Exam 1 Spinal & Epidural Neuraxial Anesthesia [06/03/24] Flashcards

1
Q

What is the effect of neuraxial anesthesia on the pulmonary system?

A
  • Usually minimal impact
  • Even with high (T4) thoracic level dermatome spread of local anesthetic: Tidal volume, RR, inspiratory reserve volume, or ABG unchanged.
  • ERV decreased
  • Small decreases in vital capacity (Loss of abdominal muscle contribution in forced expiration)
  • High thoracic blockade can result in the blockade of accessory muscles of respiration (intercostal and abdominal muscles)

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2
Q

What are special considerations for neuraxial anesthesia for the pulmonary system?

A
  • Use caution in COPD, Pickwickian syndrome
  • Feelings of dyspnea in normal population (extremely common); very troublesome.
  • This is due to the loss of sensory feedback from the chest area
  • Lose ability take big breaths and strong cough

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image from the internet
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3
Q

What causes apnea in regards to neuraxial anesthesia?

A
  • Apnea is typically due to reduced blood flow to the brainstem, affecting the brain’s breathing centers.
  • High concentrations of local anesthetics in the spinal fluid rarely cause nerve paralysis that stops breathing.

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4
Q

Flow volume loops graph

A

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5
Q

What are the componets of vital capacity?

A
  • VT
  • IRV
  • ERV

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6
Q

Phrenic nerve orginates from what levels of the spine?

A
  • C3, C4, C5

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7
Q

For the GI system, parasympathetic innervation is primarily via what? Sympathetic innervation?

A
  • Parasympathetic innervation is via the vagus nerve (originates medulla)
  • Sympathetic innervation of GI tract stems from T5-L2

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8
Q

What is the function of parasympathetic afferent and parasympathetic efferent?

A
  • Parasympathetic AFFERENT: transmits sensations of satiety, distension, and nausea
  • Parasympathetic EFFERENT: tonic contractions, sphincter relaxation, peristalsis, and secretion.

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9
Q

What is the function of sympathetic afferent and sympathetic efferent for the GI system?

A
  • Sympathetic AFFERENT: transmit visceral pain
  • Sympathetic EFFERENT: inhibit peristalsis and gastric secretion and cause sphincter contraction and vasoconstriction

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10
Q

Sympathetic innervation of GI tract stems from

A
  • T5-L2

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11
Q

What is the Impact of Neuraxial Anesthesia on GI system?

A
  • Reduces Sympathetic Tone: Local anesthetics used in neuraxial blocks decrease the activity of sympathetic nerves.
  • Increases Parasympathetic Activity: With less sympathetic inhibition, the parasympathetic system becomes more dominant.
  • Resulting Changes in Unopposed Vagal Tone[this is parasympathetic]

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12
Q

The unopposed vagal tone on the GI system from neuraxial anesthesia results in?

A
  • Relaxes Sphincters
  • Increases Peristalsis
  • Small, contracted gut with active peristalsis
  • 20% incidence of N/V
  • Increased GI blood flow
  • Nausea and vomiting (20% of the patients)
  • Reduces postoperative incidence of ileus in abdominal surgery

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13
Q

20% of nausea related to central neuraxial is d/t unopposed effect. What is the cause of the other 80% of nausea?

A

The remaining 80% is from sympathethecomy due to reduced blood supply in the chemotaxis center resulting in nausea.

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14
Q

What are the genitourinary effects of Neuraxial Anesthesia.

A
  • No change in renal blood flow when MAP is maintained
  • Sympathetic blockade above T10 affects bladder control
  • Urinary sphincter tone relaxed

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15
Q

How does the addition of Neuraxial Opioids affects the GU system?

A

Addition of Neuraxial Opioids:
* Decrease in detrusor contraction
* Increase in bladder capacitance
* These changes lead to urinary retention/incontinence and need for foley catheter with neuraxial anesthesia

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16
Q

What are the metabolic/endocrine effects of Neuraxial Anesthesia.

A
  • Neuraxial blockade can partially suppress (major invasive surgery) or totally block (lower extremity) neuroendocrine response.
  • Maximal benefits occurs if the neuraxial blockade occurs before the surgical stimulus
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17
Q

The activation of somatic and visceral afferent fibers from pain, tissue trauma, and inflammation causes?

What does neuraxial anesthesia do?

A
  • Elevated cortisol, epinephrine, norepinephrine, vasopressin, activation of renin-angiotensin-aldosterone system.
  • neuraxial anesthesia reduces this which is good.

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18
Q

What are local anesthetics made of?

A
  1. Aromatic or beneze ring
  2. Intermediate chain
  3. Tertiary amine

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19
Q

What does the aromatic ring, intermediate chain, and tertiary amine group determine?

A
  1. Aromatic - lipophilic
  2. Intermediate - drug class, metabolism, allergic potential.
  3. Tertiary amine - hydrophilic, accepts protons.

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20
Q

What metabolizes esters?
What metabolizes amides?

A
  • Esteres: pseudocholinesterase
  • Amides: Hepatic P450

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21
Q

What LA is an exception to the metabolization rule?

A
  • Cocaine
  • even though its an ester, it is also metabolized by the liver.

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22
Q

Allergies with LA are seen with esters or amides? why?

A
  • More Common Allergy is with Esters
  • Produces para-aminobenzoic acid (PABA)
  • There’s cross-sensitivity in esters

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23
Q

Can you have an allergic reaction to amides?

A
  • Amide allergic reaction is rare
  • Contains preservative methylparaben, similar to PABA.

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24
Q

T/F: There is no cross sensitivity between esters and amides

A

True

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25
Onset of action of LA is relies on?
* relies on PKA * LA are all basic [most] * the closer the pK to physiologic pH [7.4], the faster the med goes to the cell. | S62
26
Potency of LA is related to?
* related to lipid solubility. * if staying in the lipophillic part of the muscles,the tissue, or in spine = stays in longer so potency is greater. | S62
27
Duration of action of LA is realted to?
* Protein binding [A1-acid glycoprotein] | S62
28
What is the sequence of how blockage of fibers occur when you put LA in central neuroaxial?
* LA inhibition of peripheral nerves occurs in the following order: 1st: B fibers 2nd: C fibers 3rd: Small diameter A fibers 4th: Large diameter A fibers | s62
29
Structure of amides vs esteres
| S62
30
List the esters and amides mentioned on the powerpoint.
| S62
31
T/F: Local anesthetic agents are weak bases, compounds with a pKa close to physiologic pH will have a faster onset of blockade as more molecules remain in the nonionized state.
True | S62
32
List the Factors Influencing Vascular Uptake and Plasma Concentration of Local Anesthetics
1. Site of Injection 1. Tissue Blood Flow 1. Physiochemical Properties 1. Metabolism 1. Addition of Vasoconstrictor: | S64 ## Footnote -if area is vasoconstriction, there is less absorption and there’s is more LA in the system.
33
List the uptake of LA based from high to low blood concentration
1. Intravenous 2. Tracheal 3. Intercostal 4. Caudal 5. Paracervicle 6. Epidural 7. Brachial 8. Sciatic 9. SubQ | S64 ## Footnote **I**f **T**here **I**s **C**hest **P**ain **E**pidurals **B**lock **S**ign/**S**ymptoms
34
What do you do if a bier block leaks?
* do not deflate the cuff * gives benzos for seizures if needed. * administeed lipid emulsion. | S64
35
What is baracity?
* Baricity refers to the density of a local anesthetic solution compared to the CSF. | S65
36
Isobaric
* Density Equal to CSF * An isobaric solution has a baricity of 1, meaning its density matches that of CSF. * Behavior: Tends to stay in place where it is injected. | S65
37
Hyperbaric
* Density Greater than CSF * A hyperbaric solution has a baricity greater than 1. * Behavior: Sinks within the CSF, moving downward from the point of injection. | S65
38
Hypobaric
* Density Less than CSF * A hypobaric solution has a baricity less than 1. * Behavior: Rises within the CSF, moving upward from the point of injection. | S65
39
Hyperbaric, isobaric, hypobaric LA solution chart
| S65
40
When giving hyperbaric solutions, and the pt is supine what happens?
* Baracity is related to spinals. * the LA will go to the lowest level which is trough. * the LA will go to the higherst level which is apex. * Trough: T6 and S2 * Apex: C3 and L3 | S66
41
# SAB pharmacology * A ____ amount of LA produces a profound block of nerve transmission * Spinal Cord uptake of LA occurs d/t ____ nature of the drug * Spread of LA occurs in a ____ and ____ direction from the site of injection ____
* small * lipid soluble * cephalad and caudad, simultaneously | S67
42
# SAB pharmacology What kind of metabolism occurs in the CSF? How are LA eliminated?
* NO metabolism occurs in the CSF * All LA are eliminated by reuptake [Vascular reabsorption via vessels in the pia mater] | S67
43
# SAB pharmacology Lipophillic drugs have ____ reuptake b/c they have ____ affinity for epidural fat
slow, high | S67
44
# SAB pharmacology ____ has a longer duration of action than lidocaine
Bupivicaine | S67
45
# SAB dosing Spinal Dose at T10 for the following medications: * Bupivicaine 0.5%-0.75% * Levobupivicaine 0.5% * Ropivacaine 0.5%-1% * 2-Chloroprocaine 3% * Tetracaine 0.5%-1%
* Bupivicaine 0.5%-0.75%: 10-15mg * Levobupivicaine 0.5%: 10-15mg * Ropivacaine 0.5%-1%: 12-18mg * 2-Chloroprocaine 3%: 30-40mg * Tetracaine 0.5%-1%: 6-10mg | S67
46
# SAB dosing Spinal Dose at T4 for the following medications: * Bupivicaine 0.5%-0.75% * Levobupivicaine 0.5% * Ropivacaine 0.5%-1% * 2-Chloroprocaine 3% * Tetracaine 0.5%-1%
* Bupivicaine 0.5%-0.75%: 12-20mg * Levobupivicaine 0.5%: 12-20mg * Ropivacaine 0.5%-1%: 18-25mg * 2-Chloroprocaine 3%: 40-60mg * Tetracaine 0.5%-1%: 12-16mg | S67
47
# SAB pharmacology Onset for the following spinal medications: * Bupivicaine 0.5%-0.75% * Levobupivicaine 0.5% * Ropivacaine 0.5%-1% * 2-Chloroprocaine 3% * Tetracaine 0.5%-1% * All are relatively how long???
* Bupivicaine 0.5%-0.75%: 4-8min * Levobupivicaine 0.5%: 4-8min * Ropivacaine 0.5%-1%: 3-8min * 2-Chloroprocaine 3%: 2-4min * Tetracaine 0.5%-1%: 3-5min * 5 min | S67
48
Duration of the following spinal medications: * Bupivicaine 0.5%-0.75% * Levobupivicaine 0.5% * Ropivacaine 0.5%-1% * 2-Chloroprocaine 3% * Tetracaine 0.5%-1%
* Bupivicaine 0.5%-0.75%: 130-220min * Levobupivicaine 0.5%: 140-230min * Ropivacaine 0.5%-1%: 80-210min * 2-Chloroprocaine 3%: 40-90min * Tetracaine 0.5%-1%: 90-120min | S67
49
What 2 medications can have epinephrine added to them for spinal blocks? how much longer does the block last with epi added?
* bupivicaine 0.5%-0.75% and tetracaine 0.5%-1% * duration increases by 20-50% for each | S67
50
Which LA medication is not given in spinals?
Lidocaine! | S67
51
For epidurals, the spread of LA is ____ and ____ from the catheter insertion site
cephalad and caudad | S68
52
How is incremental dosing helpful in epidurals? what does it avoid?
* it avoids: accidental "high spinal," hypotension from rapid autonomic blockade (cardiac arrest), & LA toxiity * **giving a little bit at a time avoids all of the above and ensures we dont give a whopping dose in the wrong place in addition!** | S68
53
How do we incrementally dose epidurals?
5mL at a time -if you calculate needing a 20mL dose, give 5mL at a time (not all 20mL at once) | S68
54
If epi is added to an epidural, it can be used as what?
an IV marker | S68
55
when is the onset of an epidural?
10-25min | S68
56
# Epidural Pharmacology In what concentration can we find 2-chloroprocaine? which concentration is best for surgical anesthesia?
comes in 2% and 3%, but 3% is used for surgical anesthesia | S69
57
# Epidural pharmacology Which LA is popular for OB anesthesia? is it an ester or amide?
2-Chloroprocaine, which is an ester LA | S69
58
# Epidural pharmacology While 2-chloroprocaine has a pka around 8.7 (which is farther from physioologic pH than some other drugs), it still has rapid onset! Why??
cocentration!! 3% makes its speed of onset very fast | S69
59
Does 2-Chloroprocaine have a short or long duration? why? how often will it need to be redosed?
duration is short lived b/c it is metabolized by plasma cholinesterase THEREFORE... we need to redose Q45min | S69
60
* How do we alkalanize LA solutions? * What 4 things does alkalinazation cause?
* Adding NaHCO3 of 1mEq/ml **4 factors** 1) increases pH of LA 2) increases concentration of nonionized free base 3) increases rate of diffusion of the drug 4) increases speed of onset of the block | S70
61
# Epidural pharmacology dosing ____ of LA is crucial for determining how ____ the anesthetic block reaches
Volume, high | S71
62
The initial dose of an epidural LA is typically ____mL/ ____ of the spine
1-2ml/segment | S71
63
What kind of dose is used to maintain epidural blocks without letting it wear off too much? how much is it? when should it be administered?
Top-up dose 50-75% of the initial dose Should be administered before the block decreases more than 2 dermatomes | S71
64
The space available in the epidural area varies. It is smaller in the ____ region than in the ____ so we have greater spread in the ____ meaning we need a ____ dose in the ____ region
thoracic lumbar thoracic smaller thoracic | S71
65
What determines the density/strength of block in an epidural? What is an easy example to remember this by?
Concentration walking epidural: uses low concentration that manages pain but allows some motor function (ideal for labor) | S71
66
List the LA epidural drugs in order from fast onset/short duration to slow onset/long duration with their concentrations
2-Chloroprocaine 3% lidocaine 2% ropivacaine 0.1-0.75% bupivacaine 0.0625-0.5% levobupivacaine 0.0625-0.5% | S71
67
List the duration for the following epidural LA: 2-Chloroprocaine 3% lidocaine 2% ropivacaine 0.1-0.75% bupivacaine 0.0625-0.5% levobupivacaine 0.0625-0.5%
30-90 min 60-120min 140-220min 160-220min 150-225min | S71
68
List the onset for the following epidural LA: 2-Chloroprocaine 3% lidocaine 2% ropivacaine 0.1-0.75% bupivacaine 0.0625-0.5% levobupivacaine 0.0625-0.5%
5-15min 10-20min 15-20min 15-20min 15-20min | S71
69
for epidural surgical anesthesia, which concentrations of the LA should be used?
the higher concentrations: 2-Chloroprocaine 3% lidocaine 2% ropivacaine 0.75% bupivacaine 0.5% levobupivacaine 0.5% | S71
70
What is the best choice LA drug for epidural? 2nd best if that's not available?
2-Chloroprocaine 3% lidocaine 2% | S71
71
neuraxial pharmacologic adjuncts provide ____ ____, extends ____, and improves ____ of the block
postoperative analgesia extends duration density | S72
72
Opioids, as an adjunct to neuraxial LA, help with ____ and ____, but do not ____ ____ of the block
analgesia and density of the block, but do not extend duration | S72
73
alpha 2 agonists (____ and ____), as adjuncts to LA, improves ____, ____, and ____
clonidine and precedex duration, density, and analgesia | S72
74
Vasopressors (____ and ____), as adjuncts to LA, extends ____, but has no effect on ____ or ____. ____, specifically, is a good IV marker epidurals: initial ____
phenylephrine and epinephrine duration, but no effect on density or analgesia epinephrine, bolusing | S72
75
what agents are currently be investigated as good adjuncts to LA in spinals and epidurals?
neostigmine, magnesium, ketamine, and versed | S72
76
neuraxial opioids have different Pk/PD realtionships when compared to ____, ____, or ____. We categorized neuraxial opioids into more ____ or ____.
IV, IM, or PO hydrophilic or lipophilic | S73
77
Which part of the SC is targeted by opioids?
substantia gelatinosa of the dorsal horn (Lamina 2) | S73
78
opioids, as a neuraxial adjunct: neurotransmission is reduced by decreased ____ and ____, and increased ____
cAMP and Ca++ conductance increased K+ conductance | S73
79
Opioids mixed with LA results what improvements to a block? Neuraxial opioids also ____ into ____ ____ and affects opioid receptors throughout the body, providing broader pain relief
stronger and more dense diffuses, general circulation | S73
80
# Neuraxial Opioids What are the hydrophilic opioids? Lipophilic?
morphine, hydromorphone, and meperidine fentanyl and sufentanil | S74
81
# Comparing neuraxial opioids Duration in CSF: hydrophilic v lipophilic
hydrophilic stays longer, lipophilic stays shorter | S74
82
# Comparing neuraxial opioids Spread in the CSF: hydrophilic v. lipophilic
hydrophilic: spreads widely affecting a larger area for pain relief (ROSTRAL spread) lipophilic: limited spread, less rostral spread | S74
83
# Comparing neuraxial opioids Onset hydrophilic v. lipophilic
hydrophilic takes longer to start working (30-60min) lipophilic starts working quickly (5-10min) | S74
84
# Comparing neuraxial opioids Duration of hydrophilic v lipophilic
hydrophilic: lasts longer 6-24hrs lipophilic: shorter effect 2-4hrs | S74
85
# Comparing neuraxial opioids Systemic absorption of hydrophilic v lipophilic
hydrophilic: less, hence it stays longer in the CSF lipophilic: absorbed more by the body | S74
86
# Comparing neuraxial opioids respiratory depression in hydrophilic vs lipophilic agents Which is better to use for a patient that is going to be going home same day?
hydrophilic: occurs later lipophilic: typically occurs only early after administration (therefore better to use for pts that will be going home) | S74
87
# Intrathecal and Epidural dosing of opioids List the IT, epidural and epidural infusiong doses for the following opioids sufentanil fentanyl hydromorphone meperidine morphine
sufentanil: 5-10mcg IT, 25-50mcg epidural, 10-20mcg/hr infusion fentanyl: 10-20mcg IT, 50-100mcg epidural, 25-100mcg/hr infusion hydromorphone: no IT, 0.5-1mg epidural, 0.1-0.2mg/hr meperidine: 10mg IT, 25-50mg epidural, 10-60mg/hr infusion morphine: 0.1-1mg/hr | S75
88
Intrathecal administration: Location? how fast does the drug move? What is the effectiveness?
location: directly into IT space drug movement: opioid quickly diffuses into the SC effectiveness: more direct and immediate effect on pain b/c it is closer to the nerve roots | S75
89
Epidural administration: Location? drug movement? dosing?
Location: Into the epidural space Drug Movement: The opioid diffuses through the fatty tissue of the epidural space. It then slowly crosses into the dural cuff and into the CSF to reach the spinal cord. Some of the drug also enters the bloodstream. Dosing: A higher dose is often required because only a portion of the drug reaches the target area in the spinal cord. | S75
90
In what instances might we use an epidural infusion?
OB or as an adjunct to GETA | S75
91
Which side effect of neuraxial adjuncts has a 30-100% incidence?
pruritis | S76
92
What is the treatment for pruritis r/t neuraxial adjuncts? (3 medications and dose)
Benadryl 25-50 mg IV Naloxone 0.1 mg IV (best) Buprenex (mixed agonist/antagonist) | S76
93
What can be used as prophylaxis for pruritis r/t neuraxial adjuncts? (3 doses)
Minimize the dose of morphine < 300 mcg Ondansetron 4 mg IV Nubain 2.5-5.0 mg IV | S76
94
When can respiratory depression happen with opioid use in neruaxial anesthesia?
can be delayed [morphine] or immediate first 24 hours [fentanyl/ sufentanil] | slide 77
95
what medication has a higher incidence of respiratory depression for neuraxial adjuncts? Why?
* Higher incidence with morphine (hydrophilic properties) * because Hydrophilic nature causes cephalad spread | slide 77
96
what monitoring equipment would you use if pt received intrathecal morphine?
**Apnea monitoring** * Capnography * Pulse oximetry * Alarms | slide 77
97
what is the medication and dose used for reversal of respiratory depression with opioids in neuraxial anesthesia?
nalaoxone 0.1-0.2 mg | slide 77
98
what are we worried about with repiratory depression with outpatient surgery?
legal implications | slide 77
99
* What dose of morphine in neuroaxail anesthesia has high insidence of nausea? * What dose is nauses almost absent?
* Morphine < 300 mcg * doses of < 100 [*50-75*] mcg almost absent. | slide 78
100
what medication when used in combination during neuraxial anesthesia has high incidence of nausea?
Fentanyl/Sufentanil + Morphine has a very high incidence | slide 78
101
What is the treatmeant for nausea r/t opioids used in spinals/epidurals?
* Ondansetron (5 HT antagonist) * Naloxone 0.1 mg * Phenergan 12.5- 25 mg IM | slide 78
102
what is the percent incidence of urinary retention when using opiods as a pharmacologic adjunct?
30-40% | slide 78
103
What are 2 alpha 2 agonists that can be used as neuraxail adjuncts?
Clonidine and Dexmedetomidine | slide 79
104
A2 agonist being used as adjuncts do what 2 things to the block?
Intensifies and prolongs the block | slide 79
105
A2 agonists prolong sensory and motor blockage by approximately how long?
1 hour | slide 79
106
what are common side effects of A2 agonist? [in neuraxial]
* hypotension * bradycardia * sedation | slide 79
107
what is the dose of dexmedetomidine when used as a neuraxial adjunct?
3 mcg | slide 79
108
what is the dose of clonidine when used as a neuraxial adjunct?
15-45 mcg | slide 79
109
what is the benefit of using a vasoconstrictor as a neuraxail adjunct?
Prolongs action of the LA by reducing blood flow | slide 80
110
Vasoconstrictor Neuraxail Adjunct: Epinephrine dose?
0.2- 03 mg "epi wash" | slide 80
111
Vasoconstrictor Neuraxail Adjunct: Phenylephrine Dose?
2-5 mg | slide 80
112
When using vasoconstrictors as a neraxial adjunct: * what is the effect when added with tetracaine? * What is the effect when added with bupivacain or lidocaine?
* When added with tetracaine - profound increase * With bupivacaine or lidocaine - variable increase | slide 80
113
Patients on anticoagulants should avoid neuraxial anesthesia due to the risk of epidural hematoma, whcich can cause what?
Can compress the spinal cord, leading to ischemia and permanent neurological damage. | slide 81
114
what are the symptoms of epidural hematomas?
* Lower extremity weakness, numbness. * Low back pain. * Bowel and bladder dysfunction. | slide 81
115
what is the treatmeant for epidural hematomas?
Surgical decompression within 8 hours to optimize recovery chances. | slide 81
116
what are the challenges with anticoags/antiplts with pts who have cardiac stents?
* Patients with stents face difficulties with neuraxial anesthesia. * Stopping antiplatelets and anticoagulants increases stent thrombosis risk. * Continuing these medications raises bleeding risk, including epidural hematoma. | slide 81
117
guidance note for anticoags/antiplts
* The provided information aligns with consensus statements from the American Society for Regional Anesthesia and Pain Medicine. * It is essential to stay updated with the latest guidelines as clinical practices evolve. | slide 81 ## Footnote dont think we need to know this but just in case
118
* what do COX inhibitors do? * what are examples?
* Inhibits cyclooxygenase which prevents the formation of the potent platelet aggregation of thromboxane-A2. * NSAIDs, Aspirin | slide 82
119
this medication is a COX inhibtor and antiplatelt
aspirin [ASA] | slide 82
120
why is it cricial to determin if aspirin is primary or secondary prophhylaxis?
Crucial to determine if aspirin is used for primary (preventing first event) or secondary (preventing recurrent event) prophylaxis. | slide 82
121
with secondary prophylaxis, what is the risk of discontinuation?
High risk associated with stopping aspirin; 10% of acute cardiovascular syndromes are preceded by aspirin withdrawal. | slide 82
122
Guidelines by Procedure Risk Level (General Surgery) * High-Risk & Intermediate-Risk Procedures hold ASA for how long? * Low-Risk Procedures hold ASA for how long? * Central neuraxial blocks hold ASA for how long?
* High-Risk & Intermediate-Risk Procedures: Hold aspirin for 4-6 days * Low-Risk Procedures: Generally, do not need to hold aspirin * Central neuraxial blocks: No additional precautions | slide 82
123
is there a distinction in guidelines between low dose ASA [81mg} and regular dose ASA[ 325mg]?
no distinction in guidelines | slide 82
124
What surgeries have a low cardiac risk [< 1%]?
* Endoscopic procedures * Cataract surgery * Superficial surgeries * Breast surgeries * Ambulatory surgeries | slide 83
125
What surgeries have an intermediate cardiac risk [1-5%]?
* Carotid endarterectomy * Head and neck surgeries * Intrathoracic or intra-abdominal surgeries * Orthopedic surgeries * Prostate surgery | slide 83
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What surgeries have a high cardiac risk [>5%]?
* Emergency surgeries (especially in elderly patients) * Open aortic surgeries * Peripheral vascular surgeries * Long surgeries with significant volume shifts and/or blood loss | slide 83
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When should NSAIDs be stoped for: * High risk procedures? * Intermediate risk procedures? * Low risk procedures? * Central neuraxial blocks?
* High risk procedures: hold for 5 half-lives * Intermediate risk procedures: consider holding for cervical ESI and stellate ganglion block * Low risk procedures: do not need to routinely hold * Central neuraxial blocks: No additional precautions | slide 83
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* what do glycoprotein IIB/IIIA Antagonist do? * what are examples?
* Inhibits platelet aggregation via surface receptors * Tirofiban (Aggrastat), Eptifibatide (Integrilin), Abciximab (ReoPro) | slide 84
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Glycoprotein IIb/IIIa Antagonists Regional Anesthesia Considerations: * Avoid until? * Tirofiban and Eptifibatide: Hold for ____ hours. * Abciximab: Hold for ____ hours.
* Avoid until platelet function has recovered. * Tirofiban and Eptifibatide: Hold for 4-8 hours. * Abciximab: Hold for 24-48 hours. | slide 84
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* what do Thienopyridine Derivatives do? * what are examples?
* Inhibits platelet aggregation by blocking ADP transferase * Clopidogrel (Plavix), Prasugrel (Effient), Ticlopidine (Ticlid) | slide 85
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Thienopyridine Derivatives Regional Anesthesia Considerations: * Clopidogrel: Hold for ____ days. * Prasugrel: Hold for ____ days. * Ticlopidine: Hold for ____ days.
* Clopidogrel: Hold for 5-7 days. * Prasugrel: Hold for 7-10 days. * Ticlopidine: Hold for 10 days. | slide 85
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* what does Unfractionated Heparin do? * what are examples?
* Potentiates antithrombin (enzyme inhibitor), inhibiting thrombin (factor 2) and factors 9, 10, 11, 12. * SQ (subcutaneous) heparin for DVT (Deep Vein Thrombosis) prophylaxis & IV (intravenous) heparin. | slide 86
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Unfractionated Heparin Regional Anesthesia Considerations: * Low-dose ( < 5,000 U): Hold ____ hours. * Higher-dose (≤ 20,000 U daily): Hold ____ hours. * Therapeutic dose (>20,000 U daily or in pregnant patients): Hold ____ hours. * UFH >____ days should have a platelet count before central neuraxial block
* Low-dose ( < 5,000 U): Hold 4-6 hours. * Higher-dose (≤ 20,000 U daily): Hold 12 hours. * Therapeutic dose (>20,000 U daily or in pregnant patients): Hold 24 hours. * UFH >4 days should have a platelet count before central neuraxial block | slide 86
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Low Molecular weight Heparin (LMWH) includes which3 drugs, and inhibits what?
* Enoxaparin (Lovenox), Dalteparin (Fragmin), Tinzaparin (INNOHEP) * Inhibits factor 10a | slide 87
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Regional Anesthesia Considerations for LMWH
* Ensure coagulation status appears normal. * No other blood thinners should be in use. * Check platelet count if on LMWH for more than 4 days. | slide 87
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When the pt is on LMWH, what should you do before the block?
* Delay block at least 12 hours after a prophylactic dose. * Delay block at least 24 hours after a therapeutic dose. * Consider checking anti-factor 10a activity in elderly or if renal insufficiency. | Slide 87
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What are the factors that are vitamin-k dependent?
2,7,9,10 | slide 88
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Regional Anesthesia considerations for Warfarin
* Hold for 5 days * verify normal INR (want <1.5) | slide 88
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MOA for thrombolytic agents
Activates plasminogen: converts plasminogen to plasmin which cleaves fibrin - thereby, causeing clot dissolution | slide 88
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Thrombolytic Agent regional anesthesia consideration
Absolute contraindication to neuraxial anesthesia | slide 88
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Drugs and MOA for Direct anticoags
* Apixaban (Eliquis), Betrixaban (Bevyxxa), Edoxaban (Lixiana), Rivaroxaban (Xarelto), Dabigatran (Pradaxa) * Inhibits facotr 10a | slide 89
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Direct oral anticoagulants regional anesthesia consideration
* Discontinue at least 72 hours before block * Consider checking drug level or anti-factor 10a activity if < 72 hours | slide 89
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Herbal therapies MOA
Activate plasminogen (Garlic, Ginkgo, Ginseng) *herbal therapies are similar action to tPA because it activates plasminogen* (Tito during lecture) | Slide 89
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Herbal therapies regional anesthesia consideration
Proceed with Neuraxial anesthesia of the pt is not on other blood-thinning drugs | slide 89
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How does a postdural puncture headache (PDPH) develop?
* Failure of a dura puncture site to properly “seal over” once breeched by a needle * Continuous leak of CSF causes an overall reduction in CSF volume * This leak lowers the pressure in the brain area, causing the brain to sag slightly and stretch the surrounding membranes, leading to a headache *this will stretch the brain meninges* (Tito in lecture) | slide 91
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Symptomes of Postdural puncture headache
* Headache that feels worse when sitting or standing and better when lying down. * Headache occurs 2-3 days post puncture. The headache is usually felt from the forehead to the back of the head. (Frontal-Occipital) * Other possible symptoms include **nausea, sensitivity to light**, double vision, and ringing in the ears (comes and goes per Tito). | slide 91
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PDPH Factors increasing risk (both pt and practitioner factors)
Patient Factors: * younger * female * preggers Practitioner Factors: * Using a needle with a cutting tip. * Using a large diameter needle. * Using air for LOR with epidural. * Positioning the needle perpendicular to the spine's long axis. | Slide 91
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The ____ needle is the cutting needle and can have a ____ to ____
* Quincke needle * 36^128% chance with a 22 gauge to 0.4^46% chance with a 32 gauge | slide 91
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Treatment for Postdural Puncture Headache
* Red rest * NSAIDs * Caffeine (Tito said soda or coffee) * Epidural blood patch * Sphenopalatine Ganglion block | Slide 92
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Epidural Blood patch: what do they do
**Main treatment for severe headaches after dural puncture** * Same level as the epidural was is a good insertion site for the blood patch * get an IV (from nurse) fresh blood - 10-20mL of pts own bloodand **must be sterile IV** * prep pt for epidural * When you hit epidural space - ask for the blood -at 10cc of the pt blood - HA likely will go away, but the first few mLs will be the worst headache of their life becuase of increased pressure * lay pt back to bed and monitor | Slide 92
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When to give the blood patch?
* 48 hours after the dural puncture * Per Tito: sometimes when they start having a headache, you can start the non-invasive stuff (soda or coffee) | slide 92
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Sphenopalatine Ganglion block (SPG) procedure
**A simpler, low-risk treatment alternative.** Procedure: * Soak a cotton swab with LA (1-2% Lidocaine or 0.5% bupivacaine). * With the patient's head tilted back, insert the swab into the nose towards the back throat wall. * Leave it there for about 5 to 10 minutes. * This can quickly reduce headache symptoms. | slide 92
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Which nerves are we blocking with the airway block or the SPG block?
SPG block: Trigeminal nerve (V2) Airway block: CN V, IX, X | lecture
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Paresthesia: * There is a higher incidence if ____ * Deficit usually is in the area ____ * Epidural Catheter are ____ risk * higher incidence with ____ techniques
* paresthesia if it was encountered during placement * where the paresthesia occures * much lower risk * CSE techniques (Combined spinal/epidural) **Usually we have paresthesia when we aren't midline** | slide 93
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What to do when your pt has paresthesias?
* redirect needle * document * noncooperative or moving pt can increase the risk * midline can help guide placement | slide 93
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Failed spinal: what do you do?
No Anesthesia Effect * If spinal has not set up after after 15-20 minutes, it may be necessary to redo the block. | slide 93
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Patchy or unilateral block with spinals (Failed spinal)
* Patchy block Avoid Repeating: May cause neurotoxicity Consider IV sedation or general anesthesia. * Unilateral Block Adjust Position If still ineffective, consider IV sedation or general anesthesia. | slide 93
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Post-Spinal Bacterial Meningitis: how infections can happen
* Not following sterile or aseptic technique * bacteria in the blood: common bacteria involved *streptococcus viridans* (found in mouth and on hands) *mask and washing hands are essential to preventing the spread of these bacteria* | slide 94
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3 preps for pt's back duirng neuraxial to prevent bacterial meningitis
Skin Preparation Options: * Iodine, Alcohol, Chlorhexidine Must be allowed to dry before the procedure begins to avoid arachnoiditis. Considered neurotoxic if not used properly. Recommended Combination (Miller) **Alcohol and Chlorhexidine**: This mix is highly effective in preventing bacterial meningitis when used correctly to prepare the skin before a spinal procedure. | slide 94
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Cauda Equina Syndrome: nerves involved, and cause
* Nerves affected: "cauda" L2-S5 + coccygeal nerves * Cause: Neurotoxicity which can happen due to high levels of local anesthetic drugs affecting nerve function | slide 95
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Factors that increase risk of developing cauda equina syndrome
* High concentration of LA (i.e. using lidocaine 5% in SAB) * Microcatheters: These catheters deliver the drug on a small area, increasing risk of nerve damage by exposing the area with a high concentration of LA. * Whiticare 25/26 needle have been associated with this syndrome | slide 95
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Signs and symptomes of cauda equina syndrome
* Serious neurologic complication that can be permanent * Bowel and Bladder Dysfunction * Sensory Deficits: Loss of feeling in the legs or feet. (Tito: numbness in the caudal/sacral area that wont go away) * Back pain * Saddle anesthesia * Sexual dysfunction * Weakness or Paralysis * Can lead to paraplegia (late sign) | slide 95
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Treatment for Cauda Equina Syndrome
Supportive care * or if compression is a factor, immediate laminectomy in <6 hrs (ex disc, hematoma etc) | slide 95
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* To prevent epidural catheter shearing, always ____ * If there are issues removing an epidural catheter try: (3 things)
* withdraw the needle and the catheter at the same time Issues removing Epidural: * positioning: put the pt in the same position they were in during insertion or lateral decubitus * Traciton: apply gentle and continuous pulling * Taps traction: tape the catheter to the skin and gently pull | slide 97
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Transient Neurologic symtpoms: cause and factors that increase risk
* cause: Patient Positioning- Improper positioning during procedures can stretch nerves, like the sciatic nerve, causing temporary symptoms. Myofascial Strain and Spasms * Factors increasing risk: Higher incidence when using **Lidocaine 5%** (around 19%) Surgical Positions: Such as the **lithotomy position** (hip o knee flex) **Outpatient surgeries** and knee arthroscopy are associated with higher risks. | slide 96
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Factors that do not increase the risk of developing Transient neurologic symptoms
* Early ambulation * LA concentration * Baricity | slide 96
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Signs, symptoms, and treament of transient neurologic symptoms
S/S: * Pain: Severe radicular pain in the back and buttocks that spreads down both legs. * Timing: Pain usually starts within 6 to 36 hours after surgery and lasts from 1 to 7 days. (Resolves within a week 90% of cases) Treatment: * NSAIDs and opioid pain killers (per Tito really does work) * Trigger point injections - can relieve muscle spasm and pain | slide 96
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If a catheter breaks, what do you do? (epidural)
* inform the pt * Monitoring: if the pt doesn't show s/s, they can often live safely with the fragment * Complicaitons: if neurological symptomes develop, surgery may be needed to remove the piece | slide 97
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* If blood is in the epidural needle: ____ * If blood is in the epidural catheter: ____
* Needle: needle could be too internal **solution: adjust the needle to aim more midline** * Catheter: pulling blood into catheter **slightly pull back the catheter and flush with saline** repeat this until no more blood is drawn or the catheter cant be adjusted further safely | slide 98
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Risk factors with epidural vein cannulation (4)
* Multiple Attempts * Pregnancy * Catheter Type: Stiffer catheters are harder to maneuver and more likely to puncture a vein. * Trauma to epidural vein during block procedure | slide 98