LOCAL ANAESTHESIA

BY- DR. AVIRAL VERMAP.G. 1st year

Department Of Oral And Maxillofacial Surgery

block transmission of impulses along nerves

short to medium duration of action (1-6 hrs)

useful for pain control

overdoses may cause convulsions

Applied in the vicinity of peripheral nerve ending or major nerve trunks

inhibits action potential generation and propagation

Prevent conduction of electrical impulses from the periphery to the CNS

Produce transient loss of sensory, motor, and autonomic function in a discrete portion of the body without producing unconsciousness

Structural Classification of local anaesthetics

•Examples of amides include lidocaine, bupivacaine and prilocaine. Examples of esters include cocaine, procaine and amethocaine.

The structure of local anesthetics

Cocain Procain Lidocain

Bupivacain MepivacainArticain

Ester

Amides

Esters vs Amides The ester linkage is more easily broken so the ester drugs are

less stable in solution and cannot be stored for as long as amides.

Amide anaesthetics are also heat-stable.  The metabolism of most esters results in the production of

para-aminobenzoate (PABA) which is associated with allergic reaction.

Amides, in contrast, very rarely cause allergic phenomena. For these reasons amides are now more commonly used than esters.

Chemistry

esters vs amides • of simple benzene derivatives

weak bases All carry at least one amine function Administered as hydrochloride salts

the degree of ionization – pKa vs pH– pKa – pH = log proton/unprot

pKa of most local anesthetics is between 8.0 and 9.0

Properties of ideal LA

Reversible action. Non-irritant. No allergic reaction. No systemic toxicity. Rapid onset of action. Sufficient duration of action. Potent. Stable in solutions. Not interfere with healing of tissue. Have a vasoconstrictor action or compatible with VC. Not expensive

Fundamentals Of Impulse Generation And Transmission

Concept behind action of local anaesthesia- prevent conduction and generation of nerve impulse, set up chemical roadblock between the source of impulse and the brain.

NEURON is the fundamental unit of nerve cell. It transmits messages between CNS and all parts of the

body. It is of 2 types:-

Sensory (afferent) Motor (efferent)

Sensory Neuron

It transmits pain sensation with 3 major portions:- Peripheral process (dendritic zone) composed of an

arborisation of free nerve endings in the most distal segment of sensory neuron.

Axon- Thin cable like structure, has free nerve endings that respond to stimulation produced in the tissues in which they lie provoking an impulse transmitted via axon.

Cell Body- located at a distance from axon, provide vital metabolic support for the entire neuron.

Motor Neuron

They transmit nerve impulses from the CNS to the periphery

Their cell body is interposed between axon and dendrites.

Axon branches with each branch ending as a bulbous axon terminal (or button)

Axon terminals synapse with muscle cells.

Physiology Of Peripheral Nerves

The function of nerve is to carry messages from one part of the body to another in the form of electrical action potential called IMPULSES initiated by chemical, mechanical, thermal or electrical stimuli.

Action Potential- transient depolarization of membrane which leads to brief increase in permeability of membrane with delayed increase in permeability of potassium.

THE ELECTRICAL IMPULSE

Nerve impulses are conducted by a wave of action potentials. When a stimulus is great enough to reach the threshold potential of -55mV, sodium ions flow into the neurone. It does so via sodium gates to produce depolarisation. When depolarised, the membrane potential is reversed to +40 mV.

At the same time, there is passive outwards diffusion of potassium ions to bring about repolarisation and the membrane potential is again reversed to -70mV

Electrophysiology Of Nerve Conduction

Nerve possesses a resting potential which is negative electrical potential of -70mV because of differing in concentration of ions on either side of membrane.

Internal to the membrane is negative in respect to the outer part.

STEP 1

Stimulation excites the nerve cells. Initial phase of slow depolarization, the electrical potential

in the nerve becomes slightly less negative. Falling electrical potential reaches a critical level.

Extremely rapid phase of depolarisation results reaches to a threshold potential or firing potential where reversal of electrical potential across nerve membrane occurs.

Internal to the membrane becomes positive in respect to the outside (+40mV)

STEP 2

This is a phase of Repolarisation. Electrical potential gradually becomes more

negative in respect to the outside until -70mv is achieved.

Step1- 0.3msec Step2- 0.7msec

Mechanism of action

- Inhibiting excitation of nerve endings or blocking conduction in peripheral nerves. Binding to and inactivating sodium channels.

- Local Anaesthetics are alkaloid bases that are combined with acids, usually hydrochloric, to form water soluble salts. All anaesthetic salts are formed by a combination of weak base and a strong acid. The salts are used because they are stable and soluble in water; water solubility isnecessary for their diffusion through interstitial fluids to the nerve fibers.

- Sodium influx through these channels is necessary for the depolarization of nerve cell membranes and subsequent propagation of impulses along the course of the nerve.

- when a nerve loses depolarization and capacity to propagate an impulse, the individual loses sensation in the area supplied by the nerve

- block nerve fiber conduction by acting on nerve membranes

- inhibit sodium ion activity

- blocks depolarization--> blocks nerve conduction

When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited. LA drugs bind more readily to sodium channels in activated state, thus onset of neuronal blockade is faster in neurons that are rapidly firing. This is referred to as state dependent blockade.

Fig.

Effect of PH

Local anesthetics are weak bases and are usually formulated as the hydrochloride salt to render them water-soluble. At the chemical's pKa the protonated (ionized) and unprotonated (unionized) forms of the molecule exist in an equilibrium but only the unprotonated molecule diffuses readily across cell membranes. Once inside the cell the local anesthetic will be in equilibrium, with the formation of the protonated (ionized form), which does not readily pass back out of the cell. This is referred to as "ion-trapping".

Effect of PH

LA are weak bases and their activity increases by increasing PH

This because if large amount of a drug is unpolar, it will facilitate its penetration through the cell membrane

Once the drug has penetrated the lipid barrier and reach its site of action it ionized and the ionized form is responsible for LA activity

Acidosis such as caused by inflammation at a wound partly reduces the action of local anesthetics. This is partly because most of the anesthetic is ionized and therefore unable to cross the cell membrane to reach its cytoplasmic-facing site of action on the sodium channel.

Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying nociceptive impulses), non-myelinated axons, then large myelinated axons. Thus, a differential block can be achieved (i.e. pain sensation is blocked more readily than other sensory modalities).

Disruption of ion channel function via specific binding to sodium channels, holding them in an inactive state.

Disruption of ion channel function by the incorporation of local anaesthetic molecules into the cell membrane .

Small nerve fibres are more sensitive than large nerve fibres

Myelinated fibres are blocked before non-myelinated fibres of the same diameter.

Thus the loss of nerve function proceeds as loss of

pain, temperature, touch, proprioception, and then skeletal muscle tone. This is why people may still feel touch but not pain when using local anaesthesia.

LA and pH

All local anaesthetic agents are weak bases, meaning that they exist in two forms: unionised (B) and ionised (BH+).

The pKa of a weak base defines the pH at which both forms exist in equal amounts.

As the pH of the tissues differs from the pKa of the specific drug, more of the drug exists either in its charged or uncharged form.

Physicochemical characteristics of a local anaesthetic affect its function

The aromatic ring structure and hydrocarbon chain length determine the lipid solubility of the drug.

The more lipid soluble drug penetrates the cell membrane more easily to exert its effect.

Thus bupivacaine – which is highly lipid soluble – is approximately four times more potent than lidocaine.

Binding of local anesthetic to receptor

The affinity of the receptor site within the sodium channel for the LA is a function of the state of the channel

drugs binds to open and inactivated channels, therefore for those with higher activity/firing

use dependence - rapidly firing fibers are usually blocked before slowly firing fibers.

There are two theories on the subject of how sodium channels are blocked:

1. Non-specific membrane expansion theory2. Specific receptor theory

Non-specific membrane expansion theory: The lipophilic part of the local

anaesthetic attaches to the cell membrane to cause swelling. This then reduces the size of the sodium channel to obstruct the flow of sodium ions.

Specific receptor theory:

The hydrophilic charged amino terminal binds to specific receptors of the sodium gates to block the passage of sodium ions

The duration of action

The duration of action of the drug is also related to the length of the intermediate chain joining the aromatic and amine groups.

Protein binding , Procaine is only 6% protein bound and has a very short duration of action, wherease bupivacaine is 95% protein bound. bupivacaine have a longer duration of action .

Absorption and distribution

Some of the drug will be absorbed into the systemic circulation: how much will depend on the vascularity of the area to which the drug has been applied.

The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. the more protein bound the agent, the longer the duration of action as free drug is more slowly made available for metabolism. 

Metabolism and excretion 

Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver. Ester metabolite excretion is renal. 

Amides are metabolised hepatically by amidases. This is a slower process, hence their half-life is longer and they can accumulate if given in repeated doses or by infusion.

Adverse Effects

CNS: excitation followed by depression (drowsiness to unconsciousness and death due to respiratory depression.

Cardiovascular System: bradycardia, heart block, vasodilation (hypotension)

Allergic reactions: allergic dermatitis to anaphylaxis (rare, but occur most often by ester-type drugs).

Uses

Local anesthesia.

Ventricular arrhythmia.

Decrease haemodynamic response to tracheal intubation also decrease cough.

Treatment of epileptic fits.

Surface/topical

anesthesia

Local infiltration

Peripheral nerve block

 Bier block (IV regional anesthesia)

 Epidural anesthesia

 Spinal anesthesia

Six Placement Sites

Topical/Surface anesthesia

For Application to mucous membranes:

 Nose- Mouth- Esophagus- Tracheobronchial tree- Genitourinary tract.

Commonly used drugs: Cocaine (4%-10%).  > 50% of rhinolaryngologic

cases (USA).  Unique pharmacological

property: produces localized vasoconstriction as well as anesthesia.

 Localized vasoconstriction: less bleeding. improved surgical field

visualization.

Cocaine substitution:  lidocaine (Xylocaine) -

oxymetazoline (Afrin) combinations.

 tetracaine (pontocaine)-oxymetazoline (Afrin) combinations.

Tetracaine (pontocaine) (1%-2%).

Lidocaine (Xylocaine) (2%-4%).

Ineffective agents: Procaine (Novocain) &

chloroprocaine (Nesacaine): poor mucous membrane penetration.

Nebulized lidocaine (Xylocaine)-- surface anesthesia

• Upper & lower respiratory tract prior to bronchoscopy or fiber-optic Laryngoscope.

• Treatment for intractable cough.

• Normal subjects: No effect on airflow resistance (they produce some bronchodilation).

• Patients with asthma: nebulized lidocaine (Xylocaine) may increase airflow resistance (bronchoconstriction)-- concern if bronchoscopy is intended for this patient group.

Systemic concentration following nebulized lidocaine (Xylocaine)

Following mucosal absorption: systemic. concentration may be similar to IV injection.

Reasons:

Large surface area. Significant vascularity of tracheobronchial region.

Skin Surface Application

Barrier: keratinized skin layer

Higher local anesthetic concentrations required:

o  5% lidocaine (Xylocaine)-prilocaine (Citanest) cream {2.5% lidocaine (Xylocaine) & 2.5% prilocaine (Citanest)}

no local irritation. even absorption. no systemic toxicity.

Combination of local anesthetic:

Definition: eutectic mixture of local anesthetics (EMLA) .General definition: eutectic--said of a mixture which has the

lowest melting point which it is possible to obtain by the combination of the given components. 

Melting point of combined drug is lower then either lidocaine (Xylocaine) or prilocaine (Citanest) alone.

Clinical uses of EMLA applications-- pain relief for:

Venipuncture

 Lumbar puncture

 Arterial cannulation

Local Infiltration

Definition: Extravascular placement of the local anesthetic in the region to be anesthetized.

 Example: subcutaneous local anesthetic injection in support of intravascular cannula placement.

Preferred local anesthetics for local infiltration:

 Most common: lidocaine (Xylocaine).  Other choices: 0.25% Ropivacaine (Naropin) or

Bupivacaine (Marcaine) (effective for pain management at inguinal operative location),

Duration of action: 

Duration extended by 2x using 1:200,000 epinephrine.

Caution: Epinephrine-containing local anesthetic solution should not be injected intracutaneously (intradermal) or into tissues supplied by "end-arteries" such as ears, nose, fingers because vasoconstriction may be sufficiently severe to produce tissue ischemia and gangrene.

LOCAL ANAESTHESIA

VASOCONSTRICTORSREGIONAL ANALGESIA

TOXICITY

DATE: 09/12/13

Presented By-

Dr. Aviral Verma

P.G. 1st Year

Department Of Oral And Maxillofacial Surgery

SLIDES_68

DEFINITION

- Local Anaesthesia is defined as a transient reversible loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves.

- A Local Anesthetic is a drug that causes reversible local anesthesia and a loss of nociception. when it is used on specific nerve pathways (nerve block), effects such as analgesia (loss of pain sensation) and paralysis (loss of muscle power) can be achieved.

CLASSIFICATION OF LOCAL ANAESTHESIA

1. Esters (of benzoic acid)

-Butacaine

-Cocaine

-Benzocaine

-Hexylcaine

-Piperocaine

-Tetracaine

2. Esters (of paraaminobenzoic acid)

-Chloroprocaine

-Procaine

-Propoxycaine

3. Amides

-Articaine

-Bupivacaine

-Dibocaine

-Etidocaine

-Lidocaine

-Mepivacaine

-Prilocaine

4. Quinoline

-Centbucridine

3- Combinations

- Lidocaine/Prilocaine(emla)

4- Natural local anesthetics

- Saxitoxin and Tetrodotoxin

-Naturally occurring local anesthetics not derived from cocaine are usually neurotoxins, and have the suffix -toxin in their names.

-Unlike cocaine produced local anesthetics which are intracellular in effect,

-Saxitoxin & Tetrodotoxin bind to the extracellular side of sodium channels.

Indications for local anesthesia

-Most frequent use: regional anesthesia.

- Analgesic espescially post operative pain.

- Lidocaine (xylocaine) also reduces blood pressure response to direct laryngoscopic tracheal intubation, an effect probably secondary to generalized cardiovascular depression.

- Treatment of intractable cough.

Contraindications for local anaesthesia

- Heart block, second or third degree (without pacemaker)

- Severe sinoatrial block (without pacemaker).

- Serious adverse drug reaction to lidocaine or amide local anaesthetics.

- Concurrent treatment with quinidine, flecainide, disopyramide, procainamide (class 1 antiarrhythmic agents).

- Prior use of amiodarone hydrochloride

- Hypotension not due to arrhythmia.

- Bradycardia.

- Accelerated Idioventricular Rhythm.

VASOCONSTRICTORS

- Vasoconstrictors are the drugs that constricts the blood vessels and thereby control tissue perfusion.

- They are added to local anaesthesia to oppose the vasodilatory action of local anesthetic agent.

What happens if you don’t use a vasoconstrictor?

*Plain local anesthetics are vasodilators by nature

1) Blood vessels in the area dilate2) Increase absorption of the local anesthetic into the cardiovascular system (redistribution)3) Higher plasma levels increased risk of toxicity4) Decreased depth and duration of anesthesia diffusion from site5) Increased bleeding due to increased blood perfusion to the area

1) Patient is not numb as long without

epinephrine

2) Patient is simply not as numb

3) More anesthetic goes into the circulation

4) Increased bleeding; more blood to area

Why You Need Vasoconstrictors Vasoconstrictors resemble adrenergic drugs and are called

sympathomimetic, or adrenergic drugs

1) Constrict blood vessels decrease blood flow to the surgical site

2) Cardiovascular absorption is slowed lower anesthetic blood levels

3) Local anesthetic blood levels are lowered lower risk of toxicity

4) Local anesthetic remains around the nerve for longer periods increased duration of anesthesia

5) Decreases bleeding

Vasoconstrictors should not be used in the following locations

Fingers Toes Nose Ear lobes

CLASSIFICATIONChemical Structure

Catecholamines Noncatecholamines*Epinephrine Amphetamine*Norepinephrine Methamphetamine*Levonordefrin Ephedrine Isoproterenol Mephentermine Dopamine Hydroxyamphetamine

Metaraminol Methoxamine Phenylephrine

Felypressin synthetic analogue of vasopressin (ADH); not in U.S.

Modes of Action

3 Classes of Sympathomimetic Amines:

1)*Direct Acting directly on adrenergic receptors

2) Indirect Acting use norepinephrine release

3) Mixed Acting both direct and indirect actions

The dilution of vasoconstrictors is commonly referred to as a ratio i.e., 1:50,000; 1:100,000; 1:200,000 etc,…

A concentration of 1:1,000 means that there is 1 gram

(1000 mg) of solute (drug) contained in 1000 ml (1 L) of

solution, therefore, 1:1,000 dilution contains 1000 mg

in 1000 ml or 1.0 mg/ml of solution (1000 ug/ml)

The concentration of 1:1,000 is very concentrated

(strong); a much more dilute form is used in dentistry

for example, 1:50,000 > 1:100,000 > 1:200,000

(1:100,000 = 0.01 mg/1 ml of solution)

1:50,000 epinephrine is used to stop bleeding in a surgical area; this amount of epinephrine is not used for block anesthesia

- Resting plasma epinephrine levels are doubled when one cartridge of 2% Lidocaine 1:100,000 epinephrine is injected

- Recent evidence suggests that epinephrine plasma levels equivalent to those achieved during moderate to heavy exercise occur after intraoral injection

- Moderate increase in cardiac output and stroke volume occurs

- Blood pressure and heart rate are minimally affected

- IV administration of .015 mg of epinephrine with Lidocaine can increase heart rate 25 to 75 beats and increase systolic blood pressure 20 to 70 mmHg

“Epinephrine reaction” causes tachycardia, sweating, apprehensionand pounding in the chest (palpitations)

2 Types of Adrenergic Receptors:

1) Alpha -contraction of smooth muscle in blood vessels

-vasoconstriction -Alpha 1 excitatory; post-synaptic -Alpha 2 inhibitory; post-synaptic

2) Beta -smooth muscle relaxation -vasodilation/bronchodilation -cardiac stimulation, i.e., increased

rate and strength of contraction

2 Types of Beta Receptors:

1) Beta 1-found in heart and small intestines-produces cardiac stimulation and lipolysis

2) Beta 2-found in bronchi of the lung, vascular beds

and uterus-produces bronchodilation and vasodilation

NOREPINEPHRINE Norepinephrine lacks Beta 2 actions (bronchodilation and

vasodilation) and produces intense peripheral vasoconstriction with possible dramatic elevations in blood pressure

Norepinephrine’s side effect ratio is 9 times higher than epinephrine

Norepinephrine’s use in dentistry is not recommended and its use is diminishing around the world

Epinephrine remains the vasopressor of choice in dentistry

*Norepinephrine is not used because of its many side effects

Norepinephrine

Epinephrine Sodium Bisulfite antioxidant added 18 months shelf life Acts directly on Alpha and Beta receptors Beta effects predominate Increases force / rate of contraction Increases stroke volume Increases myocardial O2 use Increases cardiac output / heart rate Increases dysrhythmias and PVCs Increases coronary artery perfusion Increases systolic blood pressure Decrease in cardiac efficiency

Alpha receptor stimulation leads to hemostasis initially

Beta 2 actions predominate leading to vasodilation 6 hours after a surgical procedure

Potent bronchodilator (asthma)

Not a potent CNS stimulant

Increases oxygen consumption in all tissues of the body

Reuptake by adrenergic nerves terminates epinephrine action

Ventricular fibrillation is possible

Epinephrine

1.8 ml Cartridge of 2% Lidocaine 1:100,000 epi

Maximum Epinephrine: 11 Cartridges

Maximum Anesthetic: 300 mg

1.8 ml Cartridge of 2% Lidocaine 1:200,000 epi

Maximum Epinephrine: 22 Cartridges

Maximum Anesthetic: 300 mg

The maximum amount of 2% Lidocaine 1:100,000 epinephrine that can be used is 300 mg which is 8.3 cartridges regardless of the patient’s weight; so the maximum epinephrine will only be achieved after you have already surpassed the maximum amount of anesthetic allowable

8.3 cartridges

American Heart Association says that the

typical concentrations of vasoconstrictors

in local anesthetics are not contraindicated

in patients with cardiovascular disease so

long as aspiration, slow injection and the

smallest effective dose is administered;

ASA III and ASA IV pose the largest risk

How much Epinephrine in CV patients?

Maximum Epinephrine

.04 mgTwo cartridges of 1:100,000 epinephrine

Clinical Applications of Epinephrine

1) Management of acute allergic reactions2) Management of bronchospasm3) Management of cardiac arrest4) Vasoconstrictor for hemostasis5) Vasoconstrictor to decrease absorption into CVS6) Vasoconstrictor to increase depth of anesthesia7) Vasoconstrictor to increase duration of anesthesia8) To produce mydriasis (excessive pupil dilation)

Contraindications to Using Vasoconstrictors

1) Blood pressure > 200/115 mm Hg

2) Severe cardiovascular disease ASA IV+

3) Acute myocardial infarction in the last 6 months

4) Anginal episodes at rest

5) Cardiac dysrhythmias that are refractory to drug treatment

6) Patient is in a hyperthyroid state of observable distress

7) Levonordefrin and Norepinephrine are absolutely contraindicated in patients taking tricyclic antidepressants (Elavil, Sinequan)

Epinephrine Norepinephrine

Receptor activity Powerful stimulant of α and β receptorsWith higher doses α effects predominates, whereas lower doses primarily produce β receptor activity

Stimulates both α and β receptors, but α effect predominates

Blood Pressure (BP) Lesser effect Greater increase in BP than epinephrine

Central Nervous System Greater effect of stimulation of central nervous system in large doses

Does not stimulate central nervous system in therapeutic doses

Cardiovascular system Greater effect of stimulation of CVS

Bronchi Dilatation Little or no effect

Heart Rate (HR) Increase in HR is of greater degree

Increase in HR is of lesser degree

Various dilutions available in India and MRD (in terms of m) for normal healthy adult individuals and medically compromised individuals

Dilutions Normal adult healthy individuals

(0.2 mg/appointment)(ml)

Medically compromised individuals

(0.04 mg/appointment)(ml)

1:80,000 16 3.2

1:1,00,000 20 4

1:2,00,000 40 8

REGIONAL ANAESTHESIA

Regional anesthesia - Definition

Rendering a specific area of the body, e.g. foot, arm, lower extremities, insensate to stimulus of surgery or other instrumentation

Regional anesthesia - Uses

Provide anesthesia for a surgical procedure

Provide analgesia post-operatively or during labor and delivery

Diagnosis or therapy for patients with chronic pain syndromes

Regional anesthesia - types

Topical

Local/Field

Intravenous block (“Bier” block)

Peripheral (named) nerve, e.g. radial n.

Plexus - brachial, lumbar

Central neuraxial - epidural, spinal

Topical Anesthesia Application of local anesthetic to mucous membrane - cornea,

nasal/oral mucosa

Uses : awake oral intubation, nasal intubation, superficial surgical procedure

Advantages : technically easy minimal equipment

Disadvantages : potential for large doses leading to toxicity

Local/Field Anesthesia

Application of local anesthesia subcutaneously to anesthetize distal nerve endings

Uses: Suturing, minor superficial surgery, line placement, more extensive

surgery with sedation

Advantages: minimal equipment, technically easy, rapid onset

Disadvantages: potential for toxicity if large field

IV Block - “Bier” block

Injection of local anesthetic intravenously for anesthesia of an extremity

Uses any surgical procedure on an extremity

Advantages: technically simple, minimal equipment, rapid onset

Disadvantages: duration limited by tolerance of tourniquet pain and Toxicity.

Peripheral nerve block

Injecting local anesthetic near the course of a named nerve

Uses: Surgical procedures in the distribution of the blocked nerve

Advantages: relatively small dose of local anesthetic to cover large area; rapid onset

Disadvantages: technical complexity, neuropathy

Plexus Blockade

Injection of local anesthetic adjacent to a plexus, e.g cervical, brachial or lumbar plexus

Uses : surgical anesthesia or post-operative analgesia in the distribution of the plexus

Advantages: large area of anesthesia with relatively small dose of agent

Disadvantages: technically complex, potential for toxicity and neuropathy.

Central Neuraxial Blockade - “Spinal”

Injection of local anesthetic into CSF

Uses: profound anesthesia of lower abdomen and extremities

Advantages: technically easy (LP technique), high success rate, rapid onset

Disadvantages: “high spinal”, hypotension due to sympathetic block, post dural puncture

headache.

Spinal Anesthesia

Definition

Anesthesia following local anesthetic injection into lumbar subarachnoid space

Site of action:

 Primary: preganglionic fibers leading the spinal cord in the anterior rami  Secondary: superficial spinal cord layers

Spinal anesthesia

Central Neuraxial Blockade - “epidural”

Injection of local anesthetic in to the epidural space at any level of the spinal column

Uses: Anesthesia/analgesia of the thorax, abdomen, lower extremities

Advantages: Controlled onset of blockade, long duration when catheter is placed, post-operative

analgesia.

Disadvantages: Technically complex, toxicity, “spinal headache”

Epidural Anesthesia

Definition

Anesthesia caused by local anesthetic solutions injected into epidural space.

Mechanism

  Direct action on nerve roots and spinal cord following local anesthetic diffusion across the dura.

Epidural anesthesia

Toxicity of local anaesthesia

1- Causes

2- Factors reducing toxicity.

3- Signs and symptoms.

4- Treatment of toxicity.

CAUSES

Accidental rapid intravenous injection.

Rapid absorption, such as from a very vascular site ie mucous membranes.

Overdose .

FACTORS REDUCING TOXICITY

Decide on the concentration of the local anaesthetic that is required for the block to be performed. Calculation of the total volume of drug should be done.

Use the least toxic drug available.

Use lower doses in frail patients or at the extremes of ages.

Always inject the drug slowly (around 10ml /minute) and aspirate regularly looking for blood to indicate an accidental intravenous injection

If Injection of a test dose of 2-3ml of local anaesthetic containing adrenaline is accidentally given intravenously it will often (but not always) cause significant tachycardia.

Add adrenaline (epinephrine) to reduce the speed of absorption. The addition of adrenaline will reduce the maximum blood concentration by about 50%. Usually adrenaline is added in a concentration of 1:200,000, with a maximum dose of 200 micrograms.

Make sure that the patient is monitored closely by the anaesthetist or a trained nurse during the administration of the local anaesthetic and following the surgery.

SIGNS AND SYMPTOMS OF LOCAL ANAESTHETIC TOXICITY:

1-CNS toxicity :

Early or mild toxicity: light-headedness, dizziness, tinnitus, circumoral numbness, abnormal taste, confusion and drowsiness.

Severe toxicity: tonic-clonic convulsion leading to progressive loss of consciousness, coma,.respiratory depression, and respiratory arrest.

2-CVS toxicity:

Early or mild toxicity: tachycardia and rise in blood pressure. This will usually only occur if there is adrenaline in the local anaesthetic. If no adrenaline is added then bradycardia with hypotension will occur.

Severe toxicity: Usually about 4 - 7 times the convulsant dose needs to be injected before cardiovascular collapse occurs. Collapse is due to the depressant effect of the local anaesthetic acting directly on the myocardium.

ADVANTAGES OF LOCAL ANAESTHESIA

During local anesthesia the patient remains conscious

Maintains his own airway.

Excellent muscle relaxant effect.

It requires less skilled nursing care as compared to other anesthesia like general anesthesia.

Non inflammable.

Less pulmonary complications

Aspiration of gastric contents unlikely.

Less nausea and vomiting.

Contracted bowel so helpful in abdominal and pelvic surgery.

Postoperative  analgesia.

There is reduction surgical stress.

Earlier discharge for outpatients.

Suitable for patients who recently ingested food or fluids.

Local anesthesia is useful for ambulatory patients having minor procedures.

Ideal for procedures in which it is desirable to have the patient awake and cooperative.

Less bleeding.

Expenses are less.

DISADVANTAGES OF LOCAL ANAESTHESIA

There are individual variations in response to local anesthetic drugs.

Rapid absorption of the drug into the bloodstream can cause severe, potentially fatal reactions.

Apprehension may be increased by the patient's ability to see and hear. Some patients prefer to be unconscious and unaware.

Direct damage of nerve.

Post-dural headache from CSF leak.

Hypotension and bradycardia through blockade of the sympathetic nervous system.

Not suitable for extremes of ages.

Multiple needle pricks may be needed.

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