Exam 3: Local Anesthetics Flashcards
(132 cards)
1
Q
What are the determinants of systemic absorption of local anesthetics?
A
The determinants include site of injection, dose, physicochemical properties, and addition of epinephrine.
2
Q
What is the effect of decreased absorption of local anesthetics?
A
Decreased absorption leads to decreased systemic toxicity.
3
Q
How does vascularity affect the uptake of local anesthetics?
A
Greater vascularity leads to more rapid uptake than areas with more fat.
4
Q
What are the rates of absorption for local anesthetics in different areas?
A
The rates of absorption are: interpleural > intercostal > caudal > epidural > brachial plexus > sciatic/femoral > subcutaneous.
5
Q
What affects systemic absorption of local anesthetics? What will increase absorption? What will decrease it?
A
Greater the total dose, the greater the absorption. Higher lipid solubility and protein bound compounds have decreased absorption.
Footnote**
Giving more drug increases absorption, but lipid solubility and protein binding act like “traps,” slowing down how fast the drug moves into the bloodstream.
6
Q
How do local anesthetics distribute in the body?
A
They distribute rapidly throughout all body tissues.
7
Q
Which organs are most vulnerable to local anesthetics?
A
The cardiovascular and central nervous systems are most vulnerable.
**Footnote
Doesn’t have blood brain barrier = make in vulnerable
8
Q
What factors contribute to Local Anesthetics distribution rapidly throughout all body tissues?
A
-Organ perfusion
– Partition coefficient
– Plasma protein binding
9
Q
What is the rate of absorption for interpleural local anesthetics?
A
Interpleural has the highest rate of absorption.
10
Q
What is the order of local anesthetic absorption rates from highest to lowest?
A
Interpleural > intercoastal > caudal > epidural > brachial plexus > sciatic/femoral > subcutaneous.
11
Q
Which local anesthetic has a lower absorption rate than caudal?
A
Epidural has a lower absorption rate than caudal.
12
Q
Which local anesthetic has the lowest absorption rate?
A
Subcutaneous has the lowest absorption rate.
13
Q
What is the elimination method for esters in local anesthetics?
A
Hydrolysis of ester by plasma cholinesterases.
14
Q
What is the elimination method for amides in local anesthetics?
A
Mixed function oxidase system of liver (i.e., p450).
15
Q
How does age affect toxicity of local anesthetics?
A
Increased in young and old due to decreased clearance and increased absorption.
16
Q
How does pregnancy affect the clearance of local anesthetics?
A
Decreased clearance in pregnancy increases potential for toxicity.
17
Q
What conditions lead to decreased clearance of local anesthetics?
A
Hepatic disease and decreased cardiac output.
18
Q
What is the relative potency of local anesthetics ranking?
A
Bupivicaine = levobupivicaine > etidocaine > ropivicaine > mepivicaine = lidocaine = prilocaine > esters
19
Q
How do local anesthetics affect the Central Nervous System?
A
They readily cross the blood-brain barrier and have dose-dependent toxicity.
20
Q
What are the effects of low and high plasma levels of local anesthetics on the CNS?
A
CNS depression occurs at low plasma levels, while CNS excitation can progress to seizures at higher concentrations.
21
Q
How can overt toxicity of local anesthetics be managed?
A
It may be avoided or masked by benzodiazepines and barbiturates, which raise the seizure threshold.
22
Q
What factors increase the potential for CNS toxicity in local anesthetics?
A
Decreased protein binding, decreased clearance, rapid rate of intravenous administration, acidosis, and increased pCO2.
23
Q
How does the dose affect toxicity in the cardiovascular system compared to the CNS?
A
Generally higher doses lead to toxicity when compared to CNS toxicity.
24
Q
What increases the risk for toxicity in the cardiovascular system?
A
Higher relative potency (lipophilicity) increases the risk for toxicity.
25
A 3-year-old child and an 80-year-old adult both receive similar weight-based doses of lidocaine for a minor procedure. Despite appropriate dosing, both patients show signs of systemic local anesthetic toxicity. Which of the following best explains why children and the elderly are at higher risk for local anesthetic toxicity?
A) Increased metabolism of local anesthetics
B) Increased protein binding of local anesthetics
C) Altered distribution and reduced clearance of the drug
D) Enhanced renal elimination of the drug
E) Increased pain sensitivity requiring higher doses
Correct Answer: C) Altered distribution and reduced clearance of the drug
⸻
Rationale:
Children have a high total body water content and immature liver enzymes, leading to slower metabolism and higher plasma levels of local anesthetics. They also have lower plasma protein levels (e.g., alpha-1-acid glycoprotein), which means more free drug is available to cause toxicity.
Elderly patients have reduced lean body mass and subcutaneous fat, decreased hepatic metabolism, and less protein binding, which also leads to higher active drug levels in the bloodstream. Additionally, impaired tissue perfusion (e.g., “skin tenting”) can affect drug absorption and clearance.
Thus, despite correct dosing, both populations have altered pharmacokinetics that increase their risk for systemic toxicity.
26
Which of the following patients is at increased risk of local anesthetic systemic toxicity (LAST) due to altered pharmacokinetics?
A) A healthy 25-year-old male
B) A pregnant woman in her third trimester
C) A 30-year-old with normal cardiac function undergoing minor surgery
D) A healthy adolescent
E) A patient receiving regional anesthesia with normal hepatic function
Correct Answer: B) A pregnant woman in her third trimester
⸻
Rationale:
Several conditions increase the risk of local anesthetic systemic toxicity (LAST) due to decreased clearance and/or increased absorption:
• Young (especially neonates/infants) and elderly patients have impaired clearance due to immature or diminished hepatic function, lower plasma protein levels, and altered body composition.
• Pregnancy reduces local anesthetic clearance due to hormonal changes affecting liver enzymes, increased cardiac output (leading to increased distribution), and increased sensitivity to anesthetics, all of which increase the potential for toxicity.
• Hepatic disease impairs metabolism of amide anesthetics (e.g., lidocaine, bupivacaine), increasing drug levels.
• Decreased cardiac output reduces hepatic blood flow, further slowing clearance and increasing toxicity risk.
In contrast, healthy young adults with normal hepatic and cardiac function have efficient metabolism and clearance, making them less susceptible.
27
A 60-year-old man with a history of cirrhosis and congestive heart failure is scheduled to undergo a procedure using local anesthesia with bupivacaine. Why is this patient at increased risk for local anesthetic systemic toxicity (LAST)?
A) Increased renal excretion of the drug
B) Increased protein binding of the anesthetic
C) Decreased clearance due to impaired hepatic metabolism and reduced perfusion
D) Enhanced enzymatic metabolism due to liver disease
E) Faster redistribution of the drug due to increased cardiac output
Correct Answer: C) Decreased clearance due to impaired hepatic metabolism and reduced perfusion
⸻
Rationale:
Local anesthetics, especially amide-type agents like bupivacaine, are primarily metabolized in the liver. In patients with hepatic disease, such as cirrhosis, the liver’s ability to metabolize these drugs is compromised, leading to accumulation and increased systemic levels.
Additionally, in conditions like heart failure, decreased cardiac output leads to reduced hepatic perfusion, which further limits the liver’s ability to clear the drug. Together, these factors significantly increase the risk of local anesthetic systemic toxicity (LAST), even at standard doses.
28
Which of the following patients is most likely to experience local anesthetic systemic toxicity (LAST) due to decreased clearance of an amide-type local anesthetic?
A) A 28-year-old woman in early pregnancy with no medical history
B) A 40-year-old man with mild asthma receiving a nerve block
C) A 65-year-old woman with decompensated liver cirrhosis and low ejection fraction
D) A 12-year-old child undergoing dental anesthesia
E) A healthy 35-year-old athlete undergoing minor skin excision
Correct Answer: C) A 65-year-old woman with decompensated liver cirrhosis and low ejection fraction
⸻
Rationale:
Amide-type local anesthetics (like lidocaine, bupivacaine, ropivacaine) are primarily metabolized in the liver. In patients with hepatic dysfunction, clearance of these drugs is significantly reduced, increasing the risk of systemic toxicity.
Additionally, low cardiac output further reduces hepatic blood flow, compounding the impaired clearance. This combination of liver disease and heart failure puts this patient at the highest risk for drug accumulation and systemic toxicity.
Other patients listed may have slight increases in sensitivity or altered distribution (like pregnancy or pediatrics), but they do not have the dual impairment of metabolism and perfusion seen in choice C.
29
A 72-year-old man with a history of congestive heart failure (ejection fraction 30%) is undergoing a procedure under local anesthesia with lidocaine. Despite receiving a standard dose, he begins to exhibit signs of central nervous system toxicity. Which of the following best explains his increased susceptibility?
A) Increased renal clearance of lidocaine
B) Increased distribution to adipose tissue
C) Decreased hepatic perfusion leading to reduced drug clearance
D) Enhanced protein binding of lidocaine
E) Increased metabolism by plasma cholinesterase
Correct Answer: C) Decreased hepatic perfusion leading to reduced drug clearance
⸻
Rationale:
In patients with decreased cardiac output, such as those with heart failure, there is reduced blood flow to the liver. Since amide local anesthetics like lidocaine are metabolized in the liver, reduced perfusion results in slower metabolism and clearance of the drug. This leads to accumulation in the plasma and a higher risk of local anesthetic systemic toxicity (LAST), even at standard or appropriately weight-based doses.
The other options are incorrect because:
• Lidocaine is not primarily cleared renally.
• Adipose tissue distribution does not explain the rapid onset of toxicity.
• Lower perfusion doesn’t increase protein binding.
• Lidocaine (an amide) is not metabolized by plasma cholinesterase — that applies to ester anesthetics.
30
What cardiovascular toxicity does lidocaine exhibit?
Lidocaine typically exhibits cardiovascular toxicity as hypotension, bradycardia, and hypoxia.
31
What cardiovascular toxicity does bupivicaine demonstrate?
Bupivicaine demonstrates sudden cardiovascular collapse secondary to ventricular arrhythmias that are resistant to treatment, characterized by widened QRS width/duration.
32
How does bupivicaine dissociate during diastole?
Bupivicaine dissociates slower during diastole.
33
What central effects does bupivicaine have on?
Bupivicaine has central effects on the nucleus tractus solitarius.
34
What peripheral effects does bupivicaine cause?
Bupivicaine causes peripheral sympathetic inhibition and direct vasodilation.
35
What is neurotoxicity in the context of local anesthetics?
Neurotoxicity refers to injury to Schwann cells, inhibition of fast axonal transport, disruption of the blood/nerve barrier, and decreased blood flow with ischemia.
36
Which nerves are typically more resistant to damage from local anesthetics?
Peripheral nerves are typically more resistant to damage than the spinal cord.
37
What are transient neurologic symptoms (TNS) after spinal anesthesia?
TNS includes pain radiating from the lower back to the buttocks and lower extremities.
38
What are the risk factors for Transient Neurologic Symptoms after Spinal Anesthesia
TNS?
Risk factors include spinal administration of lidocaine (up to 40%), lithotomy position, ambulatory surgical status, arthroscopic knee surgery, and obesity.
39
In which patient group is the lowest incidence of Transient Neurologic Symptoms after Spinal Anesthesia (TNS) observed?
The lowest incidence of TNS is observed in obstetrical patients undergoing c-section.
40
When do Transient Neurologic Symptoms after Spinal Anesthesia (TNS) symptoms typically occur after surgery?
TNS symptoms typically occur 12-23 hours after surgery.
41
What is the usual recovery time for Transient Neurologic Symptoms after Spinal Anesthesia
(TNS)?
Recovery from TNS is usually within a week.
42
What are ester local anesthetics?
Ester local anesthetics are weak and short-acting.
43
Are ester local anesthetics good for regional anesthesia?
No, they are not good for regional anesthesia.
44
What are ester local anesthetics good for?
They are good for fast local anesthesia.
45
What are Transient Neurologic Symptoms after Spinal Anesthesia (TNS) treatments?
Treatment consists of opioids, NSAIDs, muscle relaxants, warm heat and positioning, and possible trigger point injections.
46
What is Procaine? Dosing for kids? Adults? Max?
Procaine is a local anesthetic that is a derivative of para-aminobenzoic acid.
## Footnote
Kids dose = 7mg/kg (unless kids is over 50kg) 350 mg for kids
Adults = 350- 600mg (Max 600mg)
47
What are the characteristics of Procaine?
Procaine has a high pKa and poor lipid solubility, making it a relatively weak local anesthetic with a slow onset and a short duration of action (30-60 minutes).
## Footnote
Toxicity is limited by rapid hydrolysis.
48
What are the common uses and dosages for Procaine spinally & infiltration?
Procaine is used for infiltration (0.25-1%), spinal (50-200 mg), but is not used topically and has very limited use in epidural, peripheral block, and intravenous regional anesthesia (IVRA).
49
What do you need to rule out with Transient Neurologic Symptoms after Spinal Anesthesia
(TNS)?
Must rule out other causes such as hematoma, abscess, or cauda equina syndrome.
50
What is the onset and duration of action for Procaine? Toxicity?
Procaine has a slow onset and a short duration of action of 30-60 minutes. Toxicity is limited by rapid hydrolysis
51
A 47-year-old man presents to the emergency department with sudden onset of severe lower back pain radiating down both legs, numbness in the perineal (“saddle”) region, and new-onset urinary retention. Which of the following is the most appropriate next step in management? Treatment?
Correct Answer: D) Immediate lumbar CT scan or MRI to evaluate for cauda equina syndrome
⸻
Rationale:
This patient presents with classic red flag symptoms of cauda equina syndrome (CES):
• Sudden bilateral sciatica
• Saddle anesthesia
• Bladder dysfunction (e.g., urinary retention)
TX: per Dave with steroids, muscle relaxant, acetaminophen, opioids last
CES is a surgical emergency. Delay in diagnosis or treatment can result in permanent neurological damage, including bowel/bladder incontinence and paralysis.
• MRI is the imaging of choice due to its high resolution for soft tissues, but CT may be used if MRI is unavailable.
• Urgent neurosurgical consultation and decompression (often within 24–48 hours) is critical for preventing irreversible damage.
• Conservative management or outpatient referral is inappropriate and dangerous in this scenario.
52
Extra: classic red flag symptoms of cauda equina syndrome (CES)?
• Sudden bilateral sciatica
• Saddle anesthesia
• Bladder dysfunction (e.g., urinary retention)
CES is a surgical emergency. Delay in diagnosis or treatment can result in permanent neurological damage, including bowel/bladder incontinence and paralysis.
• MRI is the imaging of choice due to its high resolution for soft tissues, but CT may be used if MRI is unavailable.
• Urgent neurosurgical consultation and decompression (often within 24–48 hours) is critical for preventing irreversible damage.
• Conservative management or outpatient referral is inappropriate and dangerous in this scenario.
53
What is Chloroprocaine?
Chloroprocaine is a derivative of procaine, used as a local anesthetic.
54
What is the maximum single dose of Chloroprocaine? With Epi?
The maximum single dose is 11mg/kg or 800 mg, (14mg/kg or 1000 mg with epinephrine).
55
What is the onset of action for Chloroprocaine?
Chloroprocaine has a rapid onset of action with a plasma half-life of 30 seconds.
56
What are the typical concentrations of Chloroprocaine for infiltration and nerve blocks?
For infiltration, the concentration is 1%. For epidural and peripheral nerve blocks, it is 2-3%.
57
How does Chloroprocaine affect sympathetic response during intubation?
Chloroprocaine inhibits sympathetic response to laryngoscopy and intubation.
58
What is the primary clinical use of Chloroprocaine?
Chloroprocaine is primarily used for epidural anesthesia during c-section.
59
What are the benefits of using Chloroprocaine?
Chloroprocaine has rapid onset, decreased toxicity, and allows for rapid recovery and discharge.
60
What can happen if EDTA is used as a preservative in Chloroprocaine?
Using EDTA as a preservative in doses greater than 40 ml can cause severe paravertebral muscle spasm after resolution of the epidural block.
**Footnote
You can avoid: use less than 25 ml preservative or none at all
61
How can the risk of muscle spasm from EDTA be avoided?
The risk can be avoided by using less than 25 ml of a preservative-free formulation.
62
What is Tetracaine?
A butylaminobenzoic acid derivative of procaine.
63
What is the maximum single dose of Tetracaine?
20 mg.
64
How potent and long acting is Tetracaine?
It is potent and long acting.
65
What is the concentration and onset time for spinal administration of Tetracaine?
0.5-1% concentration with a 3-5 minute onset.
66
What is the duration of action for Tetracaine?
2-3 hours, increased to 4-6 hours if co-administered with epinephrine.
67
What is the hydrolysis rate of Tetracaine? Half life?
Tetracaine has the slowest rate of hydrolysis but its half-life is still shorter than any of the amides.
68
What are the topical properties of Tetracaine?
Tetracaine has excellent topical properties, particularly for topical ophthalmologic anesthesia.
69
What limits the use of Tetracaine?
Toxicity concerns limit the use of Tetracaine by epidural, peripheral nerve, or IVRA.
70
What is cocaine classified as?
Local anesthetic with intense vasoconstriction
71
What is the maximum single dose of cocaine?
150 mg
72
What concentration of cocaine solution is used prior to nasopharyngeal or otolaryngologic manipulation?
4-10% solution
73
What limits the use of cocaine?
Low therapeutic index and abuse potential limit its use to topical only
74
What is Benzocaine? Why is it different?
Benzocaine is a local anesthetic that differs from others in its class due to possessing a secondary amine and being a weak acid with a pKa of 3.5.
75
What is the pKa of Benzocaine?
The pKa of Benzocaine is 3.5.
76
What is the maximum single dose of Benzocaine?
The maximum single dose of Benzocaine is 200 mg.
77
What is the ideal application of Benzocaine?
Benzocaine is ideal for topical application to mucous membranes prior to endoscopy or bronchoscopy in a 20% solution.
78
What is the onset and duration of action for Benzocaine?
Benzocaine has a rapid onset of action with a duration of 30-60 minutes.
79
What adverse effect can occur with doses of 200-300 mg of Benzocaine?
Doses of 200-300 mg of Benzocaine can cause methemoglobinemia, which is characterized by cyanosis and decreased oxygen carrying capacity.
80
Who is at the most risk for methemoglobinemia from Benzocaine?
Neonates are at the most risk for methemoglobinemia from Benzocaine.
81
How can methemoglobinemia caused by Benzocaine be treated?
Methemoglobinemia can be treated with 1% methylene blue at a dosage of 1-2 mg/kg over 20 minutes.
82
What is the maximum single dose of Lidocaine?
The maximum single dose is 4.5 mg/kg or 300 mg (7 mg/kg or 500 mg with epinephrine).
83
What concentration of Lidocaine provides rapid onset anesthesia?
0.5-1% Lidocaine provides anesthesia of rapid onset with a duration of 60-120 minutes.
84
What is the concentration of topical Lidocaine?
Topical Lidocaine is available in a concentration of 4%.
85
What is Tumescent Lidocaine used for? Peak effects?
Tumescent Lidocaine involves large volumes of dilute Lidocaine/epinephrine combination injected into subcutaneous tissue; it is useful for liposuction.
## Footnote
Peak effects may not occur for 10-12 hours.
86
What is the dosage of Lidocaine for IVRA?
For IVRA, 50 ml of 0.5% Lidocaine provides 45-60 minutes of anesthesia for upper extremity surgery.
87
What is the use of Spinal/Epidural Lidocaine?
Spinal/Epidural Lidocaine is popular for dense sensory anesthesia and motor block for surgery of the trunk and lower extremities.
## Footnote
There is controversial neurotoxicity with spinal use; maximum single dose is 100 mg.
88
How is Lidocaine administered to blunt the effects of tracheal intubation? What is the dose?
Lidocaine can be administered intravenously or via laryngotracheal route to blunt the effects of tracheal intubation at a dose of 2-2.5 mg/kg.
89
What effects does Lidocaine prevent during intubation?
Lidocaine prevents elevations in intraocular pressure (IOP), intracranial pressure (ICP), and intra-abdominal pressure (IAP).
90
91
What is the primary use of Lidocaine relating to cardiac function? What is the bolus? Infusion?
It suppresses ventricular ectopy.
## Footnote
Administered as a 100-200 mg bolus followed by a 1-4 mg/min infusion.
92
What dosage of Lidocaine can be used as a systemic analgesic?
1-5 mg/kg may be used for acute postoperative and chronic neuropathic pain.
**Footnote
Max Dose: 300mg given over 20-30 mins
93
How effective is transdermal Lidocaine?
Transdermal Lidocaine is very effective.
**Footnote
Lidocaine free period ~ 12 hrs
94
What is Prilocaine similar to?
Prilocaine is similar to lidocaine but has less vasodilation and doesn’t require co-administration with epinephrine.
95
What is the maximum single dose of Prilocaine?
The maximum single dose of Prilocaine is 600 mg.
96
How is Prilocaine used topically?
Prilocaine is used in a combination with lidocaine for topical applications.
97
How long does it take for anesthesia to be realized with Prilocaine under occlusive dressing?
Anesthesia for painful procedures is realized after 60-90 minutes under occlusive dressing.
98
What procedures can benefit from Prilocaine anesthesia?
Prilocaine anesthesia can be used for painful procedures such as vascular cannulation or spinal puncture.
99
What is notable about the metabolism of Prilocaine?
Prilocaine has a rapid metabolism and is the least toxic of the amides.
100
What metabolite of Prilocaine is implicated in methemoglobinemia?
The metabolite o-toluidine is implicated in methemoglobinemia.
101
What is Mepivicaine similar to?
Mepivicaine is similar to lidocaine, with a slightly longer duration.
102
What is the maximum single dose of Mepivicaine?
Max single dose 7 mg/kg or 400 mg (500 mg with epi and 100 mg for spinal)
103
What types of anesthesia can Mepivicaine be used for?
Mepivicaine can be used for topical or infiltration anesthesia.
104
What concentration of Mepivicaine is used for epidural anesthesia?
A concentration of 1.5-2% provides surgical anesthesia within 10-15 minutes with a duration of 70-90 minutes.
105
What concentration of Mepivicaine is used for peripheral block?
A concentration of 1-1.5% provides anesthesia for 2-4 hours.
106
What is a risk associated with Mepivicaine in obstetrics?
There is an increased toxicity risk in obstetrics due to poor metabolism in the fetus.
107
What is Levobupivicaine?
S-enantimor of racemic bupivicaine with similar potency.
108
What is the systemic toxicity of Levobupivicaine compared to bupivicaine?
Levobupivicaine has 30-40% less systemic toxicity.
109
What is the maximum single dose of Levobupivicaine?
The max single dose is 2mg/kg or 150 mg.
110
What concentration of Levobupivicaine is used for labor analgesia?
Epidural—0.125-0.25% for labor analgesia.
111
What 3 has its own vasoconstriction properties?
Levobupivicaine, Ropivicaine, cocaine
112
What is Ropivicaine?
Ropivicaine is an anesthetic with a 3-carbon substitution on the tertiary amine, similar to mepivicaine and bupivicaine.
113
How does Ropivicaine compare to Bupivicaine in terms of lipid solubility?
Ropivicaine has decreased lipid solubility compared to bupivicaine, resulting in less motor block.
114
What is the cardiotoxicity of Ropivicaine compared to Bupivicaine?
Ropivicaine is 30-40% less cardiotoxic than bupivicaine.
115
What is the maximum single dose of Ropivicaine?
The maximum single dose of Ropivicaine is 3 mg/kg or 200 mg.
116
What concentration of Ropivicaine is used for labor analgesia in epidurals?
For labor analgesia, Ropivicaine is used at a concentration of 0.1-0.25%.
117
What effect does Ropivicaine have on blood vessels?
Ropivicaine causes vasoconstriction.
118
What is Etidocaine used for?
Etidocaine is used for infiltration, epidural, and peripheral nerve block.
## Footnote
It provides selective more potent motor blockade than sensory anesthesia.
119
What are the properties of Etidocaine?
Etidocaine is a potent, highly lipophilic agent with a rapid onset and duration similar to bupivacaine.
120
What is Bupivicaine?
A long-acting local anesthetic with a slow onset except for infiltration and spinal use.
121
What is a drawback of Bupivicaine?
It has an increased risk of toxicity despite being a very potent local anesthetic.
122
What is the maximum single dose of Bupivicaine?
2.5 mg/kg or 175 mg (3 mg/kg or 200 mg with epinephrine).
123
What concentration of Bupivicaine is used for infiltration into surgical wounds?
0.25%.
124
What is the onset and duration of Bupivicaine for spinal use?
Fast onset within 5 minutes, lasting 1-4 hours.
125
What is Bupivicaine ideal for?
Continuous epidural use in labor and post-operatively.
126
What happens to the degree of motor block with Bupivicaine below 0.25% concentration?
The degree of motor block decreases, while 0.1% provides sensory analgesia with minimal motor block.
127
What is the duration of a peripheral block with Bupivicaine?
4-12 hours, may last up to 24 hours.
128
What are some examples of delivery systems in local anesthesia?
Examples include ambulatory pumps, encapsulation with liposomes, microspheres, or polymers with slow degradation and release.
129
What is Lipid Rescue?
A treatment for local anesthetic-induced cardiac arrest that is unresponsive to standard therapy.
## Footnote
This protocol should be attached to the Intralipid bag.
130
What should be done in the event of local anesthetic-induced cardiac arrest?
In addition to standard cardio-pulmonary resuscitation, Lipid Rescue may be used if unresponsive to standard therapy.
131
Intralipid 20% should be given i.v. in the following dose regime:
– Intralipid 20% 1.5 mL/kg over 1 minute
– Follow immediately with an infusion at a rate of 0.25 mL/kg/min,
– Continue chest compressions (lipid must circulate)
– Repeat bolus every 3-5 minutes up to 3 mL/kg total dose until circulation is restored
– Continue infusion until hemodynamic stability is restored. Increase the rate to 0.5 mL/kg/min if BP declines
– A maximum total dose of 10 mL/kg is recommended
132
Lipid Rescue In practice, in resuscitating an adult weighing 70kg:
– Take a 500ml bag of Intralipid 20% and a 50ml syringe.
– Draw up 50ml and give stat i.v., X2
– Then attach the Intralipid bag to an iv administration set (macrodrip)and run it .i.v over the next 15 minutes
– Repeat the initial bolus up to twice more – if spontaneous circulation has not returned.
**Footnote
If you use Intralipid to treat a case of local anaesthetic toxicity, please report it at www.lipidrescue.org. Remember to restock the lipid. Ver 7/06
