5.1.

1 Regional Anesthesia
Dr. Payawal

January 6, 2014
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LEGEND:
Old trans/book notes/recording

o
Objectives
1. Introduce the principles of regional anesthesia
2. Present the different techniques in regional anesthesia
3. Discuss the complications of this technique

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o
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REGIONAL ANESTHESIA

Regional anesthesia or block is the reversible blockade of

conduction of painful impulses on the site of
administration of local anesthetic.
Provides only two of the three major components of
anesthesiaanalgesia and muscle relaxation. Anxiolysis,
amnesia, or sedation must be attained by supplemental IV
administration of other drugs (e.g., the benzodiazepines or
propofol infusion).

TYPES OF REGIONAL BLOCK

CENTRAL NEURAL AXIS ANESTHESIA/
CENTRAL REGIONAL ANESTHESIA

Blocks spinal nerves as they exit the spinal cord.

The effect is centered on the central nervous system.
Types:
o Spinal anesthesia Administration of the
anesthetic in the spinal canal. Will last from 1 2
hours.
Most useful technique for regional
anesthesia
Usually used for abdominal operations
o Epidural anesthesia Administration of the
anesthetic into the epidural space. Stays in the
epidural space.
Could last up to several hours provided that
you place an epidural catheter
o Caudal analgesia Administration of the
anesthesia into the caudal space.
o Continuous spinal/epidural anesthesia

A catheter is left in place in the spinal canal

or epidural space to continuously give
anesthetic drugs.

CSA Continuous Spinal Anesthesia

CEA/CLEA Continuous Epidural

Anesthesia / Combined Lumbar and
Epidural Anesthesia

INFILTRATION ANESTHESIA

Local anesthetic is deposited near a large nerve or a plexus

of nerves.
o Brachial plexus block For arm and hand
surgery.
Can be approached either through supra or
infraclavicular approach or via axillary area.
This is becoming popular nowadays due to
ultrasound machines.

DOREEN. CARMI. JAMES. HENNA. LOUIE

Accumulation of the anesthesia in the surrounding tissues

of where the incision is to be made.
Just infiltrating the area around the site of incision
Most common technique in the clinics. Can be used in any
excision of tumor or mass that is superficial in the body.

IV
REGIONAL
ANESTHESIA
TECHNIQUE/ BIERS BLOCK)

(BIERS

IV administration of a local anesthetic into the vein of a

tourniquet-occluded limb. Local anesthesia diffuses from
the peripheral vascular bed to nonvascular tissue such as
axons and nerve endings.
o Ankle block
o Intercostal
o Cervical plexus
The anesthesia is prevented from reaching the systemic
circulation to prevent systemic toxicity.
It is quite dangerous when the tourniquet is advertently
loosened.

LOCAL ANESTHESIA

PERIPHERAL NERVE BLOCK

Femoral nerve block For lower extremity

analgesia
Sciatic nerve block For lower extremity
analgesia
Ankle block For the foot surgery
Intercostal block anesthesia is injected 2 mm under
the ribs
Cervical plexus block

Local anesthesia produces transient and reversible loss of

sensation in a certain part of the body without loss of
consciousness.
Can produce differential blockade which means
differential inhibition of the motor and sensory activity
based on the concentration of the local anesthetic used.
Using full-strength anesthetic inhibits the sensory, motor
and sympathetic activities while diluting the anesthesia
will just produce sensory blockade with no or very limited
motor paralysis.
Initial effect is analgesia or sensory blockade followed by
temperature, touch, pressure and lastly motor. The most
difficult to block are the motor nerves referred to as the a peripheral nerves.
Local anesthetics block nerve conduction by stabilizing
sodium channels in their closed state preventing action
potentials from propagating along the nerve. The
individual local anesthetic agents have different recovery
times based on lipid solubility and tissue binding but
return of neural function is spontaneous as the drug is
metabolized or removed from the nerve by the vascular
system.

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SURGERY II: 5.1.1 Regional Anesthesia

INDICATIONS OF LOCAL ANESTHESIA

Abdominal operation
Urologic procedure
Rectal surgery
Perineal procedure
Lower extremity procedure

Newer anesthetics like your Lidocaine has a PKA

value of 7.9 will be able to have a rapid onset than
ester type of anesthetics such as Tetracaine which has
a PKA value of 8.6.
An area with an abscess will usually have a low
pH(acidic). Hence, there is a decrease in effect of your
local anesthetic. It is the cation form that is
responsible for the nerve block which prevents the
depolarization of nerve impulses. However you need
the base form for it to penetrate the tissues to reach the
nerves. If it is acidic area there would be less
penetration of local anesthetics to the nerve. So its
very difficult for you to block an area with an abscess.

STRUCTURE ACTIVITY RELATIONSHIP

Fig. 1 structure of local anesthetics

Aromatic Ring
o Responsible for lipophilicity of compounds.
o Lipophilicity Tendency of the compound to
associate with membrane lipids and penetrate the
lipid membrane.
Amine portion
o Secondary and tertiary amine is associated with water
solubility
o Compounds lacking the amine portion are insoluble
in water (ex. Benzocaine)
Intermediate linkage (Ester and Amide)
Determines what type the anesthetic drug will be.
o Anesthetics are connected to the aromatic molecule
via an ester or amide linkage.
o Ester portions are derivatives of para-aminobenzoic
acid (known allergen).
Tetracaine is the only ester anesthetics that is
commonly used nowadays in the clinic
o Esters are hydrolyzed by plasma cholinesterase (or
pseudocholinesterase) and the metabolites formed are
associated with some allergic reactions.
o Amides undergo enzymatic degradation in the liver
and are more stable in solution. Does not produce
anaphylactic reaction.
Newer local anesthetics are usually amides
o Basis for classification of local anesthetics.
o Determines the route of metabolism.
o Determines allergic potential.

MOLECULAR BASIS OF ANESTHETIC

ACTION

fig.2 Action of Local Anesthetics

Nonionized base crosses the nerve sheath and membrane,
and internal surface of the membrane. There is reequilibration of internal pH of the axon.
The cationic form is quantitatively the predominant form
of anesthetic in the internal membrane. Cationic form
enters the sodium channel from the internal (axoplasmic)
surface of the membrane and attaches to a specific binding
site within the channel. Na movement is blocked.
The base is responsible for membrane penetration because
it is more lipophilic. When it gets inside the cell membrane,
it is again depolarized in the presence of hydrogen to form
the cationic form which from the inside blocks the sodium
channel. Remember this diagram because it is very
important so that you will know the reasons for toxicity of
local anesthetics.

LOCAL ANESTHETIC DRUGS

LA

Local anesthetics are weak bases.

The more basic the anesthetic is, the more easily it can
penetrate in the tissue.
Exists as a non-ionized base and cationic form in
physiological pH.
The mechanism of action of local anesthetics is dosedependent blockade of sodium currents in nerve fibers.
The non-ionized form is responsible for the lipid
penetration and when inside, the charged form is
responsible for the local anesthetic effect.
Remember that local anesthetics are weak bases and exists
as a non-ionized base in physiologic pH. Note the
Henderson-Hasselbach equation for pH. The ionic form
and the base form are shown. Addition of the H ion forms
the cationic form

DOREEN. CARMI. JAMES. HENNA. LOUIE

Esters

SPECIFIC
DRUGS
Cocaine
(first local
anesthetic that is
used into the
clinical practice)

SIDE EFFECTS
Vasoconstrictor (in
areas where there is
bleeding),
hypertension, topical
use only

Procaine

Short duration, For

infiltration use

Chlorprocaine

Short duration, For

spinal use

Tetracaine
(commonly
used)

Long duration, For

spinal use only, not
epidural

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EFFECT

Analgesia,
muscle
relaxation
and NOT
amnesia or
hypnosis

SURGERY II: 5.1.1 Regional Anesthesia

Benzocaine
Amides

Lidocaine

Rapid onset and short

duration, Can be used
for infiltration/ spinal/
epidural and peripheral
nerve block

Bupivacaine

For
infiltration/spinal/
epidural use

Mepivacaine

Produces a metabolite
Toluidine

Prilocaine

Causes
methemoglobinemia*
secondary to its
metabolite

Ropivacaine

For topical use only

CLINICAL PROPERTIES OF LOCAL

ANESTHETICS

Potency
o Correlates with lipid solubility
o Directly proportional; The more lipid soluble the drug
is, the more potent it is.
o Lipid solubility determines whether the molecule is
able to penetrate the nerve membrane. The more lipid
soluble the drug, the more it is able to penetrate the
nerve membrane.
o Anesthetic molecule must penetrate the nerve
membrane and bind at a partially hydrophobic site in
the Na channel.
Lipid Solubility
Potency
Lidocaine
46
Intermediate
Bupivacaine
390
High

Duration of Action
o Correlates with protein binding
o Molecules bound to plasma proteins are not
pharmacologically active.
o Albumin has lower affinity and has higher capacity
for binding while alpha1 acid glycoprotein has higher
affinity and lower capacity for binding.
o Local anesthetic with higher protein binding stays in
the protein receptor longer.
o Influenced by peripheral vascular effects
Protein Binding
Duration
Lidocaine
64
Intermediate
Bupivacaine
95
Long

Onset of Action
o Correlates with lower ionization, pKa or dissociation
constant
o Dissociation Constant is a measure of the strength of
an acid or a base.
o The pKa range of local anesthetics: 7.8 9.2

The higher the pKa, the more relatively acidic

physiologic pH will be, and therefore the
direction of the Hasselbach equation is toward
formation of the cation hence less base therefore
less membrane penetration and prolonged onset.
o Physiologic pH is ~ 7.4

The idea is the farther away you are from

physiologic pH, the more relatively acidic
physiologic pH is. Therefore, in physiologic pH,
if you inject the local anesthetic in that milieu,
youre going to have a relatively higher
hydrogen ion concentration. Going back to the
equation a while ago, a very high H+
concentration pushes the equation towards
formation of the cation. When it is mostly in the
cationic form, it will not penetrate the nerve
membrane, therefore, the onset will be longer.
o Lower pKa = lower ionization = shorter time of onset
o The non-ionized form responsible for membrane
penetration.
During
INFLAMMATION,
local
anesthetic exists in ionized form.
o What happens when you inject the local anesthetic
into inflamed tissue? Inflammation increases
hydrogen ions thus lowering the pH, forming more of
ionized form and a longer onset.

Sister of Mepivacaine,
Less cardiotoxic, For
OB analgesia

The only ester anesthetic type available now is tetracaine.

This is used as spinal anesthesia.
Prilocaine is not used anymore since it can cause
methemoglobinemia*.
Most common used now is lidocaine and bupivacaine.

*METHEMOGLOBINEMIA

Increase in methemoglobin portion of hemoglobin in the

blood.

Normal concentration: 1%. More than that is

methemoglobinemia.
Under normal circumstances, most of the hemoglobin
iron exists in the ferrous (Fe+2) state and a small
fraction of the hemoglobin present in erythrocytes
undergoes oxidation. As a result of this process, some
of the hemoglobin iron is converted to the ferric (Fe +3)
state, forming methemoglobin. Oxidized hemoglobin
cannot bind or carry oxygen. The physiologic level of
methemoglobin is less than or equal to 1% of total
hemoglobin concentration and when greater than 1%
of hemoglobin is oxidized to methemoglobin, a
hemoglobin deficiency occurs. In normal blood, the
methemoglobin
reductase
system
maintains
methemoglobin in equilibrium with deoxygenated
hemoglobin.

Hallmark: Cyanosis unresponsive to high-flow oxygen

in the absence of cardiac or pulmonary disorders.

Results when hemoglobins oxygen-carrying capacity is

greatly decreased due to an increased amount of
methemoglobin in the blood.

Frequently seen in PRILOCAINE (which fortunately is not

available in the Philippines).

Oxidizing agents known to induce methemoglobinemia

are Articaine, Benzocaine, EMLA, Lidocaine, Methylene
blue, Prilocaine and Propitocaine. EMLA is a topical
anesthetic that can penetrate the skin which is useful for minor
excisions of small tumors and also used for those who are not
able to stand the pain of IV injection where it is applied with an
occlusive dressing for about 45 minutes before the IV insertion.
They are local anesthetics except methylene blue.

Lidocaine
DOREEN. CARMI. JAMES. HENNA. LOUIE

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pKa
7.8

Onset
Quick
3

SURGERY II: 5.1.1 Regional Anesthesia

Bupivacaine

8.1
Intermediate
Correlates with Concentration
Concentration
Onset
Bupivacaine
0.5%
Quick
0.75%
Intermediate

Differential Blockade
o The ability of local anesthetics to cause a differential
inhibition of sensory and motor activity. Not all
sensations are blocked. Blockade depends on the
thickness of the nerve sheet.
o Not all sensations are blocked. Blockade depends on
the thickness of nerve sheet. A fibers should be,
theoretically, blocked by higher concentrations.

Duration of action can be prolonged with epinephrine.

o If the procedure would last for less than 30 minutes,
then you dont need epinephrine.
Infiltration is placement of anesthetic near (or in) the area
you want anesthetized. Usually, the anesthetic is affecting
the terminal branches of the nerves (but not always) in
that area. Typically, an infiltration will only affect that
area and not beyond. It is induced by injecting the
anesthetic solution directly into or around the tissues to be
anesthetized. It is used for operative procedures on the
maxillary premolar, anterior teeth and mandibular
incisors.

TOPICAL ANESTHESIA

An example is dropping of anesthetic in the eye or the use

of anesthetic cream for the skin.

PERIPHERAL REGIONAL BLOCKS

fig.3 differential blockades of anesthetics

o
o

At low concentrations, there is selective blockade of

preganglionic sympathetic nervous system B fibers.
At high concentrations, there is an interruption in the
conduction of small C fibers and small/medium-sized
A fibers.
Application: Labor analgesia

A dilute solution of local anesthesia can cause

sensory blockade without motor blockade. This is
especially useful for labor when you want to
have analgesia without motor blockade so that
the mother can be walking around while in labor.
Hierarchy: Sympathetics are blocked first then pain,
temperature,
touch,
pressure,
motor
and
proprioception.
In some instances, the doctor was able to block
everything and the patient retains proprioception
because it was not blocked, or it was blocked later on.
The patient retains the feeling of her or his previous
position before proprioception was blocked.
In some instances, it corresponds to the time that the
catheter is being inserted; therefore, if this happens,
the patient will be asking the doctor to straighten
their legs because they feel that they are still in the
lithotomy position.

Simplest
Extravascular placement of local anesthetic to the area to
be anesthetized
Dosage Requirements:
o Volume depends on the area to be anesthetized.
o More volume may be given in dilute concentrations.
o Particular attention to toxic dose of the local
anesthetic (always bear this in mind!).
Onset is almost immediate.

DOREEN. CARMI. JAMES. HENNA. LOUIE

INFILTRATION

REGIONAL ANESTHETIC TECHNIQUES

Blockade of brachial plexus, lumbar plexus, and specific

peripheral nerves via injection of local anesthetic solutions
into tissues surrounding individual peripheral nerve or
nerve plexuses.
Commonly used for awake craniotomies and other awake
surgeries in the face like rhinoplasty, blepharoplasty and other
cosmetic surgeries.
Brachial Plexus Block For arm and hand surgery (Note!)
Hypogastric and ilioinguinal nerve block - For hernia surgery
Pudendal nerve block Given before episiotomies and repair
Local anesthetics deposited near the vicinity of the nerve
diffuse from the outer surface to the center of the nerve
along a concentration gradient.
o Proximal structure: mantle
o Distal structure: core
Advantages
o Reduced physical stress (compared to central
neuroaxis anesthesia)
o Avoids airway manipulation and complications
associated with endotracheal intubation.
o Indwelling catheters may be placed for prolonged
block and analgesia.
o Provides surgical anesthesia and postoperative
analgesia.
Head and Neck (intracranial blocks, neurosurgery and
scalp surgeries are amenable to just local anesthesia, eye
blocks, face blocks, ophthalmic nerve block, maxillary
nerve block, mandibular nerve blocks, cervical plexus
blocks)
Thorax and Abdomen (epidural anesthesia, ilioinguinaliliohypogastric block, peri-umbilical & rectus sheath block,
pudendal block commonly used by obstetricians for
episiotomy and repair in the perineal area.)
Upper Limb Blocks (interscalene block, supraclavicular
block, infraclavicular blocks, axillary block)
Lower Limb Blocks (lumbar plexus block, iliofascial block,
obturator block, sciatic blocks, ankle blocks)
Complications
o Local anesthetic toxicity
o Neurologic injury From mechanical, pressure, chemical
and vascular factors.
o Inadvertent neuraxial block
o Intravascular injection of local anesthetics
o Nerve blocks of the thorax run the risk of causing
pneumothorax.

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CENTRAL REGIONAL ANESTHESIA

Two main types: Subarachnoid block and epidural

anesthesia
The main objective is to look for spinal canal which is
marked by the flow of the spinal fluid then the
anesthetic is administered.
Provides anesthesia for the lower half of the body.
Especially useful for genitourinary, gynecologic, inguinal
hernia, or lower-extremity procedures.
A. Subarachnoid block (Spinal Block)

The temporary interruption of nerve transmission

produced by injection of a small amount of local
anesthetic solution into the subarachnoid space.
Provides sensory and motor blockade below the level of
the block.
Only a small amount is needed because were dealing here
with naked nerve roots that come out of the spinal cord.
Indications: operations on the abdomen, urologic, rectum,
perineum, and lower extremity procedures that are
amenable to spinal anesthesia.
Spinal cord membranes from outside in: dura,
arachnoid then pia mater. When you puncture the
dura, its actually the dura-arachnoid that youre
puncturing because the dura is very tightly adhered to
the arachnoid therefore another name for spinal
anesthesia is subarachnoid block.
Just after the dura, there is a great number of blood
vessels. When you puncture the dura, youll have
backflow of CSF. This technique is very good for
operations in the abdomen, the rectum, perineal area
and lower extremities.
Local anesthetic is injected directly into the dural sac
surrounding the spinal cord. The level of injection is
usually below L1 to L2, where the spinal cord ends in
most adults. Because the local anesthetic is injected
directly into the cerebrospinal fluid surrounding the
spinal cord, only a small dose is needed, the onset of
anesthesia is rapid, and the blockade thorough. The block
wears off naturally via drug uptake by the cerebrospinal
fluid, bloodstream, or diffusion into fat. Epinephrine as an
additive to the local anesthetic will significantly prolong
the blockade
Factors Affecting Subarachnoid Block (SAB)
o Local anesthetic blockade
o Volume and dose
o Patient position and local anesthetic baricity

Influences the spread and level of the block

Baricity is the specific gravity of the anesthetic

solution relative to the CSF. If the anesthetic
solution has a lower SG than the CSF, it is known
as a hypobaric solution. If the SG is almost the
same, it is isobaric; if SG is higher than CSF, then
it is hyperbaric.
In the clinics, the baricity is varied by using tetracaine
which comes in a powder form. When a hypobaric
solution is needed, it is diluted with water. When an
isobaric solution is needed, it is diluted with CSF and
when a hyperbaric solution is needed, it is diluted with
an 8-10% dextrose solution.
In a hyperbaric solution, the anesthetic would tend to
gravitate, therefore to accomplish a higher level of
spinal anesthesia, the patient is placed on a head down

DOREEN. CARMI. JAMES. HENNA. LOUIE

position. If the solution is hypobaric, patient is placed

in the head up position.
o Addition of vasoconstrictors
o Addition of opioids

Opioids prolong duration of analgesia and

increase tolerance for tourniquet pain.
o Anatomic and physiologic factors

Examples:
obesity,
pregnancy,
increased
intraabdominal pressure, previous spine surgery,
spine deformities, age

All of these will increase the level of spinal anesthesia.

Spine deformities can cause problems when the

anesthetic gravitates or floats on the CSF either way
when its hypobaric or hyperbaric. There will be some
problems later on in terms of producing the level block
needed.
Advantages of SAB
o Avoids manipulation of airways.
o Difficult intubation would not be a problem.
o Avoids side effects of general anesthesia like nausea,
vomiting, prolonged emergence or drowsiness.
o Technique is simple.
Absolute Contraindications to SAB
o Infection and other lesions at the site of injection
o Sepsis
o Shock or severe hypovolemia

The anesthesia will cause vasodilation as one of the

physiologic effect of the drug so in a person with shock,
the state of hypovolemia will be aggravated and can
result to cardiovascular collapse.

Because one of the things that happen in spinal

anesthesia, is you block the sympathetics
therefore you expect some hypotension in the
presence of existing hypotension, you may
probably cause early demise of the patient
o Preexisting disease of the spinal cord

The spinal cord is more susceptible to the

neurotoxicity of the local anesthetic like the
demyelinating disease.
o Increased intracranial pressure

Doing a tap in the lumbar area decreases the

pressure inside the subarachnoid space causing a
decrease in the CSF pressure resulting to uncal
herniation and ultimately, death.
o Coagulopathies

Doing a tap and inadvertently puncturing a

vessel causes a hematoma formation and can
cause compression in the small space of the
spinal canal causing neurologic damage if not
drained in a timely manner.
o Refusal of patient, patients who are psychologically
or psychiatrically unsuited
o Lack of skill and experience of the anesthesiologist
Relative Contraindications to SAB
o Deformities of the spinal column because of the
perceived difficulty in access.
o Chronic severe headache or backache because the
patient might claim that the anesthetic aggravated the
preexisting ache.
o Blood in the CSF that fails to clear after 5 to 10 ml of
CSF have been aspirated.
o Failed spinal tap after three attempts, unless the
assistance of another experienced colleague can be
sought.

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Minor abnormalities of blood clotting, including

"mini" doses of heparin administered up to the time
of surgery.
Complications of SAB
o Infection
(Meningitis,
Encephalitis,
Adhesive
Arachnoiditis)
o Neuropathy happens when the nerve is hit and
traumatized.
o Hematoma

Most large nerves are adjacent to large blood

vessels.
o Systemic toxicity or the inadvertent deposition of large
volume of local anesthetic into the systemic circulation.
Preventing Complications
o Do not exceed the maximal dose of the local
anesthetic to avoid toxicity.
o Use the minimal effective drug concentration.
o Stay within the recommended total maximal dose.
o Avoid injecting intravenously.
o Use of sedative as adjunct to local anesthetic is with
risk because the symptoms will be picked up at a later
time. In a patient with sedative, closed monitoring is
needed.
NOTE: Intravascular technique has the greatest risk of systemic
toxicity followed by intrapleural blocks, intercostal, epidural and
the most minimal is subcutaneous block.
B.

Epidural Anesthesia

Injection of a certain amount of local anesthetic (with or

without opiates) into the lumbar or thoracic epidural
space via a catheter taped on the patients back.
Indications: abdominal, thoracic and lower extremity
procedures.
Requires re-dosing of anesthesia for long procedures.
The epidural space is just a potential space. As long as nothing
is injected there, it only contains a lot of fat and blood vessels. So
when a larger volume is injected, as compared to the
subarachnoid block, there will be anesthesia in the area that is
covered by the particular volume of anesthetic. The levels that
are blocked are dependent a lot on the total volume of the local
anesthetic that has been given.
Also called extradural anesthesia, because local
anesthetics are injected into the epidural space
surrounding the dural sac of the spinal cord.
Much greater volumes of anesthetic are required than
with spinal anesthesia, and the onset of the block is
longer10 to 15 minutes
Advantages of EB
o Decreased blood loss and incidence of deep venous
thrombosis during hip surgery.
o Superior pain control, less sedation and better
pulmonary function for thoracic surgery.
o Rapid recovery of GI function.
o Early ambulation.
Can be continuously administrated so there is no
limitation on the duration of the local anesthetic
deposited because more anesthetic can be added
through a catheter.
Procedure
o Patient is positioned.
o The landmarks are identified.
o Aseptic Preparation.
o Local infiltration of LA at injection site.
o Epidural puncture with Tuohy needle.

DOREEN. CARMI. JAMES. HENNA. LOUIE

A Tuohy needle is a hollow hypodermic needle,

very slightly curved at the end, suitable for
inserting epidural catheters.
o Epidural space is identified.

Note +/- of CSF, blood, paresthesia.

Epidural anesthesia is something similar to

spinal anesthesia, only, the epidural space is
identified by the LORT (loss of resistance
technique) or the hanging drop technique.
Loss of resistance is when the epidural needle
is inserted and the ligamentum flavum is
identified which immediately precedes the dura.
The ligamentum flavum is identified by its
resistance to the air or fluid inside the syringe.
The needle is continually pushed while applying
pressure to the plunger. As soon as there is loss
of resistance, it is the epidural space. As
compared to spinal anesthesia, this is less
accurate. The endpoint is not definite because it
is the loss of resistance so there is problem when
there is no resistance to begin with. There are
patients wherein resistance is not too good.
o Spinal anesthesia is the simpler technique because the
endpoint is much better, much more consistent and
much accurate.
o Epidural catheter is threaded into the space.
o Test for inadvertent intravascular and intrathecal
placement of catheter.
o Epidural injection of LA.
Complications of EB
o Similar to that of spinal block/SAB
o Total spinal anesthesia
A dose of about 1-4cc of LA is given for spinal
anesthesia. With epidural, it is about 20-30cc.
With this volume, the level of anesthesia that will
be able to achieve can actually result to a total
spinal anesthesia. When there is total blockade of
the sympathetics, expect a cardiovascular collapse
and respiratory paralysis.
o Local anesthetic toxicity
o Systemic toxicity
Heralded by CNS symptoms. The dose
required to produce CNS toxicity is lower
than the dose needed to produce
cardiovascular collapse. If you suspect
systemic toxicity, observe for CNS effects
first because they are manifested earlier than
CV effects. To prevent systemic toxicity,
aspirate first to make sure that a vein or
artery is not hit before administering the
anesthesia with the addition of a
vasoconstrictor.

Spinal/epidural hematoma

Epidural abscess
o High Block

Inadvertent injection of local anesthetic into a

dural tear will result in a high block, manifesting
as unconsciousness, severe hypotension, and
respiratory paralysis requiring immediate
aggressive hemodynamic management and
control of the airway.
o Severe headache

Epidural-introducing needles are of a much

larger diameter (17- or 18-gauge) than spinal
needles, and accidental dural puncture more

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often results in a severe headache that may last
up to 10 days if left untreated.

Minor abnormalities of blood clotting, including mini

doses of heparin administered up to the time of surgery

DERMATOMAL LEVEL AND BLOCKS

Fig.5 Toxic plasma levels in different sites

fig.4 Dermatomal levels

Dermatome
Level
T4-T5
T6-T8

Nipple Area
(T4)
Xiphoid
(T6)

T10

Umbilicus

L1

Inguinal
Ligament

L2-L3

Knee and
below
Perineum

S2-S5

Procedures
Upper abdominal surgeries
(cholecystectomy, gastrectomy)
Intestinal surgery (including
appendectomy), gynecologic
pelvic surgery, and ureter
explorations
Transurethral resection, vaginal
delivery, hip surgery
Transurethral resection without
bladder distension; thigh
surgery; lower limb
amputations
Foot surgery (Achilles tendon
repair)
Perineal surgery,
hemorrhoidectomy, anal dilation

How to control the level of the block? By positioning the patient,

providing varying amounts of anesthesia, giving same
concentration but different volumes of anesthesia.

CONTRAINDICATIONS
Absolute contraindications

Infection and other lesions at the site of injection

Sepsis

Shock or severe hypovolemia

Disease of the spinal cord

Increase intracranial pressure (due to possible brain

herniation)

Coagulopathies

Refusal of the patient

Lack of skill and experience of the anesthesiologist

Relative Contraindications

Deformities of the spinal column

Chronic severe headache or backache

Blood in the CSF that fails to clear after 5 to 10 ml of CSF

have been aspirated

Failed spinal tap after three attempts

DOREEN. CARMI. JAMES. HENNA. LOUIE

When you do your intercostal blocks you have to have at

least 5 sites to block it very well. Subcutaneous will have
the very least because it is superficial.
Neurological signs will occur first before cardiovascular
toxicity
You need 2 3 times of neurological toxicity before CVS
toxicity. Hence do not sedate patient to see the common
signs of neurologic toxicity such as ringing in the ear and
metallic taste. If this occurs, stop local anesthetic
immediately. If local anesthesia goes to plasma, convulsions,
hypotension and cardiac arrest can happen. Bupivacaine
will be very difficult to reverse once CVS toxicity occurs
since it binds to Ca receptors. It is easier to reverse the
effects of Lidocaine because it is metabolized faster and is
easier to dislodge from Ca receptors of the heart.
Ropivacaine is better than Bupivacaine since they are
isomers. They produce good effect minus the bad effect of
local anesthetics.

Physiologic Effects of Local Anesthesia

o Hypotension as a consequence of sympathectomy and
vasodilatation but this can be treated with fluids and
vasopressors.
o Bradycardia as a consequence of sympathectomy and
blockade of cardiac acceleration fibers from the upper
thoracic spine.
o Respiratory inadequacy

Respiratory inadequacy is secondary to blockade and

paralysis of intercostal muscles. This is especially true
for patients with increased intraabdominal pressure
such as pregnant women which prevents full
movement of the diaphragm.
o High spinal anesthesia
o Postdural puncture headache

This was highly prevalent in pregnant women with

the use of large-sized needles but it can be prevented
by the use of finer needles which are readily available
now.

Postdural puncture headache is caused by leakage of

CSF. In CSF hypovolemia, in an erect position, there
will be traction of the pain sensitive areas of the brain
which includes the cranial nerves and dura resulting
to headache. The treatment of choice would be
hydration and prevent further CSF losses.
o Urinary retention

It is caused by the action of the detrusor muscle. With

spinal anesthesia, theres a tendency to retain urine.
Its very important that after the anesthetic, the

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o
o
o
o

urinary bladder should be palpated to see if theres

retention.
Transient radicular neuropathy associated with
lidocaine use for spinal anesthesia but is self-limiting.
Frank neurologic injury
Meningitis / encephalitis
Adhesive arachnoiditis

ADVERSE EFFECTS OF LOCAL

ANESTHETICS
SYSTEMIC TOXICITY

CNS is more susceptible to the actions of systemic local

anesthetics than the CVS.
The dose required to produce CNS toxicity is lower than
levels producing cardiovascular collapse.
Prevention: aspiration to detect inadvertent vascular entry;
addition of a vasoconstrictor (epinephrine)
Exception: Bupivacaine (CVS before CNS)
CNS side effects: metallic taste, ringing in the ears,
convulsions (Reversed with Pentothal or Benzodiazepine).
CVS side effects: sinus bradycardia, 3rd degree AV block,
cardiac arrest
With hypercapnia and acidosis, there will have greater
incidences of local anesthetic toxicity, especially CNS
toxicity.
Elevation in PaCO2 enhances cerebral blood flow (CO2 is a
very potent cerebral vasodilator) Enhancing local
anesthetic delivery to the brain CNS toxicity will occur
earlier.
Diffusion of carbon dioxide decreases intracellular pH
Promoting the conversion of the base form to the cationic
form (which cannot penetrate the lipoprotein membrane)
Causing ION TRAPPING (ions are trapped inside the
nerve) increasing the CNS toxicity.
Decreased plasma protein binding Increases the free
drug available for diffusion into the brain that may
produce toxicity.
Spectrum of local anesthetic and toxic doses

fig.7 Mechanism of action for CNS toxicity

fig.6 toxicity levels of different local anesthetics

CENTRAL NERVOUS SYSTEM TOXICITY

DOREEN. CARMI. JAMES. HENNA. LOUIE

An increased dose of local anesthetics can produce an

initial blockade of inhibitory pathways in the Cerebral
Cortex. This may also be a result of the stimulation of
glutamate release, which is an excitatory neurotransmitter.
This blockade of inhibitory pathways leads to an
unopposed excitatory activity which may present with the
following signs (see excitatory signs), leading to seizures.
Further doses of local anesthetics will eventually inhibit
the activity of both inhibitory and facilitatory circuits,
resulting to depression of the CNS via (1) a desensitization
of receptors, or (2) a depletion of neurotransmitters.
Excitatory
o Circumoral numbness. This is the first thing to ask
patient when you suspect local anesthesia toxicity if
the patient is awake.
o Tongue paresthesia
o Dizziness
o Blurred vision
o Tinnitus
o Restlessness /Confusion/Agitation
o Shivering
o Muscular twitching
o Generalized convulsions (tonic-clonic)
Depression
o Cessation of seizure activity
o Respiratory depression
o Respiratory arrest
o A precaution for patients receiving CNS depressants:
CNS toxicity secondary to local anesthetics may not
be heralded by signs of CNS Excitation.
What to do in the presence of LA-induced CNS Toxicity?
o Assist ventilation mask ventilation.
o Circulatory support Give vasoactive drugs by IV.
o Prevent or correct hypercapnia and acidosis by giving
sodium bicarbonate.
o Prevent or correct hypoxemia.
o Control convulsions:

Benzodiazepines

Thiopental

Propofol
Equipment necessary prior performance of major
conduction blockade:
o Monitors
o Oxygen supply
o Airway Equipment
o Drugs to terminate convulsions
Cardiovascular System Toxicity
o Direct Cardiac Effects

Decrease in the rate of depolarization.

There is initially bradycardia followed by cardiac
arrest in the fast conducting tissues of Purkinje
fibers and ventricular muscle.

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SURGERY II: 5.1.1 Regional Anesthesia

Decrease in action potential duration and

effective refractory period.

Due to a decrease in the availability of fast

sodium channels in cardiac membranes.

Bupivacaine is more cardiotoxic. It has a direct

effect on ventricular muscle and because it is
more lipid soluble than lidocaine, it binds tightly
to sodium channels (it is called the fast-in, slowout local anesthetic). Patients who have received
an inadvertent intravascular injection of
bupivacaine
have
experienced
profound
hypotension,
ventricular tachycardia and
fibrillation, and complete atrioventricular heart
block that is extremely refractory to treatment.
The toxic dose of lidocaine is approximately 5
mg/kg; that of bupivacaine is approximately 3
mg/kg.

It is helpful to remember that for any drug or

solution, 1% = 10 mg/mL. For a 50-kg person, the
toxic
dose of
bupivacaine
would
be
approximately 3 mg/kg, or 3 x 50 = 150 mg. A 0.5%
solution of bupivacaine is 5 mg/mL, so 150 mL/5
mg/mL = 30 mL as the upper limit for infiltration.
For lidocaine in the same patient, the calculation
is 50 kg x 5 mg/mL = 250 mg toxic dose. If a 1%
solution is used, the allowed amount would be
250 mg/10 mg/mL = 25 mL..
Direct Peripheral Vascular Effects

Biphasic effect on peripheral vascular smooth

muscle:
Low doses of lidocaine and bupivaine:
vasoconstriction.
Higher doses: vasodilatation with increased
arteriolar diameter.
COCAINE
consistently
causes
vasoconstriction at all concentrations by
inhibiting the uptake of norepinephrine by
premotor
neurons
(Vasogenic
vasoconstriction).
Prevention

Aspiration to detect inadvertent vascular entry

Use of anesthetics with less cardiotoxicity that

are levoisomers which are less cardiotoxic than
the racemic local anesthetic solution
Levobupivacaine
Ropivacaine
Cardiac Resuscitation:

1. Secure the airway

2. Provide oxygenation and ventilation mask

ventilation, intubation

3. Institute cardiac compressions

The effect of local anesthetics on the heart is
just like in other areas of the body: transient
and reversible, therefore, somebody who is
into CVS toxicity from local anesthesia can
be saved by just supporting the physiology.
Cardiac compression and ventilation would
suffice.

Medications
Epinephrine, first line
Amiodarone, may be beneficial
Bretylium

Do not exceed the maximal dose of LA to avoid

toxicity. Use the minimal effective drug concentration
and stay within the recommended total maximal dose
Avoid intravascular injection
Use of sedatives as adjunct to the LA is not without
risk. Hypoxia and hypercarbia may develop and
precipitate cardiac arrest.
Close monitoring is mandatory.

RECOVERY

Score
1
2
3
4
5
6

After the procedure, the patient is sent to the recovery

room for monitoring. To monitor for recovery from
motor blockade, use the Modified Bromage Scoring.
MB Score of 4 with full flexion is a good marker for full
recovery.
Modified Bromage Score as used by Breen et al
Criteria
Complete block (unable to move feet or knees)
Almost complete block (able to move feet only)
Partial block (just able to move knees)
Detectable weakness of hip flexion while supine (full
flexion of knees)
No detectable weakness of hip flexion while supine
Able to perform partial knee bend
Fig.8 Modified Bromage Scoring

GUIDELINES

DOREEN. CARMI. JAMES. HENNA. LOUIE

UERM MEDICINE 2015 B