2. Slide 2
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Agenda
Review physiology of nerve impulse conduction
Identify equipment and preparation to provide
peripheral nerve blocks
Identify types of local anesthetic agents,
characteristics, and risk factors
Indentify techniques of risk mitigation in
performance of regional blocks
Identify nerve stimulation theory
3. Slide 3
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
References
Military Advanced Regional Anesthesia and
Analgesia Ch. 2 – 4, & 25
Pathophysiology for the Health Professions 4th
Edition Ch. 6 p.126
Basis Guide to Anesthesia for Developing
Countries, Volume 2, Daniel D. Moos
(International Federation of Nurse
Anesthetists, ifna-int.org)
7. Slide 7
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
The goal in regional anesthesia
Target nerves proximal to source of pain
• Surround “targeted” nerve with agents thus
preventing depolarization prior to perception by
CNS
• Lowering or eliminating systemic pain medications
• Lowering or eliminating negative CNS side effects of
systemic medications
8. Slide 8
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Methods of targeting proximal nerves
Paraesthesia “Blind” or “anatomical”
• Less equipment
• More suitable for distal blocks
Nerve Stimulation *
• Specialized equipment
• Allows very proximal blocks
Ultrasound guided
• Specialized equipment
• Allows visualization of targeted nerves
10. Slide 10
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
"This technology can only confirm and
refine correct needle placement for
regional blocks; it should never be
considered a substitute for the
physician's understanding of the
anatomical basis for each block.”
Military Advanced Regional Anesthesia and Analgesia
11. Slide 11
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Regional Block Contraindications
Adamant refusal by the patient
Infants, children, or the elderly
Localized infection at the injection site
Systemic anticoagulation / coagulopathy
Obese patients
Pre-existing neurological disease
Inadequate communication capability
History of traumatic injury at block site
12. Slide 12
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Preparation (Patient consent and
education)
Avoid using blocked extremity for 24 hours
Protective reflexes and proprioception
decreased
Location
• Calm/Quiet location
• Adequate “set up” time
The most common cause of “failed” regional anesthesia is
impatience
17. Slide 17
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local Anesthetics Agents
Lidocaine (30-60 minute duration)
• Short to medium acting, most versatile, considered
too short acting for post operative pain
management
Mepivacaine (45-90 minute duration)
• Medium acting, less neurotoxic and cardiotoxic
than lidocaine; very attractive agent due to low
toxicity, rapid onset, and a dense block
18. Slide 18
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local Anesthetics Agents
Ropivacaine (120-360 minute duration)
• Considered the safest long acting agent, long acting
agent of choice at Walter Reed due to safety profile
and efficacy
Bupivacaine (120-240 minute duration)
• Considered a long acting agent, longest latency to
onset time frame, low cost, propensity for sensory
versus motor blockade; cardiac toxicity high if
intravascular injection occurs
20. Slide 20
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local Anesthetics(Risk Factors)
Neurotoxicity
CNS Toxicity
Cardiac Toxicity
Stay out of vessels and keep the dosing in
prescribed ranges
For every clinical situation, the use of regional
anesthesia must be carefully evaluated as a
matter of risk versus benefit
21. Slide 21
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Neurotoxicity
Evidence suggests that local anesthetics can be
myotoxic and neurotixic
Usually associated with long term catheter
placement and infusion pumps
Unintentional direct injection into the nerve
sheath can cause nerve damage.
Unintentional direct needle penetration of the
nerve can cause damage
27. Slide 27
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Neurological Function Assessment
Upper Extremity Neurological Check
If you can’t remember anything, note sensory deficit
comparing good to bad and note prior to block
28. Slide 28
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local anesthetics(Risk mitigation)
Standard monitoring with audible O₂ saturation
tone
O₂ supplementation
Slow, incremental injection(5ml every 10-15sec)
Initial injection of local “test dose” observe HR >
10 beats/min, BP> 15mmHg, or T-wave
decrease
Pretreatment with benzodiazepines increase
seizure threshold
29. Slide 29
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local anesthetics(Risk mitigation)cont.
Patient either awake or sedated, but still able to
communicate
Resuscitation equipment and drugs available
If seizure occur, airway maintenance, O₂ and
seizure termination with propofol (25-50mg)
If cardiovascular collapse, ACLS
Intralipid 20% 1ml/kg every 3-5 minutes up to
3ml/kg in conjunction with ACLS treatments
Military Advanced Regional Anesthesia and Analgesia, TABLE 3-2
30. Slide 30
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Local anesthetics(Risk mitigation) cont.
“test dose” 10ml of regional agent with
epinephrine 1:400,000 (0.5ml 1:000 in 10ml)
• Aspirate for blood, inject 1ml
• If resistance felt, reposition repeat aspirate
Inject 3-5ml of local with epinephrine
1:400,000
Transfer to “clean” agent syringe
• Aspirate every 3-5ml
32. Slide 32
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Conduction of Nerve Impulse
Locating Nerves with Stimulation
Advancing needles (1.2mA to 0.5mA)
33. Slide 33
JSOMTC, SWMG(A)
Putting it Together Nerve Stimulation
Motor as a Proxy
Regional Anesthesia - Principles
34. Slide 34
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
Agenda
Review physiology of nerve impulse conduction
Identify equipment and preparation to provide
peripheral nerve blocks
Identify types of local anesthetic agents,
characteristics, and risk factors
Indentify techniques of risk mitigation in
performance of regional blocks
Identify nerve stimulation theory
35. Slide 35
JSOMTC, SWMG(A)
Regional Anesthesia - Principles
References
Military Advanced Regional Anesthesia and
Analgesia Ch. 2 – 4
Pathophysiology for the Health Professions 4th
Edition Ch. 6 p.126
Basis Guide to Anesthesia for Developing
Countries, Volume 1, Daniel D. Moos
(International Federation of Nurse
Anesthetists, ifna-int.org)
Students should be encouraged to read all of the references multiple times as part of written test preparation.
BGAD volume 2 is very basic and easy to read with testable information
Pathophysiology for Health Professional, page 126 discusses normal nerve conduction
The figure on slide represents a peripheral nerve. The left side of figure represents the resting state of “polarization.” The outside of the nerve is positively charged by the presence of sodium ions Na+. The inside is negatively charged by the presence of potassium ions K+. For discussion our figure is a sensory nerve. When stimulation is applied to the nerve, Na+ channels open, and sodium enters the nerve starting an impulse that moving along nerve terminating at the spine and CNS.
In order to return to resting state, in order to send additional signals or not send signals when painful stimulus is removed the nerve must “repolarize” by having sodium leave the nerve cells and potassium enter via sodium potassium pump.
Local anesthetics are valued for the ability to prevent membrane depolarization of nerve cells. Local anesthetics prevent depolarization of nerve cells by binding to cell membrane sodium channels and inhibiting the passage of sodium ions. Military Advanced Regional Anesthesia and Analgesia p.11
Compared to general anesthesia with opioid-based perioperative pain management, can provide superior pain control, improved patient satisfaction, decreased stress response to surgery, reduced operative and post operative blood loss, diminished post operative nausea and vomiting, and decreased logistical requirements. Military Advanced Regional Anesthesia and Analgesia p.11
Instructor Notes: Remind students that MARAA was written for level three and above facility work, but regional anesthesia can be used at any phase from point of injury forward.
"This technology can only confirm and refine correct needle placement for regional blocks; it should never be considered a substitute for the physician's understanding of the anatomical basis for each block."
Paraesthesia: Oldest regional technique uses anatomical knowledge of the location of peripheral nerves in relation to anatomic structures to guide needle placement in proximity of nerves. Actually contacting the nerve is a goal of this technique eliciting a “paraesthesia” to gage placement. This technique has the least logistical requirements, but can be challenging because the provider has no feed back to get needle closer to nerve other than painful nerve response. More appropriate for more superficial sensory nerves of distal extremities.
Nerve stimulation: Although an old technique, it has become standardized with the widespread use of specific nerve stimulator devices and specialized needles. Although anatomic knowledge is required, this technique uses motor response of specific muscles to gage placement of needles close to targeted nerves. This technique requires specific needles and nerve stimulators to work, and is suitable for deep nerves, but probably not appropriate for superficial sensory nerves.
Ultrasound guided: This technique uses ultrasound technology to visualize nerves and other anatomic structures to gage placement of needles and locals "real time." This technique requires the skill in use of ultrasound and ability to manipulate needles using the 2-D image of the screen.
Note: In SFMS/SOIDC, you will start out using nerve stimulators on human role models and conclude using nerve stimulators and paraesthesia techniques on each other.
Use this rough diagram of a femoral cross section to explain the three different techniques. Remind the students that knowledge of anatomy is a critical skill to performing any regional anesthesia.
Using longer acting agents can have significant effect on patients for many hours. Because the patient feels no pain they may they can move around. For example, with a high sciatic block the patient will have no motor function for 6-8 hours and will have a “weird” sensation that will have to explain to them or they may get panicky.
In your practice, you may not have a separate “regional” area, but you must allow for 10-20 minutes of regional “set-up” time before it will provide adequate sensory and motor blockade.
The use of regional anesthesia by anyone other than a CRNA or anesthesiologist is controversial at the least
There are many MD board certified physicians who do not do this. Very much a specialty which can be requested by those not skilled in applying it
There are many contraindications for the novice provider that may not exist for the true professional
Regional anesthesia is very anatomy dependent; you have to know where you are on the human body. MARAA provides good ways to approach many different blocks, but you have to know what the reference is describing in order to use it. Laying out of land marks is key to the development of regional skills. You may see some providers not mark out landmarks, however this is not recommended, especially for the novice provider.
Regional anesthesia is not a sterile procedure, but is clean and precautions should be taken to maintain cleanliness
Local anesthetics are valued for the ability to prevent membrane depolarization of nerve cells. Local anesthetics prevent depolarization of nerve cells by binding to cell membrane sodium channels and inhibiting the passage of sodium ions.
The sodium channel is most susceptible to local anesthetic binding in the open state, so frequently stimulated nerves tend to be more easily blocked. The ability of a given local anesthetic to block a nerve is related to the length of the nerve exposed, the diameter of the nerve, the presence of myelination, and anesthetic used. Small or myelinated nerves are more easily blocked than large or unmyelinated nerves.
An example of this the A-d (fibers (sharp pain/temperature) of the finger are easier to block than the C fibers (chronic pain) of that same finger. Another example, the C fibers of the foot would be easier to block than the C fibers of the high sciatic.
Potency (lipid solubility) - The potency (how quickly it works and binds with Na+ channels) of local anesthetics is determined by lipid solubility. As lipid solubility increases, the ability of the local anesthetic molecule to penetrate connective tissue and cell membrane increases, causing the increase in potency.
Duration-(protein binding) – The duration of action (how long it works) is determined by protein binding. Local anesthetics with high affinity for protein binding remain bound to nerve membranes longer, resulting in an increased duration of action.
Lidocaine- (30-60 minutes) – Is considered a short to medium acting agent. Lidocaine is the most versatile and widely used local anesthetic. Subcutaneous infiltration is commonly done. Not considered a good agent for regional anesthesia because the analgesia is considered too short of action to be of benefit in the post operative period.
Mepivacaine- (45-90 minutes) – Is considered a medium acting agent. Mepivacaine has similar onset of lidocaine but has longer duration and also less neurotoxic and cardiotoxic than lidocaine. Low toxicity, rapid onset, and dense motor block can make it an attractive for surgical applications.
Ropivacaine- (120-360 minutes) – Is considered a long acting agent. Ropivacaine is considered the safest long-acting local anesthetic currently available. Ropivacaine is the long-acting anesthetic of choice at Walter Reed Army Medical Center because of its favorable safety profile and efficacy.
Bupivacaine- (120-240 minutes) - Is considered a long acting agent. Bupivacaine has the longest latency to onset of block. Bupivacaine is noted for having a propensity for sensory block over motor (desirable characteristic). It is low in cost. The cardiac toxicity with this agent post intravascular injection has been reported, in fact, it is the most common agent with cardiovascular collapse occurring.
Duration of action times Basic Guide to Anesthesia for Developing Countries, Volume 1 and would be considered very conservative
Lidocaine- (30-60 minutes) – Is considered a short to medium acting agent. Lidocaine is the most versatile and widely used local anesthetic. Subcutaneous infiltration is commonly done. Not considered a good agent for regional anesthesia because the analgesia is considered too short of action to be of benefit in the post operative period.
Mepivacaine- (45-90 minutes) – Is considered a medium acting agent. Mepivacaine has similar onset of lidocaine but has longer duration and also less neurotoxic and cardiotoxic than lidocaine. Low toxicity, rapid onset, and dense motor block can make it an attractive for surgical applications.
Ropivacaine- (120-360 minutes) – Is considered a long acting agent. Ropivacaine is considered the safest long-acting local anesthetic currently available. Ropivacaine is the long-acting anesthetic of choice at Walter Reed Army Medical Center because of its favorable safety profile and efficacy.
Bupivacaine- (120-240 minutes) - Is considered a long acting agent. Bupivacaine has the longest latency to onset of block. Bupivacaine is noted for having a propensity for sensory block over motor (desirable characteristic). It is low in cost. The cardiac toxicity with this agent post intravascular injection has been reported, in fact, it is the most common agent with cardiovascular collapse occurring.
Duration of action times Basic Guide to Anesthesia for Developing Countries, Volume 1 and would be considered very conservative
The basic equipment is considered necessity to do any anesthesia. CNS toxicity is the most common risk and this is exacerbated by hypoxia, hence the airway equipment. The advanced gear includes on top of ACLS capability includes Intralipids. Intralipid is a brand name for a fat emulsion for human use. It was approved in the United States in 1972. It is used as a component of parenteral nutrition for patients who are unable to get nutrition via an oral diet. It is an emulsion of soy bean oil, egg phospholipids and glycerin. It is the same emulsion in propofol, however Intralipid is 20% and Propofol is 10%. The thought is free locals bind with the fat in the emulsion preferentially compared to the CNS. It is very safe to administer.
Neurotoxicity
Local anesthetics are shown to be both myotoxic and neurotoxic. The significance is not really known, but long term regional with pumps can in theory cause muscle dysfunction. Also injecting directly into nerve can cause nerve death.
CNS Toxicity
Local anesthetics are indispensable to the successful to the successful practice of regional anesthesia, and providers who use these techniques must be familiar with the signs of and symptoms of local anesthetic toxicity. Initial excitatory symptoms of local anesthetic toxicity are manifestations of escalating drug concentrations in the central nervous system, specifically blocking the inhibitory pathways, resulting in unopposed excitatory neuron function. This is manifested clinically as symptoms:
Muscular twitching
Visual disturbances
Tinnitus
Light-headedness
Tongue and lip numbness
Extreme anxiety, screaming, and impending death feelings
As the blood concentration increases, these initial symptoms, without intervention, will progress:
Generalized tonic-clonic convulsions
Coma
Respiratory arrest
Death
Cardiac Toxicity
The cardiovascular system, though significantly more resistant to local anesthetic toxicity than CNS, will exhibit arrhythmias and eventual collapse. In general, agents with longer duration of action Ropivacaine and especially Bupivacaine have greater potential for causing cardiac depression and arrhythmias.
What is the risk? One study stated 7.5-20 cases per 10,000 of cardiovascular collapse associated with regional anesthesia.
Neurotoxicity
Local anesthetics are shown to be both myotoxic and neurotoxic. The significance is not really known, but long term regional with pumps can in theory cause muscle dysfunction. Also injecting directly into nerve can cause nerve death.
CNS Toxicity
Local anesthetics are indispensable to the successful to the successful practice of regional anesthesia, and providers who use these techniques must be familiar with the signs of and symptoms of local anesthetic toxicity. Initial excitatory symptoms of local anesthetic toxicity are manifestations of escalating drug concentrations in the central nervous system, specifically blocking the inhibitory pathways, resulting in unopposed excitatory neuron function. This is manifested clinically as symptoms:
Muscular twitching
Visual disturbances
Tinnitus
Light-headedness
Tongue and lip numbness
Extreme anxiety, screaming, and impending death feelings
As the blood concentration increases, these initial symptoms, without intervention, will progress:
Generalized tonic-clonic convulsions
Coma
Respiratory arrest
Death
Cardiac Toxicity
The cardiovascular system, though significantly more resistant to local anesthetic toxicity than CNS, will exhibit arrhythmias and eventual collapse. In general, agents with longer duration of action Ropivacaine and especially Bupivacaine have greater potential for causing cardiac depression and arrhythmias.
What is the risk? One study stated 7.5-20 cases per 10,000 of cardiovascular collapse associated with regional anesthesia.
Neurotoxicity
Local anesthetics are shown to be both myotoxic and neurotoxic. The significance is not really known, but long term regional with pumps can in theory cause muscle dysfunction. Also injecting directly into nerve can cause nerve death.
CNS Toxicity
Local anesthetics are indispensable to the successful to the successful practice of regional anesthesia, and providers who use these techniques must be familiar with the signs of and symptoms of local anesthetic toxicity. Initial excitatory symptoms of local anesthetic toxicity are manifestations of escalating drug concentrations in the central nervous system, specifically blocking the inhibitory pathways, resulting in unopposed excitatory neuron function. This is manifested clinically as symptoms:
Muscular twitching
Visual disturbances
Tinnitus
Light-headedness
Tongue and lip numbness
Extreme anxiety, screaming, and impending death feelings
As the blood concentration increases, these initial symptoms, without intervention, will progress:
Generalized tonic-clonic convulsions
Coma
Respiratory arrest
Death
Cardiac Toxicity
The cardiovascular system, though significantly more resistant to local anesthetic toxicity than CNS, will exhibit arrhythmias and eventual collapse. In general, agents with longer duration of action Ropivacaine and especially Bupivacaine have greater potential for causing cardiac depression and arrhythmias.
What is the risk? One study stated 7.5-20 cases per 10,000 of cardiovascular collapse associated with regional anesthesia.
Neurotoxicity
Local anesthetics are shown to be both myotoxic and neurotoxic. The significance is not really known, but long term regional with pumps can in theory cause muscle dysfunction. Also injecting directly into nerve can cause nerve death.
CNS Toxicity
Local anesthetics are indispensable to the successful to the successful practice of regional anesthesia, and providers who use these techniques must be familiar with the signs of and symptoms of local anesthetic toxicity. Initial excitatory symptoms of local anesthetic toxicity are manifestations of escalating drug concentrations in the central nervous system, specifically blocking the inhibitory pathways, resulting in unopposed excitatory neuron function. This is manifested clinically as symptoms:
Muscular twitching
Visual disturbances
Tinnitus
Light-headedness
Tongue and lip numbness
Extreme anxiety, screaming, and impending death feelings
As the blood concentration increases, these initial symptoms, without intervention, will progress:
Generalized tonic-clonic convulsions
Coma
Respiratory arrest
Death
Cardiac Toxicity
The cardiovascular system, though significantly more resistant to local anesthetic toxicity than CNS, will exhibit arrhythmias and eventual collapse. In general, agents with longer duration of action Ropivacaine and especially Bupivacaine have greater potential for causing cardiac depression and arrhythmias.
What is the risk? One study stated 7.5-20 cases per 10,000 of cardiovascular collapse associated with regional anesthesia.
Neurotoxicity
Local anesthetics are shown to be both myotoxic and neurotoxic. The significance is not really known, but long term regional with pumps can in theory cause muscle dysfunction. Also injecting directly into nerve can cause nerve death.
CNS Toxicity
Local anesthetics are indispensable to the successful to the successful practice of regional anesthesia, and providers who use these techniques must be familiar with the signs of and symptoms of local anesthetic toxicity. Initial excitatory symptoms of local anesthetic toxicity are manifestations of escalating drug concentrations in the central nervous system, specifically blocking the inhibitory pathways, resulting in unopposed excitatory neuron function. This is manifested clinically as symptoms:
Muscular twitching
Visual disturbances
Tinnitus
Light-headedness
Tongue and lip numbness
Extreme anxiety, screaming, and impending death feelings
As the blood concentration increases, these initial symptoms, without intervention, will progress:
Generalized tonic-clonic convulsions
Coma
Respiratory arrest
Death
Cardiac Toxicity
The cardiovascular system, though significantly more resistant to local anesthetic toxicity than CNS, will exhibit arrhythmias and eventual collapse. In general, agents with longer duration of action Ropivacaine and especially Bupivacaine have greater potential for causing cardiac depression and arrhythmias.
What is the risk? One study stated 7.5-20 cases per 10,000 of cardiovascular collapse associated with regional anesthesia.
Blocked Extremities(Risk Factors)
Neurological Function
Prior to performing a regional block one should test motor and sensory deficits prior to performing a block (especially if being done for exclusively for pain control), so receiving facility is aware of nerve damage/deficit prior to block
Splinting
Remember, if you perform a correct block the patient will not have sensory or motor function. If an extremity is splinted and there are pressure points created, that patient cannot provide feedback to you about a poor splint job. Long term this could be bad to both the soft tissue and superficial neurovascular beds
Compartment Syndrome
The same problem with splinting carries over to injuries that could be at risk of compartment syndrome. This has been observed in regionally block patients during transport from Europe to stateside medical facilities.
Establish your baseline before you begin
Table 3-2 Military Advanced Regional Anesthesia and Analgesia p.14
Table 3-2 Military Advanced Regional Anesthesia and Analgesia p.14
This represents one example of ways of accessing intravascular penetration; it is a modification of "Raj" test found on Figure 2-3 Military Advanced Regional Anesthesia and Analgesia p.7
Note: The students may make an inquiry of higher doses of epinephrine namely 1:100,000 to increase block time and allow for greater volume of agents. The use of epinephrine based solutions to prolong regional blocks is discouraged because of vasoconstrictive effects on the nerves themselves ~ 80%. If a longer block is desired, select a more potent agent.
We have talked about background information about regional anesthesia. Now let's talk specifically about "nerve stimulation" The figure on slide represents a peripheral nerve with different fibers. Fibers that we have already addressed are A-d (sharp pain) and C (chronic or aching pain). One more that is essential for nerve stimulation is A-a (motor). The threshold for response for these motor fibers is less than the pain fibers, when specific electrical stimulation in milliamps is applied to the nerve it depolarizes terminating with a motor/muscle response. The milliamp setting should be low enough to get motor response but not pain. Pain with stimulators is usually associated with sensory stimulation of small superficial nerves. Smarter people than I have determined what muscle response is appropriate for a given fiber. All the different nerve fibers are collocated. The motor of response of the sciatic nerve with our needle corresponds with being close to the sciatic nerve. If I am close to the nerve and deliver my agent, I will get motor and sensory blockade. The patient will not move (motor) (areflexia) and will not feel anything (sensory) (analgesia).
Continuation of slide 23
A-d and C fibers are “afferent” nerves, A-a with motor stimulation is an efferent effect
