Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_612_Библиотеки_им_академика_М_И_Перельмана
.pdf
such as epinephrine cause decreased plasma distribution, leading to decreased clearance
and increased durations of action.
TABLE 11.1. WEIGHT-BASED DOSAGE AND DURATION OF LOCAL ANESTHETICS
Plain
With
Epinephrine
Anesthetic Maximum
Dose (mg)
Duration of
Action
(minutes)
Maximum
Dose (mg)
Duration of
Action
(minutes)
Bupivacaine 2 mg/kg 120-240 3 mg/kg 180-420
Levobupivacaine 2 mg/kg 120-240 3 mg/kg 180-420
Lidocaine 5 mg/kg 30-60 7 mg/kg 120-360
Mepivacaine 5 mg/kg 45-90 7 mg/kg 120-360
Ropivacaine 3 mg/kg 120-240 3 mg/kg 180-420
Prilocaine 8 mg/kg 30-90 8 mg/kg 210-360
Data Compiled from El-Boghdadly K, Pawa A, Chin KJ. Local anesthetic systemic toxicity: current
perspectives. Local Reg Anesth. 2018; 11:35-44; Strichartz GR, Covino BG. Local anesthetics. In: Miller RD,
ed. Anesthesia. 4th ed. New York, NY: Churchill Livingstone; 1994.
The addition of epinephrine in local anesthetics is traditionally used to prolong the
duration of action while decreasing the toxicity secondary to decreased plasma levels.
Traditionally, epinephrine is added to an anesthetic solution into a concentration of
1:200,000 or 1:100,000. The addition of epinephrine improves hemostasis through
vasoconstriction, enhances visualization, and decreases blood loss during local anesthesia
procedures. The effect on the pharmacokinetics of epinephrine with different agents can be
seen in Table 11.1. Previously, there were significant concerns utilizing epinephrine in
proximity to end arteries with small-caliber vessels (eg, fingers, toes, penis, nose, and
ears). The fear was that the vasoconstrictive effects of epinephrine on the end arteries
would result in potentially critical ischemia and subsequent necrosis of these appendages.
Current evidence demonstrates the contrary.6 Epinephrine is safe to use in the vicinity of
end arteries with extremely low rates of complications noted with their use.7 In fact, more
recent data demonstrate that epinephrine is not only safe for use, but its use, particularly in
hand surgery, may also be associated with lower complications including decreased risk of
bleeding, better visualization with increased ease of surgery, and prolonged procedural pain
relief.
1,7
In situations where ischemia persists and is of concern, phentolamine or terbutaline
are alpha antagonists that are used to reverse the ischemic effects. However, the need for
this is rare. Overall, the use of epinephrine in distal appendages anesthesia is safe and
recommended.
Toxicity
Toxicity of local anesthetics typically manifests as symptoms affecting primarily the central
nervous system (CNS) and the cardiovascular system (CVS). As plasma concentrations of
local anesthetics increase, the blockade of sodium channels initially affects inhibitory
https://t.me/med1917
pathways within the CNS.8 This results in initial excitatory symptoms including visual
changes, agitation, restlessness, confusion, tinnitus, muscle twitches, and paranoia. This
may eventually progress to seizure activity. With increased plasma concentrations, the
depression on excitatory pathways then begins, resulting in circumoral numbness, tongue
paresthesia, dizziness, and eventual loss of consciousness with respiratory arrest. CVS
toxicity primarily results from rhythm disturbances and myocardial dysfunction. The rhythm
disturbances result from the blockade of sodium conduction, impeding signal propagation
from the pacemaker cells to the myocardium, resulting in prolonged intervals that may be
evident on an electrocardiogram. Local anesthetic effects on intracellular calcium signaling
produce reduced myocardial contractility. The combination of impeded cardiac conduction
with reduced myocyte contractility results in cardiac electrical lability, arrhythmias, reduced
cardiac output, decreased peripheral vascular tone, and hypotension.
Dosing
The safe dosing of local anesthetics requires the maintenance of safe plasma levels so as
to achieve drug effect while minimizing systemic toxicities. As real-time monitoring of
plasma concentrations remains impractical, dosing guidelines standardly use weight-based
calculations for safe administration. In this setting, the patient’s weight is used as a
surrogate by which to estimate the patient’s volume of distribution. Patients with greater
body mass and subsequent volume represent greater volumes of distribution for the
medications, and therefore, lower plasma concentrations will be achieved for a given dose
of a particular agent. Typical weight-based dosing recommendations and durations of
action can be seen in Table 11.1. These dosing guidelines must be adjusted within the
setting of patient physiology and comorbidities as these may alter medication metabolism
and therefore subsequent plasma levels.
Patient age has been associated with the need to alter dosing guidelines, particularly in
the young and elderly. Infants have decreased α1-acid glycoprotein and hepatic enzyme
activity. This results in greater free plasma concentrations of agents at given weight-based
dosing. Therefore, a 15% reduction in dose is recommended for patients less than
4 months of age.4 Similarly, elderly patients often present with multiple comorbidities and
reduced skeletal muscle mass and adiposity. This results in decreased metabolism and
higher free plasma levels at given doses. A 10% to 20% dose reduction is therefore
recommended in these patients.
9
Dosing is also dependent on the technique of administration. Techniques that result in
greater access of the agent to the blood stream require lower dosing and have shorter
durations of action than those that direct the agent to reservoirs such as skeletal muscle
and adipose tissue. The maximum dosing and duration of action for epinephrine- and non–
epinephrine-containing anesthetics differ for subcutaneous infiltration (Table 11.2), minor
nerve blocks (Table 11.3), and major nerve blocks (Table 11.4).
TABLE 11.2. DOSAGE AND DURATION CHARACTERISTICS OF THE LOCAL
ANESTHETICS WHEN USED FOR INFILTRATION ANESTHESIA (EG,
INFILTRATION AROUND THE PERIPHERY OF A SKIN LESION BEFORE
EXCISION)
Plain Solution Epinephrine-Containing Solution
https://t.me/med1917
Drug Concentration
(%)
Maximal
Dose
(mg)
Duration
(min)
Maximal
Dose
(mg)
Duration
(min)
Duration
Procaine
Chloroprocaine 1.0-2.0 800 15-30 1000 30-90
Moderate Duration
Lidocaine 0.5-1.0 300 30-60 500 120-360
Mepivacaine 0.5-1.0 300 45-90 500 120-360
Prilocaine 0.5-1.0 500 30-90 600 120-360
Long Duration
Bupivacaine 0.25-0.5 175 120-240 225 180-420
Etidocaine 0.5-1.0 300 120-180 400 180-420
Reprinted with permission from Strichartz GR, Covino BG. Local anesthetics. In: Miller RD, ed. Anesthesia.
4th ed. New York, NY: Churchill Livingstone; 1994.
TABLE 11.3. DOSAGE AND DURATION CHARACTERISTICS OF THE LOCAL
ANESTHETICS WHEN USED FOR MINOR NERVE BLOCKS (EG, MEDIAN NERVE
BLOCK AT THE WRIST)
Plain Solutions
EpinephrineContaining
Solutions
Drug Usual
Concentration
(%)
Usual
Volume
(mL)
Dosage
(mg)
Average
Duration
(min)
Average
Duration
(min)
Procaine 2 5-20 100-
400
15-30 30-60
Chloroprocaine
Lidocaine
Mepivacaine 1 5-20 50-200 60-120 120-180
Prilocaine
Bupivacaine 0.25 5-20 12.5-50 180-360 240-480
Etidocaine 0.5 5-20 25-100 120-240 180-420
TABLE 11.4. DOSAGE AND DURATION CHARACTERISTICS OF THE LOCAL
ANESTHETICS WHEN USED FOR MAJOR NERVE BLOCKS (EG, AXILLARY
https://t.me/med1917
BLOCK OF THE BRACHIAL PLEXUS)
Drug With
Epinephrine
1:200,000
Usual
Concentration
(%)
Usual
Volume
(mL)
Maximal
Dose
(mg)
Usual
Onset
(min)
Usual
Duration
(min)
Lidocaine 1-1.5 30-50 500 10-20 120-240
Mepivacaine 1-1.5 30-50 500 10-20 180-300
Prilocaine 1-2 30-50 600 10-20 180-300
Bupivacaine 0.25-0.5 30-50 225 15-30 360-720
Etidocaine 0.5-1.0 30-50 400 10-20 360-720
Tetracaine 0.25-0.5 30-50 200 20-30 300-600
Reprinted with permission from Strichartz GR, Covino BG. Local anesthetics. In: Miller RD, ed. Anesthesia.
4th ed. New York, NY: Churchill Livingstone; 1994.
Tumescent Anesthesia
Tumescent anesthesia typically injects high-volume dilute local anesthetic solutions
containing epinephrine to facilitate procedures such as liposuction. Typical compositions of
tumescent solution are formulated with 300 to 1000 mg of lidocaine per 1 L of solution
(normal saline or lactated Ringer solution) mixed with epinephrine (1:500,000-1:100,000).
The infiltration is focused on the adipose and subcutaneous tissues, which act as reservoirs
for the agents, resulting in a prolonged release to the blood plasma. The American Society
for Dermatologic Surgery Guidelines of Care for Liposuction recommend a maximal safe
dosage of lidocaine in the tumescent solution during liposuction cases of 55 mg/kg,10 but
other studies have recommended a maximum of 45 and 28 mg/kg if liposuction is not
performed.11 The timing of peak doses of local anesthetics used in tumescent techniques is
dependent on the location of infiltration. Injection to sites above the clavicle (highly vascular
areas) typically demonstrates peak plasma concentrations 6 hours after administration but
can peak as late as 10 to 14 hours. Peak concentrations in areas injected below the
clavicles (less vascular areas) typically occur at 12 hours but may peak as late as 12 to 24
hours after infiltration. Mortality from tumescent anesthesia has nearly exclusively been
reported in patients who underwent concomitant general anesthesia at the time of their
procedures, but symptoms of toxicity can present late secondary to delayed peak
concentration times. Thus, practitioners must be aware as the increase in office-based
procedures may result in patients presenting signs of toxicity after discharge.
Allergies
Allergic reactions to anesthetic agents themselves are extremely rare. Reactions to local
anesthetics traditionally are attributed to adverse responses to epinephrine, toxicity from
the local anesthetics, or vasovagal syncope. Allergies have been reported to preservatives
added in the compounding process such as metabisulfite and methylparaben (paraaminobenzoic acid derivatives). True allergies are rare but have been reported and are
noted to occur more frequently with amino esters than amino amides.
12
Treatment of Local Anesthesia Toxicities
https://t.me/med1917
The initial treatments of a patient experiencing local anesthetic systemic toxicity (LAST) are
recognizing the toxicity, cessation of the agent, activating the appropriate emergency
systems, and providing supportive treatment. Initial supportive efforts focus on establishing
an airway while maintaining breathing and circulation. The airway should be secured and
the patient intubated if needed. Oxygenation should begin with 100% O2 as hypercarbia
can worsen CNS toxicity. Hypercarbia lowers seizure threshold and therefore increased
ventilation may terminate seizures via reversal of the lowered threshold. However, it is
important to avoid over hyperventilation as this may cause a respiratory alkalosis, which
has also been demonstrated to increase morbidity.13 In the seizing patient, the convulsing
activity exacerbates a metabolic acidosis, worsening the condition. The first line of
treatment in LAST seizures remains benzodiazepines as they are cardiac stable. Diazepam
(0.1 mg/kg) is often the first-line agent.14 Propofol should be limited to small doses to treat
seizures as large doses are associated with cardiovascular depression and compromise.
4
LAST may cause cardiovascular collapse and hypotension. Therapy with intravenous
fluids should be initiated immediately with Advanced Cardiovascular Life Support protocols.
Maintenance of end-organ perfusion and blood pressure if needed can occur with positive
inotropes and vasopressor agents such as epinephrine and phenylephrine. Vasopressin
should be avoided as it has been associated with adverse outcomes in animal models.4 In
severe cardiovascular collapse that is unresponsive, cardiopulmonary bypass may be
initiated.
Early administration of intravenous lipid (IntralipidÒ) is essential in the management of a
severe LAST episode. Lipid emulsion therapy should be initiated immediately after securing
an airway. IntralipidÒ is a 20% intravenous lipid emulsion that has been used in safety
protocols for local anesthetic toxicity since 2008. The mechanism by which lipid emulsion
treats LAST is multipronged. First, lipid emulsion sequesters local anesthetic agents from
organs such as the heart and brain and shuttles it to end organs such as skeletal muscle
and the liver where it is metabolized.15 This functions to lower the CNS and CVS toxicities
and promote clearance of the anesthetic agents. Additionally, lipid emulsion therapy directly
stimulates cardiac output with positive ionotropic and pressor effects, helping to counteract
the CVS toxicities while providing postconditioning myocardial protection.
16,17
The lipid
emulsion protocol recommended by the American Society of Regional Anesthesia and Pain
Medicine protocol18 is demonstrated in Figure 11.1. Practitioners who use local anesthetics
should familiarize themselves with these protocols.
https://t.me/med1917
FIGURE 11.1 American society of regional anesthesia and pain medicine lipid
emulsion protocol for local anesthetic toxicity. (Reproduced from Neal JM, Gravel
Sullivan A, Rosenquist RW, Kopacz DJ. Regional anesthesia and pain medicine:
US anesthesiology resident training-the year 2015. Reg Anesth Pain Med.
2017;42:437-441. With permission from BMJ Publishing Group Ltd.)
Liposomal Bupivacaine
Liposomal bupivacaine is currently available and marketed under the trade name Exparel
by Pacira Pharmaceuticals for the nonopioid treatment of postoperative pain. Exparel uses
proprietary multivesicular liposomal technology to encapsulate bupivacaine and release the
agent over 72 hours from a single injection. It is currently approved by the US Food and
Drug Administration (FDA) for local infiltration and interscalene blocks performed at the
brachial plexus for patients older than 6 years of age. Initial data for the support of its use
were based on early trials that demonstrated improvement in pain post injection for 24
hours in patients who underwent bunionectomy and hemorrhoidectomy.
19,20
More recent
https://t.me/med1917
studies have demonstrated improved pain control for 72 hours when used as a fascial block
in patients undergoing C-sections and when used for regional anesthesia in patients
undergoing total shoulder arthroplasty, total knee arthroplasty, and rotator cuff repair.21-23 In
these studies, reduction in narcotic usage was noted over these same time periods.
Liposomal bupivacaine has been used in plastic surgery for cosmetic procedures,
peripheral nerve blocks, regional blocks, and breast surgery. It has been proposed as an
alternative to more traditional pain management protocols including indwelling catheters,
patient-controlled analgesia devices, and even intravenous narcotics. Studies assessing
the effectiveness of liposomal bupivacaine for use in breast reconstruction, augmentation
mammaplasty, abdominal wall reconstruction, mastectomy, and abdominoplasty
demonstrated adequate safety with equivalent to improved pain control as compared to
traditional analgesia modalities.24 Studies of the effect of Exparel on pain and opioid
consumption in patients undergoing distal radius fracture fixation noted decreased pain and
opioid consumption only on the day of surgery and not further.25 Unfortunately, large
systematic reviews of articles examining the effectiveness of liposomal bupivacaine
demonstrate that while it does decrease postoperative pain as compared to placebo, the
limited evidence available at this time does not demonstrate greater effectiveness than
standard bupivacaine.26 Therefore, though liposomal bupivacaine may represent an agent
that can provide delivery of anesthesia and pain control over a longer period of time for
plastic surgical procedures, further studies are required to determine the true efficacy and
benefits.
Liposomal bupivacaine toxicity studies in the peer reviewed literature remain sparse.
Limited published data reported maximum plasma concentration levels that were noted to
remain well below the maximum FDA-recommended dose.27 It is important to note that
liposomal bupivacaine may interact with other anesthetic agents, and therefore, the
manufacturer recommends that liposomal bupivacaine not be combined with other
nonbupivacaine local anesthetics for simultaneous administration. Nonbupivacaine local
anesthetics facilitate the release of the encapsulated bupivacaine, thus hastening rises in
drug levels. LAST events with liposomal bupivacaine have been reported and mirror those
for nonliposomal bupivacaine.28 Therefore, practitioners must exercise the same caution
and vigilance when utilizing these products.
MINOR NERVE BLOCKS
Minor nerve block refers to the direct infiltration of local anesthetic in the vicinity of a
specific distal nerve to induce analgesia and anesthesia. Minor nerve blocks contrast with
infiltrative anesthesia in that instead of providing untargeted anesthetic to a generalized
area resulting in diffusion-limited analgesia, these blocks hone in on a nerve(s) to
completely anesthetize its dermatome. This allows for lower injected volumes with possible
larger fields of anesthesia but does suffer from the decreased benefit of the
vasoconstrictive properties of epinephrine. Minor nerve blocks increase patient comfort and
provide immediate postprocedural pain relief with minimal morbidity. The use of minor
nerve blocks has become an essential practice for plastic and reconstructive surgeons.
These blocks can be used in conjunction with general anesthesia to reduce the narcotic
and general anesthetic needs during and after an operative procedure. Minor nerve blocks
also allow procedures to be performed in the clinic, emergency department, or office
operating room setting without the need of anesthesiologists and invasive monitoring.
Applications of minor nerve blocks in plastic surgery include trigeminal nerve blocks for the
completion of facial reconstructive/cosmetic surgery, facial injectables, and laceration
https://t.me/med1917
repair; distal nerve blocks for the repair of finger, hand, wrist, and elbow injuries; fascial
blocks for cosmetic and reconstructive abdominal surgeries; and diagnostic peripheral
nerve blocks for migraines and chronic peripheral nerve pain. Minor nerve blocks for these
procedures demonstrate many advantages as compared to general anesthesia including
reductions in postoperative pain, narcotic use, and PONV. Additionally, surgery centers and
offices may benefit with quicker discharges, fewer nursing interventions, lower rates of
hospital readmission, and overall lower costs.
29
Successful minor nerve blocks require a thorough understanding of the pertinent
anatomical location of the targeted nerve as well as surrounding vascular structures.
Precise injection ensures maximal anesthesia of the targeted nerve while minimizing side
effects from intravascular injection or unwanted motor nerve inhibition. As minor nerve
blockade depends on a single injection to achieve anesthesia, the duration of action is
limited by the pharmacokinetics of the chosen anesthetic agent. Short-acting agents with
fast recovery profiles may be selected to minimize the duration of unwanted motor nerve
blockade and if early return of sensation is required. Long-acting agents can provide
extended analgesia. Regardless of the anesthetic used, rebound pain on block regression
occurs and must be managed appropriately with adjuvant pain control.
Facial Blocks
Minor nerve blocks play a major role in reconstructive and cosmetic facial surgery. In the
face, infiltrative anesthesia is often employed secondary to the vasoconstrictive effects of
epinephrine-containing anesthetics. This provides for decreased bleeding, increased
visualization, and better identification of vital structures. However, minor nerve blocks often
are preferable in certain clinical scenarios. As minor nerve blocks can provide anesthesia
over an entire dermatome with smaller volumes of anesthetic, they are often favored when
procedures are performed on large areas of tissue where the volumes of infiltrative
anesthesia required for a field block to the area would be impractical or unsafe. Additionally,
infiltrative anesthesia typically results in deformation of the tissues secondary to volume
effects from the infiltrated solution. This may be undesirable, especially in the face, where
the goal of the repair is based on restoration of the natural appearance and symmetry. For
example, in lip laceration repairs, correct alignment of essential anatomic structure such as
the vermillion border may be more difficult if the tissues are expanded with local anesthetic.
In such a clinic scenario, a more distant minor nerve block may provide adequate
anesthesia to perform the repair without tissue warping, facilitating realignment of the
tissues. It should be noted that the use of infiltrative anesthesia and minor nerve blocks are
not mutually exclusive. These techniques may be used in tandem to create the optimal
operative field if care is taken to ensure LAST does not occur.
Minor nerve blocks in the face are often used for reconstructive/cosmetic procedures and
facial fillers. Filler injections in the face can be painful because of the highly sensitive skin
of this area. Sensory nerve blocks of the trigeminal nerves used in conjunction with fillers
can decrease pain and increase tolerability of the injections.30 Cosmetic procedures that
have been performed safely with minor nerve blocks include but are not limited to cleft lip
surgery,31 otoplasty,29 rhytidectomy,32 blepharoplasty,33 and brow lift.34 Minor nerve blocks
are also essential in Mohs surgery reconstruction. Mohs surgery defects can be repaired in
the office setting utilizing trigeminal nerve blocks, allowing for skin grafts, complex closures,
local flaps, and even paramedian forehead flaps.35 Upper face blocks can also be used to
facilitate scalp laceration repairs.
https://t.me/med1917
The success of performing facial procedures under minor nerve block depends on correct
identification and isolation of the dermatomal nerve. Nerves that are commonly blocked for
these procedures include the supraorbital nerve, supratrochlear nerve, infraorbital nerve,
infratrochlear nerve, mental nerve, anterior ethmoidal nerve, inferior alveolar nerve, and
auriculotemporal nerve. Approaches to individual nerve blockades in the face are
demonstrated in Figure 11.2. Auricular blocks are also essential to facilitate repair of ear
lacerations in the emergency department, close cancer defects including Mohs surgical
defects, and perform cosmetic ear procedures such as otoplasty and lobule reduction. The
ear derives its sensation from five different nerves: the superficial temporal nerve, the
auriculotemporal nerve, the lesser occipital nerve, the great auricular nerve, and Arnold
nerve (a branch of the vagus nerve) (Figure 11.3). Blockade of the ear may be
accomplished via infiltration of the greater auricular and lesser occipital nerves in the neck
along the posterior border of the sternocleidomastoid muscle. Blockade of the
auriculotemporal and superficial temporal nerves may be accomplished just anterior to the
tragus. Blockade of Arnold nerve requires infiltration in the otic canal and conchal bowl if
intervention is required in the central ear.
https://t.me/med1917
FIGURE 11.2 Location of nerves for minor nerve blocks of the face.
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана