Neurosurgery Flashcards

1
Q

Brain metabolism (% of O2 consumption)

A

20%

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2
Q

What is CMRO2?

A

Cerebral Metabolic Rate of O2 consumption

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3
Q

What is the CMRO2 of the average brain?

A

3-3.8mL/100g/min or 50mL/min

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4
Q

Where is the the CMRO2 the highest and why

A

Grey matter because the myelin sheath is present

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5
Q

Why is the brain so sensitive to hypoxia?

A

No O2 reserves

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6
Q

What is CBF?

A

Cerebral blood flow

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7
Q

What is the average CBF?

A

15-20% of CO

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8
Q

Circle of Willis Anatomy

A
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9
Q

What is CPP?

A

Cerebral Perfusion Pressure

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10
Q

CPP formula?

A

CPP=MAP-ICP or CVP

Whichever is greater

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11
Q

Normal CPP pressure?

A

80-100mmHG

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12
Q

What CPP value shows slowing on an EEG?

A

< 50mmHG

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13
Q

Autoregulation for the brain?

A

60-160mmHg

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14
Q

Relationship with MAP / PaO2 / PaCO2

A
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15
Q

Average PaC02 for the brain?

A

20-80mmHG

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16
Q

Why doesn’t metabolic acidosis affect CBF?

A

Ions do not cross the BBB but CO2 does

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17
Q

A reduction in temp does what two things in the brain?

A

Reduces CBF and CMRO2

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18
Q

A decrease in 10°C is a what reduction in CMRO2?

A

50%

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19
Q

An increase in 10°C is a what rise in CMRO2?

A

Double the CMRO2

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20
Q

Why is blood viscous?

A

The hematocrit

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21
Q

An increase in blood viscocity does what?

A

Reduces blood flow

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22
Q

What do tight junctions regulate?

A

Size
Charge
Lipid solubility
Protein binding

H2O moves freely throught tight junctions

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23
Q

What disrupts tight junctions selectivity?

SHITTSS

A

Severe HTN
Hypercapnia/Hypoxia
Infection
Tumors
Trauma
Stroke
Sustained seizures

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24
Q

What is CSF

A

Cerebrospinal Fluid

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25
Q

How much CSF is made per day?

A

500mL

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26
Q

Total volume of CSF?

A

150mL

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27
Q

Why do we make more CSF than the total volume?

A

It is constantly being reabsorbed in the arachnid layer

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28
Q

Where is CSF made?

A

Choroid Plexus
ependymal cells in ventricles

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29
Q

The skull is a fixed volume, what are some mechanism to help with increased pressure?

4 things

A

Displacment of CSF into spinal column
Increase in CSF absorption
Decrease in CSF production
Decrease in cerebral blood volume

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30
Q

What is considered a significant midline shift?

A

> 0.5cm

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31
Q

What is luxury perfusion?

A

A decrease in CMRO2 and increase in CBF

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32
Q

What is circulatory steal phenonmenon?

A

When there is vasodilation and ischemic areas, blood is shunted or “stolen” away from the narrowed vessels to the dilated ones

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33
Q

How can we protect the brain from furthter deline during periods of less O2 delivery?

6 things HAAAAN

A
  • Hypothermia
  • Anesthetics
  • Adequate CPP
  • Avoid hypotension
  • Avoid blood sugars of 180mg/dl and above
  • Nimodipine (prevents spasms)
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34
Q

Neuromonitoring Types: Blood Flow

CIT-JIT

A
  • Cerebral Oximetry
  • IV Tracer Flow
  • Transcranial doppler ultrasound
  • Jugular bulb venous O2 saturation
  • Invasive tissue blood flow
  • Tissue partial pressure of O2

Bold most common and the only one Adam has seen

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35
Q

Neuromonitoring Types: Nerve Function

A
  • EEG (Electroencephalogram)
  • EP (Evoked Potentials)
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36
Q

Different kind of EP’s?

A
  1. Sensory (SEPs)
  2. Motor (MEPs)
  3. Electromyograph (EMG)
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37
Q

Different kind of SEPs?

A
  1. Somatosensory Evoked Potentials (SSEPs)
  2. Brainstem Auditory Evoked Potentials (BAEPs)
  3. Visual Evoked Potentials (VEPs)
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38
Q

Different kind of MEPs?

A
  1. Transcranial Motor Evoked Potentials
  2. Spinal Motor Evoked Potentials
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39
Q

Most common cranial vessel to be involved in an acute stroke?

A

Middle cerebral artery (MCA)

neuromonitoring done by the transcranial doppler

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40
Q

What is the EEG

A

Electroencephalogram: summation of excitatory and inhibitory postsynaptic potentials of the cerebral cortex

41
Q

Brain Waves: Gamma

IPE

A

Insight
Peak focus
Expanded consciousness

42
Q

Brain Waves: Beta

ACC

A

Alertness
Concentration
Cognition

43
Q

Brain Waves: Alpha

CRV

A

Creativity
Relaxation
Visualization

44
Q

Brain Waves: Theta

MIM

A

Meditation
Intution
Memory

45
Q

Brain Waves: Delta

DH

A

Detached awareness
Healing Sleep

46
Q

Why do we care about brain waves in surgery?

A
  • Helps identify inadequate BF
  • Guides us reducing cerebral metabolism
  • Predictor of neurological outcome
  • BIS monitor
47
Q

When it comes to brain waves and ischemia, what are we looking for?

A

Slowing frequency with preserved amplitude

Height is the same, wave form lengthens

48
Q

What is BIS and what are the two types?

A

Bispectral Analysis
1. 2 Channel
2. 4 Channel

4 Channel can monitor left and right brain differences

49
Q

BIS Monitor numbers scale

A
  • 100 = Completely awake
  • 60-80 = MAC / Sedation
  • 40-60 = GA
  • 0 = Isoelectric
50
Q

Evoked potentials look for what in a stimulus?

A

Amplitude: Tall and potent
Latency: Short and fast

51
Q

Can we paralyze if using MEPs?

A

No, sensory types only

52
Q

Basic rule about anesthetc drugs and evoked potentials

A

Increased latency and decreased amplitude

53
Q

5 Generalities of anesthetic drugs on evoked potentials

A
  1. IV agents have significantly less effect that equal potent doses of inhalation agents
  2. Combination of drug effects are additive
  3. Subcortical SEPs are very resistant to the effects of anesthetic agents
  4. MEPs are very sensitive to inhaled agents
  5. Des has stronger inhibitor effects than Sevo at high doses
54
Q

Types of spine surgeries

RSSF-DVT

A
  • Radiculopathy: compression on nerve root
  • Spondylosis: wear on bone or cartlidge
  • Scoliosis: congenital defect
  • Fusions
  • Decompression
  • Vascular malformations
  • Tumor resection
55
Q

Spine surgery pre-op

A

Always evaluate neurological defecits
Neuromonitoring?
Airway issues? (C-Spine collar?)
multi-modal analgesia

56
Q

Spinal surgery positioning

A

Usually prone arms out like superman
Difficult line access after positioned
POVL (Perioperative Vision Loss)
Hypotension due to abdominal compression
Facial edema

57
Q

What is POVL

A

Perioperative Vision Loss

58
Q

What is OIH

A

Opioid Induced Hyperalgesia
Hyper increase of pain sensation by short acting opiods

Opiods cause an increase in pain

59
Q

Adams Neuromonitoring regiment for spine cases

A

PO Hydrocodone preop
Propofol infusion
low dose narcotic infusion
ketamine infusion
0.5 gas MAC

60
Q

Neurogenic shock

A

Low blood pressure, bradycardia, and hypothermia due to disruption of the sympathetic nervous system with preserved parasympathetic activity.

Trauma to T6 and above

61
Q

Neurogenic Shock Pathway

A

Spinal cord injury above T6

Decreased sympathetic output = vasodilation = decreased preload = decreased stroke volume -=decreased CO

Unopposed parasympathetic output = bradycardia = decreased CO

both add up to profound hypotension

treat with volume, then Levophed

62
Q

AH and AD (same thing):
Autonomic Hyperreflexia / Dysreflexia

A

Usually injury to T6 or above
Sympathetic stimulaiton below injury causes increased BP
Above injury baroreceptors decrease HR

Causes high aferload: LV failure, Pulmonary edema, and arryhtmias

reduce affernent stimulus, treat with narcs, vaso dilators or propofol

63
Q

Brain masses or lesions: Supratentorial

Presentations

Supratentorial = Cerebrum or all the lobes

A

Increase seizure activity
hemiplegia (weakness or loss of fuction on one side)
Aphasia (inability to understand language or articulate thoughts to language)

64
Q

Brain masses or lesions: Infratentorial

Presentations

Infratentorial = Cerebellum and brainstem

A

Cerebellar:
Ataxia (lack of voluntary coordination of muscle movements)
Nystagmus (involuntary eye movements)
Dysarthria (muscle dysfunction in the lips, tongue and other speech muscles making it hard to pronounce words)

Brainstem:
Basic human funtion abnormalities (respiratory, conciousness, cranial nerve sensations)

65
Q

Brain mass or lesion pre-op

A

ICP?
Neurological assesments
What meds? (steroids, diuretics, anticonvulsants)
Check sodium levels and glucose levels
Avoid pre-op medication, can cause issues post-op for assesments

66
Q

Brain mass or lesion intra-op

A

ASA Monitors
Foley (diuretic for relaxed brain)
±Neuromonitoring
A-Line
±Central line
EVD (external ventricular drain)

67
Q

What is an EVD and what does it monitor?

A

External Ventricular Drain
Monitors CSF pressure and allows acces to test and drain CSF

Draining CSF reduces pressure

68
Q

Induction for brain masses

A

Extra propofol
phenylephrine
esmolol
Avoid succs if not a difficult airway (succs can potentially increase ICP)

69
Q

Crani positioning

A

Variable but usually in mayfields (aka pinning)

70
Q

When a patient is in mayfields (aka pinned) what do we need to make sure they do not do and how?

A

Do not let them cough, they can die
Propofol and esmolol at the ready

71
Q

Crani maintenance

A

Paralyze if you can
limit fluids
avoid hyperglycemia
normocarbia
normotensive

72
Q

Hypertension in a crani does what?

A

Increased brain mass and EBL

73
Q

Hypotension in a crani does what?

A

greater chance of ischemia

74
Q

Hypercarbia in a crani does what?

A

Increase CBF

75
Q

Hypocarbia in a crani does what?

A

Decrease CBF

76
Q

How does an increase/decrease of CBF affect ICP?

A

Increse/decrease ICP respectivly

77
Q

Hyperventilation will only transceintly decrease CBF and ICP beauce of the bicarb buffering system. How long does this take?

A

6-8 hours

78
Q

Relaxing the brain can cause what that makes the surgeon annoyed?

A

Changes in the imgaing when using naviagation

79
Q

Crani emergence

A

Avoid coughing
rapid wakeup (no precedex, they are slow to emerge) for neuro assesment
Pain should not be too bad, dont over narc
Off to ICU after

80
Q

Brainstem masses disrupt what

A

breathing
conciousness
BP/HR
Sleep

81
Q

Cheyne-Stokes Respiration?

A
82
Q

Biot Respiration

A
83
Q

10 steps to an awake Crani mass

A
  1. ASA Monitors, facemask c̅ O2
  2. Sedation
  3. Scalp Block by doc (propofol before he starts helps)
  4. Pins placed
  5. Positioned then woken up
  6. Asked about comfort
  7. Sedation again, surgery starts
  8. Woken up for neural mapping (put back to sleep when done)
  9. Mass removed
  10. Sedated until emergence
84
Q

Crani mass tidbits

A

Avoid benzos, slow wakeup
short acting agents
educate patients
lots of local used
Dura manipulations most painful
communication with doc

85
Q

Unruptured aneurysms can be treated what two ways

A
  1. Coiling
  2. Clipping
86
Q

Unruptured Aneurysm Pre-op

A
  • Neuro assesment
  • Type and Cross
  • 4 units PRBC and 4 FFP in room and ready
  • Avoid benzos if any altered mental status (othweise beneficial)
87
Q

Unruptured Aneurysm Intra-Op

A
  • Large bore IV
  • A-Line
  • Central Line
88
Q

Unruptured Aneurysm Induction

A

Gentle
MAP strict control 60-60 mmHg
ETCO2: 35 mmHg
Propofol
Esmolol
Phenylephrine
Cardene
Labetalol

89
Q

Unruptured Aneurysm Maintenance

A

Neuromonitoring
possible lumbar drain
if clipping cool patient to 34-35 °C

90
Q

Temporary Clipping

A

Burst supression just prior to it
Then increase MAP to 90-100 mmHg to test it
After clip removed bring MAP back to 60-80 mmHg

91
Q

Final Clipping

A

ICG dye to make sure its working
MAP goals of 70-90 mmHg

92
Q

ICG Dye concentration and dosing

A

25mg in 10mL of normal saline
(2.5mg/1mL)

Dosing is 5mL with rapid saline flush(20mL)

93
Q

Unrupture Aneurysm Emergence

A

No coughing
Pressors and dilators in line to control BP
Neuro assesment before xfer to ICU

94
Q

Intra-op Aneurysm Rupture

A

Doc lets room know it busted
Immediate MAP of 40-50

If surgical intervention fails then:
Propofol for decreased CBF
Adenoside (6,12,18 mg)
Xfusion of PRBC

95
Q

Ruptured Aneurysm brought in

A

Lare bore IV
PRBC stat
Art Line
Brain relaxation (Decadron, Mannitol, Lasix, Hyperventilate)
Keppra

96
Q

What is Keppra

A

Anticonvolusant

97
Q

What is AVM

A

Ateriovenous Malformation

98
Q

AVM basic info

A

Differnet types of abnormalities, may increase or decrease bleeding risk depending on flow rate
Treat similar to unruptured aneurysm
Higher flow rare = higher bleeding risk / surgical risk