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Carlo D. Franco, MD
Chairman Orthopedic Anesthesia
JHS Hospital of Cook County

Associate Professor Anesthesiology and Anatomy

Rush University Medical Center

Chicago, IL

Third Edition
This manual is intended for Anesthesiology Residents, Nurse Anesthetists and
Faculty of the Department of Anesthesiology and Pain Management, Cook County
Hospital of Chicago. The writing in these pages reflects the author’s own experience, as
well as his understanding and interpretation of the available literature. The author made
every effort to give proper credit to outside sources.
The persons depicted in pictures in this manual gave 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, come from dissections performed by the author in the
Anatomy Laboratory of Rush University Medical Center in Chicago, in compliance with
Rush University 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 April 2008.
However, recommendations and guidelines change, therefore the reader is urged to check
for new indications, warnings and precautions.

To my residents,
who make my coming to work
intellectually challenging and pleasurable
to the memory of my father

Chapter 1: Introduction

General considerations………………………………………………………………….. 8
Patient selection and premedication……………………………………………………. 8
Monitoring……………………………………………………………………………..… 9
Outcome issues…………………………………………………........................................9
Airway and regional anesthesia………………………………………………………….11

Chapter 2: Local Anesthetics

Historical perspective………………..…………………………………………………...14
Chemical structure ……………………………………………………………………....15
Structure-activity relationship………………………….………………………………...16
Mechanism of action and Na+ channels……………….………………………………....17
Frequency-dependent blockade…..………………….…………………………………..17
Pregnancy and local anesthetics……………………………………………………….....18
Fiber size and pattern of blockade………………….…………………………………....18
Modulating local anesthetic action…….………………………………………………...19
Local anesthetics additives…………….……………………….………………………..20
Tumescent anesthesia……………………………………………………………….........26
Toxic plasma concentrations………………………………………………………..…....26
Toxicity management……………………………………………………………….........27
Lipid emulsion……………………………………………………………………....…...27
Maximum dose…………………………………………………………………………...28
Allergy ………………………………………………………………………………......29
Profile summary of selected agents………………………………………..……….…....30

Chapter 3: Neuraxial Anesthesia

Spinal anesthesia
Cerebrospinal fluid………………………………………………………….........38
Site of action and indications…………………………………….........................39
Determinants of spread………………………………………………………..…39
Techniques (median, paramedian, Taylor’s)………………………………..…...40

Anesthesia duration…………………………………………………………........31
Side effects and complications……………………………………………..…….41
Other physiological effects……………………………………………………....42
Postdural puncture headache………………………………………………….….43
Transient neurological symptoms……………………………………………......44
Cauda equina syndrome…………………………………………………….........45
Back pain ………………………………………………………………….…….45
Spinal in the outpatient………………………………………………………..…46
Intrathecal adjuncts………………………………………………........................46

Epidural Anesthesia
Blockade characteristics………………………………………….........................47
Spread of local anesthetics……………………………………….........................47
Type of needles and catheters……………………………………………………48
Test dose…………………………………………………………........................48
Activating an epidural………………………………………………………........48

Chapter 4: Regional Anesthesia and Anticoagulation

Guidelines summary…………………………………………………………………......52
2002 consensus highlights………………………………………………………...……..52
New anticoagulants…………………………………………………………………........57

Chapter 5: Peripheral Nerve Blocks

Bringing the needle close to its target………………………….....……………………...54

Nerve stimulators……………………………………………………………………...…54
Insulated versus non-insulated needles……………………………………………......…56
Short versus long-bevel needles……………………………………….............................56
Nerve injury……………………………………………………………………….…......57

Chapter 6: Upper Extremity Blocks

Anatomy of the brachial plexus…………………………………………………...……..71

Scalene muscles……………………………………………...………………………......71
Brachial plexus structure…………………………………………………………..….....72
Interscalene block…………………………………………………………………...…...74
Supraclavicular block…………………………………………………………………….78
Infraclavicular block…………………………………………………………………......84

Axillary block………………………………………………………………………...….87

Chapter 7: Lower Extremity Blocks

Subgluteal fold…………………………………………………………………………...94
Male and female pelvis issue…………………………………………………………….95
Lateral femoral cutaneous nerve block…………………………………………………..96
Femoral block…………………………………………………………………………....97
Obturator nerve block………………………………………………………………....…99
Lumbar plexus block…………………………………………………………………....100
Sciatic nerve block, classic (Labat-Winnie)…………………………………………....102
Sciatic nerve block, Franco’s…………………………………………………………...104
Sciatic subgluteal nerve block, di Benedetto’s………………………………………....107
Sciatic subgluteal nerve block, Franco’s…………………………………………….....109
Popliteal nerve block, Franco’s………………………………………………………....111
Popliteal nerve block, lateral approach………………………………………………....113

Chapter 8: Continuous Nerve Blocks

Stimulating versus non-stimulating catheters………………………………………….117
Catheter-related problems………………………………………………………………117



General considerations

Regional anesthesia refers to anesthesia of a segment of the body, achieved by

selective interruption of nerve transmission (i.e., peripheral or neuraxial) without the need
to alter the patient’s level of consciousness. In this manual I discuss several aspects
related to regional anesthesia, according to the techniques most commonly used in the
United States, although with special emphasis in the techniques we perform daily at Cook
County Hospital of Chicago.
Regional anesthesia has been traditionally considered an “art”. As such, it is
usually practiced by “artists”, who use their particular talents to produce results difficult
to reproduce by anesthesiologists devoid of such artistic talents. We have a great respect
and admiration for all the pioneers who introduced and/or helped popularized the various
regional anesthesia techniques available to us now. We owe them a debt of gratitude. It is
the foundation on which we build our practice today. However, we also believe that the
practice of regional anesthesia in the 21st century should be based more on science than
art, taking advantage of all the various technologies available to us now. Using objective
tools to help our work, does not demean our practice, in the contrary, it makes it more
rational, reproducible, and potentially easier and safer. The recent introduction of
ultrasound to assist peripheral nerve blocks is an example of that.
The nerve blocks that we perform, and which I describe in these pages, are based
on anatomical, physiological, and pharmacological facts. The endpoints chosen are
objective. The local anesthetic solutions are used in volumes and concentrations
considered adequate and safe by clinical experience. Regional anesthesia practiced in this
manner, should likely lead to results that are predictable and reproducible.
Regional anesthesia carries the risks and complications associated with the use of
local anesthetics (i.e., local anesthetic toxicity), the risks and complications of using
needles and drugs in the proximity of nerves (e.g., neuropraxia, irreversible nerve
damage) and those risks associated with a particular technique (e.g., pneumothorax, total
As with any other anesthetic technique, choosing regional anesthesia requires a
thorough assessment that involves the patient, the surgeon, the nature of the procedure
and its estimated duration, as well as the level of experience of the anesthesiologist with
regional anesthesia and its management.

Patient selection and premedication

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 vast and 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. A conscious and cooperative patient may also potentially decrease the
chances of complications (e.g., pain at injection, early subjective symptoms indicating
impending systemic toxicity, etc).


Every nerve block, whether it is performed in holding area, OR, PACU or office,
must be treated as potentially dangerous. Monitoring blood pressure, heart rate and pulse
oxymetry, as well as the establishment of 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.

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
insufficient data. 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 bias at the time of technique selection (i.e., sicker patients
receiving more regional anesthesia).
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
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 of 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) there is
also some evidence that the values obtained are frequently better 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.

Procedures where regional anesthesia has not shown benefits as compared to

general anesthesia include:

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 and fewer side effects (nausea
and vomiting), especially immediately after surgery. This difference rapidly
disappears at 24 h.

An interesting meta-analysis on the subject of comparative outcome was

published in December 2000 in the British Medical Journal, by Rodgers et al from New
Zealand. The authors reviewed the literature looking for randomized trials with or
without use of neuraxial anesthesia (spinal or epidural) before 1997. A total of 141 trials
including 9,559 patients were included in this meta-analysis. The following are the main

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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 of whether neuraxial was used alone or in combination with general
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”, adding that 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 numbers, therefore infrequent
clinical events can be studied. However, it also means putting together trials from
different settings. They not only include data from different institutions, but also in some
cases different countries and cultures. It remains to be seen whether these very
encouraging results can be duplicated, and whether they could apply more generally to
regional anesthesia beyond neuraxial blocks (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 having increased importance in today’s
cost-conscious practice.

Airway and regional anesthesia

For some anesthesiologists managing a difficult airway usually means always

securing it. This approach negates the benefits that regional anesthesia can provide when
it is judiciously used. Evidence does not exist to support either claim.
We believe, that regional anesthesia, with its capacity to produce safe and dense
surgical anesthesia with minimal physiological derangements, should be carefully
contemplated, on a case by case basis, in all kind of patients. This does not mean that the
anesthesiologist should not be prepared at all times to manage the airway, and have at his/
her immediate disposal all necessary equipment and personnel to do it. We do need to
remember though, that “securing” the airway in all patients is not completely devoid of
In our practice we routinely provide regional anesthesia to patients with
challenging airways. These patients include the obese, as well as trauma patients wearing
halos and cervical collars. These patients are assessed individually. The discussion needs
to involve the patient and the surgeons and must take into account the anesthesiologist’s
expertise and familiarity with regional anesthesia. If a regional anesthesia option is
selected, a backup plan, that can be readily implemented, needs to be available at all

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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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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 neurotoxic, if injected intraneurally, and the damage
caused is 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

Anesthesia by compression was common in the antiquity. Cold as an anesthetic

was widely used until the 1800s, and then it came cocaine. The native Indians of Peru
chewed coca leaves and knew about their cerebral-stimulating effects. The leaves of
erythroxylon coca were taken to Europe where Niemann in Germany isolated cocaine in
1860. Carl Koller, a contemporary and friend of Sigmund Freud, is credited with the
introduction of cocaine as a topical ophthalmic local anesthetic in Austria in 1884. In
1888 Koller came to the US and established a successful ophthalmology practice at
Mount Sinai Hospital in New York until the year of his death in 1944.
Recognition of cocaine’s cardiovascular side effects, as well as its potential for
dependency and abuse, led to a search for better local anesthetic drugs. Cocaine is a good
topical local anesthetic that also produces vasoconstriction and for this reason it is still
used by some, for topical anesthesia of the nose and other mucous membranes. Cocaine
blocks the reuptake of cathecolamines from nerve endings. Total dose should not exceed
100 mg (2.5 mL of a 4% solution), to avoid systemic effects (hypertension, tachycardia,
cardiac arrhythmias).
Ropivacaine is the only other local anesthetic able to produce some
vasoconstriction, and that effect is weak.

Some highlights on local anesthesia

1850s Invention of the syringe and hypodermic hollow needle.

1884 Halsted, an American surgeon, blocks the brachial plexus with a solution of cocaine
under direct surgical exposure.

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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 from 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 founds the first American Society of Regional Anesthesia.
1953 Daniel Moore, from Virginia Mason Clinic in Seattle, publishes his book “Regional
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.

Date of introduction in clinical practice of some local anesthetics:

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.

Chemical structure of local anesthetics

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 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 local anesthetic

15 | P a g e
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.

Physicochemical properties-activity relationship

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

16 | P a g e
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 used in clinical practice (3%) that are possible thanks to its low
toxicity. It is also claimed that 2-chloroprocaine has better “tissue penetrability”.

Mechanism of action and sodium channels

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.

Pregnancy and local anesthetics

Increased sensitivity to local anesthetics, demonstrated as faster onset and more

profound block, may be present during pregnancy.
Alterations in protein binding of bupivacaine, may result in increased
concentrations of active unbound drug in the pregnant patient, increasing its potential for
Placental transfer is also more active for lipid soluble local anesthetics. In any
case, agents with a pka closer to physiologic pH have a higher placental transfer. For
example the umbilical vein/maternal vein ratio for mepivacaine is 0.8 (pka 7.6) while for
bupivacaine is 0.3 (pka 8.1).
In the presence of fetal acidosis, local anesthetics cross the placenta and become
ionized in higher proportion than at normal pH. The ionized fraction cannot cross back to
the maternal circulation, originating what is called “ion trapping”. Therefore, 2-
chloroprocaine, with its very short maternal and fetal half-lives, is an ideal local
anesthetic in the presence of fetal acidosis.

Fiber size and pattern of blockade

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.

18 | P a g e
(Figure from Morgan’s Clinical Anesthesiology, 3rd edition, 2006, reproduced with permission)

Modulating local anesthetic action

pH adjustment

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

19 | P a g e
(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).


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.



Epinephrine is the most common vasoconstrictor added to local anesthetics to

prolong the anesthetic effect and to decrease absorption. Epinephrine is also used to
detect intravascular injection. Without beta-blockers on board, 15 mcg of epinephrine
should produce a 30% increase in heart rate within 30 seconds.
Vasoconstrictors may also improve the quality and density of the block, especially
with spinal and epidural anesthesia. This has been demonstrated with tetracaine, lidocaine
and bupivacaine. The mechanism is unclear. Epinephrine may simply increase the
amount of local anesthetic available by reducing absorption. It could also have some local
anesthetic effect by means of its α2-agonist actions. Subarachnoid epinephrine also
delays voiding and discharge readiness.
The prolongation of effect in peripheral nerve blocks can be 30-60%, depending
on site of injection and type of local anesthetics (more vascular sites like intercostal see
more effect, and intermediate agents like lidocaine benefit more). Peripherally
epinephrine does not have any significant alpha-2 effect.
In general, epinephrine added to spinal anesthesia prolongs the effect of the less
lipid soluble agents like lidocaine and mepivacaine (20-30%). The exception to this rule
is tetracaine, a highly lipid soluble agent, that gets the largest prolongation of all spinal
local anesthetics (up to 60% in lumbar dermatomes).
The usual dose of intrathecal epinephrine is 200 mcg, but doses as small as 50
mcg can be sufficient. In the epidural space the usual dose is 5 mcg/mL. Epinephrine,
other than intrathecal, is absorbed systemically and may produce adverse cardiovascular
effects. In small doses the beta-adrenergic effects predominate, with increased cardiac
output and heart rate. Dose larger than 0.25 mg (250 mcg) may be associated with
arrhythmias or other undesirable cardiac effects.
The potential risk for peripheral nerve ischemia, as a result of epinephrine acting
on epineural vessels and vaso nervorum has to be balanced against the lower risk of
systemic toxicity, the ability to detect intravascular injection and the prolongation of

20 | P a g e
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
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

Dilution/concentration issues

By definition a 1:1,000 dilution means 1 g solute in 1,000 mL of solution. That is

the same than to say 1 mg/mL or 1,000 mcg/mL.
o 1:10,000 equals 100 mcg/mL
o 1:100,000 equals 10 mcg/mL
o 1:200,000 equals 5 mcg/mL
o 1:400,000 equals 2.5 mcg/mL


1. Neuraxial use: The addition of opioids to local anesthetics has a synergistic

effect, both in anesthesia and postoperative analgesia (especially visceral pain).
They block pain pathways without significantly affecting motor or sympathetic
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

21 | P a g e
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.

Extended-release epidural morphine (DepoDur): is a new liposomal

formulation designed for epidural use, providing 48 h of pain relief. DepoDur was
approved in 2004. It is supplied in a 2 mL vial containing 10 mg/mL dose in
sterile saline. It is only approved as a single lumbar epidural dose prior to
surgery or after clamping of the umbilical cord during C-section. The
recommended dose is 10 mg for C-section, 10-15 mg for lower abdominal surgery
and 15 mg for major orthopedic surgery of the lower extremities. Respiratory
depression is dose-related. The most common adverse events reported during
clinical trials were decreased oxygen saturation, hypotension, urinary retention,
nausea and vomiting, constipation and pruritus.

2. Peripheral nerve blocks: The usefulness of opioids in peripheral nerve blocks is

mostly unsupported by the evidence. Opioids have been shown useful when
injected in the intra-articular space.


Alpha-2 agonists have central (sedation, analgesia, bradycardia) and peripheral

effects (vasoconstriction/vasodilation with net hypotension, anti shivering, diuresis). The
site for sedative action is the locus ceruleus of the brain stem, while the principal site for
analgesia seems to be the spinal cord.
The main alpha-2 effect on the heart is decreased tachycardia by blocking
cardioacelerator fibers, and bradycardia through a vagomimetic effect. In the periphery
clonidine produces both vasodilation via sympatholysis and vasoconstriction through
receptors on smooth muscle. The cause for its anti shivering and diuretic effects are yet to
be established.
Side effects, including sedation, hypotension and bradycardia, limit alpha-2
agonists use. Small doses of clonidine (50-75 mcg) have shown to significantly prolong
analgesia in spinal, epidural, IV regional, and peripheral nerve blocks, both when injected
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

22 | P a g e
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

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. Currently it is approved only for sedation in the ICU.

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).

N-methyl-D-aspartate (NMDA) receptor antagonists

Activation of NMDA receptors makes the neurons of the spinal cord more
responsive to all types of input including pain stimuli (central sensitization). NMDA
receptor antagonists, like ketamine, have shown analgesic activity. In fact in IV regional
0.1 mg/kg of ketamine is superior to clonidine (1 mcg/kg) in preventing tourniquet pain.
Errando in Spain showed that commercially available ketamine containing benzethonium
chloride is toxic in swine (Reg Anesth Pain Med 1999; 24:146-52). Preservative-free
solutions of ketamine have proven safe.

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 and other high-molecular-weight compounds have been advocated to
increase the duration of local anesthetics. The evidence is lacking.


Ester local anesthetics

They are rapidly hydrolyzed at the ester linkage by plasma pseudocholinesterase,

the same enzyme that hydrolyses acetylcholine and succinylcholine. The hydrolysis of 2-
chloroprocaine is about four times faster than procaine, which in turn is hydrolyzed about

23 | P a g e
four times faster than tetracaine. However, even tetracaine has a metabolic half-life of
only 2.5-3.0 min (Tetzlatt JE. In: Ambulatory Anesthesia Perioperative Analgesia. New
York, McGraw-Hill, 2005, p 193).
In individuals with atypical plasma pseudocholinesterase the half-life of these
drugs is prolonged and potentially could lead to plasma accumulation. Cerebrospinal
fluid does not contain esterase enzymes, so if an ester is used for spinal anesthesia (e.g.,
tetracaine) its termination of action depends on blood absorption.
The hydrolysis of all ester local anesthetics leads to the formation of para-
aminobenzoic acid (PABA), which is associated with a low potential for allergic
reactions. Allergic reactions may also develop from the use of multiple dose vials of
amide local anesthetics that contain methylparaben (PABA derivative) as a preservative.
As opposed to other ester type anesthetics, cocaine is partially metabolized in the
liver and partially excreted unchanged in the urine.

Amide 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 dibucaine number

People with atypical plasma pseudocholinesterase exhibit prolonged recovery

after a dose of succinylcholine or mivacurium. Dibucaine is an amide local anesthetic that
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

24 | P a g e
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).

The capacity of a local anesthetic to produce systemic toxicity is directly related

to plasma level of unbound drug. This plasma level depends on:

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

Brown et al reported a 1.2 in 10,000 incidence of systemic toxicity after epidural

anesthesia and 19 in 10,000 after peripheral nerve blocks.
According to Mather et al, central nervous system (CNS) and cardiovascular (CV)
effects are “poorly correlated with arterial drug concentrations” and better correlated with
the “respective regional venous drainage”. According to them, lung uptake reduces the
drug concentration by 40% and slower injection (3 min compared to 1 min) achieves
similar decreases (Reg Anesth Pain Med 2005; 30: 553-66). CNS signs of toxicity usually
precedes CV manifestations.
Peak local anesthetic blood levels are directly related to the dose administered at
any given site. However the vascularity of the site at similar doses is very important in
determining different plasma levels. The absorption of local anesthetics from different
sites is from highest to lowest: endotracheal > intercostal > caudal > epidural > plexus
blocks > sciatic/femoral > subcutaneous infiltration.
Generally the administration of a 100-mg dose of lidocaine in the epidural or
caudal space results in approximately a 1 mcg/mL peak blood level in an average adult.
The same dose injected into less vascular areas (e.g., brachial plexus axillary approach or
subcutaneous infiltration) produces a peak blood level of app 0.5 mcg/mL. The same
dose injected in the intercostal space produces a 1.5 mcg/mL plasma level.
Peak blood levels may also be affected by the rate of biotransformation and
elimination. In general this is the case only for very actively metabolized drugs such as 2-
chloroprocaine, which has a plasma half-life of about 45- 60 seconds.
For amide local anesthetics like lidocaine peak plasma levels after regional
anesthesia primarily result from absorption and in general occur within 1 h (please see
difference with tumescent anesthesia).
Rodriguez et al studied 10 end-stage renal disease patients coming for A-V fistula
(Eur J Anaesthesiol 2001; 18: 171-6). The patients received an axillary block with a total
of 650 mg of plain mepivacaine. Plasma levels were studied during 150 min. Peak levels
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.

25 | P a g e
Tumescent (diluted) anesthesia for liposuction

The use of highly diluted concentrations of lidocaine (0.1% or less) plus

epinephrine (usually 1 mg per liter or 1:1,000,000) allows for painless and bloodless
liposuction procedures. Lidocaine bounds to tissue proteins in this subdermal drug
reservoir from where it is subsequently slowly released into the systemic circulation.
Diluted lidocaine, along with epinephrine-induced vasoconstriction, makes
systemic uptake so slow as to match the liver maximum lidocaine clearance capacity of
250 mg/h. Therefore, according to de Jong, “the blood level remains below 5 mcg/mL
toxic threshold, despite the administration of many times (e.g., 35 mg/kg) the
conventional upper dose limit of undiluted full strength lidocaine” (Int J Cosmetic Surg
2002; 4: 3-7).
Peak plasma levels of lidocaine using tumescent technique occur between 5-17
hours compared to less than 1 h for common infiltration.

Central nervous system toxicity

Toxic plasma levels are usually produced by inadvertent intravascular injection.

This is the basis for fractionating of the dose and the use of vasoconstrictors. Toxic
plasma levels could rarely result from the slow absorption from the injection site. A
sequence of symptoms may include numbness of the tongue, lightheadedness, tinnitus,
restlessness, tachycardia, convulsions and respiratory arrest. Interestingly enough, there is
no evidence that patients suffering from seizure disorders are at any increased risk for
CNS local anesthetic toxicity, including seizures.
The site of action for local anesthetic-induced seizures seems to be the amigdala,
part of the limbic system, in the base of the brain.

Cardiovascular system toxicity

• The cardiovascular manifestations usually follow the CNS effects (therapeutic

index). The exception is bupivacaine, which can produce cardiac toxicity at sub
convulsant concentrations.
• Rhythm and conduction are rarely affected by lidocaine, mepivacaine and
tetracaine, but bupivacaine and etidocaine can produce ventricular arrhythmias.
• EKG shows a prolongation of PR and widening of the QRS
• The incidence of CV toxicity with local anesthetics is higher in pregnancy due to
higher proportion of unbound fraction.
• CV toxicity is increased under conditions of hypoxia and acidosis.

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

26 | P a g e
Management of systemic toxicity

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.

Bupivacaine toxicity and use of lipid emulsion to treat it

Bupivacaine cardiac toxicity was highlighted in an editorial report by Albright in

1979, in which he described several cases of refractory cardiac arrests in association with
the use of bupivacaine (Anesthesiology 1979; 51:285-7). In 2003, Weinberg and
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

27 | P a g e
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
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
depression. Therefore, propofol is not indicated to treat local anesthetic-induced
cardiac toxicity.

Maximum dose

Regional anesthesiologists perform peripheral nerve blocks with an amount of

local anesthetics that usually exceeds what traditionally have been considered “maximum

28 | P a g e
recommended doses”. However the traditional recommendations are based on
extrapolation from animal data that do not necessarily apply to clinical practice.
According to Rosenberg et al, the common recommendations for maximum doses, as
suggested by the literature, “are not evidence based” (Reg Anesth Pain Med 2004; 29:
564-575), and according to Milroy have proven to be “poor approximation of safety”
(Reg Anesth Pain Med 2005; 30: 513-515).
It is known that peak plasma levels do not correlate with patient size or body
weight. Many practitioners have called to review these guidelines to better reflect the
reality of clinical practice. The American Society of Regional Anesthesia convened a
“Conference in Local Anesthetic Toxicity” with a panel of experts in 2001, to discuss the
subject. Many papers related to that conference have been published. In a review article
by Rosenberg et al (just cited) the authors argue that the safe doses instead should be
block specific and related to patient’s age (e.g., epidural), organ dysfunction (especially
for repeated doses) and whether the patient is pregnant. They suggest also adding
epinephrine 2.5 to 5 mcg/mL, when not contraindicated.
The fact is that most of the systemic toxicity occurs with unintentional direct
intravascular injection (Mather et al, Reg Anesth Pain Med 2005; 30: 553-566).


Normal hemoglobin contains an iron molecule in the reduced or ferrous form

(Fe ), the only form suitable for oxygen transport by hemoglobin. When hemoglobin is
oxidized, the iron molecule is converted into the ferric state (Fe 3+) or methemoglobin.
Methemoglobin lacks the electron that is needed to form a bond with oxygen and
therefore it is incapable of oxygen transport. Because red blood cells are continuously
exposed to various oxidant stresses, blood normally contains approximately 1%
methemoglobin levels. Prilocaine and benzocaine can oxidize the ferrous form of the
hemoglobin to the ferric form, creating methemoglobin. It is more frequently seen with
nitrates like nitroglycerin. When MetHb exceeds 4 g/dL cyanosis can occur.
Prilocaine doses of more than 600 mg are needed to produce clinically significant
methemoglobinemia. Depending on the degree, methemoglobinemia can lead to tissue
hypoxia. The oxyHb curve shifts to the left (P50 < 27 mmHg). MetHb has a larger
absorbance than Hb and 02Hb at 940 nm, but simulates Hb at 660 nm. In the presence of
high MetHb concentrations the SaO2 falsely approaches 85%, independent of the actual
arterial oxygenation. Diagnosis needs clinical suspicion and confirmation by blood
Methemoglobinemia is easily treated by the administration of methylene blue
(1-2mg/kg of a 1% solution over 5 min) or less successfully with ascorbic acid (2 mg/kg).


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

29 | P a g e
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).

Eutectic mixture of local anesthetics (EMLA)

EMLA cream is a 1:1 mixture of 5% lidocaine and 5% prilocaine. One gram of

EMLA contains 25 mg of lidocaine, 25 mg of prilocaine, an emulsifier, a thickener and
distilled water. EMLA is a liquid at room temperature, containing up to 80%
concentration of the uncharged base form of local anesthetic, which confers better dermal
penetration. Anesthesia onset takes between 45 to 60 minutes. Its main use is in children.
One or 2 grams of EMLA cream are applied per 10 cm2 of skin and covered with an
occlusive dressing (maximum application area 2000 cm2 or 100 cm2 in children less than
10 kg).

Drug interactions

Local anesthetics potentiate the effects of non-depolarizing muscle relaxants.

Simultaneous administration of succinylcholine and ester local anesthetics, both
metabolized by pseudocholinesterases, may potentiate the effect of each other.
Cimetidine and propranolol decrease hepatic blood flow and amide local anesthetic
clearance increasing the potential for systemic toxicity. Opioids and alpha-2 adrenergic
agonists potentiate the effects of local anesthetics and vice versa.

Profile summary of selected agents

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).

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).

30 | P a g e
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.
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

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Characteristics: slow onset, short duration and the only LA with a secondary
amine structure that limits its ability to pass through membranes (topical use
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 seems to produce 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.

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.
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%

32 | P a g e
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.

33 | P a g e

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
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:
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 α2-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

35 | P a g e


36 | P a g e

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


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 8 th 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.

Planes between the surface of the skin and subarachnoid space

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.

Composition of cerebrospinal fluid and serum in humans

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.

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.

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.

Determinants of local anesthetics spread in the spinal fluid

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

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).

Side effects and Complications

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 with spinal anesthesia the decrease in systemic vascular
resistance is < 15%. This is because arterioles retain intrinsic tone and do not
dilate maximally.
The extent of decrease in BP is dependent 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 the drug of choice because it
produces vasoconstriction and increased cardiac output.
Phenylephrine is a good second choice especially if tachycardia is present. It
causes vasoconstriction, but it could decrease the cardiac output.
Trendelenburg position can alleviate the venous pooling, but may produce an
even higher spinal level. Flexion of the operating table with legs and back up is a
good compromise.

2. Bradycardia
When the sympathetic block reaches T2 level the cardioacelerator fibers are

41 | P a g e
blocked and the vagus action is unopposed. The extent to which hear 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,
use of vasopressors, atropine and fluid replacement as needed.

Miscellaneous physiologic effects

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.

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

42 | P a g e
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.

Other effects and complications

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.

2. Post dural puncture headache (PDPH)

PDPH is due to CSF leak through the dural puncture site. The subsequent loss of
CSF pressure produces stretching of the meningeal coverings of intracranial
nerves whenever the upright position is assumed. The pain characteristics,
involving exacerbation in the upright position and relief in the recumbent
position, remain the main diagnostic tool. It is more frequent in females, in
younger patients and during pregnancy. The size and type of needle are proven
factors. Pencil point needles significantly reduce the risk.
Spinal needles are either cut-bevel (Quincke-type) or pencil-point (Whitacre-
type). It has been usually accepted that the collagen fibers of the duramater are
oriented longitudinally and that the bevel of a cutting needle should be oriented
vertically to reduce trauma to the dural fibers. This concept has been challenged
by Reina and collaborators (6). They found that dural fibers are arranged in
laminas with fibers in all different directions and not necessarily longitudinal.
They also showed that pencil point needles produce a more traumatic lesion in the
dura than cutting-point needles. They hypothesized that a more traumatic lesion
may stimulate more inflammation than a cleaner cut does. The inflammatory
response and edema would then limit the leakage of CSF. This observation agrees
with the surprisingly low incidence of PDPH after continuous spinal anesthesia
with an 18-gauge epidural needle and a 20-gauge epidural catheter. The catheter
might act as foreign object producing an inflammatory reaction. This low
incidence can also, at least in part, reflect the fact that continuous spinal are more
frequently performed in older patients. Older age is accompanied by a decreased
risk of PDPH.
In the issue 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%.

43 | P a g e
• 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.

3. Transient neurological symptoms (TNS)

Usually appears 12- 24 hrs after surgery and consist of mild to moderate pain or
sensory abnormalities in the lower back, buttocks or lower extremities. It resolves
between 6 hrs and 4 days. No patient with TNS has ever been reported to develop
neurological deficits or motor weakness. If present, other more serious diagnosis
must be ruled out: epidural hematoma, nerve root damage, cauda equine
syndrome. The first report appeared in the literature in 1993 when Schneider et al
published a series of 4 patients with buttocks pain after spinal.
Prospective, randomized studies have shown:

• A higher (but variable) incidence after lidocaine spinal. Decreasing the

concentration of lidocaine to 0.5% does not appear to change this
• Its incidence seems related to other factors like: lithotomy (30-36%), knee
arthroscopy (18-22%), whereas the risk after supine position appears to be
relatively low (5 to 8%).

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.
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.

44 | P a g e
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.

4. Cauda equina syndrome

It is a rare but devastating complication resulting in perineal anesthesia and
possible loss of bowel and bladder control. Most of the reported cases have been
associated with the use of continuous spinal with microcatheters (30-gauge and
smaller) along with use of 5% hyperbaric lidocaine. Low flow rates promoting
pooling of concentrated drug around the sacral roots have been postulated as the
reason for this condition. In 1992 the FDA issued a safety alert that resulted in the
withdrawal of these catheters from the US market.
The incidence of CES increases with increased concentration of local anesthetics
as well as the addition of vasoconstrictors. There have been reports of cauda
equina syndrome after epidural anesthesia.
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.

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.

45 | P a g e
Spinal anesthesia in the outpatient setting

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 of action 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 concentrates 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 and other anesthetics 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 (as opposed to epinephrine). 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.

4. Clonidine and neostigmine

They potentiate spinal local anesthetics and produce postoperative analgesia, but
they produce unacceptably high rates of hypotension and sedation (clonidine) and
protracted vomiting (neostigmine).

46 | P a g e

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.

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.

Characteristic of an epidural blockade

Epidural anesthesia produces a band of segmental anesthesia spreading cephalad
and caudad from the site of injection. Epidural anesthesia has a slower onset and usually
it is not as dense as spinal. This characteristic can be used as an advantage to obtain a
more pronounced differential blockade. Dilute concentrations can spare the motor fibers
while still able to produce sensory analgesia. This is commonly employed in labor
epidural analgesia.

Factors affecting the spread of local anesthetics in the epidural space

In general 1-2 mL of local anesthetic is needed per every segment to be blocked.
Thus, to achieve a T4 level from an L4-5 injection 12-24 mL of local anesthetic is
1. Dose and volume: The total dose and the volume affect the height of the block.
The effect of volume is linear but it plateaus at about 20 mL, after which there is
a greater loss through intervertebral foramina, especially in younger patients.
2. Age: As opposed to spinal, age is a major factor in the spread of epidural
anesthesia with smaller volumes producing a higher spread in older patients.
This may be due to the narrowing of the intervertebral foramina with age.
3. The site of injection influences the spread. Volumes as small as 6-8 mL of
solution injected at the thoracic level can produce anesthesia due to smaller
volume of the epidural space.
4. Body weight: heavier patients have smaller volume requirements.
5. Height: Plays a small role with taller patients requiring higher volumes.
6. Gravity: is not a very important factor, as sitting position does not appear to
enhance sacral spread.

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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

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 5 th 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.

Activating an epidural, Incremental dosing

After a negative test dose most of practitioners will inject incremental doses of 5
mL at a time. This technique helps decrease the risk of systemic toxicity in case of
catheter migration (intravascular or intrathecal).

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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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;
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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Regional Anesthesia in the anticoagulated patient

The American Society of Regional Anesthesia (ASRA) developed the 2nd

consensus statement on this topic in April 2002, which was published 2003. The
statement focuses on anticoagulation and neuraxial blocks (spinal and epidural). The
risk following plexus and peripheral techniques remains undefined.
Epidural hematoma is defined as a rare but potentially catastrophic complication
of spinal or epidural anesthesia. Although, it can happen spontaneously, its incidence
dramatically increased in the US after the introduction of low molecular weight heparin.
The following is a summary of pharmacological anticoagulation options for DVT
prophylaxis and treatment, as well as treatment for acute coronary syndromes, according
to the 2nd consensus statement:

Total hip or knee replacement, DVT prophylaxis

Unfractionated heparin: 3,500 U SC q8 hours, started 2h prior to surgery.

After surgery, dose adjusted to maintain the
aPTT within the upper normal range.

Low molecular weight heparin:

Ardeparin sodium (Normiflow®): 50 U/kg SC q 12h, started 12-24h after surgery
Dalteparin sodium (Fragmin®): 5,000 U SC qd, started 12h before surgery, or
2,500 U SC 7h after surgery,
then 5,000 U SC qd
Danaparoid sodium (Orgaran®): 750 U SC q 12h, started 2h before surgery
Enoxaparin sodium (Lovenox®): 30 mg SC q 12h, started 12-24h after surgery, or
40 mg SC qd, started 10-12h before surgery
Tinzaparin (Innohep®): 75U/kg SC qd, started 10-12h before surgery

Warfarin sodium: 5 m orally, started the night before, or

immediately after surgery.
Adjusted to prolong the INR = 2.0-3.0

General surgery, DVT prophylaxis

Unfractionated heparin: 5,000 U SC q8-12h, started 2h before surgery

Low molecular weight heparin:

Dalteparin sodium (Fragmin®): 2,500 U SC qd, stated 1-2h before surgery
Enoxaparin sodium (Lovenox®): 40 mg SC qd, started 2h before surgery

Acute Coronary Syndrome and DVT therapy

Enoxaparin sodium (Lovenox®): 1 mg/kg SC q12h, (outpatient DVT and non q-

wave MI)
1 mg/kg SC q12h, or 1.5 mg/kg SC qd (inpatient
treatment of DVT or PE)
Dalteparin sodium (Fragmin®): 120 U/kg q12h or 200 U/kg qd (non q-wave MI)
Tinzaparin (Innohep®): 175 U/kg qd

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The following is a summary of the 2002 ASRA guidelines adapted with
permission from Neal JM: Neural Blockade and Anticoagulation. In: Regional
Anesthesia, The Requisites in Anesthesiology. Rathmell J, Neal J, Viscomi C (eds).
Philadelphia, Elsevier Mosby, 2004

Anticoagulant ASRA guideline Catheter removal Evidence strength

LMWH Single preop dose: Delay Single daily dosing: Pharmacokinetic data
block 10-12 h. Remove 10-12 h Large series of case
Postop single daily dosing: after last dose; reports
Delay block 6-8 h. Wait ≥ 2 h before
Postop twice daily dosing: next dose
Delay block 24 h Twice daily dosing:
Remove ≥ 2 h before
first dose.
Standard heparin SQ 5,000 U/first dose: Delay Discontinue heparin Pharmacokinetic data
heparin for 1-2 h after block. for 2-4 h Prospective and
IV/first dose: Delay 1 h after Check aPTT prior to retrospective case
block. removal. surveys and case
IV/continuous: discontinue reports
2-4 h. Check aPTT prior to
Warfarin New dose: check INR if 1st If used for > 36 h, Case series and case
dose given >24 h before or if remove with INR reports
2nd dose given. <1.5
Chronic use: discontinue for
4-5 days. Check INR
Aspirin/NSAIDs/COX-2 No issues if patient is not No issues Retrospective case
inhibitors taking other anticoagulants surveys
Other antiplatelet agents Discontinue for: No recommendation Pharmacokinetic data
Ticlopidine (Ticlid): 14 days
Clopidogrel (Plavix): 7 days
Eptifibatide/tirofiban: 8 hrs
Abciximab: 48 hrs

Thrombolytics/ Avoid a block within 10 days No recommendation Surgical

Fibrinolytics of drug administration. recommendation
Avoid giving the drugs for 10
days after the block.
If block was received around
the time drug given, check
neurological status ≤ 2 h
Fondaparinux (Arixtra) Do not combine with No recommendation No data
neuraxial anesthesia
Herbal supplements No specific concerns No issues No data

I encourage you to read the 2002 consensus statement as published in Regional

Anesthesia and Pain Medicine in May-June 2003. Some highlights are:

1. Fibrinolytic and thrombolytic therapy: plasmin originates from plasminogen

and dissolves intravascular clots. Exogenous plasminogen activators, such as
streptokinase and urokinase dissolve thrombus and affect circulating
plasminogen. Endogenous t-PA formulations (alteplase and tenecteplase) are

52 | P a g e
more fibrin-selective and have less effect on plasminogen. While the plasma half-
life of thrombolytic drugs is only hours, it can take days for the thrombolytic
effect to resolve; fibrinogen and plasminogen are maximally depressed at 5 hours
after this therapy and remain significantly depressed at 27 hours.
Contraindications to thrombolytic therapy include surgery or puncture of non-
compressible vessels within 10 days.
• Patients on fibrinolytic and thrombolytic drugs should not receive spinal
or epidural procedures. Data are not available to recommend a precise
number of days. Ten days has been the usual recommendation.

2. Unfractionated heparin: the major anticoagulant effect of heparin is due to

binding with antithrombin (AT). This effect leads to inactivation of thrombin
(factor IIa), factor Xa, and factor IXa. Intravenous injection results in immediate
anticoagulant activity, whereas SC injection results in a 1 to 2 hour delay. The
anticoagulant effect of heparin is typically monitored with aPTT. Administration
of a small dose (5,000 U) SC heparin for prophylaxis of DVT generally does not
prolong the aPTT, and is typically not monitored. It can result in unpredictable
10-fold variability and therapeutic blood concentrations in some patients within 2
hours after administration.
Intraoperative systemic heparinization: usually IV injection of 5 to 10,000 U.
• Performance of neuraxial procedure at least 1 hour prior to administration
of heparin.
• Bloody or difficult placement may increase risk, but there are no data to
support mandatory cancellation of a case. Communication with the
surgeon plus risk-benefit decision about proceeding is warranted.
• Heparinization into the postoperative may be continued and the risk of
bleeding may be increased and so is the risk of spinal hematomas in the
presence of a catheter (increased risk at removal).
• Indwelling neuraxial catheters should be removed 2 to 4 hours after the
last heparin dose. Evaluation of the patient’s coagulation status should be
assessed before manipulation. Re heparinization should occur not before 1
hour after catheter removal
• Avoid neuraxial block in patients with other coagulopathies.
• Monitor the patient postoperatively for at least 12 hours

3. Complete anticoagulation during cardiopulmonary bypass: To date there are

no cases of spinal hematomas associated with cardiopulmonary bypass. A review
has recommended the following precautions:
• Avoid neuraxial blocks in patients with known coagulopathy of any cause
• Delay surgery for 24 hours in the event of a traumatic tap.
• Perform procedure at least 1 hour prior to systemic heparinization.
• Tightly control heparin doses and reversal doses to shortest duration compatible
with desired effect
• Remove epidural catheter when normal coagulation is restored

53 | P a g e
• Closely monitor patients postoperatively for signs and symptoms of spinal

4. Low-Dose SC heparin: commonly used for DVT prophylaxis in general and

urologic surgery. A dose of 5,000 U of heparin every 12 hours has been used
effectively. There is often no detectable change in aPTT. Small percentage of
patients (2-4%) may become therapeutically anticoagulated during SC heparin
therapy. There is extensive experience in the US and Europe without
complications. There are only 4 case reports of neuraxial hematomas in
concomitance to the use of SC heparin.
• Performance of neuraxial block before the injection of SC heparin may be
preferable, although
• There does not appear to be an increased risk of bleeding in the presence
of SC heparin. The risk may be increased in debilitated patients after
prolonged therapy.

5. Low molecular weight heparin (LMWH): The biochemical and

pharmacological properties of LMWH differ from those of unfractionated
heparin. Most relevant are: no measured effect on anti-Xa level, prolonged half-
life and non-reversibility with protamine. Since the introduction of LMWH in the
United States in 1993 over 40 spinal hematomas were reported in association with
its use over a 5-year period. This is in contrast with the European experience of
only 13 spinal hematomas reported over a decade of extensive use. It should be
noted that European dosing of LMWH is once daily, with the first dose
administered 10 to 12 hours preoperatively.
• On patients receiving preoperative LMWH needle placement should occur
at least 12 hr after last dose or 24 hr with higher doses
• Avoid neuraxial blocks in those patients receiving a dose of LMWH 2 hr
preoperatively because needle placement would occur at peak
anticoagulant activity.
• First dose of postoperative LMWH should be administered no earlier than
24 hr after the neuraxial procedure.
• Catheters should be removed prior to initiation of LMWH and first dose
administered 2 hr after catheter removal
• If patient has been receiving a single daily dose catheter can be safely
maintained. However it should be removed a minimum of 12 hr after the
last dose and the subsequent dose a minimum of 2 hr after catheter

6. Oral anticoagulants (warfarin): They interfere with the synthesis of vitamin K-

dependent clotting factors: II (thrombin), VII, IX, X. The effects of warfarin are
not apparent until a significant amount of biologically inactive factors are
accumulated and is dependent on factor half-life:
• Factor VII: 6 to 8 hr

54 | P a g e
• Factor IX: 24 hr
• Factor X: 25 to 60 hr
• Factor 2: 50 to 80 hr

Factor activity level of 40% for each factor is adequate for normal hemostasis.
The PT and INR are most sensitive to the activities of factors VII and X and are
relatively insensitive to factor II.
Because factor VII has a short half-life prolongation of PT and INR may occur in
24 to 36 hr. Prolongation of the INR (More than 1.2) occurs when factor VII is
down to 55% of baseline, while an INR of 1.5 is associated with factor VII
activity of 40%. Thus an INR of more than 1.5 should be associated with normal
Upon discontinuation of warfarin factor VII activity will rapidly increase and the
INR will decrease. However factor II and X recover much more slowly, thus
hemostasis may not be adequate even though the INR is 1.4 or less. Adequate
levels of all vitamin K-dependent factors are typically present when the INR is
less than 1.2.
In emergency situations the effect of warfarin can be reversed by vitamin K
injection and/or transfusion of fresh frozen plasma.

• Do not perform neuraxial blocks on patients who have been on chronic
warfarin therapy.
• Caution should be exercised when patients have had their warfarin
discontinued prior to surgery. Ideally 4 or 5 days should elapse and PT
and INR should be measured prior to any neuraxial block. Remember
that early after warfarin discontinuation the PT/INR reflects
predominantly factor VII levels while the rest of factors activity is still
inadequate. Wait until PT and INR are normal.
• Concurrent use of medications that affect other components of the clotting
mechanism may increase the risk of bleeding and do so without affecting
PT/INR (aspirin and other NSAIDs, ticlopidine and clopidogrel).
• Patients receiving one initial dose more than 24 hr prior to block should
have PT/INR checked before proceeding.
• As thromboprophylaxis with warfarin is initiated with a catheter in place
during low dose warfarin therapy, PT/INR should be checked daily and
before catheter removal. The INR prior to removal should be less than 1.5.
• Continue neurological exams at least 24 hr after removal.

7. Antiplatelets medications: include:

• NSAIDs (aspirin, ibuprofen, others)
• Thienopyridine derivatives like ticlopidine (Ticlid) and clopidogrel (Plavix)
• Platelet GP IIb/IIIa receptor antagonists (abciximab, eptifibatide and
- NSAIDs inhibit platelet cyclooxygenase (COX) and prevent the synthesis of
thromboxane A2. COX exists in 2 forms; COX-1 regulates constitutive

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mechanisms, while COX-2 mediates pain and inflammation (no effect on
platelets). Platelet function is affected for the life of the platelet following aspirin;
other nonsteroidals (naproxen, ibuprofen) have a short-term effect (3 days).
- COX-2 inhibitors like celecoxib (Celebrex) and rofecoxib (Vioxx) are anti-
inflammatory agents that affect COX-2 an enzyme not present in platelets, and
thus do not cause platelet dysfunction.
- The thienopyridine derivatives have antiplatelet effect from inhibition of
ADP-induced platelet aggregation. These agents are used in the prevention of
cerebrovascular thromboembolic events. Labeling recommends, “if a patient is to
undergo elective surgery, and an antiplatelet effect is not desired, clopidogrel
should be discontinued 7 days and ticlopidine 10-14 days prior to surgery.”
- Platelet GP IIb/IIIa receptor antagonists inhibit platelet aggregation by
interfering with platelet-fibrinogen and platelet-von Willebrand factor binding.
Time to normal platelet aggregation ranges from 8 hr (eptifibatide, tirofiban) to 24
to 48 hr (abciximab). Labeling precautions recommend that puncture of non-
compressible sites and “epidural” be avoided.
• Difficult to generalize because these drugs have different effects
• There is no accepted test to guide antiplatelet therapy.
• NSAIDs: their use alone does not seem to create a level of risk that will
interfere with the performance of neuroaxial blocks.
At this time there is no specific concern as to the timing of single-shot or
catheter techniques or the timing of catheter removal in conjunction with
• Thyenopyridine derivatives: risk unknown. Follow labeling precautions:
clopidogrel (Plavix) 7days and ticlopidine (Ticlid) 14 days.
• GP IIb/IIIa antagonists: risk unknown. Follow label precautions: 48 hr for
abciximab and 4-8 hr for eptifibatide and tirofiban
• The concurrent use of other medications affecting clotting may increase
the risk of bleeding complications.

8. Effect of herbal therapies on coagulation: The use of herbal medications is

widespread in surgical patients.
• Garlic: inhibits platelet aggregation in a dose dependent fashion. Its effect
appears to be irreversible and may potentiate the effect of other platelet
inhibitors. There is one case of epidural hematoma in an octogenarian that
was attributed to heavy garlic use.
• Ginkgo: Appears to inhibit platelet-activating factor (PAF). Four cases of
spontaneous intracranial bleeding have been associated with ginkgo use.
• Ginseng: inhibit platelet aggregation in vitro and prolongs Thrombin time
and activated partial thromboplastin time in rats. These findings need to be
confirmed in humans. On the other hand it was associated to a significant
decrease in warfarin anticoagulation in 1 reported case.
• Herbal drugs by themselves appear to represent no added significant risk
for spinal hematomas in neuraxial blocks.

56 | P a g e
• Mandatory discontinuation or cancellation of surgery is not supported by
available data.
• Concurrent use of other medications affecting clotting may increase the
risk of bleeding.
• No specific concern about timing of neuraxial catheter removal.

New Anticoagulants (Direct Thrombin Inhibitors and Fondaparinux), from ASRA

website (January 2006):

New antithrombotic drugs which target various steps in the hemostatic system, are
continually under development. The most extensively studied are antagonists of specific
platelet receptors and direct thrombin inhibitors. Many of these agents have prolonged
half-lives and are difficult to reverse without administration of blood components.

Thrombin inhibitors

Recombinant hirudin derivatives, including desirudin, lepirudin, and bivalirudin

inhibit both free and clot-bound thrombin. Argatroban, an L-arginine derivative, has a
similar mechanism of action. Although there are no case reports of spinal hematoma
related to neuraxial anesthesia among patients who have received a thrombin inhibitor,
spontaneous intracranial bleeding has been reported. Due to the lack of information
available, no statement regarding risk assessment and patient management can be made.
Identification of interventional cardiac and surgical risk factors associated with bleeding
following invasive procedures may be helpful.


Fondaparinux produces its antithrombotic effect through factor Xa inhibition. The

FDA released fondaparinux with a black box warning similar to that of the LMWHs and
heparinoids. The actual risk of spinal hematoma with fondaparinux is unknown.
Consensus statements are based on the sustained and irreversible antithrombotic effect,
early postoperative dosing, and the spinal hematoma reported during initial clinical trials.
Close monitoring of the surgical literature for risk factors associated with surgical
bleeding may be helpful in risk assessment and patient management. Until further clinical
experience is available, performance of neuraxial techniques should occur under
conditions utilized in clinical trials (single needle pass, atraumatic needle placement,
avoidance of indwelling neuraxial catheters). If this is not feasible, an alternate method of
prophylaxis should be considered.

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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

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Peripheral Nerve Blocks

A successful peripheral nerve block results from injecting an adequate volume of

an adequate concentration of local anesthetic in the proximity of the target nerve(s).
Intraneural injection (especially intrafascicular) is harmful to the nerve and can lead to
permanent damage. Therefore, a balance must be achieved between the need to get close
to a nerve and safety.

Bringing the needle close to the nerve(s)

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:

1. Purely anatomical: the practitioner bases his/her technique solely on anatomical

facts to bring the needle in proximity to the nerve. For example, the femoral pulse
can be used as a guidance to locate the femoral nerve. The trans-axillary
technique of brachial plexus block is another good example. Knowing that the
terminal branches of the brachial plexus surround the axillary artery in a very
predictable pattern can be used to block the terminal branches of the brachial
This anatomical method, practiced alone, has limited success, because it
does not take into account anatomical variations, lacks depth perception and can
not gauge proximity to a nerve with any degree of certainty. Therefore, the needle
might end up too far from the nerve (failed block) or too close to it (intraneural).

2. Paresthesia: this technique requires a combination of anatomical knowledge and

patient collaboration. The needle is brought to the point of physical contact with
the target nerve. The patient is instructed to acknowledge the electrical sensation
elicited (paresthesia). The location of the paresthesia, as referred by the patient,
helps the practitioner locate the position of the needle. At this time the needle is
withdrawn a few mm, before the injection is started, to decrease the risk of
intraneural injection.
For the longest time, Dr. Moore’s dictum “no paresthesia no anesthesia”,
was the “law of the land” in regional anesthesia. Works by Selander and others,
starting in the 1970s, have questioned the safety of this practice. Although, there
is not enough evidence to believe that paresthesias lead to nerve damage, there
seems to be enough circumstantial evidence to be cautious, especially if repeated
paresthesias are elicited.

3. Nerve stimulation: the idea of locating mixed nerves by electrical stimulation

was developed in Germany in the 1910’s by Perthes. However, it was not until
1962 when Greenblatt and Denson introduced a portable, transistorized nerve
stimulator that was suitable for the clinical setting.
The nerve stimulator is connected to a needle, usually insulated, that
delivers a current to its tip. The A alpha fibers (motor) are readily depolarized by
the small currents used, but not the sensory fibers. As the needle approaches a

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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. Since they do not necessarily rely on patient cooperation, they are
sometimes used in unconscious or heavily sedated patients. We do not encourage
this practice, as it can lead to complications that a conscious patient could perhaps
help prevent (e.g., intraneural injection). 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).

4. Ultrasound: It is the latest technological development available to the

practitioner of regional anesthesia and its potential is enormous. It is the only
method that provides real time assessment of the position of the needle with
respect to the nerve, as well as the surrounding structures. An added advantage is
that the practitioner is able to see the spread of the local anesthetic, giving him/her
the chance to more accurately predict the need for supplementation.
Ultrasound could theoretically produce warming of tissues or gas formation.
This technology is still expensive, and requires competency on interpretation of
cross-section anatomy from “grainy” images. However, it has been rapidly
progressing and it should be a matter of time before it becomes the method of

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). High
frequency waves are shorter and good for superficial structures. 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.
The ultrasound is delivered from a small probe that contains a transducer.
The transducer converts electrical signals into ultrasound waves. The transducer
detects the reflected waves and converts them back into electrical signals, which
are eventually the source of the image we see on the screen. Therefore, the
transducer delivers ultrasound for part of the time and for part of the time it
“listens” for the returned waves. Some of the wave sounds pass through tissues,

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while others get reflected back into the transducer. The distance is calculated as a
function of the time it takes for the wave to return. Tissues with high density like
bones, reflect most of the waves and produce a bright image. These tissues are
known as hyperechoic. The hypoechoic structures are soft tissue structures with
different degrees of echo.
The more perpendicular the probe is to the structure being searched, (e.g.,
nerve), the better the image obtained, because more bouncing sound waves can be
detected by the transducer. This is also true when trying to visualize the needle.
Changes as small as 10 degrees from the perpendicular, can distort the
echogenicity of a nerve, by reducing the amount of waves returning to the
The easiest way to identify a peripheral nerve is on a transverse scan, also
called “short axis view”. The needle, on the other hand, can be advanced with the
“out-of-plane” approach, crossing the ultrasound beam perpendicularly. The
needle becomes practically invisible as its cross section is one more of the
thousands of dots that form the ultrasound image. With the “in-plane” approach
the needle is advanced parallel to the probe. Depending on its depth and angle of
insertion the whole needle can be visualized. With either approach the needle is
aimed to the nerve surroundings.
Scanning superficial structures, like the brachial plexus, requires high
frequency probes (10-15 MHz) that provide good resolution, but limited
penetration (3-4 cm). For deeper structures like the brachial plexus in the
infraclavicular region or sciatic nerve in the buttocks, lower frequencies (4-7
MHz) are needed. Deep scanning of intra abdominal organs requires frequencies
of 3-5 MHz.

Insulated versus non insulated needles

Insulated needles (Teflon-coated) are the needles most commonly used in

conjunction with a nerve stimulator in the United States and Europe. They are also used
commonly for ultrasound-guided peripheral blocks. 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.

Short versus long-bevel 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

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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. In fact 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 are more severe.

Nerve injury

Persistent paresthesias can occur after regional anesthesia, although severe

neurologic injury is extremely rare. Neal estimates the incidence of persistent neuropathy
after regional anesthesia to be less than 0.4%.
A large survey by Auroy et al in France in 1997, involving 71,053 neuraxial
blocks and 21,278 peripheral nerve blocks, a low incidence (0.03%) of nerve
complications after regional anesthesia was confirmed. The survey showed that
neurological deficits were extremely low, but relatively more frequent after spinal (70%)
than epidural (18%) or peripheral nerve block (12%). In two third of the cases that
developed neuropathy after spinal, and 100% of the cases after epidural, a paresthesia
was elicited by the needle or during injection. Among the neurological deficits that
developed after non-traumatic spinals, 75% of them were in association with the use of
5% hyperbaric lidocaine.
Cheney et al in 1999 reviewed the American Society of Anesthesiologist closed-
claims database and found that out of 4,183 claims, 670 (16%) were considered
“anesthesia-related nerve injury. Injury to the ulnar nerve represented 28% of the total,
and in 85% of the cases it was associated to general anesthesia. Other nerve injuries were
brachial plexus in 20%, lumbosacral trunk in 16% and spinal cord 13% and they were
more related to regional anesthesia. In 31% of the brachial plexus injuries the patient had
experienced a paresthesia with the needle or after injection. They concluded that
prevention strategies are difficult because the mechanism for nerve injury, especially of
the ulnar nerve, is not apparent.
Lee et al in 2004 conducted a new review of the Closed Claims Data for the 1980
to 1999 period focusing in regional anesthesia. A total of 1,005 regional anesthesia-
related claims were reviewed. These claims were 37% obstetric related and 63% non-
obstetric. All regional anesthesia, obstetric claims were related to neuraxial
anesthesia/analgesia. In 21% of the non-obstetric claims peripheral nerve blocks were
involved. The most common block was axillary block (44%). Upper extremity blocks
were more involved in claims than lower extremity blocks. Nerve injury temporary or
permanent was claimed in 59% of the peripheral nerve injury claims. Death or brain
damage was usually the result of cardiac arrest associated with neuraxial block.
Pneumothorax accounted for 10% of the claims and “emotional distress” was claimed in
2% of the cases. Eye blocks accounted for 5% of the claims.
Regional anesthesia could result in nerve damage directly from a needle or
catheter or be the result of ischemia. Ischemia could be the potential result of
vasoconstrictor use or by an intraneural injection that produces a raise of the intraneural
pressure leading to nerve ischemia. Local anesthetic toxicity could play a role in cauda
equine and transient neurological symptoms. Another mechanism of nerve injury could
be hematoma and infection leading to scar formation.

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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

Epinephrine containing local anesthetic solutions may theoretically produce nerve

ischemia by vasoconstriction of the epineural and peri-neural blood vessels. Patients at
increased risk would be those with previous impaired microcirculation (e.g., diabetics).
There is no evidence at this time to suggest a detrimental effect of epinephrine in regional
anesthesia, as used in clinical practice. We use epinephrine 1:400,000 extensively, in all
kind of patients, and we appreciate its role in helping to diagnose an inadvertent
intravascular injection (please see discussion on epinephrine in local anesthetic chapter).

Persistent Paresthesia, Clinical presentation

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 symptoms can be mild, like
tingling and numbness that usually disappear within weeks to more rarely severe cases of
neuropathic pain and motor involvement that can last months and even years.

Pre-existing neurologic condition and regional anesthesia

A pre existing neurologic condition per se is not a contraindication to regional

anesthesia. However a careful preoperative assessment must be made, and any
neurological deficit must be documented in the patient’s chart. A thorough discussion
with the patient and the surgeon is always important.
Certain progressive neurologic conditions like multiple sclerosis, acute
poliomyelitis, amiotrophic lateral sclerosis, Guillian Barre syndrome are relative
contraindications to regional anesthesia, because the development of new symptoms
postoperatively may be confounded with a nerve block’s complication. In these cases the
risks and benefits must be carefully evaluated before proceeding with regional anesthesia.
There are other stable neurologic conditions like a preexisting peripheral
neuropathy, inactive lumbosacral radiculopathy and neurologic sequelae of stroke that
can be adequately managed with regional anesthesia, provided that all preexisting
neurological deficits are well documented in the chart.

Persistent paresthesia prevention and management

In order to minimize the risk of neurologic injury after regional anesthesia several
factors are important, including patient selection and type of surgeon. A meticulous nerve
block technique, avoiding direct trauma to the nerve and an appropriate selection of local

64 | P a g e
anesthetic concentration, is also 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 or hematoma or
infection. A neurological exam by a neurologist is also crucial.

Electrophysiological testing

Although electrophysiological studies remain normal for 14 to 21 days after the

injury, ordering them early will help to establish a baseline and rule out any preexisting
condition. These tests have limitations, as they only assess large motor and sensory fibers
and not small unmyelinated fibers. They usually include nerve conduction velocity
studies and electromyography and sometimes may include evoked potentials.

1. Sensory Nerve Conduction Studies

They assess functional integrity of sensory nerves by measuring amplitude and
velocity of peripheral nerve conduction. Injuries involving fascicular damage
primarily show a decrease in the amplitude of the action potential, a sign that the
impulses are being transmitted by a reduced amount of fibers. Conduction
velocity in these cases may be minimally affected. When the lesion is
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 muscle 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 traced back, according to Bailey, 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 the 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 use. Surgeons should be
made aware of 2-hour tourniquet time and tourniquet should be deflated at that time,

65 | P a g e
unless the surgeon is at a crucial time of the operation and requests more 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, has shown
minimal muscle damage under electron microscopy, with tourniquet times not exceeding
3 hours.
Some people advocate deflating the tourniquet at 1.5h for 5-15 minutes and then re
inflate it for an additional 1.5 h.

Tourniquet inflation pressure: It is believed that inflation pressure is even more

important a factor than time, in influencing injury. It is recommended to use the
minimum inflation pressure that accomplishes ischemia. In general 100 mmHg above the
systolic pressure is a common setting. Roekel and Thurston in 1985 showed that 200 mm
Hg for the upper extremity and 250 mm Hg for the lower extremity were adequate
parameters. Adding layers of padding is important. Wrinkles in the padding should be
avoided, since they may become pressure points.

Tourniquet associated problems: The exsanguination with an Esmarch bandage prior to

tourniquet inflation causes an increase in preload, which can be significant in cases of
bilateral lower extremity tourniquets. The elimination circulation in part of one extremity
also leads to an increase in afterload. This may cause problems in patients with cardiad
problems and decreased cardiac output. Exsanguination of lower extremities has also
been associated with pulmonary embolism and cardiovascular collapse.
Some patients may develop post-tourniquet nerve palsy, affecting more frequently larger
motor fibers than sensory fibers. These lesions are usually reversible. The magnitude of
the compression and the time of it dictate the severity of the injury.
Patients also can 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

Tourniquet pain: It is commonly observed despite signs of otherwise good anesthesia of

the extremity. Unpremedicated volunteers refer intolerable pain by 30 minutes. Signs of
tourniquet pain, manifested as a gradual rise in blood pressure, are also observed under
neuraxial blocks and general anesthesia. Patients report this pain under the tourniquet and
distal to it.
Controversy exists as to how this pain is transmitted. De Jong and Cullen in 1963
proposed that tourniquet pain was transmitted by small non-myelinated sympathetic
fibers. However tourniquet pain can arise even when high thoracic levels of anesthesia
are present.
It seems that tourniquet pain is transmitted, as other painful sensations, by A-delta
myelinated fibers and C unmyelinated fibers. Tourniquet pain is usually described as

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burning, cramping or heaviness. The burning and aching sensations, characteristics of
ischemia, are believed to be conducted by unmyelinated fibers (MacIver and Tanelian,
1992), while the sharp pain, usually a small component of tourniquet pain, is transmitted
by A-delta fibers. MacIver and Tanelian proposed that C fiber activation by ischemia-
induced alterations are responsible for tourniquet pain. They studied in an in-vitro model
the effects of ischemic alterations (i.e., hypoxia, hypoglycemia, lactic acid, and decreased
ph), on A-delta and C pain fibers. They showed that hypoxia and hypoglycemia induced
under ischemia, increased C fiber tonic action potential activity, but did not affect A-delta
fibers. Increased lactate and decreased pH did not alter the discharge frequency of C
fibers in this model. The activation of C fibers by ischemia products seems crucial in
tourniquet pain. Whether these C fibers eventually enter the spinal cord at a level above
the somatic nerve block is debatable.

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1. Mulroy MF: Complications of Regional Anesthesia, In: Mulroy MF, Regional

Anesthesia, 3rd edition. Philadelphia, Lippincott Williams & Wilkins, 2002, pp
2. Selander D, Dhuner KG, Lundborg G. Peripheral nerve injury due to injection
needles used for regional anesthesia. Acta Anaesth Scan 1977; 21: 182-188
3. Rice ASC, McMahon SB. Peripheral nerve injury caused by injection needles
used in regional anaesthesia: Influence of bevel configuration, studied in a rat
model. Br J Anaesth 1992; 69: 433-438
4. Selander D: Peripheral Nerve Injury After Regional Anesthesia, In: Finucane BT
(ed), Complications of Regional Anesthesia. New York, Churchill Livingstone,
1999, pp 105-115
5. Horlocker TT: Persistent paresthesia, In: Atlee JL (ed), Complications in
Anesthesia. Philadelphia, W.B. Saunders Company, 1999, pp 290-292
6. Auroy Y, Narchi P, Messiah A, et al. Serious complications related to regional
anesthesia. Results of a prospective survey in France. Anesthesiology 1997; 87:
7. Cheney FW, Domino KB, Caplan RA, et al. Nerve injury associated with
anesthesia: A closed claims analysis. Anesthesiology, 1999; 90: 1062-1069
8. Lee LA, Posner KL, Domino KB, et al. Injuries associated with regional
anesthesia in the 1980s and 1990s: A closed claims analysis. Anesthesiology,
2004; 101: 143-152
9. Morgan GE, Mikhail MS, Murray MJ: Clinical Anesthesiology, 4th edition. New
York, McGraw-Hill, 2006, pp324-358
10. Hebl JR: Peripheral Nerve Injury, In: Neal JM, Rathmell JP, Complications In
Regional Anesthesia and Pain Management. Philadelphia, Saunders Elsevier,
2007, pp 125-140
11. Hadzic A: Textbook of Regional Anesthesia and Acute Pain Management.
McgRaw-Hill, 2007
12. Sites BD: Introduction to Ultrasound-Guided Regional Anesthesia: Seeing Is
Believing, In: Schwartz AJ (ed), ASA Refresher Courses in Anesthesiology,
2006, pp 151-163
13. Bailey MK: Use of the Tourniquet in Orthopedic Surgery, In: Conroy JM,
Dorman H (eds), Anesthesia for Orthopedic Surgery. New York, Raven Press,
Ltd, 1994, pp 79-88
14. MacIver MB, Tanelian DL. Activation of C fibers by metabolic perturbations
associated with tourniquet ischemia. Anesthesiology 1992; 76: 617-623
15. Hamid B, Zuccherelli L: Nerve Injuries, In: Boezaart AP (ed), Anesthesia and
Orthopedic Surgery. New York, McGraw-Hill, 2006, pp 405-419
16. Darmanis S, Papanikolaou A, Pavlakis D. Fatal intra-operative pulmonary
embolism following application of an Esmarch bandage. Injury 2002; 33: 761-764
17. Lu CW, Chen YS, Wang MJ. Massive pulmonary embolism after application of
an Esmarch bandage. Anesth Analg 2004; 98: 1187-1189

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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

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Anatomy of the brachial plexus


The brachial plexus is most commonly formed by five roots originating from the
ventral divisions of spinal nerves C5 through T1. The roots of the plexus are located in
the cervical paravertebral space, between the anterior and middle scalene muscles.
Besides understanding its origins, it is also important to understand the plexus in terms of
the relative surface area occupied by its components at different levels of its trajectory.
As shown in figure 6.1 each root of the plexus emerges from an intervertebral foramen.
The C5 root appears between cervical vertebrae 4 and 5, while the T1 root emerges
between thoracic vertebrae 1 and 2.

Fig 6.1. Left supraclavicular

area, cadaver dissection. The
sternocleidomastoid and anterior
scalene muscles have been
removed. The subclavian artery
and the vertebral artery appear
painted in red. The suprascapular
nerve is the branch seen coming
off the upper trunk. The pleural
dome is painted blue.
(Own dissection).

The distance from C5 to T1 roots is large and irreducible, and it is equal to the
height of four vertebrae. This fact helps to explain why during an interscalene block,
usually performed at C5 or C6 level, dermatomes derived from C8-T1 are frequently
missed. C8-T1 roots are simply too far from the site of injection. Another important and
frequently ignored reason is the expansive, pulsatile effect of the subclavian artery over
the C8 and T1 roots, preventing the local anesthetic from reaching them.
When the five roots combine together to form three trunks, not only there is a
40% reduction in the number of nerve structures (from 5 to 3), but also the trunks become
physically contiguous. This is the point where the brachial plexus is reduced to its
smallest surface area. This area of high concentration of nerve structures helps to explain
the rapid onset and high success rate of the supraclavicular approach. This special
circumstance is only seen in the brachial plexus and has not parallel in the lower
extremity. The surface area of the plexus increases again when the trunks originate six
divisions and even further when the plexus ends up by giving off terminal branches in the

The scalene muscles

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 upper surface of the first

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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 the upper surface of the first rib,
behind the subclavian groove.

Brachial plexus structure: Trunks to terminal branches

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 (1-2 cm) 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. They carry 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
second intercostal nerve. This special arrangement is mandated by the narrow passage
between the clavicle and the first rib that the neurovascular bundle must negotiate before
getting into the axilla.
The brachial plexus enters the apex of the axilla lateral to the axillary artery,
which is the continuation of the subclavian artery. At this point the divisions rearrange
and mixed their fibers to form three cords, lateral, medial and posterior, named after their
relative position to the axillary artery. The cords travel caudally in close proximity to the
coracoid process, under the cover of the pectoralis minor muscle, which itself is covered
by the pectoralis major muscle. 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. Very often
the musculocutaneous nerve remains attached to the median nerve until reaching the
proximal arm.

Distribution of the branches of the brachial plexus

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-T1): 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

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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.

Medial antebrachial cutaneous nerve (T1): It is also a sensory nerve. It supplies the
medial side of the anterior forearm.

Musculocutaneous nerve (C5-C6-C7): gives motor innervation to the choracobrachialis,

biceps and brachialis muscles. At the elbow it becomes purely sensory innervating the
lateral anterior aspect of the forearm to the wrist.

• With the shoulder down the three trunks of the brachial plexus are located above
the clavicle, therefore during a supraclavicular block the needle should never
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.
• 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 a
supraclavicular block. To avoid this problem the injection needs to be performed
in the vicinity of the lower trunk, demonstrated by fingers twitch with a nerve
stimulator or by injecting behind the subclavian artery when using ultrasound).
• 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.
• The brachial plexus crosses the clavicle at or near its midpoint. Because of the
direction of the brachial plexus from medial to lateral as it descends, the higher in
the supraclavicular area the more medial (closer to the SCM) the plexus is

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Its main indication is anesthesia of the shoulder, lateral part of the clavicle and
proximal part of the humerus.

Point of contact of the needle with the brachial plexus

The needle approaches the plexus at the level of the roots, high in the interscalene
groove, approximately at the level of C5-C6 roots (most likely C5).

Main characteristics
This block is superficial and usually easy to perform. Characteristically it misses
the C8-T1 dermatome, which includes ulnar nerve, medial antebrachial cutaneous nerve
and medial brachial cutaneous nerve.

Patient position and landmarks

The patient is lightly sedated. Older, obese and recent trauma patients can be
expected to be extremely sensitive to the depressant effects of benzodiazepines and/or
narcotics. Titrate to effect.
The patient lies supine or on a 30-degree upright position. The ipsilateral shoulder
is down and the head is turned slightly to the opposite side. The posterior (lateral) border
of the sternocleidomastoid (SCM) muscle is identified as well as the upper border of the
cricoid cartilage, as shown in figure 6-2.

Fig 6-2. Cricoid cartilage.

The superior border of the
cricoid cartilage at the level
of the cricothyroid membrane
is marked on the skin. (On a
model with permission).

A horizontal line is drawn from the cricothyroid membrane laterally to intersect

the posterior border of the SCM. 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 6-3. This maneuver brings the palpating fingers behind 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.

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Fig 6-3. Finding the interscalene
groove. The interscalene groove
is found behind the SCM at the
horizontal level of the cricoid
(On a model with permission).

Nerve stimulator technique

The nerve stimulator is set to deliver a current of 0.8-0.9 mA, at a pulse frequency
of 1 Hz and a pulse width of 0.1 ms (100 microsec). A small skin wheal is raised with 1%
lidocaine or 1% mepivacaine using a small gauge needle (ideally 27).
A 2” (5 cm) or 1” (2.5 cm), 22-gauge, short bevel, insulated needle can be used.
The needle is introduced between the two palpating fingers in a medial direction that also
has a small (20 to 30-degree) posterior and caudal inclination, as shown in figure 6-4.

Fig 6-4. Needle insertion. The

needle is advanced medial,
posterior and caudal.
(On a model with permission).

A needle directed just medial has a bigger chance to enter the intervertebral
foramen and produce intravascular injection (vertebral artery) or penetrate the
subarachnoid and epidural spaces. This is a superficial block that should take place not
deeper than the projection of the clavicular head of the SCM. With that in mind further
penetration putting in risk the neuraxis are discouraged.
Any distal motor twitch as well as biceps, triceps or deltoid muscles are adequate.
A twitch of the abdomen signals phrenic nerve stimulation and it is evidence that the
needle is anterior to the anterior scalene. The needle should be withdrawn and redirected
posteriorly. A motor twitch of the trapezius muscle indicates stimulation of the spinal
accessory nerve and signals that the position of the needle is posterior to the brachial
plexus and needs to be repositioned anteriorly.
The injection of the local anesthesia is started slowly with frequent aspirations.
There is some confusion as to whether a shoulder twitch is acceptable. Anatomical and

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clinical evidence support accepting any twitches other than trapezius (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).

Ultrasound technique
The area is best visualized by placing the probe obliquely across the anterior and
middle scalene muscles at the level of C5-C6. The SCM is identified as well as the great
vessels (common carotid and internal jugular). The internal jugular vein is easily
collapsible by the probe, which helps with its identification. Behind and somewhat lateral
to the SCM the anterior and middle scalene are usually easily visualized and the roots of
the plexus appear in between them with a characteristic honeycomb appearance. The
needle is advanced in plane with the probe, from lateral to medial, with a slight posterior
and caudal deviation, similar to Winnie’s approach. The needle is brought under direct
visualization into the proximity of C6 root. The spread of local anesthetic should show
the interscalene space expanding.

Local anesthetic and volume

For single shot techniques in adults, 30 mL of 1.5% mepivacaine plain provides
2-3 h of anesthesia. The addition of 1:400,000 epinephrine prolongs the anesthesia to
about 3-4 h. The residual analgesia post anesthesia is variable in duration, although rarely
persists for more than 2 h after block resolution. Ropivacaine 0.5% - 0.75% can be used
in the same volume to provide 5-7 h of anesthesia. The addition of lyophilized tetracaine
to 1.5% mepivacaine, for a final concentration of 0.2% tetracaine, accomplishes similar
extended duration with shorter onset, although the onset is longer than for mepivacaine
Also 20-30 mL of 0.2% ropivacaine can be used to provide postoperative
analgesia for surgery performed under general anesthesia.

Side effects and complications

Systemic local anesthetic reaction can occur as with any block. More specific
(and frequent) side effects related to interscalene block are: Horner’s syndrome (ptosis,
miosis and anhydrosis) due to stellate ganglion block and hoarseness due to recurrent
laryngeal nerve involvement. Characteristically this block produces 100% of phrenic
nerve block with diaphragmatic paralysis (Urmey W. et al. One hundred percent
incidence of hemidiaphragmatic paresis associated with interscalene brachial plexus
anesthesia as diagnosed by ultrasonography. Anesth Analg 1991; 72: 498-503). 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. Rough
movements by the surgeon could scare the patient.

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• It must be remembered that most of these procedures are performed in positions
other than supine (e.g., beach chair, prone, lateral), therefore management of the
airway is a concern.
• Language barrier between patient and anesthesiologist is also a relative
contraindication for interscalene block as the sole anesthetic.
• This is a very superficial block. Care should be taken not to introduce the needle
more than 2 cm beyond the projection of the midpoint of the SCM muscle.

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This block is ideally suited for any surgery on the upper extremity that does not
involve the shoulder.

Point of contact of the needle with the brachial plexus

The needle approaches the plexus at the level of the trunks, and ideally the
injection should take place in the vicinity of the lower trunk.

Main characteristics
This block is considered more difficult to learn than other upper extremity blocks
and historically 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 and high success
rates. This is due to the compact arrangement of the plexus at this level. The location of
such large amount of innervation in such reduced area does not have a parallel in the
lower extremity, or anywhere else for that matter, qualifying the supraclavicular block as
the most successful plexus block in the whole body. Indeed it has been called the “spinal
of the upper extremity”.
Because of pneumothorax reports, the supraclavicular block started to lose its
appeal and by the 1960’s the axillary block started to become popular. A rational
approach should have dealt with the pneumothorax issue by finding reliable superficial
landmarks for the dome of the pleura. An anatomical approach that starts by determining
the pleura boundaries is the technique we perform and the reason for its safety and
reliability. This allows us to take advantage of such extraordinary block while limiting its
potential drawbacks. Our experience to late 2007 includes more than 3,500
supraclavicular techniques without any pneumothorax ever being demonstrated. A
common question posed to us is whether we perform routine chest X-rays after a
supraclavicular block. The fact is that we only do an X-ray when the clinical situation
calls for it (e.g., an unusually difficult technique). The literature predominantly shows
that when a pneumothorax has been found following a supraclavicular block, it has been
after the patient developed clinical symptoms and not during routine chest x-ray post
block. So our practice of performing selective chest X-rays, as needed, is comparable to
the common practice in the rest of the country.

Some history of the supraclavicular technique

The supraclavicular block was introduced into clinical practice in Germany by
Kulenkampff in 1911. A publication of his technique appeared later in the English
literature in 1928. Kulenkampff accurately described the plexus as being more compacted
in the neighborhood of the subclavian artery, where he rightly believed that a single
injection could provide adequate anesthesia of the entire upper extremity. Kulenkampff’s
technique was simple and in many ways sound. Unfortunately his recommendation to
introduce the needle toward the first rib, in the direction of the spinous process of T2 or
T3, carried an inherited risk for pneumothorax.

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Albeit with several modifications, the supraclavicular block remained a popular
choice until the early 1960’s. Eventually, the combined effect of pneumothorax risk 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 regional
anesthesia techniques ever described.
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. The 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 carried a paper by Brand and
Papper out of New York, comparing axillary and supraclavicular techniques. This article
is the source of the 6.1% pneumothorax rate frequently quoted for supraclavicular block.
In retrospect these two articles could be considered the point at which the tide definitely
turned against the supraclavicular block making the axillary route the most common
approach to the brachial plexus in the United States and the rest of the world. With some
exceptions this is still true today.
Some authors also cite the perceived complexity of supraclavicular block as the
reason for not performing it more often. However the advantages of a supraclavicular
technique, namely its rapid onset, density, high success rate along with large area of
anesthesia are too good to ignore. 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.
Ultrasound has produced a resurgence in the interest to perform supraclavicular blocks
once again.

Patient position and landmarks

The patient lies supine with the head of the bed elevated 30 degrees (fig 6.5). The
ipsilateral shoulder is down and the head is turned to the opposite side. The arm to be
blocked is flexed at the elbow and, if possible, the wrist is supinated to easily detect a
twitch of the fingers. We use the same position for ultrasound-guided technique.

Fig 6-5. Patient position. The patient

lies supine with the head of the bed
elevated 30 degrees. The head of the
patient is turned, the shoulder is down
and the arm is flexed at the elbow and
supinated at the wrist.
(On a model with permission).

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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 6-6. A parasagital (parallel to the midline) plane that
crosses this point determines an “unsafe” zone medial to it, where the risk of
pneumothorax is high and a lateral zone that is safer.

Fig 6-6. Lateral head of SCM. The

lateral (clavicular) head of the SCM at
its junction with the clavicle is marked
with an arrow. Medial to this plane the
risk of pneumothorax increases.
(On a model with permission).

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 clavicular
head to be away from the pleura, and close enough to this point to still reach the trunks,
before they disappear behind the clavicle. 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 6-7.

Fig 6-7. Safety margin

A safety margin of 1” lateral to the
lateral insertion of the SCM is marked
over the clavicle.
(On a model with permission).

This is only an orientation point because the actual point of needle entrance is
determined by palpation of the most lateral elements of the plexus in the supraclavicular
area around the orientation point. At this level the brachial plexus is usually easily
palpable, either as a groove or some type of cord. This is usually called “interscalene
groove”, but the interscalene groove only exists high in the C5-C6 level.
The palpating finger is placed parallel to the clavicle and the point of needle
entrance is marked with a downward pointing arrow, as shown in figure 6-8 (upper lateral
arrow). Over the clavicle an upward pointing arrow is also drawn, as shown in figure 6-8
(lower lateral arrow). Both arrows together show the direction of the needle, parallel to

80 | P a g e
the midline. The lower lateral arrow also marks the caudal limit for penetration of the
needle (as far caudal as we are willing to go), keeping it supraclavicular and away from
the first intercostal space.

Fig 6-8. Orientation arrows.

The medial arrow (pointing up) shows
the most lateral boundary of the pleura.
The upper lateral arrow shows the
needle entrance point, the lower lateral
arrow indicates the caudal limit for
needle penetration. The two opposing
lateral arrows (one up, one down) show
the needle trajectory (parallel to the
midline of the patient).
(On a model with permission).

Nerve stimulator technique

The needle is inserted first anteroposterior (toward the table) with a 30 degree
caudal orientation as shown in figure 6-9, for a distance of a few mm up to 1.5 cm,
depending on the amount of subcutaneous tissue. Usually a twitch of the upper trunk
(shoulder) is found as evidence that the needle is approaching the plane of the plexus.

Fig 6-9. Direction of the needle

The needle is first introduced
almost perpendicular to the skin.
(On a model with permission).

The direction of the needle is then changed from anteroposterior to caudal, to be

advanced parallel to the midline (and parallel to the most lateral pleural boundary), as
shown in figure 6-10.

Fig 6-10. Direction of the needle

And then advanced caudal, parallel
to the midline
(On a model with permission).

81 | P a g e
The reference to the midline is easy to ascertain and avoids the use of other
landmarks (e.g., nipple), which have enormous patient-to-patient location variability.
The needle is advanced caudally with a slight posterior angle. Because the trunks
are physically contiguous a twitch of the upper trunk (shoulder) is followed by middle
trunk (pectoralis, triceps, supination, pronation) and finally lower trunk (wrist and
fingers). The goal of the technique is to stimulate the fingers. Wrist flexion and extension
are acceptable responses, but supination or pronation or other more proximal twitches are
If advancing the needle, after finding a proximal trunk, makes the twitch
disappear it means that the angle of the needle is not matching the orientation of the
trunks, and that the tip of the needle is wandering away from the trunks. The needle is
slowly withdrawn until the original twitch is once again visible, 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 is reassessed starting with the
nerve stimulator and its connections. As long as a twitch from the brachial plexus is being
elicited the needle can be safely advanced caudally without regard to depth.

Ultrasound technique
We also use the semi sitting position. A linear, high frequency probe, as for the
interscalene block, is used. We usually start scanning high in the neck at above C6 to
identify SCM, scalene muscles and great vessels. The probe is then advanced caudally
and placed just above the clavicle and almost parallel to it. The angle (tilting) is adjusted
to get a good cross section of the subclavian artery and the scalene muscles. The plexus,
either trunks or divisions, are visualized behind and proximal to the artery in a
characteristic honeycomb arrangement.
The needle is directed in plane from lateral to medial under the probe. The needle
should be inserted at 1-2 cm away from the probe to avoid a steep angle of insertion that
would make its visualization harder. The needle is directed toward the lower trunk,
behind the subclavian artery. The anesthetic solution should be seen surrounding the

Local anesthetic and volume

For single shot techniques in adults, 30 mL to 40 mL of 1.5% mepivacaine plain
will provide 2-3 h of anesthesia. The addition of 1:400,000 epinephrine prolongs the
anesthesia to about 3-4 h. The residual analgesia post anesthesia is variable in duration,
although it rarely persists for more than 2 h after block resolution. Ropivacaine
0.5%-0.75% can be used in the same volume to provide 4-7 h of anesthesia. The addition
of lyophilized tetracaine to 1.5% mepivacaine, for a final concentration of 0.2%
tetracaine, accomplishes similar extended duration with shorter onset, although the onset
is longer than for mepivacaine alone.
Also 20-30 mL of 0.2% ropivacaine can be used to provide postoperative
analgesia for surgery performed under general anesthesia.

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Besides the common complications accompanying any block, the supraclavicular
technique can also be followed by Horner’s syndrome, hoarseness and phrenic nerve
palsy, but less frequently than after interscalene block. Neal et al in 1998 studied
diaphragmatic paralysis in 8 volunteers after supraclavicular block using ultrasound
(replicating what Urmey et al did in 1991 to demonstrate 100% of diaphragmatic
paralysis after interscalene block). They found an incidence of 50% of diaphragmatic
paralysis. No subject experienced changes in pulmonary function tests (PFT) values or
subjective symptoms of respiratory difficulty. This is our experience too.

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.
• 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 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.

83 | P a g e
This block is more suited for surgery distal to the elbow.

Point of contact of the needle with the brachial plexus

The needle approaches the plexus at the level of the cords in the proximity of the
terminal branches.

Main characteristics
The infraclavicular block is really an axillary block in which the needle enters the
axilla through its anterior wall (pectoralis muscles), instead of through its base. This fact
is usually unrecognized and infraclavicular block is presented as a block completely
different than axillary. It is a good place to place a catheter since it is less mobile than
neck and axilla. It also hurts more because is a deep block that requires the needle to go
through muscle. Patients should be adequately sedated.
It is widely recommended to obtain a distal twitch in the hand or wrist and to
avoid a biceps twitch (musculocutaneous nerve or lateral cord) or pronation of the
forearm (lateral cord). This is based on clinical experience. A bicepts twitch could be the
result of musculocutaneous nerve stimulation, outside the sheath, or from lateral cord
stimulation inside the sheath, and as such it is unreliable. It is theoretically possible 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
subjected to more pressure from surrounding structures, although it is more difficult to
get to it. Ultrasound, with visualization of the axillary artery, makes the injection
posterior to it easy.
Many 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.

Patient position and landmarks

The patient lies supine with the ipsilateral shoulder down. The coracoid process is
found by palpation and marked on the skin. The coracoids can be found at around 2 cm
below the clavicle, at the level of the deltopectoral sulcus (junction between the middle
third with the lateral third of the clavicle). A C-arm can be useful if available. The point
of needle entrance is marked 2 cm caudal and 2 cm medial to the coracoid process as
shown in fig 6-11.

Fig 6-11. Needle entrance point.

Two cm caudal and two cm
medial from the coracoid process.
(On a model with permission).

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Nerve stimulator technique
The nerve stimulator is set to deliver a current of 0.9-1.0 mA at a frequency of 1
Hz and 0.1 ms of pulse duration. It is frequently necessary to use a 4” (10 cm) needle to
be able to reach the plexus.
The needle attached to the nerve stimulator is advanced in the anteroposterior
direction, perpendicular to the skin, as shown in figure 6-12.

Fig 6-12. Direction of the needle

The needle is introduced
perpendicular to the skin.
(On a model with permission).

Before entering in contact with the plexus the needle passes through the 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 time) or cephalad, but maintaining the same parasagital plane without
medial or lateral deviation.

Ultrasound technique
Because the brachial plexus at this level is deep, being located under pectoralis
major and minor muscles, a lower frequency linear probe is usually used, in the range of
4-7 MHz. The probe is aligned almost perpendicular to the junction between the middle
and lateral thirds of the clavicle in the proximity of the coracoid process. This way a
cross section of the plexus and axillary vessels is obtained. The tilt is adjusted until a
clear view in cross section is obtained. The needle can be advanced in plane with the
probe from proximal to distal or vice versa. The best target, if a single injection is
desired, is the posterior cord behind the artery. Separate injections of the cords can be
done as needed.

Local anesthetic and volume

This block requires a higher volume for better results, although ultrasound
techniques do not. Usually 40 mL of 1.5% plain mepivacaine will provide 2-3 h of
anesthesia. The addition of 1:400,000 epinephrine prolongs the anesthesia to about 3-4 h.
The residual analgesia post anesthesia is variable in duration although rarely persists for
more than 2 h after block resolution. Ropivacaine 0.5% can be used in the same volume
to provide 4-6 h of anesthesia. The addition of lyophilized tetracaine to 1.5%
mepivacaine, for a final concentration of 0.2% tetracaine, accomplishes similar extended
duration with shorter onset, although the onset is longer than for mepivacaine alone.
Also 30 to 40 mL of 0.2% ropivacaine can be used to provide postoperative
analgesia for surgery performed under general anesthesia.

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Pneumothorax can occur due to injury of the pleura through an intercostal space.
Muscle pain and hematomas, which can be large in size, are not uncommon.

Clinical pearls

• This is a good place to put a catheter because it is easier to fix it.

• Use adequate sedation, as this block is more uncomfortable for patients.
• The block should not be attempted medial to the junction between the lateral third
and middle third of the clavicle, because of increased risk of pneumothorax.

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It is best suited for surgery distal to the elbow.

Point of contact of the needle with the brachial plexus

The needle approaches the plexus at the level of its terminal branches.

Main characteristics
The axillary block is not properly a plexus block, but rather a block of the
terminal branches of the brachial plexus. The distance between the different branches
plus the expanding wave of the axillary artery pulse are obstacles that the local anesthetic
must overcome to adequately reach the nerves. A single injection technique is an option,
but a second and even a third injection has shown to increase the success rate. If a single
injection is to be attempted, the epicenter of the injection if possible, has to coincide with
the specific nerve responsible for the sensory innervation of the surgical area. For
example, to deal with an extensor tendon injury of the thumb (radial nerve) the injection
should occur around the radial nerve. The same is true for lesions located in the ulnar and
median territories. If the surgical area involves more than one terminal nerve, the single
injection technique should be performed in the proximity of the radial level, because I
believe the solution diffuses more easily from back to front that vice versa. This may be
because of more resistance in the back of the plexus (muscles and scapula) than in front
(subcutaneous tissue). The anatomy lab also shows that better diffusion could be obtained
by placing a pillow under the elbow with the shoulder abducted slightly less than 90
A point usually stressed in the literature is to perform the block as proximal in the
axilla as possible. 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 plexus. This is never certain. A
better strategy is to block this nerve first before performing the block of the rest of
terminal branches.
Although some variability exists, usually the median nerve is superficial (anterior)
to the artery following its same direction, the ulnar nerve (and medial
brachial/antebrachial cutaneous) 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.

Patient position and landmarks

I do not like the transarterial technique so we will only discuss nerve stimulator
and ultrasound techniques. The patient is supine, the arm is abducted to about 80 degrees
and the elbow is elevated 30 degrees by using a small pillow or folded blanket.
The biceps muscle is identified by visualization and/or palpation, under which a
cord like structure signals the presence of the coracobrachialis muscle. Immediately
posterior to it the pulse of the axillary artery can be found. A marker is used to identify
the proximal trajectory of the artery in the upper arm/axilla junction, as shown in figure

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Fig 6-13. The arm is abducted
about 80°, the elbow is elevated
slightly with a small pillow and
the axillary artery is marked.
(On a model with permission).

Nerve stimulator technique

A 2’, 22-gauge insulated needle usually suffices. The block of the
musculocutaneous nerve is accomplished first. 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 into the substance of the choracobrachialis
muscle as shown in fig 6-14.

Fig 6-14. Blocking the

musculocutaneous nerve.
The needle is introduced under the biceps
perpendicular to the main axis of the arm.
(On a model with permission).

At some point under the biceps a motor twitch of the elbow in flexion is elicited.
The current is reduced to 0.5 mA and 5 mL of local anesthetic solution is slowly given.
The needle is then withdrawn and the nerve stimulator is set again to 0.8-0.9 mA. Using
the mark of the axillary artery on the skin as a reference, the needle is directed either
tangential to it (median), medial to it (ulnar and medial brachial/antebrachial) or posterior
to it (radial), as shown in figure 6-15.

Fig 6-15. The needle is introduced

in reference to the axillary artery
using the mark on the skin without
the need to feel for the pulse again.
(On a model with permission).

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Ultrasound technique
The brachial plexus once again is superficial here so a linear, high frequency
(10-15 MHz) probe is used. The arm is abducted and a pillow is placed under the elbow,
as described for the nerve stimulator technique. The probe is placed across the
neurovascular bundle to get a cross section image of it. The median nerve is usually seen
superficial (anterior) to the artery. The ulnar nerve is medial and somewhat posterior, the
radial nerve is posterior. 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 seen entering the coracobrachialis muscle. 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.

Local anesthetic and volume

The terminal nerves in the axilla are more separated than at more proximal
locations. The terminal branches of the plexus are enclosed in a fibrous sheath which is
filled with loose connective tissue without any defined organization or septa, as we have
recently demonstrated (Franco et al. Gross anatomy of the brachial plexus sheath in
human cadavers. Reg Anesth Pain Med, 2008; 33: 64-69). This connective tissue in itself
is an obstacle to the free diffusion of local anesthetic within the sheath. Planes of
cleavage surrounding nerves and vessels help promote longitudinal spread of local
anesthetics as opposed to circumferential spread. For these reasons an axillary block
should be performed using a higher anesthetic volume than at other more proximal
locations, 50 mL injected slowly using the usual precautions is the volume most used. A
multi injection technique is a justifiable alternative. Ultrasound techniques help to
decrease the total volume of local anesthetic used.

Pneumothorax is virtually impossible to get from this location. Hematomas from
vascular puncture are more common and can be associated with nerve damage.

• This is a block mainly indicted 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 whole arm.
• The main injection should aim for the nerve most responsible for the sensory
innervation of the surgical site.

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1. Brown DL. Brachial plexus anesthesia: an analysis of options. Yale J Biol Med
1993; 66: 415-431
2. Franco CD, Vieira Z. 1,001 subclavian perivascular brachial plexus blocks:
success with a nerve stimulator. Reg Anesth Pain Med 2000; 25: 41-46
3. Franco CD. The subclavian perivascular block. Tech Reg Anesth Pain Med 1999;
3: 212-216
4. 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
5. Greenblatt Gm, Denson GS. Needle nerve stimulator-locator: nerve blocks with a
new instrument for locating nerves. Anesth Analg 1962; 41: 599-602
6. 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
7. Brown DL. Atlas of regional anesthesia. Philadelphia, PA: W.B. Saunders, 1992
8. Mulroy MF. Regional anesthesia: An illustrated procedural guide. 3rd edition.
Philadelphia, PA; Lippincott Williams & Wilkins 2002
9. 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
10. Neal JM, Hebl JR, Gerancher JC, Hogan QH. Brachial plexus anesthesia:
Essentials of our current understanding. Reg Anesth Pain Med 2002; 27: 402-428
11. Perlas A, Chan V: Ultrasound-assisted nerve blocks. In: Textbook of Regional
Anesthesia, Hadzic A (ed). New York, McGraw Hill, 2007, pp 663-672
12. Franco CD, et al. Gross anatomy of the brachial plexus sheath in human cadavers.
Reg Anesth Pain Med 2008; 33: 64-69

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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, and they never get to be confined to a small
surface area like the trunks of the brachial plexus do. Therefore, no single peripheral
block technique is able to provide anesthesia of the whole lower extremity. This,
combined with the high success of neuraxial anesthesia, has contributed to make lower
extremity peripheral nerve blocks less popular than the techniques of the upper extremity.
The introduction of low molecular weight heparin, with its increased risk for
epidural hematoma in association with neuraxial blocks, has produced a renewed interest
in lower extremity nerve blocks.

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. 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 the psoas and the iliacus muscle. As it passes under the inguinal
ligament the nerve is superficial to the iliopsoas muscle. 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 anteromedial 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.
At it passes under the inguinal ligament the femoral nerve has the femoral artery medial
to it, followed by the femoral vein medial to the artery (VAN from medial to lateral). The
nerve is covered by the iliac fascia, which separates it from the main vessels, and more
superficially by the deep fascia of the thigh (fascia lata).
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 the pelvis is located on the
medial side of the psoas muscle. It runs along the lateral pelvis until it reaches the
obturator foramen, through which it enters the thigh. In the thigh the nerve divides into
anterior and posterior branches. The anterior division runs caudally, in front of the
obturator externus and the adductor brevis and behind the pectineus and adductor longus.
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

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the skin of the medial side of the thigh. The posterior division pierces the obturator
externus and passes downwards, behind the adductor brevis and in front of the adductor
magnus. 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 sensory branch of the obturator nerve has
contributed to the confusion about how much can be obtained from a single block
performed at the femoral level (“3-in-1” block).

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. These two components can be easily identified as
two separate nerves in about 11% of the cases However, even in those cases the two
components are surrounded by a common sheath. Therefore, this should not be confused
with a true “early” division of the nerve. The real separation of the two components of
the nerve, takes place always in the popliteal fossa.
The nerve comes out of the pelvis through the greater sciatic foramen, entering
the gluteal region anterior to the piriformis muscle and cephalad to the ischial tuberosity.
After reaching the lateral aspect of this bony prominence, the nerve turns vertically
downwards to run between the ischium medially and the greater trochanter laterally, as
shown in figure 7.1.
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 (see references 5 and 10).

Fig 7-1. The sciatic nerve (1)

travel parallel to the midline (5).
Piriformis muscle (2), ischium (3)
and greater trochanter (4) are also
shown. (Own dissection).

The nerve enters the thigh deep to the biceps femoris muscle. In the thigh, the
position of the nerve 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.

Subgluteal fold
The fold that defines the buttocks inferiorly is a fold of the skin. It 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 (see figure 7-2). 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.
Anesthesia of the posterior cutaneous nerve of the thigh is not reliable at this level,
because this nerve usually is already superficial (above the fascia) at the subgluteal fold.

Fig 7-2. The inferior border of the

gluteus maximus and subgluteal
fold are two different things. They
cross each other diagonally.
(Own dissection).

Genitofemoral nerve
It derives from the ventral rami of spinal nerves L1-L2. It provides some of the
innervation of the genital area, part of the medial upper thigh and the skin over the
femoral vessels.

Posterior cutaneous nerve of the thigh

Also known as posterior femoral cutaneous nerve. It is not a branch of the sciatic
nerve, although it has a close relationship with it in the gluteal area, before it becomes a
superficial nerve. It originates from the ventral rami of spinal nerves S1-S3. It exits the
pelvis through the greater sciatic foramen, first medial and then superficial (posterior in
anatomic position) to the sciatic nerve. Somewhere caudal to the ischium, the nerve
pierces the deep fascia (fascia lata) and becomes a superficial structure. It innervates the
lower part of the buttocks as well as the posterior thigh, frequently reaching down as far
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.

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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, 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. At a variable point caudal to the knee joint, it pierces the deep fascia to become
superficial. Below 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, before terminating around the base of the first metatarsal.

Male and female pelvis issue

The pelvis of the female is adapted to accommodate child bearing and as a result
the female inner pelvis is wider than males. However, the total width of the bony pelvis,
that is the diameter between both iliac crests (bicrestal diameter), is similar in both sexes,
measuring an average of 280 mm in males and 275 mm in females (Cunningham’s
Anatomy). The thicker bones in the male pelvis compensate for a “roomier” female
pelvis (Hollinshead’s Anatomy). According to some anthropologists (3) the human bony
pelvis is “surprisingly” similar in males and females at all ages. The difference in pelvis
size corresponds to hormone-dependent, different patterns of fat deposition in both sexes.
In other words the difference in pelvic size among the sexes is mostly due to soft tissue
and not bony pelvis. The bony pelvis determines the position of the sciatic nerve in the

Clinical pearls

• The nerves of the lower extremity are distant from each other, making it
impossible to block the entire extremity from a single injection point.
• The position of the sciatic nerve in the buttocks with respect to the midline 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 inferior border of the
gluteus maximus muscle goes diagonally from medial superior to lateral
inferior to insert in the iliotibial tract.
• The gluteus maximus is the only gluteal muscle to cover the sciatic nerve
superficially, caudal to the piriformis muscle. Gluteus medius and minimus
are located cephalad and lateral to the sciatic nerve.
• The inguinal crease does not correspond deep 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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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, that aims to
block also the lateral femoral and obturator nerves (not supported by the evidence).

Point of contact with the nerve

The nerve is approached as it emerges from under the inguinal ligament, medial
and inferior to the anterior superior iliac spine (ASIS).

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.

Patient position and landmarks

The patient lies supine. The ASIS is identified by palpation.

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
where the local anesthetic is injected in a fanwise fashion. A nerve stimulator with pulse
duration of 0.3 to 1 ms (300 to 1000 μsec) can be used to elicit a paresthesia in the lateral

Local anesthetic and volume

A volume of 5 to 10 mL of 1% mepivacaine is frequently used. A long acting
agent, as ropivacaine, can be used if necessary.

Very rare. Some patients can complain of dysesthesia in the area from minor
injury to the nerve. It usually goes away without sequelae.

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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. It is also
the point of injection for a “3-in-1” block.

Point of contact with the nerve

The nerve is usually approached just below the inguinal crease. However, if
possible, the nerve can be approached above the crease, closer to the inguinal ligament.
At this level the nerve is more compacted, prior to branching off.

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. Ultrasound provides usually an excellent image of the
nerve and neighboring vascular structures facilitating any technique to block it.

Patient position and landmarks

The patient lies supine. If necessary, the back of the bed can be elevated for
patient’s comfort. If done in combination with a sciatic nerve block, we prefer to do the
sciatic block first because this is a block that needs more time to settle than the femoral.
The femoral pulse at the inguinal crease is recognized and the trajectory of the artery is
marked. The point of entrance is marked on the skin, proximal or distal to the inguinal
crease, about 2 cm lateral to the pulse of the femoral artery.

Nerve stimulator technique

A 2”, insulated needle usually suffices. The nerve stimulator is set at 1.0 mA, a
frequency of 1 Hz and pulse duration of 0.1 ms (100 microsec). The needle is directed
45-degree cephalad and parallel to the femoral artery 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 to about 0.5 mA or less and, if the response is still
visible, 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. My own anatomic dissections fail
to make the case for this, because the point at which the block is attempted is usually
cephalad to the origin of the branch to the sartorius.

Ultrasound technique
The femoral nerve is relatively superficial in most of patients. As usual, use a high
frequency probe (more than 12 MHz) to define structures expected to be at less than 3 cm
of depth. For deeper structures use less than 10 MHz of frequency which provides deeper
penetration and less resolution.
A linear probe at 13-15 MHz can usually provide a good image of the femoral
nerve and vessels. The probe is placed parallel to the inguinal crease, The needle can be

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advanced out of plane with the image of nerve in cross section. The needle can also be
advanced in plane with the probe from lateral to medial. The femoral vein is the most
medial structure of the neurovascular bundle and is easily collapsible by the probe. The
artery is just lateral to the vein. The nerve is lateral to the artery. There is usually a gap of
about 1 cm in between.

Local anesthetic and volume

A slow injection of 20 mL of 1% or 1.5% mepivacaine is usually used for this
block. Using larger volumes, in an attempt to produce a “3-in-1” block by cephalad
spread of local anesthetic, is not supported by the available evidence.

Very rare. Hematomas from puncture of the femoral artery are possible, but
avoidable with meticulous technique, use of small gauge needles and thorough
compression of the arterial puncture when it occurs. The use of ultrasound almost
eliminates this problem.

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It is rarely performed alone. It is more often combined with femoral, lateral
femoral and/or sciatic blocks.

Point of contact with the nerve

The needle approaches the nerve after it exits the obturator foramen, below the
inguinal ligament.

Main characteristics
This is a deep block that requires good anatomical knowledge.

Patient position and landmarks

The patient lies supine. The easiest way to do it is to use the femoral artery pulse
at the inguinal ligament as the main landmark. The point of needle entrance is found
about 4 cm medial to the artery and 2 cm below the inguinal crease.

A 4”, insulated needle connected to a nerve stimulator is advanced perpendicular
to the frontal plane. A local twitch from the pectineus and or adductor longus is usually
obtained. This is just a direct muscle twitch. Deep to this level, the tip of the needle
should reach the nerve eliciting thigh adduction. The current is lowered to 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.

Local anesthetic and volume

Usually 10-15 mL of 1% to 1.5% mepivacaine or a longer acting agent is used.

Hematoma is the most frequent complication of this technique. Adductor muscles
spasm can occur.

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LUMBAR PLEXUS BLOCK (alternatively called “psoas compartment block”)
Its goal is to produce anesthesia of the lateral femoral, femoral and obturator
nerves, so it can be used along with sciatic nerve to provide anesthesia of the entire lower
extremity. It is also used to provide postoperative analgesia after hip and knee surgery.

Point of contact with the nerve(s)

The plexus is accessed deeply in the lumbar area in the space limited by the
quadratus lumborum posteriorly (more superficial) and the psoas muscle anteriorly

Main characteristics
It is the posterior approach of a “3-in-1” block. 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 superficial to the psoas
muscle, in the retroperitoneal space.
Because of the depth at which the nerves are located, the operator has little
control over the exact location of the needle tip, increasing the potential risk for
complications. It is essential that the operator be familiar with the anatomy. The epidural,
subdural and intrathecal spaces are very close to the trajectory of the needle and so is the
kidney and the iliac vessels. Cases of penetration of the peritoneal cavity with injury of
the contents have been reported.
This block should not be performed in obese patients.

Patient position and landmarks

The patient is placed in the lateral position with both hips and knees flexed like
for neuraxial block. A line joining both iliac crests is drawn (L4-L5 interspace). The
posterior superior iliac spine is identified, and a parasagital line is drawn at this level
(perpendicular to the bicrestal line). The point of intersection between the two lines
becomes the needle insertion point. Alternatively the point of entrance can be found at
4-5 cm from the midline at the bicrestal line.

Nerve stimulator technique

A 4”, insulated needle connected to a nerve stimulator is used. The needle is
advanced parallel to the midline, perpendicular to the skin. If the transverse process of L4
is contacted, the needle is “walked off” caudally. A muscle twitch of the femoral nerve or
obturator indicates good placement. It is frequent to accept higher currents (around 1 mA)
to inject. Thorough aspiration for blood or CSF is performed combined with a slow
injection, alternated with frequent aspirations.

Ultrasound technique
This is a deep block. Some people use a curved 4-5 MHz probe to delineate the
psoas and the anatomy of the lumbar plexus, but it is challenging. We do not perform it

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Local anesthetic and volume
A volume of 30-40 mL of 1% mepivacaine or 0.5% ropivacaine can be used. For
analgesia the concentration is lowered.

This is the regional anesthesia technique associated with the highest amount of
complications. Retroperitoneal hematomas, subdural and intrathecal injection, total
spinal, as well as kidney and bowel punctures have been reported.

Clinical pearls
• This is a deep block with important potential complications. It is not a block for
the novice.
• The anesthesiologist must carefully balance the potential benefits against the risks
of complications.

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Classic approach (Labat as modified by Winnie)

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.

Point of contact with the nerve

The nerve is contacted in the gluteal area at the point where it is emerging caudal
to the piriformis muscle. The needle on occasions could traverse through the piriformis.

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 an accurate approach if the operator is able to
accurately determine the actual position of the PSIS and GT, disregarding ANY soft
tissue (i.e., muscle, bursa, subcutaneous tissue).

Position of the patient and landmarks

The patient is positioned in lateral decubitus, with the side to block up. The
dependent leg is extended. The non-dependent leg is flexed at the hip and at the knee,
while the buttock is rotated anteriorly (Sim’s position).
The PSIS is marked and so is the superior aspect of the GT. The midpoint of this
PSIS-GT transverse line is determined. From this midpoint a perpendicular line
measuring 3 cm, is directed caudally and medially. This is the point of needle insertion. It
is important that the marks placed on the skin truly represent the posterior projection of
the bony prominences. Marking the GT on the lateral buttock for example, would
artificially add length to the PSIS-GT line (soft tissue), making its midpoint artificially
lateral and away from the sciatic nerve. The 3-cm length of the perpendicular line has
also been a source of problems. Several authors have modified the length of this line,
from 2-5 cm, blaming it for the difficulty with the technique.
In 1974 Winnie and collaborators published in Anesthesiology Review a
modification, which combined with the original Labat’s are known collectively now as
the “classic” technique. In order to deal with the several modifications in the length of
Labat’s 3-cm perpendicular line, they proposed an additional transverse line extending
from the sacral hiatus (SH) to the tip of the greater trochanter, to be added to the PSIS-
GT line. This way, the length of Labat’s perpendicular line would be determined by the
distance between the two transverse lines, without any need to measure it. Quoting the
authors, “with this technique the distance along the perpendicular line will vary with the
height of the patient”. This apparent solution has some problems of its own. Because, as
discussed earlier, the transverse diameter of the pelvis is fairly constant in all adults, any
prolongation of the perpendicular line would bring it closer to the midline (its direction is
caudal and medial). As a result, a taller patient (longer line) would end up with a sciatic

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nerve located closer to the midline than a shorter patient. This obviously could not be the
case. The fact is that the perpendicular line of Labat was not created to be flexible in
The combined “classic” approach (Labat-Winnie), despite its shortcomings, is the
most commonly used posterior approach to the sciatic nerve in the gluteal area.

Usually the block can be completed with a 4”, 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.

Local anesthetic and volume

We usually like to use 1.5% mepivacaine plus 1:400,000 epinephrine in a volume
of 30-35 mL to provide 3-4 hrs of anesthesia. Ropivacaine 0.5-0.75% can be used if
longer duration is needed.

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.
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 usually resolve within 1-2

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Franco’s approach

The same indications than for a classic technique.

Point of contact with the nerve

This is a mid-gluteal technique that approaches the sciatic nerve distal to the
piriformis in the proximity of the ischium (about the same level than the classic
technique). However, because caudal to the piriformis the sciatic nerve runs almost
parallel to the midline, this technique can be performed at any point between mid-gluteal
to subgluteal levels. It can also be used for continuous catheter techniques.

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 “surprisingly” similar in
males and females at any given age. Variation in hip width reflects a hormone-
dependent, gender-related different pattern of fat deposition. In fact most of the
differences in the human bony pelvis are limited to the inner pelvis. Thicker bones
in the 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. The sciatic nerve is about 10 cm from the midline (intergluteal sulcus) in all
adults. What remains highly variable is the depth at which the nerve is located and
the distance from the nerve to the lateral side of the patient. However, the distance
midline-nerve is dictated by the distance midline-ischium. As the bony pelvis
stops growing, this distance becomes fixed and unaffected by soft tissue.

Position of the patient and landmarks

This block can be performed in lateral decubitus or prone. We prefer to do it almost
100% of the times in the lateral position, because it is more comfortable for the patient
and faster to prepare for.

Fig 7-3. The patient lies on lateral

decubitus. The point of needle
entrance is easily found at 10 cm
from the midline at about
midgluteal level.
(On a patient with permission).

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The patient is placed in the lateral position with both hips and knees slightly
flexed. In a true lateral decubitus, a tangential line to the buttocks, should form a 90-
degree angle with the table. Having the patient placed at straight angles with the table,
makes his/her midline parallel to the table. The midpoint of the intergluteal sulcus, from
top to bottom, is identified. From this point, the needle insertion point is marked at 10 cm
lateral to it (see figure 7-3). This is a linear measurement that, on purpose, disregards any
particular curvature or contour in the patient’s buttocks. The insertion point, always
located at 10 cm from the midline, can be moved distally at will, as far caudal as the
subgluteal fold. This could be necessary for example, if the buttock is large and the
needle is not long enough.

Nerve stimulator technique

A skin wheal of local anesthetic is raised at 10 cm from the midline in the
midgluteal area. A small amount of subcutaneous infiltration, in the line of insertion of
the blocking needle, can also be given. A 4”, insulated needle is usually sufficient,
although in some cases a 6” needle is necessary. For this technique we set the nerve
stimulator current at 1.5 mA (1.8 mA in diabetic patients), with a frequency of 1 Hz and
pulse duration of 0.1 ms (100 microsec).
The needle is advanced slowly and parallel to the midline, until it reaches the
gluteus maximus muscle. Usually this is evidenced by a local muscular twitch of the
buttock. 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.
The needle is advanced through the gluteus muscle, with a visible local twitch that
does not disappear until the needle reaches beyond 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

Some useful tips when trying to “pinpoint” the sciatic nerve

When an adequate twitch is found, the nerve stimulator current is lowered until a
twitch is still visible at 0.5 mA or less. This is done while maintaining visual contact with

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the twitch. If the twitch becomes too weak, before reaching 0.5 mA, the current is not
lowered any further and instead the operator slowly moves the needle closer to the nerve.
It is not infrequent to see the response fade as the needle is inserted deeper. This
can be the result of a needle approaching the nerve tangentially, along one of the sides of
the nerve. We usually try to perform a small correction in order to get a “bull’s eye”
alignment with the nerve. Deciding whether to correct lateral or medial depends on what
type of response is being elicited. Eversion and dorsiflexion are responses from the
common peroneal nerve (lateral side), while inversion and plantar flexion are responses
from the tibial nerve (medial side). A small correction is then made accordingly. A more
controlled correction can be accomplished by only partially removing the needle a couple
of cm. The unburied portion of the needle is then bent and directed in the desired
direction. The buried portion of the needle keeps the needle from overcorrecting.
Bringing the needle out completely, and then reinserting it, carries a chance of
overshooting the correction.

Ultrasound technique
The nerve is identified in cross section as usual. Because of the sciatic nerve
depth, usually a curved 5-7 MHz probe is needed. The needle can be advanced cephalad
out of plane. Injecting small amounts of local anesthetic helps to localize the tip of the

Local anesthetic and volume

We commonly use 30-35 mL of 1.5% mepivacaine, usually with 1:400,000
epinephrine for a 3-4 hr duration of anesthesia. Ropivacaine can be used if needed.

Same as classic approach.

• The 10 cm measurement is a linear measurement that disregards, on purpose, the
patient’s buttock contour. This linear measurement tries to reflect only the
distance between the midline and the outer lip of the ischium, without soft tissue
• 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
of inclination of the midline with respect to the table, so the needle still may 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

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di Benedetto’s approach

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.

Point of contact with the nerve

The nerve is approached in the vicinity of the subgluteal fold.

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.

Patient position and landmarks

This block is performed in the Sim’s position, as the classic technique. The greater
trochanter and the ischium are identified and a line is drawn in between the two. The
midpoint of this line is determined. A second line is drawn from this midpoint,
perpendicularly and caudally for 4 cm. This is the needle insertion point. According to
the authors, the operator should be able to palpate at this point a “skin depression”, which
would represent “the groove between the biceps femoris and semitendinosus muscles”.
This groove supposedly represents the trajectory of the sciatic nerve. This is just one
more instance in which anesthesiologists display their love affair with grooves. In fact
cadaver dissections show:

1. Ischium and greater trochanter are located at about the same tranverse 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
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.

The authors advice to insert the needle perpendicular to the skin until a twitch
from the sciatic nerve is obtained.

Local anesthetic and volume

The same as indicated for classic approach

Common to other approaches to the sciatic nerve.

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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 7-4.

Fig 7-4. The needle insertion

point in the subgluteal fold is
found the same way than in the
mid-gluteal area.
(On a patient with permission).

The 10-cm measurement is made lateral to 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 more likely. Depending on depth, the nerve could 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 or in lateral position. The nerve is visualized in cross section and the needle
is advanced either out of plane or in line with the probe.

A few facts on subgluteal approach

1. This approach consistently misses the posterior femoral cutaneous nerve, so

anesthesia of the back of the thigh is only obtained in about 30% of the cases (our
own data, Reg Anesth Pain Med 2006; 31: 215-20). The reason is that the
posterior femoral nerve is usually already a superficial nerve (above the fascia) at
the level of the subgluteal fold.
2. As shown in fig 7-2, the inferior border of gluteus maximus and subgluteal fold
are not the same thing. Therefore, during a subgluteal approach the needle needs
to pass through the same layers of tissue than at more proximal approaches.

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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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Franco’s approach

It is especially suitable for foot surgery. Along with femoral nerve block
(saphenous) it provides complete anesthesia below the knee.

Point of contact with the nerve

The needle approaches the sciatic nerve high in the popliteal fossa, before its main
components diverge from each other.

Main characteristics
This is the only place in the trajectory of the sciatic nerve where the nerve is not
covered superficially by muscle, perhaps the only true advantage over other more
proximal approaches to the sciatic nerve. Characteristically, a sciatic block done at this
level 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 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 fuses with the fat that fills
the popliteal fossa. The fat of the popliteal fossa would “soak” away the local anesthetic,
“stealing” it from the nerve surroundings.

Patient position and landmarks

This block is most usually performed in the prone position. The patient’s patella is
palpated with two hands, to verify the neutral position of the knee on the bed (the natural
resting position of the knee is with a small degree of lateral rotation). The patient is then
asked to flex the knee slightly to make the biceps (lateral) and semitendinosus (medial)
tendons visible at the popliteal crease. A mark is placed on both tendons at the crease.
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. The needle insertion point is
marked 7-9 cm above the crease. A good orientation is to insert the needle at a distance
from the crease that is 1 cm longer than the intertendinous distance.

Nerve stimulator technique

A 2”, 22-gauge, insulated needle usually suffices. The nerve stimulator is set at
1-1.5 mA, frequency of 1 Hz and pulse duration of 0.1 ms (100 microsec). 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. 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.

Ultrasound technique
Patient is prone. A linear high frequency probe can be used, but a lower frequency
probe is usually needed. The probe is placed across the fossa to obtain a cross section of
vessels and nerves. It is easier to start scanning at the popliteal crease, where the two

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nerve components are more superficial. The probe is then moved cephalad from the
popliteal crease to identify the point at which both components come together. An
alternative method is to find the common peroneal division just medial to the biceps
tendon at the crease and follow it proximally toward the main sciatic trunk.

Local anesthetic and volume

I believe that a block of the sciatic nerve in the popliteal fossa requires a higher
volume than more proximal approaches. As a general rule I give about 10 mL more of
anesthetic solution than what I would give the same patient in more proximal locations.
This comes to about 35-45 mL of 1.5% mepivacaine or a longer acting agent if needed.
When using ultrasound there is no need to use higher volumes, if a good distribution of
local anesthetic surrounding the nerve is observed.

Small hematoma can develop. Residual dysesthesia lasting up to two weeks can
be seen.

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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

Point of contact with the nerve

Similar to the posterior technique. The needle approaches the sciatic nerve from
the lateral side, before this nerve’s main components diverge from each other. The needle
is advanced between the biceps (posteriorly) and vastus lateralis (anteriorly) into the
popliteal fossa.

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.

Patient position and landmarks

The patient lies supine in the semi sitting position. A pillow is placed under the
leg, so the hip and knee are slightly flexed. The patient can be asked to shift his/her
weight to the opposite side, so a small degree of lateral rotation is obtained. The popliteal
crease is identified and marked toward the lateral side of the knee. The cleavage between
the biceps and vastus lateralis is identified. A mark is placed in this groove 10 cm
proximal to the popliteal crease. This is the point of needle insertion.

Nerve stimulator 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.

Ultrasound technique
The patient is placed prone with a slight rotation to the opposite side. The probe is
placed across in the popliteal fossa facing anterior. A cross section of the sciatic nerve is
obtained. The needle is advanced from the lateral side, in plane with the probe.

Local anesthetic and volume

The same than for posterior approach.

The same than for posterior approach.

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1. Snell RS: Clinical anatomy for medical students, 3rd edition. Boston, MA: Little,
Brown and Company; 1986
2. Shipman P, Walker A, Bichell D: Human skeleton. Cambridge, MA: Harvard
University Press; 1985
3. Hall J, Froster-Iskenius U, Allanton J: Handbook of normal physical
measurements. Oxford: Oxford University Press; 1989
4. Labat G: Regional anesthesia: Its technique and clinical application. Philadelphia,
PA: W.B. Saunders, 1922
5. Winnie A, Ramamurthy S, Durrani Z, et al. Plexus blocks for lower extremity
surgery. Anesthesiology Review 1974; 1: 11-16
6. Franco, CD. Posterior approach to the sciatic nerve in adults: Is Euclidean
geometry still necessary? Anesthesiology 2003; 98: 723-728
7. 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
8. Rogers J, Ramamurthy S: Lower extremity blocks, Regional anesthesia and
analgesia. Edited by Brown DL. Philadelphia, PA: W.B. Saunders Company,
9. Mulroy M: Regional Anesthesia, An illustrated procedural guide, 3rd edition.
Philadelphia, PA: Lippincott Williams & Wilkins; 2002
10. 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
11. 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
12. Cunningham’s Textbook of Anatomy, 5th edition. Edited by Robinson A. New
York, William Wood and Company, 1928, pp 258
13. Hollinshead’s Textbook of Anatomy, 5th edition. Edited by Rosse C, Gaddum-
Rosse P. Philadelphia, Lippincott-Raven, 1997, pp 641–80

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Single-shot peripheral nerve blocks provide quality anesthesia for a variety of

different procedures. In most cases postoperative pain is moderate and manageable with
either IV PCA (patient controlled analgesia) or oral analgesics. However, there are
surgical procedures known to be followed by intense pain in the postoperative period.
Pain is a very important and usually not well addressed problem. It does not only affect
patients physically and emotionally, but also affects their recovery time and
In those cases in which postoperative pain is expected to be more than moderate
and lasts longer than the duration of a single shot block, the anesthesiologist needs other
means to produce and prolong the analgesia. Ideally, analgesia could be provided by
slow-released analgesic products injected along with local anesthetics during single shot
techniques. Local anesthetics and other substances like morphine have been added to
liposome systems to deliver controlled and steady doses of analgesia. However, to date
only duromorph, a liposomal system delivering morphine, is the only one available. It has
been approved by the FDA for epidural analgesia. In this context continuous peripheral
nerve blocks with perineural catheters become an excellent option for postoperative
analgesia providing the versatility in duration and effect that single shot techniques lack.
F. Paul Ansbro published in 1946 what is widely considered the first account of a
continuous peripheral nerve block technique. He described a technique in the
supraclavicular area in which he used a needle passed through a cork for stabilization.
Once the needle was inserted to an adequate level, as judged by paresthesia, the cork was
advanced to the level of the skin and taped. A tubing connected to a syringe provided the
opportunity for what Ansbro called “fractional injections”. More recently in the 1970s,
Selander introduced continuous techniques in the axillary region using an IV cannula left
in place.

Benefits of continuous perineural catheters

Many authors have demonstrated the benefits of continuous techniques, mainly

prolonged analgesia without the undesirable side effects associated with opioid use (i.e.,
nausea, vomiting, constipation, dependency), better patient satisfaction and better
ability to participate in rehabilitation. Liu and Salinas published in 2003 an excellent
review on continuous perineural blocks. After an extensive review of the available
literature they concluded that there was enough evidence to support the claim of superior
analgesia of continuous perineural blocks as compared to IV PCA “for open shoulder
procedures and total knee replacement”. It is likely that may other surgical procedures
could also benefit from the ability to extend the analgesia provided by perineural

Continuous techniques

Continuous blocks are usually performed in a similar way than single-shot

techniques with the addition of a catheter that provides the means to continuously deliver
the analgesic solution. Single-shot blocks (“primary block”) are generally associated with

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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.

Stimulating versus non-stimulating catheters

There are proponents of both techniques. The non-stimulating catheters are

commonly inserted through an insulated, Tuohy type needle. The catheter can be a single
orifice catheter in which the hole is usually at the tip, or most commonly a multiorifice
catheter with a dead end (no hole at the tip) and three side holes, the distal one at about
0.5 cm from the tip. The proximal hole is separated from the distal one by a distance of
about 1 cm. After the needle is positioned the catheter is advanced to the desired location.
The technique is generally easy, but the success of the secondary block (through the
catheter) depends on a good perineural placement of the catheter.
The stimulating catheter uses for insertion a similar Tuohy type needle, but the
catheter itself has a wire connected to its tip, allowing for stimulation through it in a
similar fashion than through a needle. The ability to stimulate a nerve as the catheter is
advanced provides a measure of catheter tip-nerve proximity. If the elicited twitch
disappears the catheter is carefully withdrawn into the housing of the needle to avoid
cutting or otherwise damaging the catheter. The position of needle is then slightly
modified by rotation or by moving it in and out a few millimeters and a new attempt is
made. The needle and catheter together as a unit can be slightly rotated in its main axis
before reinserting the catheter. This technique can be more time consuming and more
difficult, but supposedly decreases secondary failure. The introduction of ultrasound into
regional anesthesia practice with its ability to visualize the needle and catheter as well as
the spread of the local anesthetic solution, has called into question the need for
stimulating catheters.

Catheter related problems

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

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1. Ansbro FP. A method of continuous brachial plexus block. Am J Surg 1946; 71:
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