Professional Documents
Culture Documents
Carlo D. Franco, MD
Chairman Orthopedic Anesthesia
JHS Hospital of Cook County
www.CookCountyRegional.com
Chicago, IL
Fourth Edition
2010
This manual is intended for anesthesiology residents, nurse anesthetists and
fellow faculty members of the Department of Anesthesiology and Pain Management,
Cook County Hospital of Chicago. The writing in these pages reflects the author’s own
views and understanding of various regional anesthesia issues, as well as his
interpretation of the pertinent literature. The author has made every effort to give proper
credit to outside sources when applicable.
Patients and models appearing in this manual provided their written permission to
the author, to have their photographs taken for the purpose of teaching. Their decision
was voluntary and did not involve compensation of any kind. The photographs of cadaver
material shown in these pages, originate from dissections performed by the author in the
Anatomy Laboratory of Rush University Medical Center in Chicago, in compliance with
Rush University’s guidelines, as well as State and Federal laws and regulations.
Care has been taken to confirm the accuracy of the information presented.
However, the author is not responsible for errors or omissions, or for any consequences
resulting from application of the information and techniques in this manual, and makes
no warranty, expressed or implied, with respect to the contents of it.
This manual is in accordance with current recommendations, as of February 2010.
However, recommendations and guidelines change, therefore the reader is urged to check
for new indications, warnings and precautions.
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For my residents,
who make my coming to work
intellectually challenging and pleasurable
and
to the memory of my father
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CONTENTS
Chapter 1: Introduction
General considerations………………………………………………………………….. 8
Patient selection and premedication……………………………………………………. 8
Monitoring……………………………………………………………………………..… 9
Outcome issues…………………………………………………....................................... 9
Airway and regional anesthesia………………………………………………………….11
References……………………………………………………………………………..…12
Historical perspective………………..…………………………………………………..14
Chemical structure ……………………………………………………………………... 15
Mechanism of action and Na+ channels……………….………………………………....17
Pregnancy and local anesthetics……………………………………………………….....17
Fiber size and pattern of blockade………………….…………………………………....17
Local anesthetics additives…………….……………………….………………………..20
Metabolism………………………….………………………….……………………......24
Dibucaine number…………………………………………………………………...….. 24
Toxicity…………………………………………………….……………………….........25
Tumescent anesthesia……………………………………………………………….........26
Lipid emulsion……………………………………………………………………....…...27
Maximum dose…………………………………………………………………………...29
Methemoglobinemia……………………………………………………………….....….29
Allergy ………………………………………………………………………………......30
References……………………………………………………………………………......34
Spinal anesthesia
Anatomy………………………………………………………….........................37
Cerebrospinal fluid………………………………………………………….........38
Site of action and indications…………………………………….........................39
Determinants of spread………………………………………………………..…39
Anesthesia duration…………………………………………………………........41
Side effects and complications……………………………………………..…….41
Postdural puncture headache………………………………………………….….43
Transient neurological symptoms……………………………………………......44
Cauda equina syndrome…………………………………………………….........45
Back pain ………………………………………………………………….…….45
Spinal in the outpatient………………………………………………………..…46
Intrathecal adjuncts………………………………………………........................46
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Epidural Anesthesia
Anatomy………………………………………………………….........................47
Blockade characteristics………………………………………….........................47
Spread of local anesthetics……………………………………….........................47
Type of needles and catheters……………………………………………………48
Test dose…………………………………………………………........................48
Activating an epidural………………………………………………………........48
References…………………………………………………………………………......…49
Introduction…………………………………………………………………………........51
Strength and grade of recommendations…………………………………………………51
Venous thromboembolism……………………………………………………………….51
Risk of bleeding………………………………………………………………………….53
Thrombolytics……………………………………………………………………………54
Unfractionated heparin…………………………………………………………………..54
Low molecular weight heparin…………………………………………………………..55
Oral anticoagulants………………………………………………………………………56
Thrombin inhibitors……………………………………………………………………...57
References………………………………………………………………………………..59
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Chapter 7: Lower Extremity Blocks
Anatomy………………………………………………………………………………..115
Lateral femoral cutaneous nerve block………………………………………………...123
Femoral block……………………………………………………………………….….124
Obturator nerve block………………………………………………………………..... 128
Lumbar plexus block…………………………………………………………………....133
Sciatic nerve block, classic (Labat-Winnie)……………………………………….…...136
Sciatic nerve block, Franco’s…………………………………………………….……..138
Sciatic subgluteal nerve block, di Benedetto’s…………………………………….…...144
Sciatic subgluteal nerve block, Franco’s…………………………………………….....146
Popliteal nerve block, Franco’s…………………………………………………….…...148
References………………………………………………………………………….…...154
Introduction……………………………………………………………………………..156
Benefits…………………………………………………………………………………156
Stimulating versus non-stimulating catheters………………………………………….157
Catheter-related problems………………………………………………………………157
References……………………………………………………………………………....158
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CHAPTER 1
INTRODUCTION
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General considerations
The type of anesthesia for any procedure must be tailored to every individual
patient. There are patients who in general are not good candidates for regional anesthesia,
especially if they remain awake (e.g., drug abusers, pediatric patients). On the other hand,
we have a large successful experience with peripheral nerve blocks on drug abusers and
some pediatric patients, confirming that each case must be individually evaluated.
Judicious use of sedation increases patient’s cooperation and acceptance. Sedation
should be used to calm anxiety, but not to turn the patient unconscious or otherwise
unresponsive. This is especially true in blocks performed close to the neuraxis, like
interscalene blocks and lumbar plexus blocks. Keeping the patient lightly sedated, but
awake and cooperative, makes the procedure easier for both the patient and the
anesthesiologist. Traditionally it has been considered that an awaken patient would
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contribute to the safety of the technique by being able to communicate with us (e.g., pain
at injection, early subjective symptoms indicating impending systemic toxicity, etc). This
is now controversial since there is some evidence that nerves can be penetrated and
injection can be performed intraneurally, although extrafascicular, without pain.
Improvements in ultrasound technology with better imaging resolution could potentially
improve safety.
Monitoring
Every nerve block, whether it is performed in a dedicated room, holding area, OR,
PACU or office, must be treated as potentially dangerous. Monitoring blood pressure,
heart rate and pulse oximetry, as well as the establishment of an IV access must always
be considered. Supplemental oxygen should be given especially when sedation is being
used. Resuscitation equipment, including oxygen, ambu bag, airways of different sizes,
intubation equipment and tubes, along with appropriate resuscitation drugs and suction
capabilities, must always be readily available.
A clear strategy to deal with and treat complications must be in place. It is always
advisable, before starting a technique, to leave room at the head of the bed for the
anesthesiologist to manage the patient’s airway, should that become necessary.
Familiarity with the surroundings helps when dealing with emergencies.
Outcome
Is regional anesthesia safer than general anesthesia?
Every discussion on regional anesthesia must address the issue of its relative
safety compared to general anesthesia. Despite several studies suggesting it and an
intuitive feeling that regional anesthesia seems “safer’ than general anesthesia, no definite
and general answer can be given. The inability to give a clear answer comes from paucity
of evidence in the literature. Most of the outcome studies available to us have compared
the relative benefits of neuraxial anesthesia (spinal or epidural) versus general anesthesia
in intra abdominal surgery. Most of the studies lack the power (number of cases) to be
able to see a true difference, if it existed, and most of them are retrospective. Lack of
randomization raises the possibility of technique bias selection (i.e., regional anesthesia
may have been preferred in sicker patients obscuring its potential benefits).
Other problems have to do with the parameter chosen for comparison. To
compare mortality for example, the sample would have to be extremely large in order to
find a statistically significant difference, since mortality under any type of anesthesia is
extremely low. Other parameters like DVT, myocardial infarction, pneumonia seem more
adequate for comparison, but their rates vary according to the procedure and not just type
of anesthesia.
The physiological response to the stress of surgery or “surgical stress response”
involves release of local and central mediators leading to increased levels of, among
others, cathecolamines, cortisol, aldosterone and renin. It is also frequently associated
with hypercoagulability, immune response depression and protein wasting. The release of
local tissue inflammatory factors like cytokines and interleukins can be partially blocked
by non-steroidal anti-inflammatory drugs and peripheral nerve blocks using local
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anesthetics. The central response, responsible for the release of cathecolamines and
cortisol, can only be blocked by neuraxial blocks using local anesthetics. Determination
of hormonal markers for stress can be demonstrated after general anesthesia and after
certain regional anesthesia techniques. However, its impact on morbidity has not been
clearly established. If physiological parameters are measured (e.g., PO2, O2 sat) the
values obtained are frequently better (at least in the short term) after regional than general
anesthesia. However, the real impact that better postoperative physiological parameters
have on morbidity is not clear.
Nonetheless, there seems to be some agreement that regional anesthesia improves
the outcome of selective surgical procedures in a number of different ways, including
decreased rates of DVT, PE and blood loss.
Surgeries most associated with improved outcome after regional anesthesia include:
1. Hip surgery (hip fracture surgery and total hip arthroplasty): rates of DVT, PE and
blood loss are reduced after neuraxial anesthesia. The mechanism is unknown, but
may involve better peripheral circulation and less stasis.
Mortality rates also have been shown to be significantly lower with epidural
anesthesia as compared to general anesthesia.
2. Total knee arthroplasty: rates of DVT and PE are lower with neuraxial anesthesia.
3. Prostatectomy: similar reduction rates in DVT and PE and may also involve better
peripheral circulation and decreased venous stasis.
4. Peripheral vascular surgery: epidural anesthesia and postoperative epidural
analgesia have shown to improve graft patency after peripheral vascular surgery,
but does not seem to improve outcome after intra-abdominal vascular surgery.
Mechanism is not clear. Improve runoff due to vasodilatation or preservation of
normal coagulation has been mentioned.
5. Colon surgery: postoperative thoracic epidural analgesia with local anesthetics
has shown to enhance colonic activity after colon resection. If narcotics are used
in conjunction with local anesthetics this beneficial effect is lost.
1. Upper abdominal and thoracic surgery, this is despite the fact that better pain
scores and times to extubation after regional anesthesia can be demonstrated.
2. Upper and lower extremity surgery, even though the patients receiving regional
anesthesia may have a higher degree of satisfaction, better pain control and fewer
side effects like nausea and vomiting, especially immediately after surgery. This
difference rapidly disappears at 24 h.
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including 9,559 patients were included in this meta-analysis. The following are the main
findings:
1. Overall mortality was about one third less in the neuraxial group (103 deaths/4871
patients versus 144/4688 patients, P=0.006). This decrease was observed
regardless as to whether neuraxial was used alone or in combination with general
anesthesia.
2. DVT decreased by 44%
3. PE decreased by 55%
4. Transfusion requirement decreased by 50%
5. Pneumonia decreased by 39%
6. There were also reductions in myocardial infarction and renal failure.
The authors concluded that neuraxial blocks “reduce postoperative mortality and
other serious complications”. It was not clear whether these effects were due “solely to
benefits of neuraxial blockade or partly to avoidance of general anaesthesia”.
Meta-analysis has the advantage of pooling large number of patients making it
possible to study infrequent clinical events. However, it also means putting together trials
from different institutions, frequently from different countries and cultures. It remains to
be seen whether theseencouraging results can be duplicated, and whether they could
apply to other regional anesthesia techniques (i.e., peripheral nerve blocks).
Other authors, like Christopher Wu from Johns Hopkins, have shown the benefits
of regional over general anesthesia, when non-traditional outcomes are measured. These
outcome parameters include patient satisfaction (including analgesia, prevention of
nausea and vomiting and discharge readiness), ability to undergo physical rehabilitation,
and cost. These so-called “soft” parameters are very important in today’s cost-conscious
practice.
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References
1. Liu SS, Carpenter RL, Neal JM. Epidural anesthesia and analgesia. Their role in
postoperative outcome. Anesthesiology 1995; 82:1474-1506
2. Sharrock NE: Risk-Benefit Comparisons for Regional and General Anesthesia, In:
Finucane BT (ed), Complications of Regional Anesthesia. New York, Churchill
Livingstone, 1999, pp 31-38
3. Neal JM, McDonald SB. Regional Anesthesia and Analgesia: Outcome and Cost
Effectiveness. In: Neal JM, Mulroy MF, Liu SS (eds), Problems in Anesthesia,
Philadelphia, Lippincott, Williams & Wilkins, 2000, pp 188-198
4. Neal JM: Regional anesthesia and Outcome. In: Rathmell JP, Neal JM, Viscomi
CM (eds), Regional Anesthesia, The Requisites in Anesthesiology, Philadelphia,
Elsevier Mosby, 2004, pp 164-170
5. Rodgers A, Walker N, Schung S et al. Reduction of postoperative mortality and
morbidity with epidural or spinal anaesthesia: results from overview of
randomized trials. Br Med J, 2000; 321: 1493-504
6. Wu CL, Fleisher LA. Outcomes research in regional anesthesia and analgesia,
Anesth Analg 2000; 91: 1232-1242
7. Urban MK: Is Regional Anesthesia Superior to General Anesthesia for Hip
Surgery?, In: Fleisher LA (ed), Evidence-Based Practice of Anesthesiology.
Philadelphia, Saunders, 2004, pp267-269
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CHAPTER 2
LOCAL ANESTHETICS
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LOCAL ANESTHETICS
The cell membrane’s resting potential is negative and close to the potential
determined by potassium alone (-70 mV). During the transmission of an action potential,
Na+ moves into the cell through open Na+ channels depolarizing the membrane and
bringing its potential to -20 mV or more.
Local anesthetics are compounds that have the ability to interrupt the transmission
of the action potential in excitable membranes. They bind to specific receptors in the Na+
channels and their action, at clinically recommended doses, is reversible. Conduction can
still continue, although at a slower pace, with up to 90% of receptors blocked.
All local anesthetics are potentially neurotoxic if injected intraneurally, especially
if that injection is intrafascicular. The neuronal damage may be directly related to the
degree of hydrostatic pressure reached inside the axoplasma. Local anesthetics injected
around nerves could also be toxic as result of the concentration of the agent and the
duration of the exposure (e.g., cauda equina after intrathecal local anesthetics).
The local anesthetics available in clinical practice are usually racemic mixtures,
that is a mixture of both R and S enantiomers. Exceptions are lidocaine, levo-bupivacaine
and ropivacaine. The S isomer appears to have similar efficacy than the R isomer, but
lesser cardiac toxicity.
Historical perspective
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1885 Wood, in the United Kingdom, is credited with the introduction of conduction
anesthesia through hypodermic injection.
1897 Epinephrine is isolated by John Abel at Johns Hopkins Medical School.
1897 Braun in Germany relates cocaine toxicity with systemic absorption and advocates
the use of epinephrine.
1898 Bier is set to receive the first planned spinal anesthesia from his assistant
Hildebrandt. After CSF is obtained, the syringe is found not fit the needle and therefore
no injection could be performed. Bier then performs the first spinal anesthesia on
Hildebrandt using cocaine. They both experience the first spinal headaches.
1908 Bier introduces the intravenous peripheral nerve block (Bier block) with procaine.
1911 Hirschel performs the first percutaneous axillary block.
1911 Kulenkampff performs the first percutaneous supraclavicular block.
1922 Gaston Labat of France, a disciple of Pauchet, introduces in the US his book
“Regional Anesthesia Its Technic and Clinical Application”, the first manual of regional
anesthesia published in America.
1923 Labat establishes the first American Society of Regional Anesthesia.
1953 Daniel Moore, practicing at Virginia Mason Clinic in Seattle, publishes his
influential book “Regional Block”.
1975 Alon Winnie, L. Donald Bridenbaugh, Harold Carron, Jordan Katz, and P. Prithvi
Raj establish the current American Society of Regional Anesthesia (ASRA) in Chicago.
1976 The first ASRA meeting is held in Phoenix, Arizona.
1976 Regional Anesthesia Journal, volume 1, number 1 is published.
1983 Winnie introduces his book, Plexus Anesthesia, Perivascular Techniques of
Brachial Plexus Block.
1905 procaine; 1932 tetracaine; 1947 lidocaine; 1955 chloroprocaine (last ester
type that is still in clinical use); 1957 mepivacaine; 1963 bupivacaine; 1997 ropivacaine;
1999 levobupivacaine.
Local anesthetics are weak bases with a pka above 7.4 and poorly soluble in
water. They are commercially available as acidic solutions (pH 4-7) of hydrochloride
salts, which are hydrosoluble. A typical local anesthetic molecule is composed of two
parts, a benzene ring (lipid soluble, hydrophobic) and an ionizable amine group (water
soluble, hydrophilic). These two parts are linked by a chemical chain, which can be either
an ester (-CO-) or an amide (-HNC-). This is the basis for the classification of local
anesthetics as either esters or amides.
Injecting local anesthetics in the proximity of a nerve(s) triggers a sequential set
of events, which eventually culminates with the interaction of some of their molecules
with receptors located in the Na+ channels of nerve membranes. The injected local
anesthetic volume spreads initially by mass movement, moving across “points of least
resistance”, which unfortunately do not necessarily lead into the desired nerve(s). This
fact emphasizes the importance of injecting in close proximity to the target nerve(s). The
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local anesthetic solution then diffuses through tissues; each layer acting as a physical
barrier. In the process part of the solution gets absorbed into the circulation. Finally a
small percentage of the anesthetic reaches the target nerve membrane, at which point the
different physicochemical properties of the individual anesthetic will dictate the speed,
duration and nature of the interaction with the receptors.
1. Lipid solubility: determines both the potency and the duration of action of local
anesthetics, by facilitating their transfer through membranes and by keeping the
drug close to the site of action and away from metabolism. In addition, the local
anesthetic receptor site in Na+ channels is thought to be hydrophobic, so its
affinity for hydrophobic drugs is greater. Hydrophobicity also increases toxicity,
so the therapeutic index of more lipid soluble drugs is decreased.
2. Protein binding: local anesthetics are bound in large part to plasma and tissue
proteins. The bound portion is not pharmacologically active. The plasmatic
unbound fraction is responsible for systemic toxicity. The most important binding
proteins in plasma are albumins and alpha-1-acid glycoprotein (AAG). Although
albumin has a greater binding capacity than AAG, the latter has a greater affinity
for drugs with pka higher than 8, the case for most local anesthetics. Newborn
infants have very low concentration of AAG, only reaching adult values by 10
months of age. The elderly and debilitated also frequently have decreased levels
of albumin and other plasma proteins. These patient populations could be at
increased risk for toxicity.
On the other hand, AAG levels increase during stress and for several days
after the postoperative period. Higher levels of AAG lead to decreased levels of
unbound fraction of local anesthetics and a decreased potential for local anesthetic
toxicity. However, changes in protein binding are only clinically important for
drugs highly protein-bound, such as bupivacaine, which is 96% bound, and
sufentanil and alfentanil, which are both 92% bound (Booker et al, Br J Anaesth
1996; 76:365-8).
The fraction of drug bound to protein in plasma correlates with the
duration of action of local anesthetics: bupivacaine (95%) = ropivacaine (94%)>
tetracaine (85%) > mepivacaine (75%) > lidocaine 65%) > procaine (5%) and 2-
chloroprocaine (negligible). This suggests that the binding site for the local
anesthetic molecule in the sodium channel receptor protein, may share a similar
sequence of amino acids with the plasma protein binding site.
Drugs as lidocaine, tetracaine, bupivacaine and morphine (e.g., DepoDur)
have been incorporated into liposomes to prolong their duration of action.
Liposomes are vesicles with two layers of phospholipids, which slow down the
release of the drug.
3. Pka: determines the ratio between the ionized (cationic) and the uncharged (base)
forms of the drug. The pka of local anesthetics ranges from 7.6 to 9.2. By
definition the pka is the pH at which 50% of the drug is ionized and 50% is
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present as a base. The pka generally correlates with the speed of onset of most
local anesthetics. The closer the pka is to physiologic pH, the faster the onset. For
example, lidocaine with a pka of 7.7 is 25% non-ionized at pH 7.4. Its onset is
therefore faster than bupivacaine, whose pka of 8.1 makes it only 15% non-
ionized at that pH. One important exception is 2-chloroprocaine that, despite its
pka of 9.1, has a very rapid onset. This is usually attributed to the relatively high
concentrations (3%) used in clinical practice that are possible thanks to its low
toxicity. It has also been claimed that 2-chloroprocaine has better “tissue
penetrability”.
The non-charged hydrophobic fraction (B), which exists in equilibrium with the
hydrophilic charged portion (BH+), crosses the lipidic nerve membrane and initiates the
events that lead to Na+ channel blockade. Once inside the cell, the pka of the drug and the
intracellular pH dictate a new equilibrium between the two fractions. Because of the
relative more acidic intracellular environment, the relative proportion of charged fraction
(BH+) increases. This hydrophilic, charged fraction is the active form on the Na+ channel.
The Na+ channel is a protein structure that communicates the extracellular of the
nerve with its axoplasm. It consists of four repeating alpha subunits and two beta
subunits, beta-1 and beta-2. The alpha subunits are involved in ion movement and local
anesthetic activity. It is generally accepted that the main action of local anesthetics
involves interaction with specific binding sites within the Na+ channel. Local anesthetics
may also block to some degree calcium and potassium channels as well as N-methyl-
D-aspartate (NMDA) receptors. Local anesthetics do not ordinarily affect the membrane
resting potential.
The Na+ channels seem to exist in three different states, closed (resting), open and
inactivated. Under adequate stimulation, the protein molecules of the channel undergo
conformational changes, from the resting state to the ion-permeable state or open state,
allowing the inflow of extracellular Na+, which depolarizes the membrane. After a few
milliseconds the channel goes then through a transitional inactivated state, where the
proteins leave the channel closed and ion-impermeable. With repolarization the proteins
revert to their resting configuration.
Other drugs, like tricyclic antidepressants (amitriptyline), meperidine, volatile
anesthetics and ketamine, also exhibit Na+ channel-blocking properties. Tetrodotoxin and
other biotoxins also interact with the Na+ channels, although their actions are exerted on
the extracellular side of the channel.
Frequency-dependent blockade
Local anesthetics show more affinity for open Na+ channels. When a nerve is
experiencing a high frequency of depolarization, like during spontaneous pain or
voluntary muscle contractions, it becomes more sensitive to blockade, because the
chances of interaction, between local anesthetics molecules and Na+ channels, increase.
The concept of frequency-dependent blockade also explains the greater
susceptibility to blockade exhibited by small sensory fibers, as they generate long action
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potential (5 ms) at high frequency. Motor fibers on the other hand generate short action
potentials (0.5 ms) at lower frequency making them more difficult to block.
As a general rule small nerve fibers are more susceptible to local anesthetics than
large fibers. However, other factors like myelinization and relative position of the fibers
within a nerve (mantle versus core) may also play a role. The depolarization in
myelinated fibers is saltatory. About three nodes of Ranvier need to be blocked in order
to block the transmission of the action potential.
The smallest nerve fibers are nonmyelinated and are blocked more readily than
larger myelinated fibers. However at similar size, myelinated fibers are blocked before
nonmyelinated fibers. In general autonomic fibers, small nonmyelinated C fibers
(mediating pain, temperature and touch), and small myelinated A delta fibers (mediating
pain and cold temperature) are blocked before A alpha, A beta and A gamma fibers
(motor, propioception, touch, and pressure).
It has been speculated that in large nerve trunks, motor fibers would be usually
located in the outer portion (mantle) of the nerve bundle, therefore more “accessible” to
local anesthetics. This would help explain why motor fibers tend to be blocked before
sensory fibers in large mixed nerves. In contrast, the frequency-dependence of local
anesthetic action would favor block of small sensory fibers, as they generate long action
potentials at high frequency, whereas motor fibers generate short action potentials at
lower frequency.
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(Figure from Morgan’s Clinical Anesthesiology, 3rd edition, 2006, reproduced with permission)
The ionized fraction of local anesthetics is the active form in the Na+ channel,
although the rate-limiting step in this cascade is membrane penetration of local
anesthetics in its non-ionized form. Unfortunately, only a small proportion of local
anesthetic in solution exists in the non-ionized state. Changes in pH can theoretically
reduce the onset time by increasing its proportion. At a pH of 5.0 to 5.5 the cation/base
ratio is 1000:1, at a pH of 7.4 the same ratio becomes 60:40. The limiting factor for pH
adjustment is the solubility of the base form before reaching precipitation. The most lipid
soluble agents, like bupivacaine and ropivacaine, cannot be alkalinized above a pH of 6.5
because they precipitate.
DiFazio et al (Anesth Analg 1986:65; 760-64) demonstrated a more than 50%
decrease in onset of epidural anesthesia, when the pH of commercially available
lidocaine with epinephrine was raised from 4.5 to 7.2, by the addition of bicarbonate.
Capogna et al (Reg Anesth 1995; 20: 369-377) randomized 180 patients to study the
effects of alkalinizing lidocaine, mepivacaine and bupivacaine for nerve blocks. They
concluded that alkalinization of lidocaine and bupivacaine shortens the onset of epidural;
alkalinization of lidocaine shortens the onset of axillary block and alkalinization of
mepivacaine shortens the onset of sciatic/femoral blocks. However, when only small
changes in pH can be achieved, because of the limited solubility of the base, only small
decreases in onset time will occur, as when plain bupivacaine is alkalinized.
It is generally accepted that adding bicarbonate to local anesthetics, may speed the
onset of local anesthetics solutions that have epinephrine added by the manufacturer
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(vials have a lower pH), while the effect would be negligible when fresh epinephrine is
added to a plain solution.
Chloroprocaine plus 1 mL of sodium bicarbonate for 30 mL of solution raises the
pH to 6.8. Adding 1 mL of sodium bicarbonate per 10 mL of lidocaine or mepivacaine
raises the pH of the solution to 7.2 and adding 0.1 mL of bicarbonate per 10 mL of
bupivacaine raises the pH of the solution to 6.4 (from Mulroy’s Regional Anesthesia, 3rd
edition, 2002).
Carbonation
Another approach to shortening onset time has been the use of carbonated local
anesthetic solutions. These solutions contain large amounts of carbon dioxide, which
readily diffuses into the axoplasm of the nerve, lowering the pH and favoring the
formation of the cationic active form of the local anesthetic inside the cell. Carbonated
solutions are not available in the United States.
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action. According to Neal (Reg Anesth Pain Med 2003;28:124-134) adding 5 mcg/mL
(1:200,000 dilution) prolongs the duration of lidocaine for peripheral nerve blocks from
186 min to 264 min. Adding only 2.5 mcg/mL (1:400,000 dilution) prolongs the block to
240 min (almost the same prolongation), without apparent effect on nerve blood flow.
Patients with micro angiopathy (e.g., diabetics), who could be at increase risk for neural
ischemia secondary to vasoconstriction, potentially could benefit from the use of more
diluted epinephrine. Adding only 1:400,000 epinephrine to local anesthetic solutions for
nerve blocks has become the standard in our practice, in both diabetics and non-diabetics
patients. In 2006 Bigeleisen reported in Anesthesiology a study in which he demonstrated
intraneural injection by ultrasound in 72 out of 104 nerves studied in the axilla. The local
anesthetic used was a combination of bupivacaine plus lidocaine and contained 3 ucg/mL
of epinephrine. The author did not find any evidence of nerve injury in up to 6 month
follow up.
Intrathecal epinephrine does not lead to cord ischemia, because it does not
decrease spinal cord blood flow, although it decreases epidural blood flow (Kosody R, et
al. Can Anaesth Soc J; 31: 503-8, 1984). In fact spinal cord ischemia due to epinephrine
is “improbable because the cord vessels are autoregulated and show very minimal
response to endogenous or exogenous vasoactive agents” (Neal JM In: Regional
Anesthesia, The Requisites. Elsevier Mosby, Philadelphia 2004, pp 25-31)
Although epinephrine-containing local anesthetics are usually contraindicated in
areas of terminal circulation (e.g., digits) this recommendation is not based on hard
evidence. Anecdotal use of epinephrine-containing solutions in digits is cited in the
literature. Lalonde et al published a multicenter study including 3,110 consecutive cases
of use of epinephrine in the fingers and hand from 2002-2004. The authors (surgeons)
defined “low dose” epinephrine as 1:100,000 and they reported no instance “of digital
tissue loss” (J Hand Surg 2005; 30:1061-67). At this time we do not recommend this
practice.
Dilution/concentration issues
Opioids
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The hydrophilic opioid morphine can be used in doses of 0.1-0.3 mg spinal and 1-
3 mg epidural. It has a slow onset of 45 min, providing an analgesic action that
lasts 12-24 h. Morphine reaches the brainstem and 4th ventricle slowly. Delayed
respiratory depression (8-10 h) is a risk with all neuraxial opioids, but it is more
frequently seen with hydrophilic drugs like morphine, and in susceptible
populations like the elderly and debilitated. Neuraxial morphine is also associated
with higher incidence (40-50%) of nausea and vomiting than systemic opioids,
more pruritus (60-80%, 20% of it severe), and delayed voiding. It is not suitable
for outpatients.
Short-acting opioids, such as fentanyl and sufentanil, when added to spinal
anesthetics can also intensify the block, and prolong the duration of anesthesia,
beyond the duration of local anesthetics. Respiratory depression with these agents
is rare and usually early (within 4 h). Sufentanil spinal can be used in doses of
2.5-10 mcg. Fentanyl spinal is used in doses of 10-25 mcg and 25-150 mcg
epidural. Onset occurs at 5-15 min, peak effect at 10-20 min and duration of 1-3
h. Hypotension, pruritus, nausea and vomiting are some common side effects.
Clonidine
22 | P a g e
along local anesthetics and when given orally. Injected intrathecally, they also can delay
voiding and can produce orthostasis. Side effects do not occur often at clonidine doses
below 1.5 mcg/kg or a total dose less than 150 mcg.
Iskandar et al in France in 2001, showed that adding 50 mcg of clonidine to
selected nerves (median and musculocutaneous) prolonged mepivacaine sensory
anesthesia by 50%, compared to placebo, after a mid-humeral block, without prolonging
motor effect. Because the prolongation was observed only in the nerves that received
clonidine they postulated that the effect must be peripheral and not central through
absorption.
Dexmedetomidine
It is a more selective alpha-2 agonist agent with an alpha-2:alpha-1 receptor ratio
of 1,600:1, seven times greater than that of clonidine. Its elimination half-life is only 2 h
compared to more than 8 h for clonidine. Dexmedetomidine may offer extended
analgesia with lesser side effects. This drug is gaining popularity as a sedative both in the
ICU and the OR.
Neostigmine
It is an acetylcholinesterase inhibitor that prevents the breakdown of acetylcholine
promoting its accumulation. Acetylcholine is an endogenous spinal neurotransmitter that
induces analgesia. Neostigmine does not cause neural blockade nor have any action on
opioid receptors.
Spencer Liu et al in 1999 (Anesthesiology 1999; 90:710-717) studied the effects
of different doses of neostigmine added to bupivacaine spinal. They reported that 50 mcg
of neostigmine increased sensory and motor anesthesia, but also delayed discharge time
and was accompanied by 67% nausea and up to 50% vomiting. Lower doses did not show
analgesic effect, but still had significant rates of side effects (nausea and vomiting).
Hyaluronidase
It breaks down collagen bonds potentially facilitating the spread of local
anesthetic through tissue planes. However, the evidence shows that at least in the epidural
space it can decrease the quality of anesthesia. Its use seems limited to retrobulbar blocks.
Dextran
Dextran and other high-molecular-weight compounds have been advocated to
increase the duration of local anesthetics. The evidence is lacking.
23 | P a g e
METABOLISM OF LOCAL ANESTHETICS
Ester local anesthetics
They are transported into the liver before their biotransformation. The two major
factors controlling the clearance of amide local anesthetics by the liver are hepatic blood
flow and hepatic function. The metabolism of local anesthetics as well as that of many
other drugs occurs in the liver by the cytochrome P-450 enzyme system. Because of the
liver large metabolic capacity it is unlikely that drug interaction would affect the
metabolism of local anesthetics. The rate of metabolism is agent specific (prilocaine >
lidocaine > mepivacaine > ropivacaine > bupivacaine).
The metabolism of amide local anesthetics is relatively fast, although slower than
esters. Elimination half-life for lidocaine is 1.5-2 h. Drugs such as general anesthetics,
norepinephrine, cimetidine, propranolol and calcium channel blockers can decrease
hepatic blood flow and potentially increase the elimination half-life of amides. Similarly,
decreases in hepatic function caused by a lowering of body temperature, immaturity of
the hepatic enzyme system in the fetus, or liver damage (e.g., cirrhosis) can lead to
decreased rate of hepatic metabolism of the amides. Renal clearance of unchanged local
anesthetic is a minor route of elimination (e.g., lidocaine is only 3% to 5% recovered
unchanged in the urine of adults, while bupivacaine is 10% to 16%).
The primary metabolic pathway for mepivacaine is oxidation to 3-hydroxy and 4-
hydroxymepivacaine. This pathway is less developed in neonates resulting in slower
metabolism of mepivacaine in newborns than in adults (Raj’s Regional Anesthesia).
24 | P a g e
helps to identify those patients. Dibucaine binds strongly to normal plasma
pseudocholinesterase inhibiting its action. This inhibition is reported as a number from 1-
100 representing the percentage of normal enzyme inhibition, the larger the number the
larger the proportion of normal enzyme. A number of 80 or higher means that dibucaine
is able to inhibit at least 80% of the enzyme and that the patient is a normal homozygous.
A dose of succinylcholine will last 4-6 min. A dibucaine number of 50 means that the
patient is heterozygous and that the effect of succinylcholine will be prolonged to up to
30 min. A number of 20 is related to the homozygous atypical enzyme and the effect of
succinylcholine could be expected to last up to 6 h (incidence 1:3,300).
1. Total dose
2. Net absorption, which depends on: vasoactivity of the drug, site vascularity and
use of a vasoconstrictor
3. Metabolism and elimination of the drug from the circulation
25 | P a g e
of 8.28 mcg/mL (range 3.83-11.21) were obtained (normal 5 mcg/mL) within 60 min and
decreased steadily thereafter. Patients did not exhibit signs of toxicity despite these high
plasma levels.
This is in contrast with a case report by Tanoubi et al (Ann Fr Anesthe Reanim
2006; 25: 33-5), where an end-stage renal patient for A-V fistula received an axillary
block with 375 mg (25 mL) of 1.5% mepivacaine and the patient presented with
dysarthria, mental confusion and loss of consciousness without convulsions or
arrhythmia. Mepivacaine plasma level at the time of symptoms was 5.1 mcg/mL
26 | P a g e
Toxic plasma concentration thresholds
The following are accepted plasma levels of selected local anesthetics, above
which systemic effects are expected in humans:
Lidocaine 5 mcg/mL; mepivacaine 5 mcg/mL; bupivacaine 1.5 mcg/mL;
ropivacaine 4 mcg/mL
The best treatment for toxic reactions is prevention. When local anesthetic-
induced seizures occur, hypoxia, hypercarbia and acidosis develop rapidly. ABC
(Airway, Breathing and Circulation) is the mainstay of treatment. Administration of O2
by mask, or ventilation support by bag and mask, is often all that is necessary to treat
seizures. If seizures interfere with ventilation, benzodiazepines, propofol or thiopental
can be used. The use of succinylcholine effectively facilitates ventilation and, by
abolishing muscular activity, decreases the severity of acidosis. However neuronal
seizure activity is not inhibited and therefore, cerebral metabolism and oxygen
requirements remain increased.
In an interesting study by Mayr et al, out of Innsbruck, Austria (Anesth Analg
2004; 98: 1426-3), the authors induced cardiac arrest in 28 pigs by administering 5 mg/kg
of 0.5% bupivacaine and stopping ventilation until asystole occurred. CPR was initiated
after 1 min of cardiac arrest. After 2 min the animals received every 5 min either
epinephrine alone; vasopressin alone; epinephrine plus vasopressin or placebo IV. In the
vasopressin/epinephrine group all pigs survived and in the placebo group all pigs died. In
the vasopressin alone 5 of 7 survived and in the epinephrine group 4 of 7 survived. This
is in line with current ACLS recommendations of using one single dose of 40U of
vasopressin IV before using epinephrine.
Little information is available regarding the treatment of local anesthetic
cardiovascular toxicity in humans. Animal data suggest:
1. Vasopressin 40 U, IV, single dose, one time only followed by, if needed,
high doses of epinephrine (1 mg IV every 3-5 minutes) to support heart
rate and blood pressure.
2. Atropine may be useful for bradycardia.
3. DC cardioversion is often successful.
4. Ventricular arrhythmias are probably better treated with amiodarone than
with lidocaine. Amiodarone is used as for ACLS, 150 mg over 10 min,
followed by 1 mg/min for 6 hrs then 0.5 mg/min. Supplementary infusion
of 150 mg as necessary up to 2 g. For pulseless VT or VF, initial
administration is 300 mg rapid infusion in 20-30 mL of saline or dextrose
in water.
27 | P a g e
colleagues from the University of Illinois, published an interesting paper describing the
use of a 20% lipid emulsion in combination with cardiac massage to successfully return
normal hemodynamics to 9 out of 9 dogs, after asystole brought by a bolus injection of
10 mg/kg of bupivacaine (Reg Anesth Pain Med 2003; 28:198-202).
The results of this study led them to recommend treating bupivacaine-associated
cardiac arrest with a 20% lipid emulsion IV. The treatment protocol includes a 1 mL/kg
bolus of 20% lipid emulsion (such as intralipid), followed by an infusion of 0.25
mL/kg/min for 10 min, and the continuation of basic life support. The bolus can be
repeated every 5 min, up to three times as needed. The maximum dose of 20% lipid
emulsion is not known, but the authors suggest that more than 8 mL/kg would not likely
be needed, nor successful, if lower doses do not work. This protocol will deliver a
significant volume load to the patient. The paper was accompanied by an editorial by
Groban and Butterworth from Wake Forest, in Winston-Salem, North Carolina. They
believe that the most likely mechanism of action of lipid emulsion is that “in some way
the lipid is serving to more rapidly remove LA molecules from whatever binding site
serves to produce the cardiovascular depression that has come to be known as
bupivacaine toxicity”.
ACLS protocols must be followed with prompt defibrillation and use of pressors
like vasopressin followed by epinephrine, to support coronary perfusion if necessary.
Amiodarone should be favored over lidocaine to treat arrhythmias and initiate the lipid
emulsion at the “earliest sign of severe local anesthetic-induced cardiac toxicity.
In 2006 Rosenblatt et al (Anesthesiology 2006; 105: 217-8) published a case
report of successful use of 20% lipid emulsion (Intralipid, Baxter Pharmaceuticals) on a
58-year old male who developed a cardiac arrest, presumably linked to bupivacaine after
an interscalene block. They described that after 20 min of cardiac compressions and with
the patient in asystole, 100 mL of intralipid IV was given resulting in an apparent
“immediate” return of patient’s rhythm. This dose is higher than the recommended 1
mL/kg. A continuous infusion of intralipid was given at 0.5 mL/kg/min for 2 h. The
patient was extubated 2.5 after hours after the episode, without any apparent neurological
sequelae. In an accompanying editorial, Weinberg suggested having 20% lipid emulsion
available in all sites where local anesthetics are used.
Also in 2006, soon after Rosenblatt’s report, Litz et al reported a case of
successful use of intralipid after ropivacaine-induced asystole. More recently, in March
2008, McCutchen and Gerancher reported a case of ventricular tachycardia treated with
150 mg of amiodarone, 10 mL of 20% intralipid and a synchronized countershock of 120
J, after which there was a prompt return to normal sinus rhythm. The authors speculate
that the use of intralipid might have prevented the patient from going into cardiac arrest.
In summary:
1. Evidence is accumulating on the beneficial effect of a 20% lipid emulsion to treat
bupivacaine-related cardiac toxicity.
2. Propofol has the same vehicle than intralipid, but only half the concentration
(10%). Giving propofol probably will not provide enough lipids, but instead it
will produce a negative inotropic effect due to the presence of the active
ingredient di-isopropylphenol (anesthetic action), exacerbating cardiac
28 | P a g e
depression. Therefore, propofol is not indicated to treat local anesthetic-induced
cardiac toxicity.
Maximum dose
Methemoglobinemia
29 | P a g e
Allergy
True allergy (type I or IgE mediated) to local anesthetics is rare and presents
within minutes after the exposure. It is relatively more frequent with esters, which are
metabolized to para-amino-benzoic acid (PABA). PABA is frequently used in the
pharmaceutical and cosmetic industries. Allergy to amide local anesthetics is exceedingly
rare. There is no cross allergy between esters and amides. However use of methylparaben
as a preservative in multidose vials can elicit allergy in patients allergic to PABA.
Delayed hypersensitivity reactions (type IV) are T-cell mediated and present 24 to
48 h after exposure. There are few cases in the literature of delayed hypersensitivity to
lidocaine, but recent reports suggest it may be more frequent than previously reported.
The North American Contact Dermatitis Group found that 0.7 % of patients who were
patch tested in 2001-02 demonstrated delayed allergy to lidocaine (ASRA News,
February 2006).
Drug interactions
1. Procaine:
Type: ester
Pka: 8.9
Protein biding: 5%
Characteristics: intermediate onset, low potency, short duration. Very short half-
life (20 sec).
Other: it provides a short-duration spinal (potential benefit on outpatients).
30 | P a g e
2. 2-Chloroprocaine:
Type: ester
Pka: 9.3
Protein binding: negligible
Characteristics: very fast onset, despite high pka (ability to use higher
concentrations could be the reason). Short duration (it has 30 minutes 2-segment
regression in epidural). Very short half-life (30 sec).
Other: The original preparation contained sodium metabisulfite as a preservative.
It was associated with serious neurological deficits when a large injection,
planned for epidural, ended intrathecally. A second preservative, ethylenediamine
tetra-acetic acid (EDTA) was associated with severe muscle spasm after epidural
in ambulatory patients. EDTA chelates ionized calcium and this side effect may
be secondary to action on paraspinal muscles.
The present solution is prepared without preservatives, and no back spasms have
been reported.
3. Tetracaine:
Type: ester
Pka: 8.6
Protein binding: 85%
Characteristics: slow onset, high potency, long duration. Short plasma half-life
(2.5 to 4 min).
Other: early experience with this product at high doses resulted in CNS toxicity,
giving it a bad reputation, mostly undeserved. We still use it occasionally in our
practice, as lyophilized crystals dissolved in liquid mepivacaine for a final
concentration of 0.2% tetracaine. It prolongs duration of surgical anesthesia in
peripheral nerve blocks to 4-6 h. Tetracaine also is the drug that gets the longest
prolongation from adding epinephrine to spinal anesthesia (up to 60% in the
lumbar dermatomes).
4. Cocaine:
Type: ester
Pka: 8.6
Protein binding: ?
Characteristics: slow onset, short duration. Elimination half life 60-90 min.
Urinary excretion of unchanged cocaine is usually less than 1%, but it can be up
to 9% especially in acid urine. At the end of 4 hours, most of the drug is
eliminated from the plasma. Cocaine metabolites (benzoylecgonine and ecgonine)
may be present in the urine for 24-36 hours, but some metabolites may be
identified for up to 144 h after administration (Ellenhom and Barceloux, 1988).
Other: It produces vasoconstriction, while most of the LA with the exception of
ropivacaine, produce some degree of vasodilation. It interferes with the reuptake
of cathecolamines, resulting in hypertension, tachycardia, arrhythmias and
myocardial ischemia. It is used mainly for topical anesthesia of the nose. Doses
below 100 mg (2.5 mL) are usually safe.
31 | P a g e
Cocaine can potentiate cathecolamine-induced arrhythmias by halothane,
theophylline or antidepressants. Cocaine can induce coronary vasospasm and
potential myocardial ischemia, without the need for coronary artery disease.
Mixtures of lidocaine and phenylephrine are safer alternatives.
5. Benzocaine:
Type: ester
Pka 3.5
Characteristics: slow onset, short duration and the only LA with a secondary
amine structure that limits its ability to pass through membranes (topical use
only).
Other: Doses higher than 300 mg can induce methemoglobinemia.
6. Lidocaine:
Type: amide
Pka: 7.8
Protein binding: 65%
Characteristics: intermediate onset and duration, elimination half-life 45-60 min.
Other: it is versatile (topical, infiltration, IV regional, neuraxial, antiarrhythmic)
and widely used. Spinal use is associated with around 30% of TNS, especially
with lithotomy position, knee arthroscopy and obesity. Lowering the
concentration does not eliminate the problem with doses larger than 40 mg. Doses
of 25-40 mg highly reduce the incidence of TNS.
7. Mepivacaine:
Type: amide
Pka: 7.6
Protein binding: 75%
Characteristics: intermediate onset and duration. Elimination half-life is 2-3 h in
adults and 8-9 h in neonates.
Other: It produces less vasodilation than lidocaine. It has been used in spinal
anesthesia. It has lower (but not zero) incidence of TNS.
It is the agent we most commonly use for peripheral nerve blocks. A 1.5% of
plain solution provides a short onset and dense surgical anesthesia lasting 2-3 h
(3-4 h with 1:400,000 epinephrine). Prolonged postoperative analgesia, as with all
other LA, is negligible after single-shot blocks.
The primary oxidative metabolic pathway for mepivacaine is less developed in
neonates resulting in slower metabolism of mepivacaine in newborns than in
adults (Raj’s Textbook of Regional Anesthesia).
8. Bupivacaine:
Type: amide
Pka: 8.1
Protein binding: 95%
Characteristics: high potency, slow onset, long duration. Elimination half-life 3-
3.5 h in adults and around 8 h in neonates.
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Other: lower concentrations (0.25% and less) produce analgesia with increased
motor sparing (desirable in outpatients and obstetrics). Commercial bupivacaine is
a 50:50 racemic mixture of the R and S enantiomers. Cardiac arrest associated
with bupivacaine is difficult to treat possibly due to its high protein binding and
high lipid solubility (please see toxicity).
9. Ropivacaine:
Type: amide
Pka: 8.2
Protein binding: 94%
Characteristics: onset and duration similar to bupivacaine, with slight lesser
potency. Elimination half-life 1-3 h in adults.
Like bupivacaine, it is chemically related to mepivacaine, but as opposed to most
local anesthetics, it is supplied as the pure S enantiomer of the drug. The S
enantiomer is associated with less cardiac toxicity, intermediate between that of
lidocaine and bupivacaine.
Other: It is a weak vasoconstrictor (only one other than cocaine). At lower
concentrations (less than 0.5%) it may show a greater selectivity for sensory than
motor blockade than bupivacaine.
10. Levobupivacaine:
Type: amide
Pka: 8.1
Protein binding: 97%
Characteristics: S enantiomer of bupivacaine, very similar to ropivacaine.
Not available at this time in the US.
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References
1. Lou L, Sabar R, Kaye A: Local Anesthetics, In: Raj P (ed), Textbook of Regional
Anesthesia. New York, Churchill Livingstone, 2002, pp 177-213
2. Brown DL, Fink R: The History of Neural Blockade and Pain Management, In:
Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia,
Lippincott-Raven, 1998, pp 3-32
3. Strichartz GR: Neural Physiology and Local Anesthetic Action, In: Cousins MJ,
Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia, Lippincott-
Raven, 1998, pp 35-54
4. Tucker GT, Mather LE: Properties, Absorpton, and Disposition of Local
Anesthetic Agents, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd
edition. Philadelphia, Lippincott-Raven, 1998, pp 55-95
5. Covino BG, Wildsmith JAW: Clinical Pharmacology of Local Anesthetic Agents,
In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition.
Philadelphia, Lippincott-Raven, 1998, pp 97-128
6. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4th edition. New
York, McGraw-Hill, 2006, pp 263-288
7. Mulroy MF: Regional Anesthesia, 3rd edition. Philadelphia, Lippincott Williams
& Wilkins, 2002, pp 1-63
8. Liu SS, Joseph RS: Local Anesthetics, In: Barash PG, Cullen BF, Stoelting RK
(eds), Clinical Anesthesia. Philadelphia, Lippincott Williams & Wilkins, 2006, pp
453-471
9. DiFazio CA, Carron H, Grosslight KR, et al. Comparison of ph-adjusted lidocaine
solutions for epidural anesthesia. Anesth Analg 1986; 65: 760-64
10. Hilgier M. Alkalinization of bupivacaine for brachial plexus block. Reg Anesth
1985;10: 59-61
11. Booker PD, Taylor C, Saba G. Perioperative changes in α1-acid glycoprotein
concentrations in infants undergoing major surgery. Br J Anaesth 1996; 76: 365-
368
12. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice, 3rd edition.
Philadelphia, Lippincott-Raven, 1999, pp158-181
13. Tetzlaff JE: Local anesthetics and adjuvants for ambulatory anesthesia. In: Steele
SM, Nielsen KC, Klein SM (eds), Ambulatory Anesthesia Perioperative
Analgesia. New York, McGraw-Hill, 2005, pp 193-205
14. Weinberg GL et al. Lipid emulsion infusion rescues dogs from bupivacaine-
induced cardiac toxicity. Reg Anesth Pain Med 2003; 28:198-202
15. Mayr VD, Raedler C, Wenzel V, et al. A comparison of epinephrine and
vasopressin in a porcine model of cardiac arrest after rapid intravenous injection
of bupivacaine. Anesth Analg 2004; 98:1426-3
16. Neal JM. Effects of epinephrine in local anesthetics on the central and peripheral
nervous systems: Neurotoxicity and neural blood flow. Reg Anesth Pain Med
2003; 28:124-134
17. Rosenberg PH, Veering VT, Urmey WF. Maximum recommended doses of local
anesthetics: A multifactorial concept. Reg Anesth Pain Med 2004; 29: 564-575.
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18. Mulroy MF. Local anesthetics: Helpful science, but don’t forget the basic clinical
steps (editorial). Reg Anesth Pain Med 2005; 30: 513-515.
19. Mather LE, Copeland SE, Ladd LA. Acute toxicity of local anesthetics:
Underlying pharmacokinetic and pharmacodynamic concepts (A review article).
Reg Anesth Pain Med 2005; 30: 553-566
20. Horlocker TT. One hundred years later, I can still make your heart stop and your
legs weak: the relationship between regional anesthesia and local anesthetic
toxicity. Reg Anesth Pain Med 2002; 27(6): 543-4
21. Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics:
Incidence and preventative measures (editorial). Reg Anesth Pain Med 2002;
27(6): 556-61
22. Horlocker TT, Wedel DJ. Local, anesthetic toxicity-Does product labeling reflect
actual risk? Reg Anesth Pain Med 2002; 27(6): 562-567
23. Weinberg GL. Current concepts in resuscitation of patients with local anesthetic
cardiac toxicity. Reg Anesth Pain Med 2002; 27(6): 568-575
24. Myer Leonard. Carl Koller: Mankind’s greatest benefactor? The story of local
anesthesia. J Dent Res 1998; 77:535-8
25. De Jong R. Tumescent anesthesia: lidocaine dosing dichotomy. Int J Cosmetic
Surg 2002; 4: 3-7
26. Nordstrom H, Stange K. Plasma lidocaine levels and risks after liposuction with
tumescent anaesthesia. Acta Anaesthesiol Scand 2005; 49: 1487-1490
27. Rosenblatt MA, Abel M, Fischer GW, et al. Successful use of a 20% lipid
emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac
arrest. Anesthesiology 2006; 105:217-8
28. Litz RJ, Popp M, Stehr SN, et al. Succesful resuscitation of a patient with
ropivacaine-induced asystole after axillary plexus block using lipid infusion.
Anaesthesia 2006; 61: 800-801
29. Rodriguez J, Quintela O, Lopez-Rivadulla M, et al. High doses of mepivacaine
for brachial plexus block in patients with end-stage chronic renal failure. A pilot
study. Eur J Anaesthesiol 2001; 18: 171-176
30. Kamibayashi T, Maze M. Clinical uses of 2-adrenergic agonists. Anesthesiology
2000; 93:1345-9
31. Tanoubi I, Vialles N, Cuvillon P, et al. Systemic toxicity with mepivacaine
following axillary block in a patient with terminal kidney failure. Ann Fr Anesth
Reanim 2006; 25:33-5
32. McCutchen T, Gerancher JC. Early Intralipid Therapy May Have Prevented
Bupivacaine-Associated Cardiac Arrest. Reg Anesth Pain Med 2008; 33: 178-180
33. Bigeleisen PE. Nerve puncture and apparent intraneural injection during
ultrasound-guided axillary block does not invariably result in neurological injury.
Anesthesiology 2006; 105: 779-783
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CHAPTER 3
NEURAXIAL ANESTHESIA
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SPINAL ANESTHESIA
It is one of the easiest and most reliable techniques of regional anesthesia. The
very small doses of local anesthetics used to produce spinal anesthesia are devoid of
direct systemic effects.
In 1885 James Corning, an American neurologist, was the first person to use
cocaine intrathecally to treat some neurological conditions. Augustus Bier, a German
surgeon, was the first person to use intrathecal cocaine to produce surgical anesthesia. In
a classic paper published in 1899, he described the failed attempt, by his assistant
Hildebrandt, to perform a spinal anesthesia on him, and his successful spinal on
Hildebrandt. Both of them became the first patients suffering from post dural puncture
headaches.
Anatomy
The spinal canal has a protective sheath composed of three layers. From the
outside to the inside they are: duramater, arachnoid and piamater. The potential space
between the dura and arachnoid is called subdural space. The cerebrospinal fluid (CSF)
flows between the arachnoid and piamater in the space called subarachnoid space.
The spinal cord begins cranially at the foramen magnum, as a continuation of the
medulla oblongata. It terminates caudally at the conus medullaris, which in the adult
corresponds to the level of the lower border of L1, and in the young child to the upper
border of L3. From this end, a prolongation of the piamater called the filum terminale
attaches the spinal cord to the coccyx. The dural sac itself ends at the level of the second
sacral vertebra.
The spinal cord is composed of a core of gray matter surrounded by white matter.
The gray matter on cross section has an H shape, with ventral (motor) and dorsal
(sensory) horns. The white matter is described as having anterior, lateral and posterior
white columns.
There are 31 pairs of spinal nerves; each one being formed by two roots, a ventral
or motor root and a dorsal or sensory root. The dorsal root has the dorsal root ganglion.
Because the spinal cord of an adult is shorter than the vertebral column, the spinal nerves
descend a variable distance in the spinal canal before exiting through the intervertebral
foramen. The most distal lumbar and sacral nerves travel the longest distance inside the
spinal canal, forming what is known as the cauda equina. As the spinal nerve pierces the
dural sac, it draws with it a dural sleeve. The spinal nerves exit through the intervebral
foramen, formed between two vertebrae. There are 8 cervical nerves. The first cervical
nerve exits through the occipital bone and C1, the 8th cervical nerve exits between C7 and
T1. Distal to T1 each spinal nerve exits below the corresponding vertebra.
The vertebral column has a series of curvatures in the anteroposterior plane. The
cervical and lumbar curvatures have an anterior convexity (lordosis) and the thoracic and
sacral have posterior convexity (xiphosis). These curvatures play a role in the spread of
the local anesthetic solution, as we will review later.
The blood supply to the spinal cord comes from one anterior spinal artery and two
posterior spinal arteries. These arteries anastomose to form longitudinal vessels,
reinforced by segmental arteries that enter the vertebral canal trough the intervertebral
37 | P a g e
foramina. The anterior two thirds of the spinal cord are supplied by the anterior spinal
artery reinforced in the neck by branches of the vertebral artery.
In the thoracic region the anterior spinal artery receives only a few radicular
arteries from the aorta. In the lumbar region a large branch called radicularis magna or
artery of Adamkiewicz, reinforces the anterior spinal artery. It arises 78% of the times on
the left side, and typically enters the spinal canal through a single intervertebral foramen
between T8 and L3. This important branch is at risk of damage during retroperitoneal
dissections (e.g., surgery on the distal aorta), which could lead to ischemia of the spinal
cord. A case of transient paraplegia after neurolytic celiac plexus block on a pancreatic
cancer patient was reported in 1995 by Wong and Brown. The proposed mechanism was
reversible arterial spasm post injection of ethanol solution.
The needle used to perform a diagnostic spinal tap or a spinal anesthesia needs to
cross the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament,
ligamentum flavum, duramater and arachnoid, before reaching the subarachnoid space
and CSF. The space between the ligamentum flavum and duramater is the epidural space.
Cerebrospinal fluid
It is primarily formed in the choroids plexus of the cerebral ventricles. The CSF
flows from the lateral ventricles to the third and fourth ventricles, and from there to the
cisterna magna. It flows then around the brain and spinal cord, within the subarachnoid
space. The CSF is absorbed into the venous system of the brain by the villi in the
arachnoid membrane. CSF is formed and reabsorved at a rate of 0.3-0.4 mL/min.
The CSF volume in the brain is between 100-150 mL. The volume of CSF below
T12, where most of the spinal anesthetics are performed is, according to Hogan and
collaborators, widely variable among individuals, ranging from 28-80 mL. CSF volume is
decreased with increased abdominal pressure, like the one accompanying pregnancy and
obesity. Therefore, increased abdominal pressure could potentially lead to higher spread
of a neuraxial blockade.
CSF Serum
Sodium (mEq/L) 141 140
Potassium (mEq/L) 2.9 4.6
Calcium (mEq/L) 2.5 5.0
Magnesium (mEq/L) 2.4 1.7
Chloride (mEq/L) 124 101
Bicarbonate (mEq/L) 21 23
Glucose mg/100mL) 61 92
Protein (mg/100mL) 28 7000
pH 7.31 7.41
Osmolality (mOsm/kg H2O) 289 289
38 | P a g e
Site of action
The nerve root is the main site of action for both spinal and epidural anesthesia. In
spinal anesthesia the concentration of local anesthetic in CSF is thought to have minimal
effect on the spinal cord itself.
Indications
Abdominal and lower extremity procedures are the most common. It has been
used for lumbar spine surgery. Saddle blocks are frequently used for rectal surgery.
Baricity
It is the result of dividing density of the local anesthetic solution by that of the
CSF. The density of CSF has a mean value of 1.0003. If the baricity is 1.0 it is by
definition isobaric; if greater than 1 it is hyperbaric and if less than 1 it is hypobaric.
1. Hypobaric solutions
Tetracaine is the local anesthetic most frequently used for hypobaric spinal
anesthesia. Solutions of 0.1% to 0.33% tetracaine in water are reliably hypobaric
in all patients. The most common uses of hypobaric solutions are for rectal
procedures in jackknife position and for hip surgery injecting in lateral position
with the surgical side up.
2. Isobaric solutions
Tetracaine and plain bupivacaine diluted with CSF make good isobaric solutions.
These solutions stay very close to the point of injection.
3. Hyperbaric solutions
The easiest, safest and most widely used way of providing spinal anesthesia. The
solution is rendered hyperbaric by adding glucose. Gravity and patient’s position
determines the spread. In supine position L3 and T6 are the highest points of the
spine and subsequently they become the limits for spread.
1. Major factors
Baricity acting together with gravity
Position of patient (except isobaric solutions)
Dosage, rather than volume or concentration
Baricity is the main factor that determines local anesthetic spread in the
subarachnoid space. It obviously works in conjunction with gravity and patient position.
When plain local anesthetics are used, total dose is more important than injected volume
or concentration. Van Zundert et al reported in 1996, that a 70 mg dose of plain
subarachnoid lidocaine produced the same quality of spinal block over a wide range of
concentrations and volumes. Sheskey et al in 1983 demonstrated similar sensory levels
with 10 mg of plain bupivacaine, at different concentrations and volumes. However,
doses of 15-20 mg of plain bupivacaine produced higher sensory levels of spinal (T2-T4
39 | P a g e
level) than 10 mg (T5-T8 level). When hyperbaric bupivacaine or tetracaine solutions are
used, similar levels of spinal blocks are obtained at different doses, when the
concentration is maintained constant. In the case of hyperbaric bupivacaine, it seems that
this applies as long as the dose is higher than 7.5 mg. Above this dose the level is
determined by baricity acting along with the curvatures of the spine, patient position, and
gravity. In general, the higher the spread the shorter the duration of the sensory blockade,
because the concentration of the drug decreases from the point of injection.
2. Minor factors
Level of injection
Increased abdominal pressure (obesity and pregnancy)
Patient height (only at extremes)
Coughing
Direction of needle bevel can affect spread of isobaric preparations. The bevel
should be directed toward the desired region.
3. No effect
Addition of vasoconstrictors
Barbotage (aspirating and injecting technique to produce CSF turbulence)
Age
Gender
Techniques
Sitting, midline approach
Sitting position is commonly used for neuraxial blocks. It may be the preferred
position in patients whose midline may be difficult to determine, like obese patients. The
position of the iliac crest is frequently used to determine the L4-L5 interspace. However,
accumulation of adipose tissue around the patient mid section, could lead to a higher-
than-desired level for needle placement.
The Closed Claims Project shows cases of spinal cord injury by the spinal needle,
in which the level of needle placement was grossly underestimated. I suggest instead
using the upper end of the intergluteal sulcus to determine the position of the sacral
hiatus. In adults the L5-S1 interspace is around 10 cm (4 inches) cephalad to this point
(height of the sacrum). This measurement in adults should always be distal to the
termination of the spinal cord at L1.
Using a hyperbaric solution in the sitting position, and leaving the patient in that
position for at least 5 minutes, produces a saddle block. However, up to 20 minutes is
necessary to wait, in the desired position, to achieve any appreciable “saddle” or
“lateralized” distribution blockade.
Lateral position
It is the position of choice in many institutions. The patient lies on his/her side. It
is more comfortable for the patient and decreases the risk for accidental fall and
vasovagal problems. The technique otherwise is similar to sitting position
40 | P a g e
Paramedian approach
In some elderly patients, with calcified ligaments, it is difficult to advance the thin
spinal needle through the midline. The lateral approach is a good alternative in those
cases. The spinous process is identified and the point of entrance is marked about 2 cm
paramedian. The needle is directed slightly medial and cephalad.
Taylor Approach
Usually the L5-S1 interspace is the larger. A spinal technique through it is known
as Taylor approach. The entrance point is 1 cm medial and 1 cm caudal to the posterior
superior iliac spine directing the needle cephalad and toward the midline.
Anesthesia duration
The local anesthetic used and the rate at which it is removed from the
subarachnoid space determines duration. Elimination is entirely dependent on vascular
absorption and does not involve metabolism of local anesthetics within the subarachnoid
space. Absorption occurs in the subarachnoid space itself and in the epidural space (local
anesthetics cross the dura both ways).
1. Hypotension
It is the most frequent seen side effect. It is mainly the result of venous pooling
with decreased cardiac output secondary to sympathetic blockade. There is also a
small component of arteriolar dilation. However systemic blood pressure does not
decrease proportionally because of compensatory vasoconstriction, especially in
the upper extremities with intact sympathetic innervation. Even with total
sympathetic blockade after spinal anesthesia the decrease in systemic vascular
resistance is less than 15%. This is because arterioles retain intrinsic tone and do
not dilate maximally.
The magnitude of the blood pressure decrease depends on the extent of
sympathetic blockade, intravascular volume, and cardiovascular status. Preloading
the patient with 250-500 mL, while frequently used, is unsupported by the
evidence.
A mild vasopressor like ephedrine in 5-10 mg increments and fluid are all that is
usually necessary to treat hypotension. Ephedrine is usually the drug of choice
because it produces vasoconstriction and increases cardiac output.
Phenylephrine is a good second choice especially if tachycardia is present. It
causes vasoconstriction, and it could decrease the cardiac output.
Trendelenburg position can alleviate the venous pooling, but may produce an
even higher spinal level. Elevating the legs with the patient sitting at 30-45
degrees is a good compromise.
41 | P a g e
2. Bradycardia
When the sympathetic block reaches T2 level, the cardioacelerator fibers are
blocked and the vagus action is unopposed. The extent to which heart rate
decreases in response to total sympathetic block during spinal usually is moderate
(10-15%). However severe bradycardia and asystole have been reported in
normal patients during otherwise uneventful spinal anesthesia. It can occur even
in the absence of hypotension and can occur after 30-45 minutes of spinal.
The Bezold-Jarisch reflex has been implicated. This reflex would be triggered by
decreased venous return to the heart producing a paradoxical hypervagal
response. Early recognition and treatment is essential. Ephedrine, atropine and
in some cases epinephrine are indicated along with fluid replacement. |
3. Total spinal
Spinal anesthetic that involves the cervical region. It is manifested by respiratory
arrest, bradycardia, hypotension and unconsciousness. The respiratory arrest most
likely is a manifestation of ischemia of the medullary respiratory center secondary
to intense hypotension and drop in cardiac output (complete sympathetic
blockade) severe enough to compromise cerebral circulation.
Block of phrenic nerve is not a likely cause. Management involves ABC with
control of the airway, ventilator support, use of vasopressors, and atropine and
fluid replacement as needed.
1. Respiratory
Arterial gases are usually unaffected in patients breathing room air.
Tidal volume, maximum inspiratory volumes and negative intrapleural pressure
during inspiration are unaffected, despite intercostals muscle paralysis with high
thoracic levels. This is because diaphragmatic activity remains intact.
Expiratory volumes and total vital capacity are significantly diminished in high
thoracic spinal, as are maximum intrapleural pressures during forced exhalation,
and coughing. This is mainly due to paralysis of abdominal muscles.
2. Hepatic
Hepatic blood flow decreases to the extent of hypotension to a degree similar than
after general anesthesia. Spinal anesthesia has not proven to be an advantage or
disadvantage in patients with liver disease. For intraabdominal surgery the
decrease in hepatic perfusion is mainly due to surgical manipulation.
3. Renal
Renal blood flow as cerebral blood flow is autoregulated through a wide range of
arterial pressure. In the absence of renal vasoconstriction renal blood flow does
not decrease until mean arterial pressure decreases below 50 mm Hg. Thus, in the
absence of severe hypotension, renal blood flow and urinary output remain
unaffected during spinal anesthesia. Loss of autonomic bladder control results in
urinary retention. This is more frequent in males.
42 | P a g e
4. Endocrine and metabolic
Spinal anesthesia, but not general anesthesia, blocks the hormonal and metabolic
stress response associated with surgery. This response involves increases in
ACTH, cortisol, epinephrine, norepinephrine and vasopressin as well as activation
of the rennin-angiotensin-aldosterone system. However this effect seems to wear
off along with the spinal anesthesia, producing metabolic and hormonal responses
similar than after general anesthesia for the same operation.
5. Gastrointestinal
The small intestine contracts during spinal and sphincters relax due to unopposed
vagus nerve activity. The combination of contracted gut and complete relaxation
of abdominal muscle provide good surgical conditions.
1. Nausea
Frequent side effect due to imbalance of sympathetic and parasympathetic
visceral tone. Hypotension, bradycardia or hypoxia must be rule out.
Antiemetics like ondansetron or droperidol are usually effective.
43 | P a g e
In the issue of PDPH:
Pencil point needles less than or equal to 22 gauge and cut-bevel needles
less than or equal to 27 gauge produce an incidence of PDPH of
approximately 1%.
Continuous spinal with 20 gauge catheters is not likely to produce PDPH
in an older patient population.
Obstetric patients undergoing spinal anesthesia with small pencil point
needles show a 3-4% rate of post dural puncture headache. Conservative
treatment involves bed rest, IV or oral fluids, acetaminophen and NSAIDs.
Hydration and caffeine stimulates production of CSF.
Epidural blood patch with 15-20 mL of autologous blood, injected at the
same original puncture level or one space below, is a very effective
treatment. The effect can be immediate or be delayed by a few hours. A
single blood patch is about 90% effective.
The cause for TNS is not well understood and could represent a mild and
reversible form of neuropathy. Many possible causes have been postulated: local
anesthetic toxicity, needle trauma, neural ischemia secondary to sciatic nerve
stretching, patient positioning, small gauge, pencil-point needles promoting local
anesthetic pooling, muscle spasm, early mobilization, etc. Because of the low
incidence of TNS after bupivacaine spinal, we could be reasonably sure than TNS
is not the result of the subarachnoid block per se, the needle or the position for it.
Even though neurotoxicity is frequently mentioned as possible cause for TNS,
a case can be made against it. Cauda equina syndrome (CES) is known to result
from local anesthetic toxicity; however the factors that increase CES (e.g., higher
doses/concentration of local anesthetics and the addition of vasoconstrictors), do
not have an effect on TNS.
44 | P a g e
We know that TNS is mostly associated with lidocaine spinal, lithotomy
position, knee arthroscopy and ambulatory surgical status (obesity could be a
contributing factor) and that it is very rarely associated with bupivacaine spinal.
We also know that decreasing the concentration of lidocaine from 5% to 0.5%
does not decrease the incidence of TNS and that hyperosmolarity, hyperbaricity
and addition of glucose ARE NOT contributing factors.
First line of treatment is reassurance, NSAIDs, comfortable positioning and
heating pad. A second line of treatment can include narcotics and muscle
relaxants like cyclobenzaprine. Trigger point injections have been used with
reported success.
Eliminating lidocaine from subarachnoid block probably is not warranted at
this point. However do not use it for ambulatory surgery in lithotomy position or
knee arthroscopy (high risk). On the other hand, the incidence of TNS after
inguinal hernia with lidocaine spinal is only 8%, after C-section is 0-8% and after
tubal ligation is 3%, similar to non-pregnant patients undergoing surgery in the
supine position. Bupivacaine, even in small doses, increases discharge time.
Perhaps the combination of small doses of bupivacaine plus narcotics is the best
possible approach.
5. Back pain
As many as 40% of patients may complain of this annoying side effect. It is
postulated to be the result of stretching of the ligaments following the relaxation
of back muscles. This is similar to what is seen in up to 25-30% of patients
receiving general anesthesia in the supine position. It can also be the result of
localized inflammatory response with muscle spasm. Rest, local heat and
NSAIDs are the treatment of choice.
6. Hearing loss
Transient minor hearing loss has been described after spinal anesthesia. The risk
seems larger with larger-gauge needles and it might be the result of temporary
decrease in CSF pressure with traction of intracranial nerves.
The problem is mild but well documented with audiometry. It resolves on its own.
45 | P a g e
7. Infection
Abscess or meningitis is rare. The development of meningitis after lumbar
puncture in bacteremic patients is a concern. Animal models suggest that
perioperative use of antibiotics eliminates this risk. Lumbar puncture in patients
infected with HIV is controversial. Neuraxial techniques including blood patch
have been performed on these patients without apparent problems. The risk has to
be evaluated on an individual basis.
A few years ago spinal anesthesia was favored for same day surgery patients.
However, widely available, poorly-soluble general anesthetic agents and LMA have
decreased its use. Home readiness involves short duration and in many institutions,
ability to void. Duration is a function of the agent and dose used. The spread of the agent
dictates the duration at a given dermatome. It is likely that the more segments blocked by
a given dose (more spread) the shorter the duration at any given segment. Hyperbaric
solutions and isobaric solutions injected rapidly with the bevel turned caudad concentrate
around the sacral roots and can delay sensory motor recovery and the ability to void. On a
milligram basis, isobaric preparations injected rapidly with the bevel facing cephalad are
more likely to improve home readiness and voiding. Procaine and very small doses of
bupivacaine plus narcotics have been used in the outpatient setting with variable success.
Intrathecal adjuncts
1. Epinephrine
It prolongs duration, but also prolongs the recovery time and voiding time. Thus it
should not be used in the ambulatory setting.
2. Fentanyl
The lipophilic synthetic opioids appear to improve the quality of the block
without prolonging recovery. Ben-David et al in 1997 showed that 5 mg of
hyperbaric bupivacaine was inadequate in 27% of cases of spinal for knee
arthroscopy. Adding 10 ucg of fentanyl reduced the failure rate to zero.
Fentanyl produces pruritus in about 50% of the patients. Serotonin inhibitors (like
ondansetron) are being used to treat this side effect too. Respiratory effects are
unlikely with doses below 25 mcg.
3. Morphine
The use of hydrophilic intrathecal narcotics is accompanied by a longer lasting
analgesia, but also by a higher rate of complications. Among them are: delay
respiratory depression (4-6 hrs after the injected dose), increased nausea and
vomiting, pruritus and delayed voiding.
46 | P a g e
EPIDURAL ANESTHESIA
It is technically more difficult to perform than spinal and because larger doses of
local anesthetics are used it has the potential for systemic toxicity. On the other hand, it
offers a greater degree of flexibility in the extent and duration of anesthesia.
Anatomy
The spinal epidural space extends from the foramen magnum to the end of the
dural sac at the level of S2. It is bounded anteriorly by the vertebral bodies and
posteriorly by the laminae and ligamentum flavum. The epidural space outlines the spinal
canal immediately superficial to the dura. In the cervical region the epidural space is
smaller and it is wider in the lumbar area. A volume of local anesthetic about 10 times
larger is required to produce lumbar epidural anesthesia than for equivalent subarachnoid
blockade. Smaller volumes are sufficient for the thoracic space. The epidural space is
filled with connective tissue, fat and veins, which can become enlarged during
pregnancy. The spinal nerves travel through this space surrounded by a sheath of dura.
47 | P a g e
Techniques
Lumbar epidural
It is the most common site for epidural anesthesia. The midline or paramedian
approach can be used. A block below the termination of the spinal cord at L1 should be
safer. An accidental dural puncture (“wet tap”) could result in spinal cord damage at
higher levels.
Thoracic epidural
It is technically more challenging and has a greater risk for spinal cord injury. It is
rarely used as the primary anesthetic. Many people prefer the paramedian approach in the
thoracic level, because of the extreme obliquity of the thoracic spinous processes.
Epidural needles
The Tuohy needle is the most commonly used. A typical needle is 17-18 gauge,
3.5 inches long. It has a blunt bevel with a gentle curve of 15-30° at the tip. The blunt tip
helps push the dura away, “tenting” it, after the ligamentum flavum has been pierced.
Epidural catheters
They provide the means for continuous infusion. Usually they are 19-20 gauge in
size. The needle bevel is directed in the desired direction (not a guarantee for catheter
final location) and the catheter is advanced 2-6 cm. A short insertion increases the chance
for accidental dislodgement. The farther in, the greater the chance of unilateral epidural
and other complications (bloody tap, catheter knotting). Four to five cm is a good
compromise.
Test dose
It is important because of the large doses of LA injected into the epidural space.
The classic test dose is 3 mL of 1.5% lidocaine (45 mg) with 1:200,000 of epinephrine
(15 mcg). The 45 mg of lidocaine, if intrathecal, should produce spinal anesthesia. The 15
mcg of epinephrine, if intravascular, should produce at least a 20% increase in heart rate
within 30 sec or 30 beats between 20-40 sec (Barash’s, 5th edition, 2006). In patients who
are beta blocked the heart rate increase may not happen and an increase in systolic
pressure of 20 mmHg or more may be more reliable (Barash’s 5th edition, 2006). The use
of epinephrine as a test dose in obstetrics is controversial. Some suggest instead the use
of only 30 mg of lidocaine or 5 mg of bupivacaine.
Termination of action
It is related to type of drug and degree of spread. It is commonly described as the
time it takes to a two-segment regression of sensory blockade. The approximate time for
two-segment regression (sensory) for chloroprocaine is 50-70 minutes, for lidocaine is
90-150 minutes and for bupivacaine is 200-260 minutes.
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References
1. Snell R: Clinical Anatomy for Medical Students, 5th edition. Boston, Little,
Brown and Company, 1995
2. Bernards CM: Epidural and Spinal Anesthesia, In: Barash PJ, Cullen BF,
Stoelting RK, Clinical Anesthesia, 5th edition. Philadelphia, Lippincott Williams
& Wilkins, 2006, pp 691-717
3. Mulroy MF: Regional Anesthesia, 3rd edition. Philadelphia, Lippincott Williams
& Wilkins, 2002, pp 65-118
4. Wong G, Brown D. Transient paraplegia following alcohol celiac plexus block.
Reg Anesth 1995; 20: 352-355
5. Hogan QH. Magnetic resonance imaging of cerebrospinal fluid volume and the
influence of body habitus and abdominal pressure. Anesthesiology 1996; 84;
1341-1349
6. Bridenbaugh PO, Greene NM, Brull SJ, Spinal (Subarachnoid) Neural
Blockade, In: Cousins MJ, Bridenbaugh PO (eds), Neural Blockade, 3rd edition.
Philadelphia, Lippincott-Raven, 1998, pp 203-241
7. Cousins MJ, Veering BT: Epidural Neural Blockade, In: Cousins MJ,
Bridenbaugh PO (eds), Neural Blockade, 3rd edition. Philadelphia, Lippincott-
Raven, 1998, pp 243-320
8. Salinas FV: Pharmacology of Drugs Used for Spinal and Epidural Anesthesia
and Analgesia, In: Wong CA (ed), Spinal and Epidural Anesthesia. New York,
McGraw-Hill, 2007, pp 75-109
9. Sheskey MC, Rocco AG, Bizzarri-Schmid M, et al. A dose-response study of
bupivacaine for spinal anesthesia. Anesth Analg 1983; 62: 931-935
10. Van Zundert AAJ, Grouls RJE, Korsten HHM, et al. Spinal anesthesia: Volume
or concentration-What matters? Reg Anesth 1996; 21: 112-118
11. Giroux CL, Wescott DJ. Stature estimation based on dimensions of the bony
pelvis and proximal femur. J Forensic Sci, 2008; 53: 65-68
12. Reina MA, de Leon-Casasola OA, Lopez A, et al. An in vitro study of dural
lesions produced by 25-gauge Quincke and Whitacre needles evaluated by
scanning electron microscope. Reg Anesth Pain Med 2000; 25: 393-402
13. Swisher JL. Spinal Anesthesia: Past and Present. In Problems in Anesthesia,
2000:12; 141-147
14. Ben-David B, Solomon E, Levin H, et al. Intrathecal fentanyl with small-dose
dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth
Analg 1997: 85; 560-565
15. Pollock JE. Transient neurological symptoms: etiology, risk factors, and
management. Reg Anesth Pain Med 2002:27; 581-86
16. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4th edition. New
York, McGraw-Hill, 2006, pp 289-323
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CHAPTER 4
REGIONAL ANESTHESIA
AND ANTICOAGULATION
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Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy
The recommendations are also graded to indicate the strength of the guideline and the
degree of consensus:
Grade 1: represents general agreement on the efficacy.
Grade 2: Notes conflicting evidence or opinion.
Grade 3: Suggests that the procedure may not be useful and possibly harmful
(e.g., epidural procedure in a patient receiving twice-daily LMWH).
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decreased venous thrombosis after these techniques. However the beneficial effect of
neuraxial techniques on coagulation is insufficient as the sole method of
thromboprophylaxis. As a result, anticoagulants, antiplatelets and thrombolytic
medications are commonly used in the prevention and treatment of thromboembolism.
Nearly all hospitalized patients have at least one risk factor and 40% of patients
have 3 or more risk factors (according to Geerts et al, as cited by the 2010 ASRA
statement). The following is a table for risk factors for VTE taken from the 2010 ASRA
statement:
Administration of thromboprophylaxis
In terms of agents and doses, the 2010 ASRA statement recommends to follow
the American College of Chest Physicians ACCP guidelines advising the clinicians to
follow the manufacturer-suggested dosing guidelines (Evidence Grade 1C).
Risk of bleeding
Bleeding, especially intracranial, intraspinal, intraocular, mediastinal or
retroperitoneal, is the most feared complication of anticoagulant and thrombolytic
therapy. Risks factors include increased age, female sex, history of gastrointestinal
bleeding, concomitant aspirin use and length of therapy.
During warfarin therapy an INR of 2.0 to 3.0 is associated with a 3% low risk of
bleeding during a 3-month treatment period. Stronger regimens (INR >4) increase the
risk of bleeding significantly to 7%.
The incidence of hemorrhagic complications during therapeutic anticoagulation
with IV or subcutaneous heparin is less than 3% and even lower with LMWH.
Thrombolytic therapy is associated with the highest risk of bleeding, with major
bleeding occurring in 6% to 30% of patients treated with thrombolytic therapy for DVT,
ischemic stroke, or ST elevation myocardial infarction. There is no significant difference
in the risk of bleeding among thrombolytic agents.
The addition of potent anticoagulants (LMWH, hirudin) or antiplatelets
(glycoprotein IIb/IIIa agents) therapy increases even more the risk of major bleeding.
“Therefore, although thromboembolism remains a source of significant
perioperative morbidity and mortality, its prevention and treatment are also
associated with risk” (2010 ASRA statement, page 67).
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Anesthetic management of the patient receiving thrombolytic therapy
These patients are at risk of serious bleeding. We will discuss several situations:
1. Patients scheduled to receive thrombolytic therapy: Avoid performing lumbar
punctures and neuraxial anesthesia and avoid thrombolytic therapy for 10 days
if these procedures have been performed (evidence Grade 1A).
2. Patients who have received thrombolytic therapy: Do not perform spinal or
epidural procedures (Evidence Grade 1A). Data not available as to how long
we need to wait.
3. Patients who have received neuraxial blocks at or near the time of fibrinolytic
and thrombolytic therapy: Neurological monitoring every 2 hours or less “for
an appropriate interval”. If epidural catheter present avoid drugs producing
sensory and motor block to facilitate neurological assessment (Evidence
Grade 1C).
4. Patient with an epidural catheter who unexpectedly received thrombolytic
therapy: There is no definite recommendation as to when to remove it. They
suggest to measure fibrinogen levels (one of the last clotting factors to
recover) for appropriate timing of catheter removal (Evidence Grade 2C).
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d. Monitor the patient postoperatively to provide early detection of motor
blockade. Avoid local anesthetics through catheter.
e. The occurrence of bloody or difficult neuraxial technique may increase
risk, but data does not support mandatory cancellation. Risk-benefit
discussion with surgeon about proceeding.
f. Insufficient data exist about risk of bleeding when neuraxial
techniques are combined with the full anticoagulation of cardiac
surgery. They suggest neurological monitoring and avoidance of local
anesthetics (Grade 2C).
1. The anti-Xa level is not predictive of the risk of bleeding. Recommend against
the routine use of it (Grade 1A).
2. Antiplatelets and other anticoagulants administered in conjunction with
LMWH increase the risk of spinal hematoma. Avoid concomitant use of
antiplatelets drugs, unfractionated heparin, or dextran regardless of LMWH
dosing regimen (Grade 1A).
3. The presence of blood during neuraxial technique does not necessitate
postponement of surgery. Recommendation to delay initiation of LMWH for
24 hr in discussion with the surgeon (Grade 2C).
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place overnight but must be removed before initiation of LMWH, and
the first dose should be delayed for 2 hrs after catheter removal.
b. Single-daily dosing. The first postoperative LMWH dose should be
administered 6-8 hrs postoperatively and the second no sooner than 24
hrs later. Indwelling catheters may be safely maintained although it
should be removed a minimum of 10-12 hrs after the last dose of
LMWH. Subsequent dosing should not be given for at least 2 hrs after
catheter removal. No other drugs with effect in coagulation should be
given because of risk of additive effects.
1. In the first 1-3 days after warfarin discontinuation the coagulation status
(reflected primarily by factors II and X levels) may not be adequate despite a
decrease in the INR (indicating a return of factor VII activity). Adequate
levels of II, VII, IX and X may not be present until the INR is normal. The
recommendation is that warfarin must be stopped 4-5 days prior to the
procedure and the INR measured before a neuraxial block is attempted (Grade
1B).
2. Avoid using other drugs with anticoagulation effect like aspirin and other
NSAIDs, ticlopidine, and clopidogrel, UFH, and LMWH (Grade 1A).
3. In patients who are likely to have an enhanced response to the drug, it is
recommended to use the available algorithms to guide in the dosing based on
desired indication, patient factors, and surgical factors (Grade 1B).
4. In patients receiving an initial dose of warfarin before surgery, the
recommendation is to check the INR prior to neuraxial block if the first dose
of warfarin was administered more than 24 hrs earlier or if a second dose has
been administered (Grade 2C).
5. In patients receiving low-dose warfarin therapy during epidural analgesia, the
suggestion is to monitor the INR daily (Grade 2C).
6. For patients on warfarin therapy receiving epidural analgesia neurologic
testing of motor and sensory function should be performed routinely. To
facilitate the neurologic evaluation keep the local anesthetics to a minimum
(Grade 1C).
7. As warfarin therapy is initiated it is suggested that neuraxial catheters should
be removed with an INR of less than 1.5. This value correlates hemostasis
with clotting factor activity levels greater than 40%. The suggestion is to keep
neurologic testing after catheter removal for at least 24 hrs (Grade 2C).
8. In patients with INR more than 1.5 but less than 3 the suggestion is to remove
catheters with caution after reviewing medication records for other
medications affecting coagulation that may not affect the INR (e.g., NSAIDs,
clopidogrel, ticlopidine, UFH, LMWH (Grade 2C). It is also recommended to
check neurological status before catheter removal and continued until the INR
has stabilized at the desired prophylaxis level (Grade 1C).
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9. In patients with INR greater than 3 and an indwelling catheter, the
recommendation to hold or reduce the warfarin dose (Grade 1A). No
definitive recommendation can be made for removal of catheters in patients
with therapeutic levels of anticoagulation (Grade 2C).
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Anesthetic management of the patient receiving fondaparinux
The actual risk is unknown. Until further experience is available, performance of
neuraxial techniques should be avoided.
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References
1. Neal JM: Neural Blockade and Anticoagulation. In: Regional Anesthesia, The
Requisites in Anesthesiology. Rathmell J, Neal J, Viscomi C (eds). Philadelphia,
Elsevier Mosby, 2004, pp 151-156
2. Bergqvist D, Wu CL, Neal JM. Anticoagulation and Neuraxial Regional
Anesthesia: Perspectives. [Editorial] Reg Anesth Pain Med 2003; 28: 163-166
3. Horlocker tt, Wedel DJ, Benzon H, et al. Regional anesthesia in the
anticoagulated patient: Defining the risks (The Second ASRA Consensus
Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med
2003; 28: 172-197
4. Horlocker TT, Wedel DJ, Rowlingson JC, Enneking FK, Kopp SL, Benzon HT,
Brown DL, Heit JA, Mulroy MF, Rosenquist RW, Tryba M, Yuan CS. Regional
Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy.
American Society of Regional Anesthesia and Pain Medicine Evidence-Based
Guidelines (Third Edition). Reg Anesth Pain Med 2010; 35: 64-101
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CHAPTER 5
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Peripheral Nerve Blocks
There are many ways to ascertain the correct placement of a needle with respect to a
nerve. A good knowledge of the anatomy makes things easier and safer. The methods are:
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mixed nerve, a painless muscle twitch is produced. The intensity of the response
is inversely proportional to the needle tip-nerve distance (actually to the square
root of it). A visible response at lower currents (less than 0.5 mA), suggests close
proximity between the needle tip and the target nerve. There is a good amount of
clinical evidence to suggest that a current of 0.5 mA or less, capable of eliciting a
visible response, is a reliable indicator of critical proximity. However, evidence is
lacking as to what exactly that distance is, and as to whether the distance is
different for different nerves. In general it is thought that 1 mA of current will
produce depolarization of a motor nerve at a distance of about 1 cm (10 mm).
Nowadays nerve stimulator techniques are widely practiced around the
world. With modern nerve stimulators the practitioner can adjust the pulse
intensity (magnitude of the current) in mA; the pulse frequency (amount of
pulses per second) in Hz (1 or 2) and the pulse width (duration of the pulse) in
milliseconds (ms). The pulse duration most suitable for stimulating motor fibers
in a mixed nerve is 0.1 ms (100 microsec).
Characteristics of ultrasound
The human ear can hear sounds between 20 and 20,000 Hz (cycles per
second) or 20 KHz. Ultrasounds waves travel at a higher frequency than the
highest frequency detectable by the human ear. Ultrasound waves used in
medicine usually are in the 1 to 20 MHz range (1 MHz = 1 million Hz).
Ultrasound waves travel easily through fluids and soft tissue, but have
problems traveling through bone and air. Ultrasound is better reflected at the
transition between two different types of tissues like soft tissue-air, bone-air and
soft tissue-bone. This transition plane is seen as a hyperechoic line on the screen.
The ultrasound is delivered from a small probe that contains piezoelectric
crystals that under the influence of an electric current are made to vibrate
producing a wave of ultrasonic sound. The ultrasound waves in the form of a
narrow beam travel through tissues at a speed that depends on the nature of the
human tissues, but for calculations and image production is assumed to be an
average value of 1,540 m/sec. This value closely approximates the speed of
ultrasound through soft tissue (1,540 m/sec), muscle (1,580 m/sec), blood (1,560
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m/sec), but differs to the speed through bone (4,000 m/sec), lung (500 m/sec) or
air (330 m/sec).
Part of the ultrasound waves are reflected back to the transducer,
especially at tissue interfaces, where the mechanical energy is converted back to
electrical energy. The information is then processed by the software of the
ultrasound machine to generate an image. Therefore, the transducer delivers
ultrasound for part of the time and for part of the time it “listens” for the returned
waves. The distance is calculated as a function of the time it takes for the waves
to return. Tissues with high density like bone reflect most of the waves and
produce a bright image, known as hyperechoic. A tissue like blood that permits
easy passage of the ultrasound waves through it appears dark or anechoic. The
rest of tissues present intermediate characteristics between anechoic o hypoechoic
to hyperechoic.
Better images are obtained when the probe is perpendicular to the
structure being searched (e.g., nerve, needle). This is because more bouncing
sound waves can be detected by the transducer. Changes as small as 10 degrees
from the perpendicular can distort the echogenicity of a nerve, reducing the
amount of waves returning to the transducer and decreasing the quality of the
image. This is known as anisotropy, the change of the quality of the echo image
as a result of change in the angle of incidence of the probe with respect to the
target structure. Tendons characteristically have higher anisotropy than peripheral
nerves.
The needle can be advanced “in plane” or “out of plane” with respect to
the main axis of the probe. In the in plane approach the needle is advanced in
coincidence with the long axis of the probe, in the same plane of the ultrasound
beam. This makes possible the visualization of the needle as it advances toward
the target nerve(s). Good needle visualization depends on its angle of insertion,
with the best visualization obtained when the needle trajectory is parallel to the
probe. As the angle of penetration increases (deeper targets) the difficult to
visualize the needle also increases. When the insertion angle is more than 45
degrees with respect to the plane of the probe the needle cannot be visualized
anymore. At this point tissue movement and injection of small amounts of local
anesthetics can help determine the location of the needle tip.
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With the out of plane approach the needle is advanced perpendicular to the
main axis of the probe, so only the tip of the needle can be visualized at the point
where it crosses under the ultrasound beam. The tip is seen as a very hyperechoic
bright point on the screen. The main advantage of an out of plane technique, from
my perspective, is that the trajectory of the needle to the target is shorter.
Regardless of the approach the goal is to bring the tip of the needle into the
proximity of the nerve(s) for injection.
High frequency probes (8-15 MHz) are usually linear probes that provide
good resolution, but limited penetration (3-4 cm). These probes are used at
different levels of the brachial plexus, abdominal wall and at different locations in
the lower extremity. For deeper structures, lower frequency (4-7 MHz) curved
probes are needed providing a wider field and deeper penetration at the expense
of resolution. Deep scanning of intra abdominal organs requires frequencies of 3-
5 MHz The quality of the image is also affected by other factors like compound
imaging (the capture of different views of structures before producing an image)
and color Doppler.
We will refer again to ultrasound when we describe individual techniques.
Insulated needles are the needles most commonly used in conjunction with nerve
stimulation and ultrasound techniques nowadays in the United States, Europe and other
parts of the world. The current applied to this needle concentrates at its tip, making the
localization of nerves more accurate. Several brands of these needles exist in the market
and they come ready with a connection that only fits the negative electrode. Connecting
the negative electrode to the exploring needle lowers the amount of current necessary to
depolarize a nerve.
Non-insulated needles transmit the current preferentially to the tip, but also along
the shaft of the needle making the localization of nerves less accurate. Insulated needles
are more expensive than non-insulated needles.
Standard needles have a tip angle of around 14 degrees and are known as “sharp’
needles. It is frequently recommended to perform regional block with short-bevel needles
with an angle of 30 to 45 degrees. This recommendation comes from studies by Selander
et al who demonstrated more neural damage in isolated sciatic nerves when sharp needles
were used. The damage with sharp needles was also more extensive when the orientation
of the sharp bevel was perpendicular to the fibers. With short bevel needles, the damage
was less frequent as the fibers were pushed away by the advancing needle.
This concept has been challenged by Rice et al. According to these authors it may
be more difficult to penetrate a nerve fascicle with a short-bevel needle than with a sharp
needle, but should it occur, the lesions may be more severe. Recently in 2009 Sala-
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Blanch and collaborators published in Regional Anesthesia and Pain Medicine a study in
which sharp long beveled versus blunt short beveled (30 degrees) needles were
introduced into a sciatic nerve of a human cadaver. After the punctures the specimen was
investigated under the microscope for evidence of fascicular damage. They demonstrated
that with either needle was very difficult to penetrate the fascicles. In fact they found no
histological evidence of fascicular damage with short beveled needles and only 3.2% of
fascicular damage (4 fascicles) with sharp needles.
Nerve injury
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Another mechanism of nerve injury could be hematoma and infection leading to scar
formation.
It has been a common belief in regional anesthesia that nerve puncture and
intraneural injection lead to nerve damage. In 2006 Bigeleisen published in
Anesthesiology a study that seems to discredit this notion. In his study conducted under
ultrasound guidance 21 of 26 patients had nerve punctures of at least one nerve, and 72
out of 104 nerves had intraneural injection (2-3 mL). A 6 month follow up failed to
demonstrate nerve injury. Incidentally it is important to notice that the local anesthetic
mixture injected (bupivacaine plus lidocaine) contained 3 microgr/mL of epinephrine.
Since peripheral nerves are formed by neural tissue (fascicles) and connective
tissue, it is possible to penetrate the nerve (intraneural), but still be extrafascicular. In
2004 Sala-Blanch et al reported in Anesthesiology two cases of inadvertent intraneural,
extrafascicular injection after anterior approach of the sciatic nerve block with nerve
stimulation performed in two diabetic patients, as evidenced by CT scan. These two cases
also demonstrate that painless nerve punctures and even intraneural (although
extrafascicular) injections are possible without apparent sequelae.
A preexisting neurological injury should always be documented. It is important to
realize that nerve damage can occur perioperatively for a reason other than regional
anesthesia. Nerves can be injured during surgery by direct trauma, use of retractors and
tourniquets and by improper positioning. Nerves can also be damaged postoperatively by
a tight cast or splint, wound hematoma or surgical edema.
Use of epinephrine
The symptoms can appear within 24 h after the injury, but sometimes they do not
present until days or weeks after the offending procedure took place. The degree of
symptoms is usually related to the severity of the injury. The cases are usually mild with
symptoms like tingling and numbness that usually disappear within weeks, or more rarely
they can progress to severe cases of neuropathic pain and motor involvement that can last
months and even years.
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Pre-existing neurologic condition and regional anesthesia
In order to minimize the risk of neurologic injury after regional anesthesia the
anesthesiologist needs to consider several factors, including procedure, patient and
surgeon. A meticulous nerve block technique, avoiding direct trauma to the nerve and
appropriate selection of local anesthetic volume and concentration are important. The role
of vasoconstrictors, especially low dose (1:400,000), on clinical development of neural
ischemia, has not been elucidated.
When a neuropathy develops in the postoperative period, a prompt evaluation is
necessary and a multidisciplinary approach, with participation of neurology, radiology,
and surgery, is recommended. A detailed history must be obtained including the timing
and nature of symptoms. A physical exam should look for any signs of hematoma or
infection. A neurological exam by a neurologist is also crucial.
Electrophysiological testing
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demyelinating, like the ones seen after tourniquet compression, nerve conduction
velocity is greatly affected while the amplitude remains normal.
2. Electromyography
It records electrical activity in the muscles helping to locate the denervated
muscles in reference to the level at which the nerve damage has occurred. Within
2-3 weeks post injury, spontaneous activity can be recorded from the muscle, in
the form of sharp waves and muscle fibrillation. After 3 months the pattern may
change, as nerve regeneration by “sprouting” takes place. In permanent injuries,
electromyography remains abnormal.
Use of tourniquet
Use of crude compression devices to control surgical bleeding from the
extremities, can be, according to Bailey, traced back to ancient Rome. The term
“tourniquet” was apparently first used by Petit in France in 1718 to describe a mechanical
screw-like contraption that he introduced to provide surgical hemostasis. Lister in 1864
was the first surgeon who used a tourniquet to produce a bloodless surgical field. Modern
tourniquet devices have a microprocessor, use an air pump and are able to accurately and
safely maintain the desired pressure. A fail-safe mechanism protects from pressure ever
exceeding 500 mmHg.
Tourniquet time: Recommended tourniquet time varies, but the most commonly
accepted limit is 2 hours. This recommendation is based on a work by Wilgis, published
in 1971 in which he demonstrated more acidosis after 2 hours of ischemia. Surgeons
should be made aware when the 2-hour limit has been reached and the tourniquet should
be deflated at that time, unless the procedure is at a crucial time. This communication
with the surgical team needs to be documented in the chart.
Despite the widely accepted 2-hour limit, Klenerman, as cited by Bailey, showed
minimal muscle damage with tourniquet times not exceeding 3 hours, using electron
microscopy.
Some people advocate deflating the tourniquet at 1.5 h for 5-15 minutes followed by an
additional 1.5 h of inflation time.
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Some patients may develop post-tourniquet nerve palsy, affecting more frequently larger
motor fibers than sensory fibers. These lesions are usually reversible. The magnitude and
duration of the compression dictate the severity of the injury.
Patients can also develop “post-tourniquet syndrome”, a clinical picture characterized
by interstitial edema, arm weakness and numbness secondary to cell injury and alteration
or permeability. It usually resolves within a week.
When the tourniquet is deflated blood pressure drops (sudden drop in preload and
afterload) and heart rate increases as blood rushes into an ischemic, vasodilated bed
(reactive hyperemia).
Carbon dioxide and potassium levels increase and so does lactic acid leading to acidosis.
These effects peak at about 3 minutes post deflation. There is also a decreased in patient’s
temperature.
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References
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18. Martin G, Breslin D, Stevens T: Anesthesia for Orthopedic Surgery, In:
Longnecker DE, Brown DL, Newman MF, Zapol WM (eds), Anesthesiology.
New York, McGraw Hill, 2008, pp 1541-1557
19. Bigeleisen PE. Nerve puncture and apparent intraneural injection during
ultrasound-guided axillary block does not invariably result in neurological injury.
Anesthesiology 2006; 105: 779-783
20. Sala_Blanch X, Pomes J, Matute P, Valls-Sole J, Carrera A, Tomas X Garcia-
Diez A. Intraneural injection during anterior approach for sciatic nerve block.
Anesthesiology 2004; 101: 1027-1030
21. Koff MD, Cohen JA, McIntyre JJ, Carr CF, Sites BD. Severe brachial plexopathy
after an ultrasound-guided single-injection nerve block for total shoulder
arthroplasty in a patient with multiple sclerosis. Anesthesiology 2008; 108: 325-
328
22. Sala-Blanch X, Ribalta T, Rivas E, Carrera A, Gaspa A, Reina MA, Hadzic A.
Structural injury to the human sciatic nerve after intraneural needle insertion. Reg
Anesth Pain Med 2009; 34: 201-205
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CHAPTER 6
UPPER EXTREMITY NERVE BLOCKS
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UPPER EXTREMITY BLOCKS
The brachial plexus is most frequently formed by five roots originating from the
ventral divisions of spinal nerves C5 through T1. After exiting through the corresponding
intervertebral foramen, the roots of the plexus are found in the cervical paravertebral
space, between the anterior and middle scalene muscles. In the cervical region the spinal
roots emerge above the corresponding cervical vertebrae, as seen in figure 6-1. Because
there are 8 cervical nerves but only 7 cervical vertebrae, starting with T1 the spinal roots
emerge below the corresponding vertebra (e.g., T1 exits between T1 and T2).
The distance from C5 to T1 roots is large and irreducible, and equal to the height
of four vertebrae. This fact in itself could help explain the frequent lack of dense
anesthesia in the C8-T1 dermatomes after an injection performed at the level of the C5-
C6 roots (interscalene block). Another important and frequently ignored reason is the
expansive wave created by the pulse of the subclavian artery and felt mostly by the distal
roots of the plexus (C8-T1), the lower trunk and its divisions. Because the local
anesthetic diffuses to points of least resistance, this expanding pulsatile force may keep
the local anesthetic from reaching the most distal elements of the plexus.
In addition to knowing the formation of the plexus and its architecture throughout
its trajectory, it is also important from my perspective to understand the plexus in terms
of its relative surface area at different locations. The five roots occupy an area that is
elongated in the frontal plane, but very narrow in the sagittal plane (anteroposterior).
When the five roots combine together to form three trunks, not only there is a 40%
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reduction in the number of nerve structures (from 5 to 3), but also the trunks become
physically contiguous, as shown in figure 6-2, helping reduce their combined surface
area. In fact this is the point at which the brachial plexus is reduced to its smallest surface
area. This striking convergence of innervation is unique to the brachial plexus and has no
parallel in the lower extremity and helps explain the rapid onset and high success rate of
the supraclavicular approach. The surface area of the plexus increases again when the
trunks originate six divisions although they stay together so the small increase in surface
area is compensated by a larger surface of absorption. The surface area increases the most
at the level of the axilla where the plexus gives off the terminal branches.
The anterior scalene muscle originates in the anterior tubercles of the transverse
processes of C3 to C6 and inserts on the scalene tubercle of the superior aspect of the first
rib. The middle scalene muscle originates in the posterior tubercles of the transverse
processes of C2 to C7 and inserts on a large area of superior aspect of the first rib, behind
the subclavian groove.
The five roots converge toward each other to form three trunks -upper, middle and
lower- stacked one on top of the other, as they traverse the triangular interscalene space
formed between the anterior and middle scalene muscles. This space becomes wider in
the anteroposterior plane as the muscles approach their insertion on the first rib.
While the roots of the plexus are long, the trunks are almost as short (app 1cm) as
they are wide, soon giving rise to a total of six divisions (three anterior and three
posterior), as they reach the clavicle. The area of the trunks corresponds to the point
where the brachial plexus is confined to its smallest surface area, three nerve structures,
closely related to one another, carrying the entire sensory, motor and sympathetic
innervation of the upper extremity, with the exception of a small area in the axilla and
upper middle arm, which is innervated by the intercostobrachial nerve, a branch of the
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second intercostal nerve. This great reduction in surface area allows the plexus to
negotiate the narrow passage between the clavicle and the first rib at the apex of the
axilla.
The brachial plexus, represented by its divisions, enters the apex of the axilla
lateral to the axillary artery, the latter being the continuation of the subclavian artery. In
order to offer a short profile the neurovascular bundle “spread” from medial to lateral
with the axillary vein the most medial structure, followed by the axillary artery in the
center and the divisions of the plexus most lateral, as shown in figure 6-3 and 6-4.
It is important to realize that immediately below the clavicle and before arriving
at the coracoid process, the six divisions of the plexus and the origin of the three cords
are located lateral to the artery and not around it (see figures 6-3 and 6-4). This is an
important anatomical detail while considering different infraclavicular approaches.
As the cords approach the level of the coracoid process the lateral cord remains on
the lateral side while the posterior and medial cords migrate behind the artery adopting all
of them the characteristic position around it from which they take their name. At this
level the cords are covered superficially by pectoralis minor and pectoralis major
muscles. It seems to me important to mention that the rotation of the cords behind the
artery from their original lateral position is usually arrested before the medial cord
reaches a true medial position with respect to the artery and before the posterior cord get
to be truly posterior to it. So, a cross section of the neurovascular bundle at the level of
the coracoid process reveals that the cords are not exactly located at the 3, 6 and 9
o’clock position Instead, on the right side, the lateral cord is usually in position 10
(anterolateral), the posterior cord is in position 7 (posterolateral) and the medial cord is in
position 4 (posteromedial). On the left side, the lateral cord is in position 2
(anterolateral), the posterior cord in position 5 (posterolateral) and the medial cord in
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position 8 (posteromedial). This means that usually there are two cords on the lateral side
of the artery (lateral and posterior cords) and only one on its medial side (medial cord),
making the approach from the lateral side more rational, especially during blind
techniques.
At about the level of the lateral border of the pectoralis minor muscle the three
cords give off their terminal branches. The posterior cord originates the axillary and
radial nerves; the medial cord originates part of the median nerve, plus the ulnar, medial
brachial and medial antebrachial cutaneous nerves. The lateral cord originates the rest of
median nerve and musculocutaneous nerve. Sometimes the musculocutaneous nerve
remains attached to the median nerve until reaching the proximal arm.
Fig 6-5 A and B. Axillary sheath. Left axillary region dissection showing A: the axillary sheath
intact from which the musculocutaneous nerve (MCN) is seen exiting. B: shows the same specimen
after the sheath has been open. The intra sheath portion of the MCN can be seen taking off from the
lateral cord (LC). Cadaver dissection by Dr Franco. Images are copyrighted.
(On a model with permission).
Fig 6-5 C. Axillary sheath in cross section.
The axillary sheath just below the clavicle
(apex) is shown with arrows as a well defined
sturdy fascia surrounding the neurovascular
bundle. The interior is otherwise filled with
loose connective tissue. The three cords of the
plexus (c) are shown lateral to the artery.
Cadaver dissection by Dr Franco. Image is
copyrighted.
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Ultrasound, on the other hand, has confirmed that nerves and vessels in all regions
of the body, but especially in exposed places like the axilla, are embedded in a matrix of
soft connective tissue surrounded by a fascial sheath. This loose connective tissue within
the sheath “soaks” the local anesthetic towards areas of least resistance (i.e., along the
nerves) and by doing so this soft connective tissue becomes an obstacle to free
circumferential diffusion. In addition to this internal (within the sheath) factor, there are
other factors outside the sheath that may also play a role in the spread of local anesthesia
within it. Some of these factors have to do with the nature of the tissues through which
the neurovascular bundle travels through and the pressure they exert over the sheath. In
the axilla, for example, the sheath and its content are resting posteriorly over muscle and
bone (scapula). So its posterior aspect is subjected to more outside pressure or resistance
than its anterior aspect that is only covered by the complaint axillary fat. As a result local
anesthetic, which can only move to points of least resistance, will have more difficulty
spreading from the anterior aspect of the axillary sheath to its posterior aspect than vice
versa and this difficulty in the spread within the sheath has nothing to do with any
specific septa.
Axillary nerve (C5-C6): gives an articular branch to the shoulder joint, motor innervation
to the deltoid and teres minor muscles and sensory innervation to part of deltoid and
scapular regions.
Radial nerve (C5-C6-C7-C8): supplies the skin of the posterior and lateral arm down to
the elbow, the posterior forearm down to the wrist, lateral part of the dorsum of the hand
and the dorsal surface of the first three and one-half fingers proximal to the nail beds. It
also provides motor innervation to the triceps, anconeus, part of the brachialis,
brachioradialis, extensor carpi radialis and all the extensor muscles of the posterior
compartment of the forearm. Its injury produces a characteristic “wrist drop”.
Median nerve (C5-C6-C7-C8-T1): gives off no cutaneous or motor branches in the axilla
or the arm. In the forearm it provides motor innervation to the anterior compartment
except the flexor carpi ulnaris and the medial half of the flexor digitorum profundus
(ulnar nerve). In the hand provides motor innervation to the thenar eminence and the first
two lumbricals. It provides the sensory innervation of the lateral half of the palm of the
hand and dorsum of first three and one-half fingers including the nail beds.
Ulnar nerve (C8-T1): like the median nerve, the ulnar nerve does not give off branches in
the axilla or the arm. Its motor component supplies the flexor carpi ulnaris and the medial
half of the flexor digitorum profundus. In the hand it provides the motor supply to all the
small muscles of the hand except the thenar eminence and first two lumbricals (median).
Its sensory branches supply the medial third of the dorsum and palmar sides of the hand
and dorsum of the 5th finger and dorsum of the medial side of 4th finger.
Medial brachial cutaneous nerve (T1): it is solely a sensory nerve. It supplies the skin of
the medial side of the arm. It is joined here by the intercostobrachial nerve, branch of the
second intercostal.
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Medial antebrachial cutaneous nerve (C8-T1): It is also a sensory nerve. It supplies the
medial side of the anterior forearm.
Pearls
With the shoulder down the three trunks of the brachial plexus and the origin of
the divisions are located above the clavicle, therefore during a supraclavicular
block the needle does not need to reach below the clavicle.
For the most part the first intercostal space is located below the clavicle (with the
exception of the most posterior paravertebral part), therefore its penetration is
unlikely during a properly performed supraclavicular block.
During procedures using a needle in the supraclavicular area, the needle should
never cross medial to the parasagital plane of the anterior scalene muscle because
of risk of pneumothorax.
The pulsatile effect of the subclavian artery exerted mainly against C8-T1 roots
and the lower trunk explains why the C8-T1 dermatome can be spared during
interscalene and supraclavicular blocks. To avoid this problem during a
supraclavicular block the injection needs to be performed in the vicinity of the
lower trunk or its divisions, evidenced by fingers twitch with a nerve stimulator
or by injecting between the subclavian artery and the first rib when using
ultrasound. In the case of interscalene block this is usually not a problem since its
main indication is anesthesia/analgesia of the shoulder that does not require
anesthesia of C8-T1 dermatomes.
The SCM muscle inserts on the medial third of the clavicle, the trapezius muscle
on the lateral third of it, leaving the middle third for the neurovascular bundle.
These proportions are maintained regardless of patient’s size. Bigger muscle bulk
through exercise does not influence the size of the muscle insertion area.
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INTERSCALENE BLOCK
NERVE STIMULATOR TECHNIQUE
Indications
Its main indication is anesthesia or analgesia of the shoulder, including the
clavicle and proximal part of the humerus.
Main characteristics
This block is superficial and usually easy to perform. Characteristically it misses
the C8-T1 dermatomes, which include the sensory territories of ulnar, medial
antebrachial cutaneous, and medial brachial cutaneous nerves (medial side of the upper
extremity).
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Fig 6-7. Cricoid-SCM plane. The
level of the cricothyroid membrane is
projected laterally to intercept the
posterior border of the SCM.
(On a model with permission).
The index and middle fingers of the palpating hand are placed behind the SCM at
this level pushing it slightly forward (medially), as shown in figure 6-8. This maneuver
brings the palpating fingers under the SCM and on top (anterior) to the anterior scalene
muscle. The fingers are then rolled back until they fall into the interscalene groove, which
at this proximal point in the neck is a real structure and easy to identify. This is the point
of needle insertion.
Type of needle
A 2.5 cm or 5cm, 22-G, insulated needle can be used.
Needle insertion
The needle is introduced between the two palpating fingers in a medial and
slightly caudal direction, but most importantly with a 20 to 30-degree posterior direction,
as shown in figure 6-9.
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Fig 6-9. Needle insertion. The
needle is advanced medial,
caudal and posterior.
(On a model with permission).
It is important to realize that this is a superficial block that should take place
within the confines of the tips of the palpating fingers and not beyond them. In no
circumstance the needle should be introduced further than the projection of the clavicular
head of the SCM.
Any distal motor twitch as well as biceps, triceps or deltoid muscles are adequate.
There is some controversy in the literature as to whether a shoulder twitch is acceptable
for an interscalene block. Besides the usual arm twitches, anatomical and clinical
evidence support accepting deltoid twitches. Motor twitches from trapezius (spinal
accessory nerve) and levator scapulae (dorsal scapular nerve) are not acceptable. For
further reading on this issue please see: Silverstein W et al. Interscalene block with a
nerve stimulator: A deltoid motor response is a satisfactory endpoint for successful block.
Reg Anesth Pain Med 2000; 25:356-359 and accompanying editorial by William Urmey,
same journal page 340-342.
A twitch of the abdomen signals phrenic nerve stimulation and it is evidence that
the needle is anterior to the anterior scalene. In this case the needle should be withdrawn
and redirected slightly posteriorly. A motor twitch of the scapulae or trapezius muscle
indicates that the position of the needle is too posterior and needs to be repositioned
anteriorly.
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laryngeal nerve involvement. Characteristically this block produces also 100% of
phrenic nerve block with diaphragmatic paralysis (Urmey et al, Anesth Analg, 1991).
This can produce dyspnea and reductions in respiratory volumes of up to 30%.
Pneumothorax is possible, but rare with this block.
Clinical pearls
Because of the position of the shoulder, so close to the head of the patient, the
anesthesiologist must carefully evaluate the patient and surgeon before deciding
to perform an interscalene block as the only anesthesia for the case. A nervous
patient and a rough surgeon could be indications for interscalene analgesia
combined with general anesthesia.
It must be remembered that some of these procedures are performed in positions
other than supine (e.g., beach chair, lateral), which can make the management of
the airway, if needed, a bit more challenging.
A language barrier between patient and anesthesiologist is also a relative
contraindication for interscalene block as the sole anesthetic.
This is a very superficial block that can be performed at 1-2 cm from the skin in
most patients.
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INTERSCALENE BLOCK
ULTRASOUND TECHNIQUE
Indications
Shoulder anesthesia and/or analgesia, including clavicle and proximal humerus.
Patient position
The patient is placed semi seated, with the shoulder down and the head slightly
turned the opposite way, as shown in figure 6-10.
Type of needle
A 2.5 cm or 5 cm, 22-G, insulated needle is what we frequently use.
Type of transducer
This is a superficial block for which a high frequency (8-15 MHz) linear probe is
well suited.
Scanning
Two are the most frequent ways to scan the neck to visualize the roots of the
plexus. One is to start a transverse scan over the sternocleidomastoid muscle (SCM) just
lateral to the cricoid cartilage, or start more distally parallel to the clavicle and then trace
the plexus proximally to the roots. In either case the probe ends in a semi transverse
position (cephalad rotation) overlapping the SCM with a slight distal orientation as
shown in figure 6-11.
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Fig 6-11. Probe position. To get a good
perpendicular cut of the roots, the probe is
slightly rotated as shown. (On a model
with permission)
Needle insertion
The needle can be advanced in plane from medial to lateral, or lateral to medial,
or out of plane usually from cephalad to caudal. It is our preference to insert the needle in
plane from lateral to medial as shown in figures 6-13 and 6-14.
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SUPRACLAVICULAR BLOCK
NERVE STMULATOR TECHNIQUE
Indications
This block is indicated for any surgery on the upper extremity distal to the
shoulder or for analgesia of the entire upper extremity.
Main characteristics
This block is considered by some as more difficult to learn than other upper
extremity blocks and historically it has been associated with a higher risk of
pneumothorax. The literature cites pneumothorax rates between 0.5-6.1 percent. However
with good anatomy and meticulous technique we have been able to practically eliminate
this risk.
A supraclavicular block is usually associated with a short onset, dense anesthesia
and high success rate. As we discussed it in the anatomy section, this is due to the
compact arrangement of the plexus at the level of trunks and divisions. Because of these
favorable characteristics, the supraclavicular block has been called the “spinal of the
upper extremity”.
We perform our own variation of the supraclavicular block, a very anatomical
approach that starts by determining the pleura boundaries as the first step. This allows us
to take advantage of such extraordinary block while limiting its potential drawbacks. Our
experience to late 2009 includes more than 5,000 supraclavicular blocks without ever
having demonstrated a single pneumothorax. A common question posed to us is whether
we perform routine chest X-rays after a supraclavicular block. The answer is no. In fact
we only do an X-ray when the clinical situation merits it (e.g., an unusually difficult
technique and or symptomatic patient). Traditionally our anesthesiology textbooks have
left the impression that a pneumothorax following a supraclavicular block has a late
onset, making the technique a bad choice for outpatients. Our review of the literature fails
to demonstrate this. In fact most of the cases of pneumothorax associated with
supraclavicular block published in the literature, have been diagnosed within a few hours
after the block and most of them have been investigated because of the patients’ early
symptoms. We perform this technique with great success in all kinds of patients,
including same day surgery and trauma patients.
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T3, carried an inherited risk for pneumothorax that would be responsible for the
technique falling into disfavor.
Albeit with several modifications, the supraclavicular approach remained a
popular choice until the early 1960’s. Eventually, the combined effect of pneumothorax
fear and the introduction of the axillary approach by Accardo and Adriani in 1949, and
especially by Burnham in 1958, marked the beginning of the decline for one of the best
approaches in regional anesthesia.
The axillary approach introduced a good technique with its share of shortcomings
(e.g., smaller area of anesthesia than supraclavicular, tendency to produce “patchy”
blocks and lower overall success rate), but definitely devoid of pneumothorax risk. The
axillary block received a big push when in 1961 De Jong published an article in
Anesthesiology praising it. His paper was based on cadaver dissections and included the
now famous calculation of 42 mL as the volume needed to fill a cylinder 6 cm long that,
according to De Jong, “should be sufficient to completely bathe all branches of the
brachial plexus”. Coincidentally (or not) the same journal issue carried a paper by Brand
and Papper out of New York, comparing axillary and supraclavicular techniques in their
hands. This article is the source of the 6.1% pneumothorax rate frequently quoted for
supraclavicular block. The authors were determined to prove that the axillary block was
safer and better than the supraclavicular block. They succeeded by not only producing the
highest percentage of pneumothorax (6.1%), but the highest number (14 cases) for an
individual study. This study should be considered an aberration.
In retrospect these two articles could be considered the turning point at which the
axillary route became the preferred approach here in the United States and the rest of the
world. With some exceptions this is still true today. Fortunately ultrasound in regional
anesthesia has caused a renewed interest in this approach and we could not be happier.
The supraclavicular technique with its rapid onset, density, high success rate
along with large area of anesthesia are highly desirable. These good characteristics are,
according to David Brown and colleagues, “unrivaled” by other techniques. In our
practice the supraclavicular approach is the cornerstone of upper extremity regional
anesthesia.
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The point at which the clavicular head of the SCM muscle inserts in the clavicle is
then identified, as shown in fig 6-16. A parasagital (parallel to the midline) plane at this
level determines an “unsafe” zone medial to it, where the risk of pneumothorax is high
and a lateral zone that is safer.
Because the trunks are short and run in a very steep direction caudally towards the
clavicle, there is a narrow “window of opportunity” to perform the block above the
clavicle. It must be performed at enough distance from the insertion of the SCM on the
clavicle to be safely away from the pleural dome, but not too far to miss the trunks and
the plexus completely. We call this distance “the safety margin”. In adults we calculate
this distance to be about 1 inch (2.5 cm), which corresponds to the width of the author’s
thumb. This distance is marked on the skin over the clavicle for orientation, as shown in
figure 6-17.
This is only an orientation point that usually will coincide with the midpoint of
the clavicle in an adult patient. At this level the brachial plexus is usually easily palpable,
either as a groove or as some type of bump(s). This is usually called “interscalene
groove”, but the interscalene groove only exists high in the C5-C6 level. The groove is
lost more distally as the scalene muscles diverge from each other in the frontal and
sagittal planes. The palpation of the plexus is what determines the actual point of needle
entrance and not a fixed distance. The plexus can be palpated a few mm medial or
lateral to the orientation point, but never too far from it.
The palpating finger is placed parallel to the clavicle and the point of needle
entrance is located immediately cephalad to it, as shown in figure 6-18.
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Fig 6-18. Orientation arrows. The medial arrow
pointing up shows the lateral insertion of SCM
(pleura’s lateral boundary). The lateral arrow pointing
caudally shows the needle entrance point. The two
lateral arrows pointing at each other show the needle
trajectory (parallel to the patient’s midline). (On a
model with permission).
Type of needle
A 5cm, 22-G, insulated needle is used for this technique.
Needle insertion
The needle is inserted first anteroposterior (toward the bed) with a 30 degree
caudal orientation, as shown in figure 6-19, for a distance of a few mm and up to 1.5 cm,
depending on the amount of subcutaneous tissue. After a short distance, a twitch of the
upper trunk (shoulder) is usually found as evidence that the needle is approaching the
frontal plane of the plexus.
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The reference to the midline is easy to ascertain and avoids confusion. The use of
other landmarks (e.g., nipple) provides lesser accuracy because of variability among
patients.
The needle is advanced caudally with a slight posterior angle to match the slight
posterior rotation of the plexus (the upper trunk is the most anterior and the inferior trunk
the most posterior). Because the trunks are physically contiguous, as the needle is
advanced, a twitch of the upper trunk (shoulder) should be followed by one from the
middle trunk (pectoralis, triceps, supination, pronation) and finally a twitch from the
lower trunk (wrist and fingers). The goal of the technique is to produce an isolated
muscle twitch of the fingers. Wrist flexion and extension are also acceptable responses,
but supination or pronation or any other more proximal motor twitches are not.
If after advancing the needle the motor twitch of the shoulder disappears and no
twitch is elicited from the middle trunk, it usually means that the angle of insertion of the
needle is not matching the orientation of the trunks, and that the tip of the needle is
wandering away from the trunks (usually anteriorly). The needle should be slowly
withdrawn until the original twitch is elicited once again, and then redirected either
posteriorly (most of the times) or anteriorly, but always parallel to the midline.
It is very important not to advance the needle more than 2 cm in the caudal
direction if no twitch is visible. In this case the situation should be reassessed starting
with the nerve stimulator and its connections and determination of landmarks. On the
other hand, when a twitch from the brachial plexus is being elicited the depth of needle
insertion is less important as such motor twitch reveals that the needle is still in close
proximity to the plexus.
Clinical pearls
This is not a block for a practitioner that rarely performs peripheral nerve blocks.
The person interested in learning to perform it should first become familiar with
the anatomy of the supraclavicular area including the location of the dome of the
pleura. Using ultrasound makes the visualization of the pleura easier, but still
requires the operator to be familiar with the anatomy of the area.
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When using a nerve stimulator technique, the block should not be attempted
unless the insertion of the sternocleidomastoid in the clavicle is clearly
established. In fact this is a must especially for a person not experienced with the
technique. With time it becomes easier to ascertain the boundaries of the SCM.
It helps to know that the neurovascular bundle crosses the clavicle under the
midpoint of it, so this should be kept in mind as a reliable reference.
Due to the steep direction of the plexus from the neck to the axilla, the higher in
the neck (the further away from the clavicle) the more medial the plexus is. By the
same token, the further below the clavicle the more lateral to its midpoint the
plexus is.
The needle should never be inserted more than 2 cm caudal if no twitch is elicited.
This warning applies to every patient regardless of weight.
The injection should always be slow, alternated with frequent and gentle
aspirations. This technique provides time to recognize accidental intravascular
injection in those cases where blood is not aspirated. I also believe it helps to keep
the needle from moving backwards as a result of high speed flow at the tip of the
needle.
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SUPRACLAVICULAR BLOCK
ULTRASOUND TECHNIQUE
Indications
Anesthesia and/or analgesia for any procedure on the upper extremity distal to the
shoulder.
Patient position
The patient is placed in the semi seated position as shown in figure 6-21.
Type of needle
A 5cm, 22-G, insulated needle is used.
Type of transducer
This is also a superficial block for which a high frequency (8-15 MHz) is used.
Scanning
We usually start scanning medially, over the sternocleidomastoid muscle, right
above the clavicle, as shown in figure 6-22.
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At this level we get to see the dome of the pleura and above it, the subclavian vein
at that point where it is joining the internal jugular vein to form the brachiocephalic vein,
as shown in figure 6-23.
The probe is then slid laterally towards the midpoint of the clavicle, as shown in
figure 6-24,
At this level a cross section of the subclavian artery, the first rib and plexus can be
visualized, as shown in figure 6-25.
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Needle insertion
The needle is advanced in plane, from lateral to medial, as shown in figure 6-26.
The entrance point is located at about 1 cm away from the probe to decrease the angle of
insertion and improve the chances of needle visualization.
The needle is then slowly advanced under direct visualization, towards the angle
formed by the first rib and the subclavian artery, as shown in figures 6-27 A and B.
94 | P a g e
Fig 6-28. Injection. The local anesthetic
spread should be seen reaching the angle
formed by the 1st rib (vertical arrows
pointing up) and the subclavian artery
(SA). The local anesthetic is seen as a
hypoechoic (dark) shadow projecting from
the tip of the needle. (Author’s archive).
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INFRACLAVICULAR BLOCK
NERVE STIMULATOR TECHNIQUE
Indications
This block can provide anesthesia/analgesia of a large area of the upper extremity
including the elbow, especially if performed proximally near the apex of the axilla. It is
considered a good approach for continuous techniques because it offers more stability
than other more mobile locations.
Main characteristics
The infraclavicular block could be considered an axillary block in which the
needle enters the axilla through its anterior wall (pectoralis muscles), instead of through
its base. The infraclavicular space of the anesthesiologists corresponds to part of the
axillary pyramid of the anatomists. With the arm in adduction it is represented on the skin
by a triangular area whose base is superior (clavicle), a medial wall formed by the
projection on the skin of the thoracic cage and a lateral wall formed by the medial side of
the upper arm. Depending on the patient’s amount of subcutaneous tissue and/or muscle
this block can be deep. Patients should be adequately sedated.
It is widely recommended when using a nerve stimulator to obtain a distal twitch
in the hand or wrist and to avoid either a biceps twitch (musculocutaneous nerve or
lateral cord) or pronation of the forearm (lateral cord). This recommendation is based on
clinical experience. A biceps twitch could be the result of musculocutaneous nerve
stimulation, outside the sheath, or from lateral cord stimulation inside the sheath. Because
the operator cannot accurately distinguish one from the other, this response is unreliable.
It is likely that a twitch from the posterior cord (elbow, wrist and or finger
extension) could be best, because the posterior cord is located at about the same distance
from the other two, and the spread of local anesthetic from this central location might be
more even. There could be another good reason to inject behind the artery, although it
may be more difficult to get there. Because the posterior structures (including the
posterior cord) are more closely packed, the spread of local anesthetic from anterior to
posterior may be more difficult than from posterior to anterior. Ultrasound, with
visualization of the axillary artery and the cords around it, makes this injection easier to
accomplish.
Different infraclavicular techniques have been described. A simple technique is
the coracoid approach first described by Whiffler in the British Journal of Anaesthesia in
1981 and later redefined by MRI studies performed in 40 volunteers by Wilson, Brown et
al, and published in Regional Anesthesia in 1998. This is the technique we most
frequently perform when using nerve stimulation.
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Patient position and landmarks
The patient is placed semi seated with the ipsilateral shoulder down. The arm is
slightly abducted 30-45 degrees, as shown in figure 6-29, to bring the neurovascular
bundle away from the thoracic cage and decrease the chance of pneumothorax.
As the neurovascular bundle follows the arm its relationship to the coracoid
process is pretty much maintained. The coracoid process is found by palpation at the
level of the deltopectoral groove (junction between the middle third with the lateral third
of the clavicle), about 2 cm below the clavicle, and marked on the skin, as shown in
figures 6-30 and 6-31.
Fig 6-30. Coracoid palpation. The Fig 6-31. Coracoid marking. The
coracoid is found below the clavicle position of the coracoid is marked
in the deltopectoral groove. (On a on the skin. (On a model with
model with permission). permission).
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Fig 6-32. Needle entrance point.
Two cm caudal and two cm
medial from the coracoid process.
(On a model with permission).
Type of needle
It is possible to use sometimes a 5cm, 22-G insulated needle, but a 10cm, 21-G
insulated needle is usually necessary.
Needle insertion
The needle attached to the nerve stimulator is advanced in the anteroposterior
direction, towards the bed, as shown in figure 6-33.
Before entering in contact with the plexus the needle passes through pectoralis
major and pectoralis minor muscles producing a visible local twitch. The brachial plexus
is found deep to them. If not response from the plexus is obtained, the needle is redirected
caudal (most of the times) or cephalad, but maintaining the same parasagital plane
without medial or lateral deviation.
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of 2 mg/mL of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of
0.2% tetracaine provides 4-6 h of surgical anesthesia.
Ropivacaine 0.5% can be used in the same volume for more than 12 h of
anesthesia. Also 20-30 mL of 0.2% ropivacaine can be used to provide postoperative
analgesia for surgery performed under general anesthesia.
Clinical pearls
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INFRACLAVICULAR BLOCK
ULTRASOUND TECHNIQUE
Indications
The same indications mentioned for nerve stimulation techniques, basically
anesthesia/analgesia of elbow, forearm wrist and hand.
Patient position
We perform both techniques with the patient in the semi seated position with the
shoulder on the side to be blocked down and the arm in abduction of about 45 degrees, as
shown in figure 6-34. Abducting the arm improves the ultrasound image of the
neurovascular bundle, perhaps by stretching it and bringing it closer to the anterior wall.
Type of needle
A 5cm, 22-G, insulated needle can be used in some patients, but it is usually
necessary to use a 10cm, 21-G, insulated needle due to the depth of the neurovascular
bundle at this location. Because the needle crosses through muscle, good sedation is
important as well as injection of local anesthetic in the intended needle path to keep the
patient comfortable.
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PROXIMAL INFRACLAVICULAR TECHNIQUE
Type of transducer
Depending on the thickness of the patient’s chest wall the operator can use a
linear high frequency (8-15 MHz) probe or a curved low frequency (3-7 MHz) one.
Scanning
For this more proximal approach we place the transducer parallel and
immediately below to the midpoint of the clavicle, as shown in figure 6-35.
The image obtained at this proximal level is a cross section of the neurovascular
bundle as it aligns under the clavicle in a formation that has the axillary vein as the most
medial structure, followed by the axillary artery in the center and the divisions of the
plexus most laterally, as shown in figure 6-36.
Needle insertion
The needle can be advanced out of plane from caudal to cephalad, but we usually
prefer an in plane technique from lateral to medial, as shown in figure 6-37.
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Fig 6-37. Needle insertion, left side.
The needle is introduced in plane from
lateral to medial. (On a model with
permission).
Figure 6-38; A, B and C. Needle insertion/injection, left side. A (left): the divisions of the plexus
are shown surrounded by a fascial sheath lateral to the axillary artery (AA); B (center): the shadow of
the needle path (pointed by arrows) is barely seen as the needle comes in at a 45 degree angle. The two
smaller arrow heads point to the indentation of the fascia produced by the piercing needle; C: the
spread of local anesthetic is seen as a hypoechoic shadow pointed by a large arrow and the resulting
expanded sheath is shown with the smaller arrows. (Author’s archive)
Type of transducer
A linear high frequency (8-15 MHz) or a curved low frequency (3-7 MHz) probe is used
depending on the thickness of the patient’s thoracic wall.
Scanning
For this more distal approach we place the transducer in an oblique fashion in the mid
pectoral region, as shown in figure 6-39. This probe rotation is needed to get a better
cross section of the neurovascular bundle, which is traveling diagonally in the
infraclavicular region.
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Fig 6-39. Coracoid level scanning, right
side. The transducer is placed in an oblique
fashion to get a perpendicular cut of the
neurovascular bundle at the level of the
coracoid process. (On a model with
permission).
The ultrasound image obtained at this level is shown in figure 6-40. At this level
the cords of the plexus have already rotated behind the axillary artery and adopted their
arrangement around it from which they take their names, medial, posterior and lateral.
Needle insertion
As it is the case with the more proximal approach, the needle can be inserted out
of plane, from caudal to cephalad, but we usually prefer to advance it in plane, from
lateral to medial (superior to inferior), as shown in figure 6-41.
Clinical pearls
The proximal infraclavicular approach is a block of the divisions of the plexus
and as such it can resemble a supraclavicular block in onset and density of
anesthesia.
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AXILLARY BLOCK
NERVE STIMULATOR TECHNIQUE
Indications
It is best suited for anesthesia/analgesia of the upper extremity distal to the elbow.
Main characteristics
The axillary block is not properly a brachial plexus block, but rather a block of its
terminal branches. The larger surface area that the branches as a whole occupy and the
tendency for the local anesthetic to follow the paths of low resistance along individual
nerves affect the circumferential spread of the local anesthetic within the sheath (please
see discussion on axillary brachial plexus sheath in the anatomy section). A single
injection technique is an option, but multiple injections have shown to increase the
success rate at this level. If a single injection is to be attempted, the operator needs to
specifically target the nerve feeding the surgical area. If the surgical area involves more
than one terminal nerve, the single injection technique should be performed in the
proximity of the radial nerve because, as mentioned in the anatomy discussion, the local
anesthetic solution tends to spread inside the sheath more easily from back to front that
vice versa. In addition, my observations in the anatomy lab show that better
circumferential spread of local anesthetic may be obtained with a slight elevation of the
elbow, because this maneuver releases some of the stretching of the neurovascular
bundle.
Some authors advice to perform the block high in the axilla to improve its overall
success. This can be uncomfortable to the patient and challenging to the anesthesiologist.
The only perceived advantage would be to increase the chances of blocking the
musculocutaneous nerve before it leaves the sheath, but since its take off is variable the
operator could never be certain. I believe that a better strategy is to start the axillary block
by first blocking the musculocutaneous nerve in the proximal arm and then complete the
block according to what is needed.
Although some variability exists, usually the median nerve is superficial (anterior)
to the axillary artery, following its same direction; the ulnar nerve (and medial
brachial/antebrachial cutaneous nerves) are medial and somewhat posterior to the artery;
the musculocutaneous nerve is lateral to the artery (and eventually under the biceps
muscle); and the radial nerve is posterior to the artery.
I believe that in the 21st century, with the variety of tools at our disposal, there is
no good reason to perform a trans axillary technique.
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the axillary artery is found immediately under the coracobrachialis. Sometimes it helps to
displace the latter slightly anterior to feel the pulsation of the artery. Figure 6-42 shows
the arm position in abduction with a small pillow under the elbow and the trajectory of
the axillary artery marked in blue.
Type of needle
This is usually a superficial block, even in obese patients. A 5cm, 22-G, insulated
needle usually suffices.
105 | P a g e
Needle insertion
The operator identifies and holds the patient’s biceps muscle with one hand and
directs the needle with the other in a direction perpendicular to the main axis of the arm,
advancing it between biceps and coracobrachialis, as shown in figure 6-43.
Type of response
As the needle approaches the musculocutaneous nerve a motor twitch of biceps
with flexion of the elbow is obtained. The current is reduced to 0.5 mA and, if a response
is still visible at this level, the injection is started.
The median nerve is most frequently located anterior (superficial) to the axillary
artery running in the same direction, making it a very superficial block.
Needle insertion
Using the mark of the axillary artery on the skin as a reference, the needle is
introduced very tangential to the skin (shallow angle), in the same direction of the artery,
as shown in figure 6-44.
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It is better to mark the course of the artery on the skin than to keep the fingers on
the pulse to avoid bringing the artery even closer to the skin and increasing the chances
for accidental artery puncture.
The ulnar nerve is located immediately medial to the artery, slightly deeper than
the median nerve. It gives sensory innervation to the medial side of the hand. Because the
medial brachial and the medial antebrachial cutaneous nerves run along with the ulnar
nerve on the medial side of the axillary artery, the ulnar nerve technique is performed for
anesthesia of the medial arm and medial forearm.
Needle insertion
Using the mark of the axillary artery on the skin as a reference, the needle is
directed slightly medial to the artery, as shown in figure 6-45.
The radial nerve is most frequently located posterior (deeper) to the axillary
artery. It is the largest of the terminal branches of the plexus.
Needle insertion
The operator uses two fingers of one hand as “hooks” to slightly displace the
artery out of the way in order to reach the radial nerve located posterior to it. The needle
is inserted posterior with a 30 degree cephalad orientation, as shown in figure 6-46.
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Fig 6-46. Radial nerve block. The axillary
artery is displaced towards the biceps to
gain entrance to its posterior aspect. The
needle is then introduced in reference to the
mark on the skin with a 30 degree cephalad
orientation. (On a model with permission).
Complications
Pneumothorax is virtually impossible to get from this location. Hematomas from
vascular puncture are more common and can be associated with nerve damage.
Pearls
This is a block mainly indicated for surgery on the distal forearm, wrist and hand.
It is not a good choice for elbow surgery.
Tourniquet pain is an issue and not necessarily due to intercostobrachial nerve,
but mainly due to insufficient proximal anesthesia of the deeper planes of the arm.
Two and three injection techniques have proven more successful, but if a single
injection is preferred this injection should be in front of the nerve most
responsible for the sensory innervation of the surgical site. If more than one nerve
is involved the injection should be performed in front of the radial nerve.
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AXILLARY BLOCK
ULTRASOUND TECHNIQUE
Indications
The same indications mentioned for the nerve stimulation technique.
Patient position
The patient is semi seated with the arm in abduction and the elbow flexed, as
shown in figure 6-47.
Type of needle
This is a superficial block for which a 5cm, 22-G, insulated needle suffices.
Type of transducer
We use a high frequency (8-15 MHz) linear probe.
Scanning
The probe is placed across the neurovascular bundle in the proximal part of the
arm, as shown in figure 6-48.
At this level the neurovascular bundle of the axilla is usually very superficial and
the terminal nerves can be seen surrounding the axillary artery. The median nerve is
usually superficial (anterior) to the artery, the ulnar nerve is medial and somewhat
posterior, and the radial nerve is posterior, as shown in figure 6-49.
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Fig 6-49. Terminal branches. The
axillary sheath has been removed to
show the relative location of the
nerves with respect to the axillary
artery. MACN: medial antebrachial
cutaneous nerve; axi: axillary
nerve. Cadaver dissection by Dr
Franco. Image is copyrighted.
Distally in the axilla the radial nerve starts shifting more lateral, but it still
remains posterior to the artery. The musculocutaneous is lateral to the artery at all times
and it can be traced from its origin in the lateral cord proximally to its location between
biceps and coracobrachialis distally. If a single injection is planned it should be made in
the proximity of the radial nerve. Individual injections of terminal nerves can be done as
needed. An image of the neurovascular bundle of the axilla in cross section is shown in
figure 6-50.
Needle insertion
The needle is advanced in plane from lateral to medial, as shown in figure 6-51.
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We usually block first the musculocutaneous nerve located in between biceps and
coracobrachialis. To target this nerve the needle needs to be inserted at an angle of 30-45
degrees. Then the rest of the terminal branches are targeted as needed. These branches are
more superficial so they need a much smaller angle of insertion, which facilitates needle
visualization.
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References
1. Brown DL. Brachial plexus anesthesia: an analysis of options. Yale J Biol Med
1993; 66: 415-431
2. Winnie AP. Interscalene brachial plexus block. Anesth Analg 1970; 49: 455-466
3. Kulenkampff D, Persky MA. Brachial plexus anesthesia. Ann Surg 1928; 87: 883-
891
4. Winnie AP, Collins VJ. The subclavian perivascular technique of brachial plexus
anesthesia. Anesthesiology 1964; 25: 353-363
5. Franco CD, Vieira Z. 1,001 subclavian perivascular brachial plexus blocks:
success with a nerve stimulator. Reg Anesth Pain Med 2000; 25: 41-46
6. Franco CD. The subclavian perivascular block. Tech Reg Anesth Pain Med 1999;
3: 212-216
7. De Andres J, Sala-Blanch X. Peripheral nerve stimulation in the practice of
brachial plexus anesthesia: a review. Reg Anesth Pain Med 2001; 26: 478-483
8. Greenblatt Gm, Denson GS. Needle nerve stimulator-locator: nerve blocks with a
new instrument for locating nerves. Anesth Analg 1962; 41: 599-602
9. Hadzic A, Vloka J, Hadzic N, et al. Nerve stimulators used for peripheral nerve
blocks vary in their electrical characteristics. Anesthesiology 2003; 98: 969-974
10. Passannante AN. Spinal anesthesia and permanent neurologic deficit after
interscalene block. Anesth Analg 1996; 82: 873-874
11. Urmey WF, Grossi P, Sharrock NE, Stanton J, Gloeggler PJ. Digital pressure
during interscalene block is clinically ineffective in preventing anesthetic spread
to the cervical plexus. Anesth Analg 1996; 83: 366-370
12. Silverstein WB, Saiyed M, Brown AR. Interscalene block with a nerve stimulator:
A deltoid motor response is a satisfactory endpoint for successful block. Reg
Anesth pain Med 2000; 25: 356-359
13. Urmey WF, Talts KH, Sharrock NE. One hundred percent incidence of
hemidiaphragmatic paresis associated with interscalene brachial plexus anesthesia
as diagnosed by ultrasonography. Anesth Analg 1991; 72: 498-503
14. Urmey WF. Interscalene block: The truth about twitches (editorial). Reg Anesth
pain Med 2000; 25: 340-342
15. Brand L, Papper EM. A comparison of supraclavicular and axillary techniques for
brachial plexus blocks. Anesthesiology 1961; 22: 226-229
16. Brown DL. Atlas of regional anesthesia. Philadelphia, PA: W.B. Saunders, 1992
17. Mulroy MF. Regional anesthesia: An illustrated procedural guide. 3rd edition.
Philadelphia, PA; Lippincott Williams & Wilkins 2002
18. Urmey WF, Stanton J. Inability to consistently elicit a motor response following
sensory paresthesia during interscalene block administration. Anesthesiology
2002; 96: 552-554
19. Neal JM, Moore JM, Kopacz DJ, Liu SS, Kramer DJ, Plorde JJ. Quantitative
analysis of respiratory, motor, and sensory function after supraclavicular block.
Anesth Analg 1998; 86: 1239-1244
20. Franco CD, Domashevich V, Voronov G, Rafizad A, Jelev T. The supraclavicular
block with a nerve stimulator: To decrease or not to decrease, that is the question.
Anesth Analg 2004; 98: 1167-1171
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21. Franco CD, Gloss FJ, Voronov G, Tyler SG, Stojiljkovic LS. Supraclavicular
block in the obese population: An analysis of 2020 blocks. Anesth Analg 2006;
102: 1252-1254
22. Perlas A, Chan V: Ultrasound-assisted nerve blocks. In: Textbook of Regional
Anesthesia, Hadzic A (ed). New York, McGraw Hill, 2007, pp 663-672
23. Franco CD, et al. Gross anatomy of the brachial plexus sheath in human cadavers.
Reg Anesth Pain Med 2008; 33: 64-69
24. Neal JM, Gerancher JC, Hebl JR, Ilfeld BM, McCartney CJL, Franco CD, Hogan
QH. Upper Extremity Regional Anesthesia: Essentials of Our Current
Understanding. Reg Anesth Pain Med 2009; 34: 134-170
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CHAPTER 7
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LOWER EXTREMITY BLOCKS
The innervation of the lower extremity comes from the lumbar and sacral
plexuses. The different nerve elements of the lower extremity run more distant from each
other than those of the upper extremity, without having a point of convergence like the
one at the level of the brachial plexus trunks. Therefore, no single peripheral block
technique is able to provide anesthesia of the whole lower extremity. This anatomical
fact, combined with the high success of neuraxial anesthesia, has traditionally affected
the popularity of lower extremity peripheral nerve blocks.
The introduction of low molecular weight heparin (LMWH) in the United States
in the early 1990s produced a renewed interest in lower extremity nerve blocks because
of the increased risk of epidural hematoma after neuraxial anesthesia in patients receiving
LMWH. The use of ultrasound in regional anesthesia has also been a major reason for the
increased popularity of all sort of peripheral nerve blocks.
Anatomy
Lateral femoral cutaneous nerve
It is an exclusively sensory nerve originating from the ventral rami of spinal
nerves L2-L3. It appears in the pelvis, lateral to the psoas muscle, caudal to the
ilioinguinal nerve. It runs anteriorly under the iliac fascia, parallel to the iliac crest. It
emerges from the pelvis, under the inguinal ligament, between the anterior superior and
anterior inferior iliac spines, as shown in figure 7-1 and 7-2. It provides sensory
innervation to the lateral thigh.
Femoral nerve
It is a motor and sensory nerve derived from the posterior divisions of the ventral
rami of spinal nerves L2-L3-L4. In the pelvis it is also located lateral to the psoas muscle,
in the cleavage between psoas and iliacus muscles. As it passes under the inguinal
ligament the nerve is superficial to the combined iliopsoas muscle. Under the inguinal
ligament the femoral nerve has the femoral artery medial to it, while the femoral vein is
located medial to the artery (VAN from medial to lateral), as shown in figure 7-2.
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Fig 7-2. Femoral nerve, left side. The
femoral nerve (FN) passes under the
inguinal ligament lateral to the femoral
artery (A). Also shown are the femoral
vein (V) and the LFCN pointed with
arrows. Cadaver dissection by Dr
Franco. Image is copyrighted.
Approximately 3-4 cm below the inguinal ligament, the femoral nerve divides
into anterior and posterior divisions. The anterior division has two sensory branches that
supply the antero medial thigh, and two muscular branches that supply the sartorius and
pectineus muscles. The posterior division has one sensory branch, the saphenous nerve,
and muscular branches to the quadriceps. The nerve is covered by the iliac fascia, which
separates it from the main vessels, and more superficially by the fascia lata, the deep
fascia of the thigh.
The muscular branch to the rectus femoris also supplies the hip joint while the
muscular branches to the three vasti muscles also supply the knee joint.
Obturator nerve
It is usually a mixed nerve (motor and sensory) derived from the anterior
divisions of the ventral rami of spinal nerves L2-L3-L4. It emerges on the medial side of
the psoas muscle just above the pelvic brim running down between this muscle and the
lumbar spine. As the nerve enters the pelvis it turns laterally to run along its lateral wall
until it reaches the obturator foramen, through which it reaches the thigh. In the thigh the
nerve divides into anterior and posterior branches, as shown in figure 7-3.
The anterior division runs caudally, first located between the pectineus muscle in
front and the obturator externus behind. A few cm distally the nerve runs between the
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adductor longus anteriorly and the adductor brevis posteriorly. It gives innervation to the
gracilis, adductor brevis and adductor longus, and sometimes to the pectineus. It gives
also articular branches to the hip joint. On occasions it supplies the skin of the medial
side of the thigh.
The posterior division after a short trajectory it usually pierces the obturator
externus to then run caudally between the adductor brevis in front and the adductor
magnus behind. It supplies the obturator externus, the adductor magnus and the knee
joint. The anterior sensory branch can be frequently missing and in that case the medial
thigh is also supplied by the femoral nerve.
The highly variable distribution of the cutaneous branch of the obturator nerve has
contributed to the confusion about how much anesthesia can be obtained from a single
block performed at the femoral level (“3-in-1” block). Most of the studies have used
pinprick testing of the medial, anterior and lateral thigh to assess anesthesia of obturator,
femoral and lateral femoral cutaneous nerves territories. This testing does not take into
account the fact that many variations exist in the innervation patterns of the thigh
including the absence of a cutaneous branch of obturator nerve. Nevertheless many
authors believe that a block at the femoral level could also produce anesthesia of the
lateral femoral cutaneous nerve by lateral diffusion of the local anesthetic under the
fascia iliaca (“2-in-1 block”). Spread of local anesthetic to the obturator nerve either,
medially under the vessels or proximally toward the pelvis is more unlikely.
Sciatic nerve
It is the largest nerve in the body. It originates from the ventral rami of spinal
nerves L4-L5, S1-S3. Part of the anterior ramus of L4 joins the anterior ramus of L5 to
originate the lumbosacral trunk, which together with the first three sacral roots form the
sciatic nerve. The nerve has two components, the tibial nerve (on its medial side), which
is derived from the anterior divisions of the ventral rami of L4-L5, S1-S3 and the
common peroneal nerve (on its lateral side), which is derived from the posterior divisions
of the ventral rami of L4-L5, S1-S2. The nerve comes out of the pelvis through the
greater sciatic foramen, entering the gluteal region anterior (deep as seen from the gluteal
region) to the piriformis muscle. The nerve curves above the ischial tuberosity and then
turns vertically downwards to run between the ischium medially and the greater
trochanter laterally, as shown in figure 7-4.
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For most of its trajectory in the buttocks, the sciatic nerve runs parallel to the
midline, at a distance of about 10 cm in adult patients. With the hips in adduction this
distance is maintained throughout adult life, not being influenced by gender or body
weight. This previously unknown fact has simplified enormously the approach to the
sciatic nerve in our practice (for more information see Franco. Anesthesiology 2003; 98:
723-728).
The tibial and common peroneal components can be easily identified as two
separate nerves during their entire trajectory in about 11% of the cases. However, even in
those cases the two components are surrounded by a common sheath of connective tissue,
as shown in figure 7-5. Therefore, it is important not to confuse this with a true separation
of the components, which invariably takes place always in the popliteal fossa.
The sciatic nerve enters the thigh deep to the biceps femoris muscle and not
lateral to it as usually mentioned in our literature, as shown in figure 7-6.
As opposed to what happens in the gluteal region, the position of the sciatic nerve
in the thigh with respect to the midline is influenced both by the degree of hip abduction
as well as by the amount of fat accumulating in the inner thigh.
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The nerve runs in the posterior thigh under the cover of the hamstring muscles,
until it reaches the popliteal fossa. Upon entering the popliteal fossa, the two nerve
components, peroneal and tibial, finally diverge from each other, having never mixed
their fibers. The posterior tibial nerve continues to run in the direction of the main trunk,
at the center of the fossa. The common peroneal component turns laterally to run just
medial to the biceps tendon, as shown in figure 7-7.
Subgluteal fold
The fold that defines the buttocks inferiorly is a fold of the skin and does not
correspond with the lower border of the gluteus maximus muscle, as frequently thought.
In fact the inferior border of this muscle crosses the subgluteal fold diagonally as it runs
laterally to insert in the iliotibial tract, as shown in figure 7-8. Therefore, during a
subgluteal approach to the sciatic nerve, the needle crosses the same planes (fat and
gluteus maximus) than in more proximal approaches, although the fat layer can be
thinner.
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Genitofemoral nerve
It derives from the ventral rami of spinal nerves L1-L2. Its genital branch
provides some of the innervation of the genital area, while its femoral component
provides sensory innervation of the medial upper thigh and the skin over the femoral
vessels.
Fig 7-9. The posterior femoral cutaneous nerve Fig 7-10. The posterior femoral
shown with arrows is in close contact to the sciatic cutaneous nerve shown with arrows and
nerve (SN) in the gluteal area. The sheath of the sciatic nerve (SN) after removal of
nerve is partially intact. Cadaver dissection by Dr connective tissue. Cadaver dissection by
Franco. Image is copyrighted. Dr Franco. Image is copyrighted.
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The posterior femoral cutaneous nerve innervates the lower part of the buttocks as
well as the posterior thigh, frequently reaching as far down as the proximal posterior
aspect of the leg. A block of the sciatic nerve performed in the gluteal area will
predictably produce anesthesia of this cutaneous nerve as well. A block performed at the
subgluteal level on the other hand, will not reliably block it.
Saphenous nerve
It is a sensory nerve that originates from the posterior division of the femoral
nerve (L3-L4) in the inguinal region. It is the largest cutaneous branch of the femoral
nerve. It runs down the femoral canal along with the femoral vessels, under the cover of
the sartorius muscle. It emerges on the medial side of the knee between the tendons of
sartorius and gracilis, as shown in figure 7-12
At a variable distance caudal to the knee, it pierces the deep fascia to become
superficial. Distal to the knee it gives off the subpatellar branch, which supplies the
medial side of the knee (chance for injury during knee arthroscopy). Once it becomes
superficial, it runs alongside the greater saphenous vein in the leg, passing in front of the
medial malleolus in the ankle, before terminating around the base of the first metatarsal
on the medial side of the foot.
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Clinical pearls
The nerves of the lower extremity are more distant from each other than in the
upper extremity so it is not possible to block the entire lower extremity from a
single injection point.
The position of the sciatic nerve in the buttocks with respect to the midline is
dictated by the bony pelvis and as such it is not affected by gender or obesity.
Its relationship to bone structures and to the midline remains unchanged
throughout adulthood.
The inferior border of the gluteus maximus muscle does not correspond with
the subgluteal fold (Snell’s Clinical Anatomy for Medical Students, 3rd
edition, page 554). In fact both cross each other diagonally. The subgluteal
fold is a fold of the skin anchored to the deep fascia.
The gluteus maximus is the only gluteal muscle to cover the sciatic nerve
superficially, caudal to the piriformis muscle in the gluteal region. Gluteus
medius and minimus are located cephalad and lateral to the sciatic nerve.
The inguinal crease does not correspond with the inguinal ligament. Both
structures are parallel to each other. The inguinal crease runs about 1 inch (2.5
cm) caudal and parallel to the inguinal ligament.
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LATERAL FEMORAL CUTANEOUS NERVE BLOCK
Indications
This block can be performed alone to provide anesthesia of the lateral thigh (e.g.,
donor area for a skin graft). It can also be performed along with femoral, obturator and
sciatic blocks to provide anesthesia of the thigh for surgical procedures above the knee
and for thigh tourniquet. It is also one of the nerves targeted in a “3-in-1” block, a block
of the femoral nerve performed with a higher volume of local anesthetic to try to block
also the lateral femoral and obturator nerves (not supported by the evidence).
Main characteristics
This can be a superficial block (above the fascia lata) if the block is performed at
2 or more cm distal to the inguinal ligament. More proximally the nerve is under the
fascia lata. This is important because this fascia is thick enough to slow the transfer of
local anesthetic to the target nerve.
ANATOMICAL TECHNIQUE
Technique
The needle entrance point is identified about 1 cm medial and 1 cm caudal to the
ASIS. The needle is advanced perpendicular to the skin and directed deep to the fascia
lata where the local anesthetic is injected in a fanwise fashion. A nerve stimulator with
pulse duration of 0.3 to 1 msec (300 to 1000 microsec) can be used to elicit a sensory
paresthesia in the lateral thigh.
Complications
Very rare. Some patients can complain of dysesthesia in the lateral thigh that
usually goes away without sequelae.
ULTRASOUND TECHNIQUE
The use of ultrasound facilitates this block. As the lateral femoral cutaneous nerve
passes under the inguinal ligament it is located under the fascia lata in between tensor
fascia lata laterally and sartorius medially. Placing the probe across the gap in between
these two muscles usually allows a good visualization. A few centimeters distal to the
inguinal ligament the nerve can be located superficial to the sartorius muscle.
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FEMORAL NERVE BLOCK
NERVE STIMULATOR TECHNIQUE
Indications
An isolated femoral nerve block can be performed to provide anesthesia for
surgery on the anterior thigh, patella and some knee procedures. It is more commonly
performed along with sciatic to provide anesthesia of the entire lower extremity.
Main characteristics
This is a simple block performed lateral to the pulse of the femoral artery, deep to
the fascia lata (deep fascia of the thigh) and deep to the fascia iliaca (the fascia that
covers the iliopsoas muscle). The femoral artery pulse usually provides an easy and
reliable landmark to the nerve.
Type of needle
A 5 cm, 22G, insulated needle usually suffices.
The needle is advanced parallel to the midline in the direction of the inguinal
ligament. A twitch of the quadriceps muscle with movement of the patella is a good
response. The current is lowered and with a muscle twitch still visible at 0.5 mA a slow
injection is started. A response from the sartorius is usually considered not a good
response, because it could be the result of stimulation of the nerve to the sartorius, a
branch of the anterior division of the femoral nerve. If the block is performed 1 cm above
the inguinal crease, where the nerve has not branched off yet, a twitch from the sartorius
is equally acceptable.
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FEMORAL NERVE BLOCK
ULTRASOUND TECHNIQUE
Indications
The same indications than for nerve stimulator techniques.
Patient position
The patient is either supine or semi seated for more comfort.
Type of needle
Usually a 5cm, 22-G, insulated needle is used.
Type of transducer
The femoral nerve is fairly superficial in most of patients, so a high frequency (8-
15 MHz) linear probe is usually adequate.
Scanning
The probe is placed across the upper thigh over the femoral vessels, as shown in
figure 7-15.
If possible we like to place the probe immediately (1 cm) above the crease, where
the nerve is more compacted. The femoral vein is the most medial structure of the
neurovascular bundle and is easily collapsible by the probe. The artery is situated lateral
to the vein and the femoral nerve is located lateral to the artery. The characteristic image
obtained at this level is shown in figure 7-16.
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Needle insertion
The needle can be advanced out of plane, usually from caudal to cephalad, as
shown in figure 7-17, or, as we usually prefer, in plane from lateral to medial, as shown
in figure 7-18.
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OBTURATOR NERVE BLOCK
NERVE STIMULATOR TECHNIQUE
Indications
It is rarely performed alone. It is more often combined with femoral, lateral
femoral and/or sciatic blocks.
Main characteristics
Although the obturator nerve exits the obturator foramen usually already divided
into anterior and posterior branches, they both run for a short distance (2-3 cm)
physically contiguous in the plane between the pectineus anteriorly and the obturator
externus posteriorly. After reaching the lateral border of the adductor brevis muscle both
branches separate, with the anterior branch passing anterior to this muscle and the
posterior branch posterior to it. It is a common practice to perform separate injections of
both branches. However we believe that if the injection is attempted 1 cm above the
crease both main branches of the obturator nerve can be blocked by a single injection
deep to the pectineus muscle.
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Type of needle
Depending on the patient, a 5cm, 22-G or a 10cm, 21-G, insulated needle is used.
Needle insertion
The needle is inserted almost perpendicular to the frontal plane with a slight
cephalad angulation, as shown in figure 7-20.
As the needle traverses the muscular plane, a localized twitch from the pectineus
muscle is usually elicited by direct stimulation. As the needle reaches the deep face of the
muscle and the proximity of the obturator nerve a more global twitch of the thigh in
adduction is obtained. At this point the current is lowered progressively to around 0.5
mA, and if a twitch is still visible, a slow injection is started. If the needle makes contact
with the pubis ramus, it is walked off caudally.
Complications
Hematoma is the most frequent complication of this technique. Adductor muscles
spasm can occur.
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OBTURATOR NERVE BLOCK
ULTRASOUND TECHNIQUE
Indications
The same indications mentioned for nerve stimulator techniques.
Patient position
The patient lies supine with the head of the bed slightly elevated. The thigh is
slightly abducted and externally rotated.
Type of needle
Depending on the patient, a 5cm, 22-G or a 10cm, 21-G, insulated needle is used.
Type of transducer
If at all possible a high frequency (8-15 MHz) linear probe is used.
Scanning
Before performing the scanning it is useful, if possible, to locate the adductor
longus, the most superficial of the three adductor muscles, as shown in figure 7-21.
This way the determination of the location of the obturator nerve is framed
between two easily identifiable structures, the femoral vessels on the lateral side and the
medial border of the adductor longus on the medial side. The probe is placed parallel and
slightly above the inguinal crease over the femoral vessels and then traced medially until
it rests over the pectineus muscle, as shown in figure 7-22.
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With the probe over the pectineus muscle the obturator nerve can be seen as a
mostly hyperechogenic ovoid image under the pectineus muscle, as shown in figure 7-23.
If the scanning instead is performed a few centimeters more distally then the two
branches of the obturator can be seen, as shown in figure 7-24.
Needle insertion
My preferred method for this particular block is to use and out of plane technique
from distal to proximal, as shown in figure 7-25.
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Local anesthetic and volume
A volume of 10-15 mL of local anesthetic is usually used. Mepivacaine 1.5% can
be used with 1:400,000 epinephrine for 3-4 hr of anesthesia. For longer anesthesia 0.5%
ropivacaine with epinephrine can be used. For analgesia 0.2% ropivacaine is commonly
used.
Complications
Hematoma is the most frequent complication of this technique. Adductor muscles
spasm can occur.
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LUMBAR PLEXUS BLOCK (also called “psoas compartment block”)
NERVE STIMULATOR TECHNIQUE
Indications
Its goal is to produce anesthesia of the lateral femoral, femoral and obturator
nerves, so it can be used along with a proximal sciatic nerve block to provide anesthesia
of the entire lower extremity. It is also used to provide postoperative analgesia for hip and
knee surgery.
Main characteristics
It is the posterior version of what a “3-in-1” block in the femoral area intends to
accomplish. It is a deep block, in which the needle goes through several layers, including
subcutaneous tissue, the mass of paraspinal muscles, and the quadratus lumborum muscle
before ending just posterior to the psoas muscle, in the retroperitoneal space.
Because of the depth at which the nerves are located and the long needles used,
the operator has little control over the exact location of the needle tip, increasing the
potential risk for complications. The most frequent complication is to produce an epidural
block, but also cases of total spinal anesthesia have been described. Because of the
relatively large volumes of local anesthetics used systemic toxicity can also develop.
Cases of penetration of the peritoneal cavity with injury of its contents as well as large
retroperitoneal hematomas and death have been reported with this block. It is essential
that the operator be familiar with the anatomy of this region before attempting this block,
which should be performed only by experienced people.
The lumbar plexus block perhaps should not be performed in obese patients.
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Type of needle
At least a 10cm, 21-G, insulated needle is necessary for this block.
Needle insertion
The needle is inserted parallel to the midline at the junction between the lateral
third and middle third of the line joining the midline with the level of the posterior
superior iliac spine, as shown in figure 7-27.
This insertion is more medial than the original technique. It is based on a study by
Capdevila et al (Anesth Analg 2002; 94: 1606-1613) demonstrating that the point of
needle insertion at the level of the PSIS falls lateral to the plexus mandating a medial
reposition of the needle that potentially could increase the chance for epidural or spinal
anesthesia.
As the needle is inserted through the mass of the paraspinal muscles a local
contraction is usually observed. The transverse process of L4 or the nerves of the lumbar
plexus should be contacted within 3 cm from the disappearance of the twitch from the
back muscles. If not, the needle is withdrawn superficially and redirected caudally or
cephalad. If the transverse process is contacted the needle should be walked off caudally
until a quad twitch is obtained, usually no deeper than 2 cm from the transverse process.
If no response is obtained within 2 cm the needle can be redirected cephalad from the
transverse process and again advanced for up to 2 cm.
When a muscle twitch from the quad is obtained the current in the nerve
stimulator is decreased to around 0.5-0.8 mA and with a visible response a gentle
aspiration is performed for blood or CSF before injecting a “test dose” amount of 3-5 mL
of epinephrine-containing local anesthetic. If no intravascular or subarachnoid injection is
detected the rest of the local anesthetic volume is slowly injected in small increments
with frequent gentle aspirations. The preferred response in this block is quad response.
An obturator response could mean that the needle is too medial and should be redirected.
A distal response (sciatic) could mean that the lumbosacral trunk is being
stimulated and could indicate a needle too medial. A medial position of the needle could
carry an increased risk of neuraxial injection.
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Local anesthetic and volume
For anesthesia of 3-4 hours 1.5% mepivacaine with epinephrine 1:200,000 (a
larger concentration than we use at other sites) can be used. For longer anesthesia the
preferred drug is 0.5% ropivacaine plus 1:200,000 epinephrine. For analgesia 0.2%
ropivacaine is adequate.
Complications
I already mentioned that this block should be performed only by experienced
people. Epidural spread is the most common problem with an incidence of 1-16%, but
can be as high as 88% in some reports. Subarachnoid injection is a dangerous
complication not always avoided by a test dose. Death associated with total spinal has
been reported. Large retroperitoneal hematomas are also possible and therefore this block
should adhere to the same anticoagulation guidelines than neuraxial techniques. Kidney
and other injuries have also been reported.
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SCIATIC NERVE BLOCK
Classic approach (Labat as modified by Winnie)
NERVE STIMULATOR TECHNIQUE
Indications
As an isolated block, it provides anesthesia of the back of the thigh (through
anesthesia of the posterior cutaneous nerve of the thigh, a branch of the sacral plexus) and
most of the lower extremity below the knee, with the exception of the medial side of the
leg (saphenous nerve). If used along with femoral, lateral femoral and obturator nerve
blocks (lumbar plexus block), it completes the anesthesia of the entire lower extremity.
Main characteristics
Labat’s approach is a highly anatomical approach that requires the identification
of the posterior superior iliac spine (PSIS) and the greater trochanter (GT). A dissection
of the gluteal area shows that this is a reliable approach if the operator is able to
accurately determine the position of the PSIS and GT, disregarding ANY soft tissue (i.e.,
muscle, bursa, subcutaneous tissue and fat).
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widely accepted but it might have some problems of its own. Because, as discussed in the
anatomy section, the transverse diameter of the pelvis is fairly constant in all adults, any
prolongation of the perpendicular line starting from a similar point would bring it closer
to the midline (its direction is caudal and medial). This will mean that a tall patient with a
long sacrum will have a sciatic nerve located closer to the midline (long perpendicular
line due to longer sacrum) than a short patient (short perpendicular line due to shorter
sacrum). This obviously could not be the case. The fact is that Labat’s perpendicular line
was not created to be adjustable.
The combined “classic” approach (Labat-Winnie), despite its shortcomings, is the
most commonly used posterior approach to the sciatic nerve in the gluteal area.
Technique
Usually the block can be completed with a 10cm, 21-G, insulated needle, but
sometimes a longer needle needs to be used. The needle is advanced, perpendicular to all
planes until a twitch from the sciatic nerve is found. If a twitch is still visible at 0.5 mA a
slow injection is started with frequent aspirations. If the nerve is not contacted, the
technique does not have a clear strategy for reposition of the needle. In fact the nerve
could be at any point around a 360-degree radius.
Complications
The literature mentions that the absorption from this site is minimal. However, it
is important to remember that the branches of the inferior gluteal vessels at this level are
large and multiple, therefore hematomas could develop. The patient lying supine
immediately post block could theoretically help to decrease the chance for a hematoma to
develop.
It is important to inject slowly, alternated with frequent and gentle aspirations.
Dysesthesias in the territories of the sciatic or posterior femoral cutaneous nerves are
reported more frequently after this block than any other. These problems usually resolve
spontaneously within 1-2 weeks.
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SCIATIC NERVE BLOCK
Franco’s approach
NERVE STIMULATOR TECHNIQUE
Indications
The same indications than for a classic technique.
Main characteristics
This is a simple technique that relies on one simple anatomical landmark, the
intergluteal sulcus (midline), making the palpation of any buried landmarks totally
unnecessary. It is based on simple, although not universally known facts:
1. The trajectory of the sciatic nerve in the gluteal region is for the most part parallel
to the midline.
2. The width of the adult pelvis is similar in all adults and according to some
anthropologists “surprisingly” similar in males and females at any given age.
Variations in hip width are mainly the result of hormone-dependent, different
patterns of fat deposition in both sexes and are not due to significant differences
in the width of the bony pelvis. Although male and female pelvises are indeed
different, most of those differences are limited to the diameters of the minor or
inner pelvis without affecting the total diameter of the pelvis. Thicker bones in
males compensate for the wider inner pelvis of females to make the average
bicrestal diameter (total width) 280 mm in males and 275 mm in females.
3. As determined by our own study (Anesthesiology 2003; 98: 723-728), the sciatic
nerve is located about 10 cm from the midline (intergluteal sulcus) in all adults.
What remains highly variable is the amount of adipose tissue that can accumulate
in the buttocks affecting the depth of the nerve and its distance to the lateral side
of the patient. The distance midline-nerve is, on the other hand, unaffected by fat
accumulation as it is dictated by the distance between the ischium and the midline
(fixed after puberty).
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The midgluteal sulcus is identified and the point of needle insertion is marked at 10
cm from it around the midgluteal region, as shown in figure 7-28.
Type of needle
A 10cm, 21-G, insulated needle is usually sufficient, although in some cases a
15cm needle is necessary.
Needle insertion
The needle is advanced parallel to the midline, as shown in figure 7-29.
When the needle reaches the gluteus maximus muscle a local muscular twitch of
the buttock is observed. This twitch is very reassuring, telling the operator that the
needle-stimulator unit is functional and most importantly, providing information on
sciatic nerve depth. If 8 cm or more, of a 10 cm needle, have been used to reach the
gluteus maximus, it is unlikely that the needle will be long enough to reach the sciatic
nerve.
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The needle is advanced through the gluteus muscle, producing a visible local
twitch that does not disappear until the needle exits the deep surface of this muscle. The
ensuing “silence” is evidence that the needle is passing through the connective tissue that
separates the gluteus maximus from the nerve. It should be soon followed by a twitch
resulting from stimulation of the sciatic nerve. The nerve is rarely more than 2 cm deeper
to the gluteus maximus.
I believe that any of the possible responses from the sciatic nerve (i.e. eversion,
dorsiflexion, inversion and plantar flexion) are adequate, provided that the injection is
made with a visible response at 0.5 mA or less. There are few reports in the literature that
argue in favor of inversion and against eversion. This is not our experience.
If no response from the sciatic nerve is obtained deeper to the gluteus maximus,
then a reposition of the needle is necessary. Here is very important to take into account
the “vector” effect, the impact of the angle of reinsertion in the final position of the
needle. According to my own calculations, at a theoretical depth of 9 cm, a 10-degree
correction angle, moves the needle tip 1.6 cm, while a 20-degree correction moves it 3.4
cm. Because the nerve is around 1.5 cm wide, it would be very easy to “overshoot” the
correction.
Complications
Same as classic approach.
Pearls
The 10 cm measurement is a linear measurement that disregards, on purpose, the
contour of the patient’s buttock. This linear measurement tries to reflect only the
distance between the midline and the outer lip of the ischium, without soft tissue
interference.
Placing the patient in true lateral position, makes the patient’s midline parallel to
the table. If this position is not possible, the operator needs to ascertain the degree
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of inclination of the midline with respect to the table, so the needle still can be
advanced parallel to the patient’s midline.
When the nerve is not found at first attempt, it could only be located either lateral
or medial to the needle. Because of gravity, it is more frequent to underestimate
the midline-nerve distance (sagging midline). Therefore, the first correction
should be lateral.
When reposition is necessary, keep in mind the “vector” effect. At a theoretical
distance of 9 cm a 10-degree correction will move the needle app 1.6 cm. A 20-
degree correction will move it 3.4 cm. This big “jump” could easily overshoot the
correction. A small 10-degree correction usually is all it takes to localize the
nerve.
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MIDGLUTEAL SCIATIC BLOCK
ULTRASOUND TECHNIQUE
Indications
The same than for nerve stimulation techniques.
Patient position
For a midgluteal approach the patient can be placed prone, lateral or in Sim’s
position.
Type of needle
A 10 or 15cm, 21-G, insulated needle is used.
Type of transducer
Because of the depth at which the sciatic nerve is located in the gluteal area, most
of the times a curved, low frequency (5-7 MHz) probe is needed.
Scanning
The nerve is identified in cross section (short axis) by placing the transducer
across the midgluteal area at which point the sciatic nerve can be identified between the
greater trochanter and ischial tuberosity, as shown in figure 7-30.
Needle insertion
The easiest approach is to introduce the needle out of plane from distal to
proximal as observed in figure 7-31.
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Figure 7-32 shows an ultrasound image of an out of plane technique during
injection.
Complications
The same as nerve stimulation techniques.
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SCIATIC NERVE BLOCK, SUBGLUTEAL
di Benedetto’s approach
Indications
This is a block more suitable for surgery below the knee, because it does not
reliably block the posterior femoral cutaneous nerve (back of the thigh). It can also be
used for continuous catheter techniques.
Main characteristics
There are several techniques performed at or around the subgluteal fold. Some
authors mention Raj’s “supine approach” to sciatic nerve (Anesthesia & Analgesia 1975)
as being the first. In fact, this is a sciatic block performed between the ischium and
greater trochanter (mid-gluteal, not subgluteal level), just a few cm caudal to Labat’s
classic approach. In this technique the extremity is elevated and flexed at the hip and
knee, stretching the buttock tissues. This supposedly brings the sciatic nerve closer to the
skin. It is interesting to note that, even though this technique is universally known as
“Raj’s supine approach”, a completely similar technique was published a year earlier
(1974) by Winnie and colleagues in Anesthesiology Review. Raj’s technique was
correctly devised “for below-the-knee operations”. This fact is frequently forgotten and
we will revisit it later.
A popular infra or subgluteal technique is the technique introduced by di
Benedetto and colleagues in 2001.
1. Ischium and greater trochanter are located at about the same transverse plane in
the buttocks, as shown in figure 7-1. Di Benedetto’s perpendicular line going
caudal and lateral, needs to have the trochanter located significantly higher than
the ischium.
2. The subgluteal fold is about 8 cm caudal to the midpoint between ischium and
greater trochanter and not 4 cm. On the other hand, being the subgluteal fold so
evident, would it suffice to extend the line until it intercepted the subgluteal fold?
3. At the subgluteal fold the three components of the hamstring muscles are
practically fused together in one single tendon, without any evident groove in
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between. More distally in the thigh a groove can be found between biceps and
semitendinosus, but it is too subtle to be easily palpable through several layers of
tissue (skin, subcutaneous tissue and thick fascia lata).
4. A groove is visible in most people between the biceps and the iliotibial tract. This
groove has nothing to do with the trajectory of the sciatic nerve.
5. The sciatic nerve runs under the biceps femoris and not in a groove between
biceps and semitendinosus.
Technique
The authors suggest to insert the needle perpendicular to the skin until a twitch
from the sciatic nerve is obtained.
Complications
Common to other approaches to the sciatic nerve.
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SCIATIC NERVE BLOCK, SUBGLUTEAL
Franco’s approach
The subgluteal approach can be easily performed at 10 cm from the midline at the
subgluteal fold, with the patient lying in lateral decubitus, as shown in fig 7-33.
The 10-cm measurement is made from the midline at the level of the subgluteal
fold, in a way similar to the one described for the mid-gluteal approach. The needle is
advanced parallel to the midline, through the gluteus maximus muscle and into the sciatic
nerve. The current is lowered to around 0.5 mA and a slow injection is started. If the
nerve is missed at first pass it could only be located medial or lateral to the needle. The
needle is reinserted, with a small 10-degree correction in its orientation, first lateral
(toward the trochanter) and then medial (to the midline) if necessary.
Ultrasound technique
Although the same tissue layers cover the sciatic nerve at the midgluteal and
subgluteal levels, the fat layer is usually thinner. This makes the ultrasound visualization
of the sciatic nerve at this level usually easier than in the midgluteal area. Depending on
depth, the nerve can be visualized with a linear high frequency probe, but frequently a
lower frequency probe is needed. Curved low frequency probes are needed for bigger
patients. The patient is placed prone, lateral position or in Sim’s position. The nerve is
visualized in cross section (short axis) and the needle is advanced either out of plane
(usually) or in line with the probe.
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3. The sciatic nerve is relatively more superficial at the subgluteal fold because the
amount of fat decreases from mid-gluteal to subgluteal level, although the type of
layers (fat and muscle) remains the same.
4. The popliteal fossa is the only level in the trajectory of the sciatic nerve in which
the nerve is not covered superficially by muscle. Approaching the sciatic nerve,
without passing through muscle is the only true advantage of a popliteal approach.
5. In terms of anesthesia distribution, the subgluteal approach is more comparable to
the popliteal block than to other more proximal approaches.
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SCIATIC NERVE BLOCK, POPLITEAL
Franco’s approach
NERVE STIMULATOR TECHNIQUE
Indications
It is especially suitable for foot surgery. Along with femoral nerve block
(saphenous) it provides complete anesthesia below the knee.
Main characteristics
This is the only place in the trajectory of the sciatic nerve where the nerve is not
covered superficially by muscle, perhaps its only true advantage over other more
proximal approaches to the sciatic nerve. Characteristically, a sciatic block done at this
level with a blind technique has a slower onset and lower success rate than more
proximal approaches. The fact that the two components of the nerve diverge from each
other could account for some of the partial blocks. However, slower onset and lower
success rates are sometimes observed in cases where there is reasonable evidence to
believe that the main trunk has been contacted. One of the possible reasons is that the
nerve sheath at this level fuses with the fat that fills the popliteal fossa soaking the local
anesthetic away from the nerve. Ultrasound techniques have a faster onset.
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The distance between these two points in adults is usually 6-7 cm in females and
7-8 cm in males. The midpoint between the two tendons is located and marked, as shown
in figure 7-35.
The needle insertion point is then found 7-9 cm above the crease, as shown in
figure 7-36.
Type of needle
A 5cm, 22-G, insulated needle is usually adequate.
Needle insertion
The needle is introduced with a 30-45 degree cephalad orientation, as shown in
figure 7-37.
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The needle is directed approximately 45-degrees cephalad, so the contact with the
nerve happens at 1-2 cm higher from the crease than the actual entrance point, increasing
the chances that the sciatic nerve is contacted prior to its division. The distance from the
crease at which the needle is inserted varies according to the patient’s height. A good
ballpark estimation is to insert the needle at a distance from the crease that is 1 cm longer
than the intertendinous distance.
Once a response from the sciatic nerve is elicited, and still present at 0.5 mA or
less, a slow injection is started with frequent aspirations.
Complications
Small hematoma can develop. Residual dysesthesia lasting up to two weeks can
be seen.
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POPLITEAL BLOCK, LATERAL APPROACH
WITH NERVE STIMULATOR
Indications
It is especially suitable for any surgery below the knee including ankle and foot,
in patients who cannot be placed in any other position than supine
Main characteristics
Blocking the sciatic nerve with this approach is a little bit more challenging than
the posterior approach. Biceps and vastus lateralis fibers are in close physical contact so
the needle usually stimulates some muscle fibers before reaching the sciatic nerve.
Technique
The midpoint of the patella is found and a line is drawn from it proximally into
the thigh. This line represents roughly the projection of the sciatic nerve and therefore it
can be used to estimate the depth of the sciatic nerve, as measured from the lateral side.
With the thigh in slight lateral rotation the needle is advanced with a 30-degree posterior
orientation. A local twitch of biceps and/or vastus lateralis muscles can be found before
entering the popliteal fossa. If the needle overshoots the projection of the nerve without
eliciting a twitch, it is withdrawn to the skin and a small 10-degree posterior correction is
applied before reinsertion. With a visible twitch at 0.5 mA or less, a slow injection is
started with frequent aspirations.
Complications
The same than for posterior approach.
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POPLITEAL BLOCK
ULTRASOUND TECHNIQUE
Indications
The same indications than nerve stimulation techniques.
Patient position
There are basically two main positions in which this block can be performed,
supine and prone. The views obtained are similar, but in general the supine technique can
be more challenging, especially in larger patients. The supine technique usually involves
an in-plane lateral approach, while the prone technique provides the opportunity for out
of plane approaches also. Whether the technique is done supine or prone, having the
patient flex the knee improves the visualization of the sciatic nerve and its components.
Type of needle
If an out of plane technique is performed usually a 5cm, 22-G, insulated needle
suffices. If an in plane lateral approach is attempted usually a longer 10cm, 21-G,
insulated needle is needed.
Type of transducer
In most cases a linear, high frequency (8-15 MHz) is used. In larger patients it is
sometimes necessary to use a curved, low frequency (3-7 MHz) probe.
Scanning
The nerve is scanned in short axis. The scanning can be started at any level in the
popliteal fossa, but it is helpful to start at the crease where the popliteal vessels, vein and
artery, have an intimate relationship with the tibial component of the sciatic nerve. Figure
7-38 shows a sequence of images as the probe is moved from distal to proximal.
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Needle insertion
The needle can be inserted out of plane, usually from distal to proximal or in
plane from lateral to medial, as shown in figure 7-39.
A needle inserted in plane from the lateral side is easily seen in the screen as
shown in figure 7-40.
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References
1. Snell RS: Clinical anatomy for medical students, 3rd edition. Boston, MA: Little,
Brown and Company; 1986
2. Labat G: Regional anesthesia: Its technique and clinical application. Philadelphia,
PA: W.B. Saunders, 1922
3. Shipman P, Walker A, Bichell D: Human skeleton. Cambridge, MA: Harvard
University Press; 1985
4. Hall J, Froster-Iskenius U, Allanton J: Handbook of normal physical
measurements. Oxford: Oxford University Press; 1989
5. Cunningham’s Textbook of Anatomy, 5th edition. Edited by Robinson A. New
York, William Wood and Company, 1928, pp 258
6. Hollinshead’s Textbook of Anatomy, 5th edition. Edited by Rosse C, Gaddum-
Rosse P. Philadelphia, Lippincott-Raven, 1997, pp 641–80
7. Winnie A, Ramamurthy S, Durrani Z, et al. Plexus blocks for lower extremity
surgery. Anesthesiology Review 1974; 1: 11-16
8. Franco, CD. Posterior approach to the sciatic nerve in adults: Is Euclidean
geometry still necessary? Anesthesiology 2003; 98: 723-728
9. Franco CD, Choksi N, Rahman A, Voronov G, Almachnouk M. A Subgluteal
Approach to the Sciatic Nerve in Adults at 10 cm from the Midline. Reg Anesth
Pain Med 2006; 31: 215-20
10. Di Benedetto P, Bertini L, Casati A, et al. A new approach to the sciatic nerve
block: A prospective, randomized comparison with the classic posterior approach.
Anesth Analg 2001; 93: 1040-1044
11. Rogers J, Ramamurthy S: Lower extremity blocks, Regional anesthesia and
analgesia. Edited by Brown DL. Philadelphia, PA: W.B. Saunders Company,
1996
12. Mulroy M: Regional Anesthesia, An illustrated procedural guide, 3rd edition.
Philadelphia, PA: Lippincott Williams & Wilkins; 2002
13. Enneking FK, Chan V, Greger J, et al. Lower-extremity peripheral nerve
blockade: Essentials of our current understanding. Reg Anesth Pain Med 2005;
30: 4-35
14. Vloka JD, Hadzic A, Drobnik L, Ernest A, Reiss W, Thys DM. Anatomical
landmarks for femoral nerve block: A comparison of four needle insertion sites.
Anesth Analg 1999; 89: 1467-1470
15. Capdevila X, Macaire P, Dadure C, Choquet O, Biboulet P, Ryckwaert Y,
D’Athis F. Continuous psoas compartment block for postoperative analgesia after
total hip arthroplasty: New landmarks, technical guidelines, and clinical
evaluation. Anesth Analg 2002; 94: 1606-1613
16. Orebaugh SL. The femoral nerve and its relationship to the lateral circumflex
femoral artery. Anesth Analg 2006; 102: 1859-1862
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CHAPTER 8
CONTINUOUS NERVE BLOCKS
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Introduction
Continuous techniques
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a high success rate. Catheters techniques (“secondary block”) do not generally achieve
the same degree of success. Catheters need to be closely placed in the proximity of target
nerve(s) in order to decrease the “secondary block failure”, a failure to achieve the same
degree of success than single shot techniques. In general catheters should not be
advanced more than 3-4 cm because the risks for catheter-related complications (e.g.,
knotting, vascular puncture, nerve injury, etc) potentially increase.
The most common problems with catheters include inability to achieve adequate
analgesia and other technical problems like accidental dislodgement and peri-catheter
leaks. Catheters tend to have a “mind of their own”. They can advance away from nerves
and into undesirable places. Capdevila et al in 2005 in a multicenter study that included
1,416 patients identified 17.9 % of “technical problems due to catheters and devices”.
Many techniques are used to increase the resistance to accidental dislodgement.
Perhaps the most successful is the subcutaneous tunnelization of the catheter. It does not
only increase the resistance to removal but also provides the opportunity to direct the
catheter away from the surgical site.
Severe nerve damage and infection are rare complications of continuous
techniques.
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References
1. Ansbro FP. A method of continuous brachial plexus block. Am J Surg 1946; 71: 716-
722
2. Selander D. Catheter technique in axillary plexus block. Acta Anaesthesiol Scand
1977; 21: 324-329
3. Liu SS, Salinas FV. Continuous plexus and peripheral nerve blocks for postoperative
analgesia. Anesth Analg 2003; 96: 263-272
4. Boezaart AP: Continuos Peripheral Nerve Blocks, In: Boezaart AP (ed): Anesthesia
and Orthopaedic Surgery. New York, McGraw-Hill, 2006, pp 257-264
5. Capdevila X, Pirat P, Bringuier S, et al. Continuous peripheral nerve blocks in
hospital wards after orthopedic surgery: A multicenter prospective analysis of the
quality of postoperative analgesia in 1,416 patients. Anesthesiology 2005; 103: 1035-
1045
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CHAPTER 9
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TRANS ABDOMINAL PLANE (TAP) BLOCK
The innervation of the anterolateral abdominal wall is provided by the lower six
thoracic (intercostal) nerves and the first lumbar nerve. The 7th intercostal nerve swings
up and terminates around the xiphoid of the sternum in the highest point of the abdominal
wall. The 10th intercostal runs almost horizontally toward the umbilicus, while the 12th
intercostal (subcostal) innervates the area above the inguinal ligament and suprapubic
area. The first lumbar nerve originates the iliohypogastric and ilioinguinal nerves, both
branches of the lumbar plexus, which run above the iliac crest.
Main characteristics
This block was described before the use of ultrasound. It was performed in the
posterior abdominal wall at the level of the triangle of Petit. This triangle is formed
anteriorly by the posterior border of the external oblique muscle, posteriorly by the
anterior border of latissimus dorsi and inferiorly by the iliac crest. The area of the triangle
is covered superficially by the aponeurosis of insertion of the external oblique and deeper
by the external oblique and transversus abdominis muscles. The performance of this
block used to require the feeling of “pop” sensations as the needle crossed the different
fascia and muscle planes. Since the introduction of ultrasound I recommend doing this
block under direct vision.
Indications
To produce anesthesia or analgesia of the abdominal wall.
Patient position
The patient can be supine or in lateral position with the arm on the side to be
blocked elevated and turned to the opposite side.
Type of needle
A 5cm, 22-G, insulated needle is usually used. An 18-G epidural needle can also
been used with the advantage that the bigger needle is more readily seen and its curved
end could help minimize the accidental puncture of deeper planes.
Type of transducer
A linear high frequency (8-15 MHz) probe is usually sufficient. In larger patients
with thicker abdominal wall (more fat) a curved, low frequency (3-7 MHz) probe is
necessary.
Scanning
The probe is placed diagonally over the lateral abdominal wall at the level of the
mid axillary line.
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Needle insertion
The needle can be inserted in plane or out of plane. We prefer to insert the needle
in plane from anterior to posterior, as shown in figure 9-1.
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References
1. Snell RS: Clinical anatomy for medical students, 5th edition. Boston, MA: Little,
Brown and Company; 1986, pp 133-182
2. Rafi A. Abdominal field block: A new approach via the lumbar triangle.
Anaesthesia 2001; 56: 1024-26.
3. Hebbard P, Fujiwara Y, Shibata Y, Royse C. Ultrasound-guided transversus
abdominis plane (TAP) block. Anaesthesia and Intensive Care 2007; 35: 616-7.
4. Carney J, McDonnell JG, Ochana A, et al. The transversus abdominis plane block
provides effective postoperative analgesia in patients undergoing total abdominal
hysterectomy. Anesth Analg 2008; 107:2056-60
5. McDonnell JG, Curley G, Carney J, et al. The analgesic efficacy of transversus
abdominis plane block after cesarean delivery: A randomized controlled trial.
Anesth Analg 2008; 106:186–91
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