull

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46
Q

Subdural hematoma

A

blood between the dura matter and the brain

venous (burgundy, black)

top of the head

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47
Q

Intracerebral Hematoma

A

bleeding within the brain
difficult to extract and treat

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48
Q

Epidural Hematoma: Causes

A

motor accidents
sports
falls

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49
Q

Epidural Hematoma: common site of injury

A

temporal fossa (middle meningeal artery/vein)

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50
Q

Epidural Hematoma: Clinical Manifestations

A

Loss of conciousness –> lucid period (hours-days)

increasingly severe headaches
vomiting
drowsiness
confusion
seizure
hemiparesis

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51
Q

Epidural Hematoma: Tx

A

Medical emergency, surgical evacuation of hematoma

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52
Q

Subdural Hematoma: Physiology

A

caused by teating of the veins
expanding clots compress brain

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53
Q

Subdural Hematoma: Onset

A

within hours

54
Q

Subdural Hematom: CM

A

headache
drowsiness
restlessness
Aagitation
slowed cognition
confusion

symptoms get worse overtime
LOC, respiration, pupillary (dysconjugate gaze, gaze palsies)

55
Q

Subdural Hematoma: Tx

A

burr hole to remove clot
craniotomy (remove gelatnous blood)
percutanous drainage

56
Q

Subacute Subdural Hematoma: Onset

A

48 hrs- 2weeks

57
Q

Chronic Subdural Hematoma: Onset

A

weeks to months

subdural space gradually fills with blood

58
Q

Chronic Subdural Hematoma: CM

A

chronic headaches
tenderness at site of injury

59
Q

Intracerebral Hematoma: physiology

A

expanding mass, increased ICP & compression = ischemia and edema

60
Q

Intracerebral Hematoma: Onset

A

3-10 data after injury

61
Q

Intracerebral Hematoma: CM

A

decreasing levels of conciousness

62
Q

Intracerebral Hematoma: Tx

A

reduce ICP (allow hematoma to reabsorb-mannitol)
surgery

63
Q

Diffused Brain injury: Mechanisms

A

severity corresponds to amount of shearing force applied to brain

rotational & twisting movements
acceration and deceleration forces

axonal damage

64
Q

Diffuse Brain Injury: Categories

A

Mild concussion
mild TBI
moderate TBI
severe TBI

65
Q

Diffuse Brain Injury: DAI

A

AKA traumatic axonal injury OR multifocal axonal injury

occurs with all severties of brain injury

66
Q

DAI: physiology

A

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

67
Q

DAI: effects

A

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

68
Q

Is DAI visible on CT scan?

A

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

69
Q

Diffuse Brain Injury: suburachnoid hemorrhage

A

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

70
Q

Subrachnoid Hemorrhage: physiology

A

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.
71
Q

Subrachnoic Hemorrhage: CM

A

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

72
Q

Subrachanoid Hemorrhage: Tx

A

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)

73
Q

Diffuse Brain Injury: Concussion

A

mildest form of TBI
head injury causes sudden change in mental status

74
Q

Concussion: CM

A

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

75
Q

TBI Categories

A

mild
mod
severe

76
Q

Mild TBI

A

imemdiate but transitory cm

temporary axonal disturbance = attention/memory defecits
no LOC / <30 mins
confusional state = 1-couple mins
retrograde amnesia

77
Q

Mild TBI: S/S

A

ha
n/v
inability to concentrate
difficulty sleeping

78
Q

Mild TBI: GCS

A

13-15

79
Q

Moderate TBI

A

basak skull fracture, no brain stem injury

transitory decebreation/ decortication w/ unconciousness for days-weeks

80
Q

moderate TBI: CM

A

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

81
Q

Moderate TBI: GCS

A

9-12

82
Q

Severe TBI: CM

A

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

83
Q

Severe TBI: GCS

A

3-8

84
Q

Cerebral Edema Types

A

Vasogenic
Cytotoxic
Interstitial

85
Q

Vasogenic Cerebral Edema: Cause

A

increased permeability of capillaries (blood brain barrier) that form BBB

86
Q

Cytotoxic Cerebral Edema: Cause

A

ischemia/hypoxia leading to faliure of active transportation systems

87
Q

Interstitial Cerebral Edema: Cause

A

increased CSF colume and transependymal movement of CSF from ventirlces into extracellular spaces of brain tissues

88
Q

Brain Herniation Syndrom

A

shifting of brain tissue, disrupts blood flow and damages brain tissue

89
Q

Brain Herniation Syndrome: Types

A

Supratentorial herniation
- uncal
- central
- cingulate gyrus
- transcalavarial

Infratentorial herniation
- upward herniation of the cerrebellum
- cerebellar tonsil moves down through foramen magnum

90
Q

Postconcussion Syndrome

A

occurs with mild TBI

91
Q

Postconcussion Syndrome: CM

A

weeks-months

h/a
dizzy
fatigue
nervous,anxiety, irritability
insomnia
depression
inability to concentrate, forgetfullness

92
Q

Postconcussion Syndrome: Tx

A

reassurance and symptomatic relief
close observation for 24 hrs

93
Q

Post-traumatic Seizure

A

associated with focal & diffuse injury that creates epileptogenic foci

can occin within days OR 2-5 yrs + after trauma

94
Q

Postconcussion Syndrome Tx

A

phenytoin
neuromodulation

95
Q

CTE

A

progresive dementing disease that develops with repeated brain injury

tau neurofibrillary tangles present in brain

sports, blast injuries, work-related head trauma

96
Q

CTE CM

A

violent behaviour
loss of control
depresison/suicide
memory loss
cognitive changes (min 12 mo)

97
Q

CTE Dx

A

hx
clinical eval
autopsy

98
Q

Determining Extent of Brain Injury

A

LOC
Breathing
Pupillary Reaction
Oculomotor response
motor response

99
Q

LOC Changes

A

critical indec
indicate improvement/deterioration
abnormal = confusion –> coma

100
Q

Term: loss of ability to think rapidly and clearly. impaired judgement and decison making

A

confusion

101
Q

beginning loss of conciousness. disoirneted to time and place. impaire memory. recognition to self lost last.

A

disorientation

102
Q

limited spontaneous movement/speech. easy arousal with normal speech/touch. may not be oriented to time, place, person.

A

lethargy

103
Q

mild-mod reduction in arousal with limited response to environment. falls asleep unless stimulated. minimum responses.

A

obtundation

104
Q

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.

A

stupor

105
Q

associated with purposeful movement on stimulation.

A

light coma

106
Q

no verbal response to environment or stimuli. noxious stimuli yields motor movement.

A

coma

107
Q

associated with unresponsiveness or no response to any stimulus

A

deep coma

108
Q

Abnormal Respiration Patterns

A

Cheyne-Strokes Respirations

Central neurgenic hyperventilation

apneustic respiration

cluster respiration

ataxic respirations

109
Q

Cheyne-Strokes Respirations

A

alternating periods of hyperventilating and apnea

injury and lesions in forebrain and diencephalon

110
Q

Central Neurogenic Hyperventilation

A

sustained hyperventilation

lesions of midbrain, pons, or medulla

110
Q

Cluster Respirations

A

periods or clusters of rapid respirations of near equal depth

trauma or compression to medulla

110
Q

Apneustic Respirations

A

prolonged inspiratory and expiratory phases

injury to pons or upper medulla

111
Q

Ataxic Respirations

A

irregular respirations with prolonged periods of apnea

damage to medulla

112
Q

Doll’s Eyes Phenomenon

A

A positive doll’s eye reflex (eyes move in opposite direction of head movement) indicates an intact brainstem.

113
Q

Caloric Ice-Water test

A

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

114
Q

Pattern of Response can be

A

purposeful
innapropriate or not purposeful
not present

115
Q

What symptom points to a neurological problem –> Direct involvement of central neural mechanism.

A

Vomiting without nausea.

116
Q

Decorticate

A

rabbit (hands tucked inwards towards chest).

117
Q

Decerebrate

A

hands on the sides, moving outwards

118
Q

Mild GCS

A

13-15
associated with mild concussion

119
Q

Moderate GCS

A

9-12
associated with structural injury such as hemorrhage or contusion

120
Q

Severe GCS

A

3-8
associated with cognitive/physical disability or death

121
Q

Brain Death

A

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.

122
Q

Cerebral Death

A

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

123
Q

Brain Death

A

body cannot maintain internal homeostasis

irreversible cessation of entire brain (includes brainstem and cerebellum)

124
Q

Brain Death Criteria

A

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

125
Q

Survivors of Cerebral Death

A

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

  1. exhibit kinetic mutism
    - eye opening with visual tracking
    - little/no spontaneous speech/following commands
  2. minimal concious state
    - exhibits minimal but defined behavioural evidence of self or environment awareness
  3. cannot communicate either through speech/body movement but is fully concious with intact cognitive function
126
Q

Pharmacotherapy for TBI

A

osmotic diuretic: mannitol

127
Q

Mannitol: Indications of use

A

reduced ICP (after trauma)
precents/treats AKI
lowers intraocular pressure in acute glaucoma

128
Q

Mannitol: MOA

A

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)

129
Q

Mannitol: DE

A

pulls fluid out of extravascular spaces
- draws water out of brain into intravascular compartment
- decreases cerebral edema and decreases ICP

130
Q

Mannitol: AE

A

fluid and electrolyte imbalances (Na, K, Cl)
HF
pulmonary edema
hypovolemia
dehydration
tachycardia

fatigue
dizziness
convulsions

PAT401 (6 decks)

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