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Anesthesia Pharm (Spring '24) - B > Lecture 18 (Exam 4) - Local Anesthetics Pt. 3 (Toxicities) > Flashcards

Lecture 18 (Exam 4) - Local Anesthetics Pt. 3 (Toxicities) Flashcards

1
Q

Neural Tissue Toxicity a.k.a Neurotoxicity with LA use.

This can either be transient or _______.

List the three neurotox categories LA use can cause.

A

permanent 😔

  1. Transient Neurological Symptoms (TNS)
  2. Cauda Equina Syndrome (CES)
  3. Anterior Spinal Artery Syndrome

Slide 21

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2
Q

Transient Neurological Symptoms (TNS)

How do these symptoms manifest? and within what time frame?

A

Moderate to severe pain within 6-36 hours post an uneventful single-shot SAB (spinal anesthesia block) in the back, buttocks & posterior thighs…

Slide 22

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3
Q

Transient Neurological Symptoms (TNS)

What is the cause(s), aside from your LA?
Which LA is the main culprit?

What is the treatment?

A

Cause: unknown; could be positioning or vasoconstrictor use. (impedes blood flow)
Most commonly seen with Lidocaine

Treat: trigger point injections and NSAIDs - can last from 1-7 days 🥲

Slide 22

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4
Q

Cauda Equina Syndrome (CES)

What are the manifestations?
What are things that could be associated with CES?

A

This is a diffuse injury in the lumbosacral plexus - you may see bowel and bladder sphincter dysfunction and/or PARAPLEGIA.

Associated with a possible lumbar disc herniation, prolapse or sequestration of the bladder with urinary retention.

Slide 23

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5
Q

What are some causes of CES (cauda equina syndrome) post LA?

A

Causes: unknown but speculated to be from continuous Lidocaine use or the needle (usually 25 gauge)

Seems like there is a lot we don’t know…😅

Slide 23

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6
Q

True or False:
Allergic reactions to local anesthetics are rare and occur < 1% of the time.

A

True
Slide 6

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7
Q

What symptoms attributed to excess plasma levels of local anesthetics were mentioned by Dr. Castillo?

A

Metallic Taste
Ringing Ears
Seizures
Cardiac Arrest
Slide 6

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8
Q

What preservative in both esters and amides are related to allergic reactions?

A

Methylparaben
Slide 6

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9
Q

Esters have a higher incidence of allergic reactions due to what component?

A

PABA
Slide 6

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10
Q

True or False:
There is no cross sensitivity between esters and amides

A

True
Slide 6

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11
Q

Anaphylaxis related to local anesthetic administration is mediated by ______

A

IgE
Slide 6

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12
Q

The acronym LAST stands for what?

A

Local Anesthetic Systemic Toxicity
Slide 7

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13
Q

Systemic toxicity is primarily due to excess __________ concentration of the drug.

A

Plasma
Slide 7

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14
Q

Besides direct IV injection, what are other factors that can lead to systemic toxicity?

A

Patient Co-Morbidities
Medications
Location and technique of block
Local anesthetic used
Dose

Slide 7

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15
Q
  1. What is the standard of care for treating systemic toxicity of local anesthetics?
  2. What is the MOA of the treatment?
A
  1. Intralipid ~ Lipid Emulsion!
  2. MOA: creates lipid compartment where it encapsulates the drug! Also, the emulsion provides fat for myocardial metabolism! Yum!

(Slide 16)

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16
Q

When doing a lipid rescue, you do a bolus and then an infusion. What are the dosages of the bolus and infusion?

A

Bolus: 1.5 mL/kg of 20% lipid emulsion (Up to 2 boluses)
Then Infusion: 0.25 mL/kg/minute for at least 10 minutes

1st 30 minutes: 3.8 mL/kg (1.2 to 6 mL/kg) MAX

(Slide 16)

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17
Q
  1. Why do we want to give epinephrine when doing a lipid rescue?
  2. What is the dose?
  3. What happens if the patient does not respond to our interventions?
A
  1. We will give epinephrine during a lipid rescue because more than likely they are trying to go see Jesus and you will be running the code.
  2. Epinephrine dose: 10 to 100 µg (with cardiac arrest)
  3. No response: Cardiopulmonary Bypass (CPB)

(Slide 16)

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18
Q

If your patient codes because of a LA toxicity, would you ever stop the code?

A

You keep going until they have received all the lipids and hopefully they recover.

(Slide 17)

19
Q

What are the management recommendations for local anesthetic systemic toxicity provided by the American Society of Regional Anesthesia and Pain Medicine ?

A

(Slide 18)

20
Q

What is the Local Anesthetic Systemic Toxicity algorithm Castillo wants us to know?

A

(Slide 19)

21
Q
A
22
Q

What is the MOA in Cocaine toxicity?

A

Caused by SNS stimulation by blocking presynaptic uptake of NE and dopamine- which in return increased postsynaptic levels.

(slide 27)

23
Q

What are the adverse effects of Cocaine toxicity and how long can they last?

A

CV: HTN, tachycardia, coronary vasospasm, MI (infarction & ischemia), ventricular dysrhythmias (including Vfib).
Parturient: decreased UBF (uterine blood flow)- which can lead to fetal hypoxemia
Hyperpyrexia (fever)- can lead to seizures

6 weeks

(slide 27)

24
Q

What are symptoms of anterior spinal artery syndrome?

A

For whatever reason the anterior spinal artery did not get enough perfusion, which means the spinal cord did not receive enough blood flow and now we got issues.

Issues we might see is lower extremity paresis with a variable sensory deficit.

Paresis = muscle weakness, partial paralysis.
(Slide 24)

25
Q

What are some causes for anterior spinal artery syndrome?

A

Thrombosis, artery spasm, hypotension, vasoconstrictive drugs, PVD, epidural abscess or hematoma.
(Slide 24)

26
Q

What is methemoglobinemia?

A

This is a life-threatening condition in which methemoglobin levels are greater than 15%. This causes a decrease in O2 carrying capacity in the blood. (Slide 25)

27
Q

Which local anesthetics are likely to cause methemoglobinemia?

A

Prilocaine and benzocaine will more likely cause this.

Lidocaine, nitroglycerin, phenytoin, and sulfonamides can also cause methemoglobinemia but not as much as prilocaine or benzocaine could. (Slide 25)

28
Q

What is the treatment for methemoglobinemia? How long will it take for methemoglobin to change back to regular hemoglobin?

A

Trt: methylene blue 1mg/kg over 5 min, max of 7 - 8 mg/kg. This drug can take 20 - 60 min for it to convert methemoglobin to hemoglobin. (Slide 25)

29
Q

Lidocaine will do what to your ventilatory response to hypoxemia?

A

Lido will decrease ventilatory response to hypoxemia.

Watch out for those COPDers or CO2 retainers, as they are more affected by this. (Slide 26)

30
Q

Hepatotoxicity can occur with what epidural local anesthetic?

A

Epidural bupivacaine (gtt or intermittent) can cause hepatoxicity, especially when used for trt of postherpetic neuralgia.

Stop the gtt to get your liver back to normal.
(Slide 26)

31
Q

Name the 3 main goals of Systemic Toxicity Treatment:

A
  1. Prompt airway management
  2. Circulatory support
  3. Removal of LA from receptor sites

(slide 13)

32
Q

What should you do in the event of CNS toxicity secondary to systemic toxicity of LA’s?

(2 respiratory interventions, 2 meds, and 1 additive med)

A

100% O2 via NRB or closed circuit
- this inhibits hypoxemia and metabolic acidosis

hyperventilation

barbiturates

Benzodiazepines

Epinephrine as an additive

(slide 14)

33
Q

You start your shift being told that you are responsible for relieving Arthur the hasty CRNA. F**k. You enter the OR and get report from Arthur. Arthur says “don’t know why this pt is wildin’. I gave her a Wombo block and now she’s seizing. Good luck brah”

The pt is indeed seizing and Arthur vanishes from the OR. What are your 1 intervention and 4 meds that you do?

A
  1. Supplemental O2
  2. Benzo (midazolam or diazepam)
  3. Propofol (if hemodynamically stable)
  4. Muscle relaxant (Succ’s or NDMA)
  5. intralipid: lipid emulsion

(slide 15)

34
Q

What kind of side effects do you see with lidocaine at 5mcg/ml?

A

Circumoral numbness but no CV effects.
Slide 10

35
Q

What cardiac side effects do you expect to see with high plasma concentration of lidocaine?

A

Slow conduction of cardiac impulse →prolonged PR interval and QRS widening due to cardiac Na channels blockade.
Slide 10
(automaticity is depressed)

36
Q

Accidental IV Bupivacaine could cause:

A

Precipitous hypotension, AV block, and cardiac dysrhythmias (SVTs, ST- T wave changes, PVCs, widening of QRS, V-tach)

Slide 10
( they can go to asystole)

37
Q

What are predisposing factors for LA systemic toxicity on cardiovascular system effects?

A
  1. Pregnancy → ↓ plasma esterases and ↓ circulating plasma proteins
  2. Arterial hypoxemia, acidosis, or hypercarbia (shown in animals)
  3. Beta blockers, Digitalis preparations, Ca+ channel blockers → These drugs inhibit myocardial impulse propagation and affect inotropy. This effect is aggravated when LA becomes systemic or toxic.
  4. Epinephrine and Phenylephrine –> Epinephrine and phenylephrine may increase bupivacaine cardiotoxicity, reflecting bupivacaine-induced inhibition of catecholamine stimulated production of cAMP. (from the book)
    Slide 11
38
Q

Among Bupivacaine, Ropivacaine, and Lidocaine, which one has the highest cardiovascular system effect and which one has the least?

A

Bupivacaine > Ropivacaine > Lidocaine
Slide 11

39
Q

What two factors predispose our OB population to local anesthetic toxicity? (select two correct answers)
A. Decrease plasma esterases
B. Decrease plasma proteins
C. Increased plasma esterases
D. Increased plasma proteins

A

A and B

40
Q

From highest to lowest concentrations, list the routes of local anesthetic administration.

A

Intravenous
Tracheal
Caudal
Paracervical
Epidural
Brachial
Sciatic
Subcutaneous

Slide 8

41
Q

Magnitude of systemic absorption of LA depends on

A

Dose
Vascularity of site
Epinephrine use
Physiochemical properties

Slide 8

42
Q

What are the CNS effects/considerations with LA systemic toxicity?

A

Drowsiness, facial twitch prior to seizure.

Monitor plasma levels with epidural lidocaine > 900mg’s

Hyperkalemia promotes seizures with LA’s (Lower seizure threshold)

Slide 9

43
Q

In the US in 2010 how many people suffered from Cocaine Toxicity?

A

1.5 Million

(slide 27)

Anesthesia Pharm (Spring '24) - B (20 decks)

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