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UBP Pearls > Neuroanesthesia > Flashcards

Neuroanesthesia Flashcards

1
Q

What does hypercapnia do in a TBI setting/why to avoid it?

What does hyperventilation do? Should you do it for TBI pt?

A

Inc ICP! D/t inc in blood flow

Mild hypervent can help dec ICP, but not recommended during first 24 hrs after TBI (unless emergent c/f herniation) d/t inc risk of cerebral ischemia 2/2 reduction in CBF

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2
Q

Equation for CPP?
Normal CPP?
Goal CPP in TBI?

A

CPP = MAP - ICP
Normal: 80-100 (MAP ~ 100, ICP ~10)
Goal in TBI: 60-70 (balancing ARDS vs cerebral ischemia)

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3
Q

Signs of basilar skull fracture?

A

Hemotympanum, periorbital ecchymosis
Avoid nasal intubation d/t risk of hitting brain through skull fracture!

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4
Q

Things that have to be met in order to clear C spine?

A

Age > 4yo
Normal mental status
No tenderness along vertebrae
No paraesthesias/neuro deficits
No distracting pain

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5
Q

What kind of fluid(s) do you want to AVOID in TBI patients?

A

Anything containing dextrose (worsens cerebral edema)
Hypotonic solutions (LR is slightly more hypoosmolar than plasma or NS)

NS is the IVF of choice!

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6
Q

List ways to dec ICP?

A

Remove it via IVD
HOB elevated
Ensure no venous obstruction (C collar, positioning)
Mannitol
Lasix
Hyperventilation (temporary for 24-48 hrs and not advised for TBI pts d/t cerebral edema)

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7
Q

How to measure fluid status in pt?

A

Urine output
Cap refill
Mucous membranes
Blood loss
Advanced monitors (PPV, TTE, etc)

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8
Q

Effects of hypothermia?

A

Coagulopathy
Impaired wound healing
Higher infx rate
Arrhythmias
Impaired renal fxn

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9
Q

Normal values of:
CI
PAP
PCWP
Mixed venous O2 sat

A

CI: 2.6-4.2
PAP: 15-30/4-12
PCWP: 2-15
Mixed venous O2 sat: 65-75%

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10
Q

Ddx for hypoxia + b/l infiltrates on CXR?

A

Aspiration pneumonitis
ARDS (can be 2/2 to anything…head trauma, fat embolism, aspiration)
Cardiogenic pulm edema
TRALI/TACO
Neurogenic pulm edema (can happen after any insult to CNS)

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11
Q

Name and parts of the criteria for ARDS?

A

Berlin criteria:
- B/l infiltrates
- Resp failure not fully explained by heart failure
- P/F ratio < 300 (200-300 mild, 100-200 mod, <100 severe)
- acute onset (w/in a week of inciting event)

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12
Q

Difference between CSW and SIADH? Tx for both?

A

CSW usually hypovolemic - isotonic or hypertonic IVF
SIADH euvolemic - water restriction and diuresis, demeclocycline, sodium replacement

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13
Q

GCS scale, what is it associated with, and mild/mod/severe cutoffs?

A
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14
Q

Main ddx for obtunded patient? How about for pregnant obtunded pt?

A

Main:
- Stroke (hemorrhage or infarct)
- Trauma/TBI
- Seizure
- Metabolic (hypoNa, hypoglycemia)
- Medication SE/overdose
- Encephalitis/meningitis
- Cerebral tumor

Pregnant: all of the above, plus:
- placental abruption –> AFE
- Seizure (eclampsia), stroke (HELLP - low pltls, see pic) higher on ddx

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15
Q

Describe some manifestations of inc ICP?

A

Cushings response: inc BP, dec HR, irregular respirations
- Weird, sometimes unilateral cranial nerve changes (like CN III palsy, dilated and nonreactive pupil) can be 2/2 brain stem herniation

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16
Q

3 ways that mannitol dec ICP

A

1) osmotic shifting of fluid from intracranial to intravascular
2) causing dec blood viscosity (I don’t understand why this is the case, seems like it would inc viscosity?) –> reflex vasoconstriction
3) dec production of CSF

-P.S. if BBB not intact can cause worsening cerebral edema, of if intracranial hematoma then can worsen it bc of osmotic diuresis

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17
Q

Steps to take if neuro pt taking longer than expected to wake up?

A
  • Assess vital signs (make sure no Cushings)
  • Ensure adequate BP, ventilation, oxygenation, temperature, glucose/metabolic derangements if possible given clinical scenario
  • Consult NRSGY
  • Prepare for transport to CT
  • Start reducing ICP
  • Maintain adequate CPP (place art line PRN)
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18
Q
  • When to do post cardiac arrest therapeutic hypothermia?
A
  • If pt comatose following arrest (assuming already made sure that ventilation/oxygenation optimized, BP adequate, no other reason for continued AMS)
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19
Q

How to induce post cardiac arrest therapeutic hypothermia?

A
  • Use cooling blankets, ice packs, infusion of ice cold (4C) LR/NS to reduce temp to 32-34 for 12-24 hrs (have to use esophageal/bladder if making urine/PAC (consider using two sources to ensure accuracy)
20
Q

How are you going to intubate pt w/cervical spinal cord injury w/worsening sxs?

A
  • Apply manual in-line stabilization and perform awake intubation! Least distraction of the C-spine, reduce the risk for aspiration, and allows for neuro assessment after final pt positioning
21
Q

Any special monitoring for spine cases?

A
  • Remember SSEP and MEPs!!! Apparently, MEPs are not necessarily the standard of care yet technically, but have inc sensitivity than SSEPs so if spinal cord ischemia is a significant risk, you could always say that you wanted to dec the false negative rate that you’d have if only monitoring SSEPs, thus you’d want both.
  • if >4 hrs, have to remember Foley
22
Q

What’s your plan for maintenance of anesthesia for a spine case?

A
  • dependent on presence and type of NM. Goal to minimally depress SSEPs/MEPs + facilitate rapid emergence for neuro fxn exam
  • Since MEPs are most sensitive to volatiles, would do TIVA (prop/remi/+-ketamine), or at least keep MAC <0.5 and avoid varying concentration that would complicate interpretation
23
Q

How do anesthetic agents affect MEPs and SSEPs? What do each of these monitor, respectively?

A
  • Decreased amplitude and increased latency (MEPs more sensitive to volatiles) - these signal changes are also seen with spinal cord ischemia, hence why using less volatiles (and avoiding hypothermia, hypercarbia, hypoxia, and hypoTN –> all of these also dec amp and inc latency) is optimal
  • MEPs: descending motor pathways in anterior spinal cord (remember anterolateral corticospinal tract…cortex to spine so this would be motor)
  • SSEPs: ascending sensory pathways in posterior spinal tract (remember dorsal horn stuff)
24
Q

During spine sx, NM shows dec amplitude and inc latency in SSEPs and MEPs. What to do?

A
  • Correct any: hypoxemia, hypoTN, hypovol, anemia, hypo/hypercarbia in order to optimize O2 delivery to cord and reverse any conditions that may be causing false +s
  • ensure depth of anesthesia has remained constant
  • speak with surgeon and ask if any excessive traction occuring or other surgical causes
  • could perform wake up test to determine further steps..
25
Q

Which part of spinal cord is most vulnerable to ischemic injury?

A
  • Supplied by the ant spinal artery (arises from vertebral arteries), which supplies the ant 2/3 of spinal cord
26
Q

Delayed emergence with adequate ventilation ddx? What to do?

A
  • neuro deficit, hyper/hypoglycemia, alcohol w/d, hypoxia, hypo/hypercarbia, residual anesthetic/NMB, metabolic derangements
  • I’d also add hypothermia
  • ensure adequate ventilation/oxygenation, review meds given during case, confirm reversal, check glu and lytes/ABG. Consult neurologist, EEG, CT of H/N
27
Q

Is a CEA considered elective/urgent/emergent after TIA?

A
  • technically emergent, as should ideally be performed within 48hrs of TIA and definitely w/in 1 week, as benefits dec rapidly after this
28
Q

Examples of intraop neuro monitoring for cerebral ischemia (5)?

A
  • EEG (high false - and + rates)
  • SSEP (sensory cortex mostly supplied by MCA)
  • Transcranial doppler (of ipsilateral MCA…detects micro-embolic events etc)
  • stump pressure (place needle in art above clamp to measure back pressure resulting from collateral flow thru COW)
  • cerebral oximetry (measures SpO2 in entire tissue bed - brain tissue, art, vein blood. Dec of 20% or more suggests cerebral ischemia)
29
Q

Explain how you would induce a pt with cardiac disease for CEA

A
  • See pic. +/- on etomidate vs propofol…need to review
  • “etomidate would provide superior HD stability in this pt w/chronic HTN, hypovol, significant cardiac disease”
30
Q

What is the intracerebral steal phenomenon?

A
  • paradoxical vasodilatory response (in normally reactive, non-ischemic vasc beds) when an acute inc in PaCO2 happens that dec (diverts) cerebral blood flow to an impaired perfusion area where the vasculature is already maximally dilated (in hypoperfused areas, vessels dilate, but over time they exhibit blunted response to CO2 changes)
  • however, significant hypocarbia could exacerbate cerebral ischemia 2/2 intense vasoconstriction and leftward shifting of oxyHb dissociation curve (impaired delivery of O2 to tissues)
31
Q

Hemodynamic changes during CEA (carotid endarterectomy) - what changes could you see and why?

A
  • significant bradycardia and hypotension
  • manipulation of the carotid sinus –> activation of baroRs (similar to “carotid massage” as a way to break SVT) –> activates parasymp and inhibits symp –> brady and hypoTN
  • surgeon can inject LA into the carotid body area to help with further episodes (this could also lead to postop HTN though, since you’d be blunting the normal baroR response to HTN)
32
Q

What is cerebral hyperperfusion syndrome?

A
  • when previously hypoperfused areas of brain that have lost ability to autoregulate flow are then exposed to high SBPs w/restoration of blood flow (like after CEA)
    -s/s: H/A, seizure, focal neuro signs, brain edema, possibly intracerebral hemorrhage
33
Q

How would you describe a wake-up test to a patient?

A

Sometime during the case, I would whisper their name into their eat and ask them to wiggle fingers/toes. Probably won’t remember this, but if so would be very sleepy, not in pain, and go back to sleep right after

34
Q

How would the monitoring of EMG help in a scoliosis repair surgery? Talk through how it works

A
35
Q

Bunch of organ systems and considerations you’d want to consider in a pt who had cervical spinal cord injury 6 mo ago?

A
  • eval airway and ROM given injury
  • inc risk of aspiration (high spinal cord lesion –> GI paralysis)
  • autonomic hyperreflexia
  • cardiac conduction abnlties
  • pulm dysfxn (impaired diaphragm fxn 2/2 denervation of phrenic) and chronic pulm infx
  • altered thermoregulation
  • other bone fxs (osteoporosis 2/2 immobility)
  • DVTs and PEs and ulcers 2/2 immobility
  • would get cervical films, EKG, CXR, PFTs, BUN/Cr, ABG, H/H, lytes
36
Q

Can you do a MAC for a pt w/C-spine injury and no feeling in legs getting LE surgery?

A

Not really - need at least spinal/regional/GA still because of risk of autonomic hyperreflexia (spinal also suppresses the unmodulated reflex sympathetic stim)

Also higher risk for aspiration too

37
Q

Risks of utilizing MEPs in spine case?

A
  • scalp burns
  • bite injury
  • seizures
  • cardiac arrhythmias
  • cost
  • also shouldn’t be used in: pts w/cochlear implants, active seizures, or vascular clips in the brain
38
Q

Which part of the spinal cord is most vulnerable to ischemic injury?

A
  • anterior d/t limited blood supply from ant spinal artery (which arises from vertebral and augmented by flow from radicular arteries)
  • ant spinal artery supplies ant 2/3 of spinal cord. Artery of Adamkiewicz (one of the radicular arteries arising from the aorta) supplies majority to the ant, lower 2/3 of the spinal cord
  • https://www.youtube.com/watch?v=etfTHQjU2-Y (great video, could even skip to 17:00 if need fast review. Called Spinal Cord Blood SUpply by Sam Webster)
39
Q

What is the Hunt and Hess classification? Describe the 5 grades

A
  • Used to grade severity of non-traumatic subarachnoid hemorrhage
    0: unruptured aneurysm. 1-5 are ruptured
    1: asxs, minimal H/A, slight nuchal rigidity
    2: mod-severe H/A, nuchal rigidity, CN palsy
    3: drowsy, confused, focal deficit
    4: stupor, hemiparesis
    5: deep coma, moribound, decerebrate rigidity
40
Q

What cardiac sign occurs in the presence of subarachnoid hemorrhage?

A

ST depression (so if see this during aneurysm clipping case, look and ask surgeon if rupture has occurred) - has not been shown to inc M&M (weird haha)

41
Q

What to do if cerebral aneurysm ruptured intraop?

A

If bleeding not excessive:
- surgeon should apply permanent/temporary clips
- correct conditions contributing to cerebral ischemia (hyperthermia, hyperglycemia, hypoxemia)
- induce mild hypoTN to facilitate surgical repair

If massive hemorrhage:
- compress carotids
-aggressively resuscitate
- avoid deliberate hypoTN
- CBP or cardiac circ arrest (I think w/adenosine - usually 5-10mg doses, up to 30mg total?)

42
Q

Things to be concerned about if patient s/p aneurysm clipping (intraop rupture) suddenly less responsive to stimuli postop day 1-2?

A
  • vasospasm (#1 cause of M&M a/w/cerebral aneurysms)
  • delayed cerebral ischemia
  • cerebral edema
  • hematoma formation (highest risk in first 12 hrs post-aneurysm rupture)
  • pneumocephalus, hydrocephalus, seizure, lyte abnltly
43
Q

What to do if c/f cerebral vasospasm in ICU?

A
  • all of the normal stuff, optimize everything
  • urgent neuro consult
  • nimodipine
  • consider anticonvulsant
  • consider transcranial doppler of angiography to ID any cerebral vasospasm
44
Q

Steps to tx cerebral vasospasm?

A
  • inc MAP to 20-30 above baseline
  • hemodilute (dec viscosity) by administering fluids
  • used to be the “triple H” therapy (HTN, hypervol, hemodilution) but now they don’t really want hypervol d/t inc risk of cerebral edema, inc ICP, pulm edema
  • discuss w/surgeons either 1) transluminal angioplasty, or 2) intra arterial vasodilator tx (verapamil, nicardipine, nimodipine)
45
Q

Emergent crani…any premeds?

A
  • reglan and H2 blocker
  • given worsening AMS and inc ICP, avoid any CNS depressants bc could confound ability to assess further mental status changes AND can lead to further hypovent, hypercapnia –> further inc ICP
  • can give corticosteroid to dec ICP and/or dec CSF production though
46
Q
A

UBP Pearls (9 decks)

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