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Neuro Flashcards

1
Q

What is the dibucaine #

A

Dibucaine inhibits normal psuedocholinesterase enzyme to far greater extent that variant.

Homozygous normal by 80%

heterzygous by 40-60% 1/500

homozygous abnormal 20% 1/3000 4-8 hrs (anticholinerstase not proven reliable, and FFP transfusion for endogenous pseudocholinesterase not recommended)

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2
Q

reasons for fade w TOF

A
  1. nondepolarizing blockade
  2. Phase 2 blockade from depolarizing agent (excessive dose, infusion, abnormal metabolism).

3, abnormla metabolsim: 90% of dose is metabolismed before reaching NMJ, with atypical psuedo a larger dose makes it to NMJ resulting in phase 2 block

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3
Q

Causes of POVL

A

corneal abrasion: exacerbated by blinking, sensation foreign body, tearing, photophobia

Glycine toxicity: dilated nonreactive pupils, elevated glyceine levels

Acute glycoma: severe periorbital pain, dilated pupil

cortical blindess: inability to follow moving objects w head stationary, normal pupillary response, absent response to visual threat

hemorrhagic retinopathy:floaters, preretinal hemorrhages, retinal edema

retinal ischemia: edematous retina, painless visual loss;

  • central: cherry red macula, imapired light reflex
  • branch: impaired light reflex

ION:painless, ischemia of optic disk

  • anterior: optic disk edema/hemorrhage
  • posterior: normal disk initially

petroleum based oitment, laser injury

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4
Q

CI to ECT

A

intracranial mass lesions

vascular malformations

increased ICP from any cause

recent stoke <1 month

recent MI (<3 months)

Pheo

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5
Q

physioloic effects of ECT

A
  1. parasym discharge –>bradycardia, airway secretions, hypotensions (10-15 seconds
  2. sym discharge–>tachycardia, HTN, arrythmia for 2-10 min

sym sympathetic activation associated with increased cerebral blood flow, increased ICP, and cerebral oxygen consumption

IOP and intragastric presssure may also increase

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6
Q

Drugs that change seizure duration

A

Increased Duration: Etomidate

No Effect: Methohexital, ketamine, remifentanil, alfentanil

Shortened Duration: Propofol, midazolam, lorazepam, thiopental, lidocaine

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7
Q

Pros and Cons of induction drugs for ECT

optimal seziure duration

A

30sec

Methohexital – gold standard for ECT, no change of seizure duration(vs prop), blunt sympathetic surg (vs etomidate)

Propofol: decrease seizure duration but blunt hemodynamic response.

Opioids are useful in the fact that they allow a lower dose of the anesthestic agent to be used, thus allowing faster wakeup and if using propofol or thiopental it will decrease the amount so the dose related decrease will help lengthen the seizure (

Hyperventilation (hypocarbia) will lengthen seizure duration and thus effectiveness of ECT.

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8
Q

How would you treat post ictal agitation?

post ECT myalgia

A

benzo, prop, precedex

NSAIDs-ketorlac

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9
Q

DDx for delayed emergence

A
  • ABCs: hypoxia, hypercarbia, hypotensions
  • Drugs: opioids, paralysis, benzos
  • Metabolic: hypoglycemia, hyponatremia, hypermagnesium (OB), hyperosmolarity
  • Neurologic: stroke (embolic, thrombotic, ischemic), postictal, ongoing ischemia (ICP, vasospasm, herniation) hematoma, edema tension pneumocephalus, hydrocephalus
  • other: hypothermia
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10
Q

rxn between intravitreal air and N20

A

increase intraocular pressure, central retinal artery occlusion, retinal/optic nerve ischemia

air-reabsorbed in 5 days

sulfur hexafluroride-10 days

perfluropropane- 30 days

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11
Q

emergence delerium

tx, prevention

RF

A

tx

  • Secure arms to prevent pulling tubes or IV
  • Attempt to reassure
  • Create quiet stress free environment
  • Consider sedative dose: prop, ketamine, opioid, dexmedetomidine
  • Evaluate for other causes of agitation: pain, hypoxic hypercarbia, hypoglycemia, bladder distention
  • Prevent: can not be reliably prevented
    • Reduce preop anxiety
    • Pain control
    • Recover in a calm environement
    • Admin preop midaz (unclear), precedex
  • RF
    • Preop anxiety, patients underlying temperament
    • Young age 1-5
    • Type surgery: abdominal breast, prolonged duration
    • Post op pain
    • Less soluble anesthetic des and sevo
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12
Q

sx PDPH

A

neuro: frontal-occipital H/A, positional, neck stiffness, seizures, CN stretch (6th nerve impaired eye abduction)
eyes: photophobia, blurred vision,
ears: tinnitis, hearing loss

GI: N/V

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13
Q

How to treat extrapyramidal symptoms

types EPS

A

imbalance between cholinergic and dopamine activity

benztropine, diphenhydramine

dyskinesias (repetitive movements-eye blinking), akathesia (internal/external restlessness

dystonia (very strong muscle contactions that result in twisting of body)

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14
Q

Prolonged non depolarizing muscle blockade.

When to reverse? Why not admin additional reversal

resistance

A

abx: aminoglycosides (gent), tetracylins, polymixins

Volatile (Des>sevo>iso) CCB, LA

hypernatremia, hypokalemia, hypoca/CCB, hyper mag, metabolic and resp acidosis,

lithium, phenytoin (acute use)

liver/ renal impairement/hypothermia

  • reverse when 25% recovery of Neuromuscular fxn, as indicated by appearance of 4th twitch of TOF
  • ceiling effect to reversal, additional drug does not provide more antagonism and may potentiate nondepolarizing blockade
  • carbamexapine, phenytoin (chronic), steriods,burns, increased Vd (liver pregnacy, CHF, RF)
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15
Q

Use of EEG in neuro case uses (3)

waves

A

good for monitoring for (burst suppression, controlled hypotension, gauging anesthetic depth

beta (increased freq, decreased amplitude) >13hz

alpha (decreased freq) 8-13

delta (sleep)-4hz

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16
Q

why no nitrous in neuro case

A

increases CMRO2

VAE/pneumocephalus

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17
Q

Consideration HTN and neuro

A

R shift of cerebral autoregulation curve

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18
Q

What is burst suppression, what does it mean

A
  • Indicates near maximally depressed CMR02 while providing predictability of recovery/awakening when anesthetic turned off

Identified as periods of no activity punctuated by brief periods with high voltage bursts

19
Q

What monitors are available for neurological monitoring during CEA

A
  1. stump pressure: needle in artery above clamp to measure backpressure related to collateral flow from circle of willis. used to select pts for shunting; <50mmHg associated w hypoperfusion
    - The problem with this is that an adquate pressure doesn’t assure perfusion to all regions of the brain.
  2. EEG: spontaneous electrical activity of cortical surface cells (electrophysiologic 60% of cerebral metabolic demand). does not measure deeper structures. EEG deterioration begins around 15-20ml/min/100gm, and manifests as frequency slowing or amplitude attenuation (normal 50, 20 ischemia, 10 death)
  3. SSEP: measures response of sensory cortex to electrical impulse from peripheral stimulation (supplied by MCA). sees cortext and deeper structures
  4. TCD: monitors mean flow velocity of MCA and detection of micoembolic events/hyperperfusion
  5. cerebral oximetry: measures regional frontal blood saturation. misses parietal where more ishcemia tends to occur
  6. awake exam: better hemodynamic stability, most sensitive for detecting cerebal ischemia,
    - cooperation, anxious pt increase sympathetic response

***None of these have been shown to improve outcome since postoperative emboli and not intraoperative hypoperfusion are most likely cause of periop stroke, but do aid in decision to shunt and BP maintenance.***

20
Q

Why do surgeons care about SBP during CEA

A

collateral perfusion drived by SBP

21
Q

Why it important to maintain normocarbia during CEA

A
  • increased PaC02 can lead to cerebal vasodilation in normal rective nonichemic vacular beds diverting flow away from hypoperfused areas of brain where vasculature is maximally dilated (Steal)
  • hypocarbia can exacerbate cerebal ischemia 2/2 vasoconstriction and L shift of oxy Hemoglobin curve
22
Q

EEG shows slowing durig CEA what should you do

A
  • alert surgeon, ask to shunt
  • assure adeuwate MAP, sat, hct, normocarbia
  • consider raising SBP: could result in myocardial ischemia 2/2 increased afterload
23
Q

What is cerebal hyperperfusion syndrome

A
  • following removal of carotid stenosis-hyppoperfused area of brain that have lost ability to autoregulate are exposed to high SBP

H/A, AMS, seizure, focal neuro defict, intracranial hemorrhage

24
Q

causes of hyponatremia and tx

why should delay case w sodium under 130

dilutional hyponatremia

A

SIADH: euvolemic, elevated urinary sodium, elevated ADH levels, raren urine sodium >100

tx water restriction, diuresis demeclocycline, NA Replacement

CSW: hypovolemic, urine sodium >100 (release of naturetic peptide from brain)

tx:both volume repletion and sodium administration

loopdiuretics

place pt at risk of cerebral edema

25
Q

management of ICP

A
  1. Eval ABCs and etiology: avoid hypoxia and hypercarbia
  2. Increase venous drainage
    • elevate head 15-20 degrees if hemodynamically
    • ensure no venous obstruction (esp if C collar in place)
  3. diuretics
    • admin mannitol: (reduces ICP by osmotically shifting fluid from brain to intravascular space, decrease production CSF, induce reflex cerebral vasoconstriction 2/2 decreasing blood viscosity(lasts 6 hr)
      • risktransient increase intravascular volume can increase BP & decrease ICP (increase transmural pressure): hazard to unrupture aneurysm, AVM, expanding hematoma (mod elevated ICP can serve to tamponade the lesions
      • elderly: rapid diuresis shrink brain and tear bridging veinssubdural hematoma
      • increase vascular volume poorly tolerated by HF
      • cerebal edema if BBB not intact
    • furosemide
      • keep in mind that in presence of hypovolemia this an lead to hypotension and worsen cerebral ischemia
    • hypertonic saline
  4. admin barbiturate/propofol (reduced ICP 2/2 cerebral vasoconstriction) and CMR02
    • risk of hypotension when admin large doses for cerebral protection
  5. hyperventilation to PaC02 25-30 if other methods unsuccessful and ICP elevation was so severe that there was risk of brain stem herniation
    • too much cerebral vasoconstriction can leadto cerebral injury
    • effects temporary (6-12 hrs) since Hc02 levels in CSF are adjusted for the change in PaC02
    • between Pac02 20-80 CBF changes 1ml/100g per 1mmHg change PaC02
  6. If ICP severe requires immediate tx: intraventricular drainremove CSF (no more than 5cc/min).
    • Too much can cause brainstem herniationHTN/hypotension/bradycardia/tacycardia
    • if lumbar catheter can cause herniation if obstructive hydrocephalus (obstruction proximal to superior sagittal sinus
  7. steroids if brain tumor for vasogenic edema, decrease CSF production?
  8. if at risk for seizures implement seizure ppx to avoid increases CMR02
26
Q

ventric drain falls on floor. concerns?

what is slit ventricle syndrome

A

ventricular collapse

ruptured cortical veins

excessive CSF shunting occurs w brain growth leading to irreverisbly collapsed ventricles (brain grows to fill empty ventricle). noncompliant venticle place pt at increased risk for herniation due to inability to compensate for changes in intracranial volume (avoid agents that can cause cerebral edema)

27
Q

features of MD

A

Anesthesia: rhabdo to succ/volatiles, sensitive to resp depressants

cards: EKG ab (tachycardia, tall R waves in V1, Q waves in limb leads, inverted T waves), cardiomyopathy, arrthymias, MR
resp: ineffective cough/dimished airway refexes (aspiration, infections), macroglossia,

GI; delayed gastric emptying

28
Q

where is precordial dopper placed

A

R sternum between 2 and 4th rib

29
Q

risks of wake up test

A

awareness/pain

extubated, dislodgement of lines/surgical equiptment

air embolism w vigorious inhalation

30
Q

change in neuromonitoring signals what to do

A
  • alert surgeon
  • ensure not change in dept of anesthesia (prop, volatile, relaxant)
  • correct hypoxia, ensure normocarbia, correct hypovolemia, hypotension, anemia, to optimize oxygen delivery
  • surgical causes- excessive distration
  • perform wake up test
31
Q

Features of MG

A
  • Pathophysiology: destruction nicotinic acetylcholine R at post synaptic memebrane
  • Sx:
    • bulbar weakness (diplopia, ptosis, difficulty with speech and swallow, dyspnea), muscle weakness with exertion, thyoma
    • cardiac:HTN, AV block, a fib, myocarditis, cardiomyopathy, dystolic dysfunction
    • endocrine: hyperthyroid, RA, pernicious anemia, SLE, thyoma
    • neonate weakness 2-4 weeks
32
Q

MG anesthetic considerations

A
  • Consider avoiding anticholinergic drugs increased weakness
  • Resistant to succ (2mg/kg), sensitive nondepolarizing agents (reduce by ½ or 1/3)
  • pridostagmine: may prolong succ, may have unsuccesful reversal of NDMB 2/2 acteylcholestase max inhibited
  • Increased vagal reflexes
  • Emergent cases IVIG, plasma exchange
  • Succ and mivacurium may last longer in setting of pyridostigamine
  • MG exacerbation vs cholinergic crisis (recent dose pyridostigamine or reversal of NDMB
    • Edrophonium test (tensilon test)- improve strength with MG worsen with cholinergic crisis
    • Watch for signs cholinergic crisis: AMS, weakness, bradycardia, broncorhea, salivation, N/V/D/urinary freq
      • Intubate, discontinue anticholinesterase, admin anti muscarinic (atropine)
33
Q

what is GCS

scoring

A
  • Scoring system based on eye opening, motor response, and verbal response that has strong correlation with severity of head injury and patient outcome.
  • Severe 8 or less, mortality 35%
  • Moderate 9-12, mild 13-15
34
Q

how to clear c spine

A
  1. No cervical tenderness/pain
  2. No paresthesia or neuro deficit
  3. Normal mental status
  4. No distracting pain
  5. Age >4
  6. If not obtained need lateral C spine, odontoid view, anterior posterior from C1-T1, when stable enough CT cervical spine for ligamentous injury
35
Q

increased BP in a trauma pt

A

pain, increasing ICP

hypoxia, hypercarbia

hypovolemia, anemia

36
Q

ideal CPP

ICP

A

50-70

in head injurty 60-70

ICP <15

37
Q

concern with acute cervical cord injury

A

neuro: worsening spinal cord injury, hypothermic
cards: hypotension-spinal shock vasodilation, knock out cardioaccelerator fibers
pulm: respiratory inpairment 2/2 diaphagmatic impairemrnt, aspiration risk (impaired airway reflexes), difficult airway w manual in line
heme: DVT, PE (venous stasis)

38
Q

complications after anesursm rupture

A
  1. Vasospasm: TCD or angiography (more specific and shows extent and severity of vasospasm)
  2. Rebleed- monitor BP
  3. Hydrocephalus- ventric drain
  4. Seizure-anti seizure meds
  5. Increasing cererbral edema
  6. CSW, SIADH
39
Q

features of spinal shhock

A

flaccid paralysis, loss sensation, spinal reflexes,

sympathetic vasomotor tone, temp regulation below level of injury, paralytic ileus,

40
Q

How to evaluate ICP

A
  • AMS H/A,, visual changes, papillaedema, ataxia, focal deficits, cushing triad (HTN, bradycardia, change resp pattern), N/V
  • CT/MRI: small/slit like ventricles/>0.5mm midline shift
  • If ICP monitor measure it directly (intraventricular catheter is gold standard)- ICP measurement, CSF drainage but risks damage to brain, bleeding/infection.
41
Q

Point of hunt and hess score

A
  • Utility HUNT HESS Score: correlates with M&M
    • 0 unrupttured
    • 1-5 ruptured
      • 1: slight H/A and nunchal rigidity
      • 2: severe H/A nuchal rigidity + neuro deficits limited to cranial nerve palsy
      • 3: drowsy/confused, mild focal deficits
      • 4: stupor, hemiparesis
      • 5: coma, decrerebrate rigidity
42
Q

What is HHH, whats the theory, SE

A
  • Hypervolemia, HTN, hemodilution-improve delivery of blood to ischemia areas with impaired autoregulation by increase perfusion pressure and decreasing viscosity
  • Risks: cerebral edema, increase ICP, pulm edema,
43
Q

Issues w lumbar Subarachnoid cathter to drain CSF to decrease ICP

A

pressure measurements less reliable

posterior fossa tumor at increased risk of noncommuncating hydrocephalus (obstruction of CSF outflow)

AW (15 decks)

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