Local Anesthesia – Advantages, Ideal Properties


               An anesthesia is derived from the word (an-without Aisthetos-sensation it was given by oliver bendel in 1846.) Local anesthesia is a state of controllable,reversible insensibility in which sensory perception and motor responses are both markedly depressed. where as analgesia is the temporary abolition or diminution of pain reception. It allows patient to undergo surgical and dental procedures with reduced pain and distress.  It is also used for relief of non surgical pain and to enable diagnosis of the cause of some chronic pain condition. Anaesthetist sometimes combine both general and local anaesthesia techniques.

lignocaine with adrenaline

Anaesthesia is defined as  loss of sensation with or without loss of consciousness”.

There are two basic types of anesthesia

  1. General Anesthesia

general anesthesia

2. Local Anesthesia

local anesthesia

General Anesthesia Local anesthesia
Site of action CNS Peripheral nerves
Mechanism of action Block axonal conduction Depress  synaptic transmission
Route of adminstration Inhalational or I/V Topical application or local injection
Area of body involved Whole body Restricted area
Consciousness Lost Unalatered
Care of vital functions Essential Usually not needed

The effect of local anesthetic are most necessarily limited to sensory nerve fibers alone. When these drugs are brought into direct contact with the other parts of the mixed spinal nerves they can also affect in the functioning of the somatic  motor and sympathetic nerve fibers. This can then interfere with the tone of skeletol and smooth muscles innovated bthey these nerves.

In addition local aesthetis that are systematically absorbed from site of their application may be carried by the blood stream to the brain, heart, liver and other organ. The effect  of these drug on the centaral nervous system and circulatory system can then cause serious toxic reaction. Thus the anesthesiologist employs special technique of administrations which are intended to

  1. Place the local anesthetic solution at some presiced local point along the course of peripheral nerves.
  2. They will keep the drug systemic absorption at the rate so slow that it doesn’t goes up to the toxic levels.

There are many methods of inducing local anesthesia for example :

  1. Mechanical trauma
  2. Anoxia
  3. Low temperature
  4. Chemical irritants
  5. Neurolactic agent (alcohol,phenol)
  6. Chemical agents (local anesthetics)


  • The history of local anesthesia started
  • In 1859, when cocaine was isolated by “Niemann”.


  • In 1884, the ophthalmologist Koller used cocaine for topical anesthesia in ophthalmological surgery.
  • In 1884, regional anesthesia in the oral cavity was first performed by surgeon Halsted, for removing wisdom tooth without pain.


  • In 1905, Einhorn reported the synthesis of procaine, which was first ester type local anesthetic agent. Procaine was most commonly used local anesthetic for more than four decades.


  • In 1943, Lofgren synthesized lidocaine, which was first “modern” local anesthetic agent.  Lidocaine was marketed in 1948 & is upto now most commonly used local anesthetic in dentistry worldwide.
  • Other amide local anesthetics were introduced into clinical use:
  1. Mepivacaine 1957,
  2. Prilocaine 1960,
  3. Bupivacaine 1963.
  • In 1969, Articaine was synthesized by the chemist “Muschaweek” and was approved in 1975 as local anesthetic agent in Germany.


  • Local anesthesia has been defined as loss of sensation in circumscribed area of body caused by depression of excitation in nerve endings or an inhibition of conduction process in peripheral nerves.(Stanley F. Malamed)


  • Local anesthetic are the drugs have a little or no irritating effects when injected into the tissues and that will temporarily interrupt conduction when absorbed into the nerves(Monheims)


  • Local anesthesia has been defined as direct administration of anesthetic agent to tissue to include the absence of sensation in small area of body (Mosby’s dictionary)


I. Based on bioavailability

  • Natural – eg. cocaine.
  • Synthetic nitrogenous compound –  eg. procaine, benzocaine, lignocaine & bupivacane
  • Non Nitrogenous compounds – benzyl alcohol
  • Miscellaneous – clove oil , phenol.

II. According to structure:

  1. Esters  :

Benzoic acid esters:

    • Benzocaine
    • Cocaine

Para-amino benzoic esters:

    • Tetracaine
    • Chlorprocaine
    • Procaine
    • Propoxycaine

amino esters and amino amides

2. Amides :

  • Articaine
  • Bupivacaine
  • Etidocaine
  • Lidocaine
  • Mepivacaine
  • Prilocaine

3. Quinolones : Centbucridine

III. According to duration of action :

1) Ultra Short acting anesthetic – less than 30 min

  • Procaine without a vasoconstrictor
  • 2 chloroprocaine without vasoconstrictor
  • 2% lidocaine without a vasoconstrictor

2) Shot acting local anesthetic – 45 to 75 min

  • 2% lidocaine with 1:100000 epinephreine
  • 2% mepivacaine with 1: 20000 lavonordefrin
  • 4% prilocaine when used to nerve block

3) Medium acting anesthetics 90 – 150min

  • 4% prilocaine with 1:200000 epinephrive
  • 2% lidocaine and 2% mepivacaine with a vasoconstrictor
  • May produce pulpal anesthesia of this duration

4) Longer acting anesthestic – 180 min or longer 

  • 0.5% bupivacaine with 1: 200000 epinephrine
  • 0.5% or 1.5% etidocaine with 1:200000 epinephrine

IV. According to mechanism of action

  • Class A : Agents acting at receptor site on external surface of nerve membrane

    eg: Biotoxins

  • Class B : Agents acting at receptor sites on internal surface of nerve membrane

    eg: scorpion venom

  • Class C : Agents acting by receptor independent physio-chemical mechanism

    eg: Benzocaine

  • Class D :Agents acting in combination of receptor dependent-independent mechanism                     eg: Lidocaine, Mepivacaine, PrilocaineV. ACCORDING TO  MODE OF ACTION:

VIACCORDING TO ORIGIN (Vinod Kapoor 2nd Edition)

Natural :- Cocaine 

  • Synthetic nitrogenous compounds 

a) Amino esters of para amino benzoic acid :- Procaine

b) Alkyl esters of Paba (Benzocaine)

c) Amino esters of Meta amino Benzoic acid (MABA) Unacaine

d) Amino –amides (xylocaine) (Bupivacaine)

  • Systemic non nitrogenous compounds (Benzyl alcohol)
  • Miscellaneous drugs (Clove oil/Phenon) 

local anesthesia color coding



  1. Lidocaine hydrochloride (20mg/ml) –  Local anesthetic agent
  2. Adrenaline bitarterate (epinephrine) (0.012mg) –  vasoconstrictor
  3. Methylparaben (1mg) –  Preservative
  4. Thymol –  Fungicide
  5. Sodium metabisulphate (0.5mg) –  Reducing agent
  6. Sodium chloride (6mg) –  Isotonic solution
  7. Ringer’s lactate solution : Vehicle
  8. Distilled water :  Diluting agent
  9. sodium hydroxide :  ph adjuster

1) Lidocaine hydrochloride

In 1940, the first modern local anesthetic agent was lidocaine, It developed as a derivative of xylidine which belongs to amide class. It is hypo allergenic. Sets on quickly produces a desired anesthesia effect for several hours.

lidocain hydrochloride

Mechanism of action

Lidocaine stabilizes the neuronal membrane by inhibiting ionic fluxes, required for initiation and conduction of nerve impulses, thereby effecting local anesthetic action.


Excessive blood levels may cause change in output, total peripheral resistance and mean arterial pressure. These changes may be attributable to a direct depressant effect of local anesthetic agent on various components of CVS. The net effect is normally a modest hypotension when there commended dosages are not exceeded.

Pharmacokinetics & metabolism lidocanine is absorbed following topical administration to mucous membrance, its rate and extent of absorption being dependent upon concentrated and total dose administered. The specific site of application and duration of exposure. In general, the rate of absorption of local anesthetic agent is following topical application occur most rapidly after intrathecal administration. Lidocaine is also well absorbed from GIT, but little intact drug appears in circulation because of biotransformation in liver.

The plasma binding of lidocaine is dependant upon drug concentration and fraction bound decreases with increasing concentration. At concentration of 1 to 4 mcg of free base /ml ,60 to 80 % if lidocaine is protein bound. Binding is also dependent upon plasma concentration of alpha and glycoprotein.

Lidocaine crosses blood brain barriers and placental barriers presumably by passive diffusion.

Lidocaine is metabolized rapidly by liver and its metabolites and unchanged drug are excreated by kidney biotransformation include oxidative dealkylation, a major pathway of biotransformation yields the metabolites monoethylglycinxylidine and glycinexylidine. The pharmacological and toxicological action of these metabolites are similar to but less potent than those of lidocaine, Approximately 90% lidocaine administered is excreted in the form of various  metabolites and less than 10% excreted unchanged .

The primary metabolite in urine is a conjugate of 4-hydroxy,2,6-fimryhylaniline. The elimination of halflife of lignocaine as IV Bolus injection is typically 1.5 to 2 hrs. the half life may be prolonged few fold more in patient with life dysfunction. Renal dysfunction does not lignocaine kinetic but may increases the accumulation of metabolites. Factor such as acidosis and uses of CNS stimulants depressant affect CNS level of lignocaine required to produce overt systemic effects.

2) Adrenaline bitarterate (epinephrine) 

Adrenaline bitarterate is a hormone neurotransmitter. It increases the heart rate constrict the blood vessels, dilates air passage and participate in fight of flight response of the sympathetic nervous system. Chemically epieprine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenyalanine and tyrosine.

Adrenaline was first synthesized by “Friedrich Stolz” and “Henry Drysdale dakin” in the laboratory.

Epinephrine added to injectable form of a number of local anesthetics, such as bupivacaine a lignocaine, as a vasoconstrictor to retard the absorption and therefore prolong the action of the anesthetic agent. Some of the adverse effects of local anesthetic use, such as apprehension, tachycardia or tumour may be caused by epinephrine (Cannon W.B., 1129) American journal of physiology.



The addition of vasoconstrictor (Adrenaline) to a local anesthetic agent causes constriction of blood vessels and thereby controls tissue perfusion. The net effects caused by addition of vasoconstrictors to local anesthetic agents are :

  1. It decreases the blood flow to the site of injection, because of vasoconstriction.
  2. It decreases the rate of absorption of local anesthetic agent into cardiovascular system.
  3. It lowers the plasma level of local anesthetic agent (Cannall et al, 1975) and Wildsmith et al, 1977), thereby decreasing the risk of systemic toxicity of local anesthetic agent.
  4. Higher volumes of local anesthetic agent remain in and around the nerve for longer periods; thereby increasing the duration of action of most local anesthetic agents (Brown, 1968).
  5. It decreases bleeding at the site of injection because of decreased perfusion. This is useful when increased bleeding is expected during a surgical procedure (Carpenter et al, 1989; and Myers and Heckman, 1989).

3) Methylparaben

Many of  the local anesthetic solution containing  methyl paraben which is used as a known local anesthetic. Methylparaben had been associated with few allergic reaction therefore care full consideration must be given to this compound. When true allergic reaction has been manifested following the use of local anesthetic solution containing methylparaben.

It has got phenol like action, it acts by denaturation of protein and its antimetabolites present in a low conc. of 0.1 to 0.3% in local anesthetic solution.

Methylparaben, also methyl paraben, one of the parabens, is a preservative with the chemical formula CH3 (C6H4(OH)COO). It is the methyl ester of p-hydroxybenzoic acid.


Methylparaben is an anti-fungal agent often used in a variety of cosmetics and personal care products. It is also used as a food preservative. Methylparaben is commonly used as a fungicide in Drosophila food media. Usage of methylparaben is known to slow Drosophila growth rate in the larval and pupal stages.

Methylparaben is produced naturally and found in several fruits, primarily blueberries, along with other parabens. There is no evidence that methylparaben or propylparabens are harmful at concentrations typically used in body care or cosmetics. Methyl and propylparabens are considered GRAS (generally regarded as safe) for food and cosmetic antibacterial preservation. Methylparaben is readily metabolized by common soil bacteria, making it completely biodegradable.

Methylparaben is readily absorbed from the gastrointestinal tract or through the skin. It is hydrolyzed to p-hydroxybenzoic acid and rapidly excreted without accumulation in the body.Acute toxicity studies has shown that methylparaben is practically non-toxic by both oral and parenteral administration. In a population with normal skin, methylparaben is practically non-irritating and non-sensitizing; however, allergic reactions to ingested parabens have been reported. Studies indicate that methylparaben applied on the skin may react with UVB leading to increased skin aging and DNA damage.

4) Thymol

Thymol (also known as 2-isopropyl-5-methylphenol), (IPMP) is a natural monoterpene phenol derivative of cymene, C10H14O, isomeric with carvacrol, found in oil of thyme, and extracted as a white crystalline substance of a pleasant aromatic odor and strong antiseptic properties.

Thymol is part of a naturally occurring class of compounds known as biocides, with strong antimicrobial, antifungal effects. Thymol is only slightly soluble in water at neutral pH, but it is extremely soluble in alcohols and other organic solvents. It is also soluble in strongly alkaline aqueous solutions due to deprotonation of the phenol.


Thymol resembles phenol in its action, but owing to its insolubility in fluids of the body it is absorbed much more slowly. it is also less irritant to wounds, while its germicidal action is greater than that of phenol. In alcoholic solution it penetrates skin and produces local anesthesia. Compound Glycerin of Thymol is used to treat mouth ulcer. One of the active ingredients of this preparation is thymol. Thymol is also used as an antiseptic, local anesthetic, cooling agent, and as a preservative.  It acts as a local irritant and anesthetic to the skin and mucous membranes.

Thymol was in originally introduced as a disinfectant in lieu of carbolic acid having the advantage of a more pleasant odor. Thymol is employed in many of the antiseptic mixtures intended for use upon mucous cavity, especially in gargles, mouth washes, and other oral preparations and as a local anesthetic in toothache.


  • Highly perfused organs have higher blood levels of anesthetic than less highly perfused organs.
  • Skeletal muscles contains greatest percentage of local anesthetics as constitute biggest mass of tissue in body.
  • All LA’s can cross blood brain barrier and placenta.
  • Plasma concentration of local anesthetic in target organs depends on :-
    • Rate at which drug is absorbed into CVS
    • Rate of drug distribution from blood to tissues
    • Drug elimination through metabolic or excretory pathways.
    • Elimination Half life of lidocaine is 1.6 hours.


Ester local Anesthetics

  • Hydrolyzed in the plasma by enzyme Pseudocholinesterase .
  • Site – Plasma.
  • Rate of hydrolysis – Varies and inversely proportional to toxicity.
  • Action of biotransformation products.
  • Allergic reaction – PABA responsible for causing allergic reactions.
  • Atypical Pseudocholinesterases – Causes inability to hydrolyze ester local anesthetics and other chemically related drugs (Succinyl choline)

metabolism of local anesthesia

metabolism of L.A


  • Primary site – liver
  • Rate of biotransformation – influenced by liver function and hepatic perfusion.
  • Poor liver function – unable to biotransform amide local anesthetics at a normal rate.
  • Action of biotransformation products
    • Monoethylglycinexylidide
    • Glycinexylidide
    • Methemoglobinemia – in patients receiving large doses of prilocaine.
    • Produced not by prilocaine but by its primary metabolite orthotoluidine.
    • Sedative effect – Produced by two metabolites of lidocaine.


  • Primary site – kidneys
  • Esters – Appear in small concentration as parent compound in urine since hydrolyzed completely in plasma.
  • Amides – Present in urine as parent compound in a greater percentage because of their more complex process of biotransformation.
  • Renal disease – Relative contraindication to local anesthetic administration.
  • Increase blood levels and potential for toxicity of local anesthetic compounds esp. cocaine.

amino esters and amino amides


Physical properties

1. Non-flammable, non-explosive at room temperature

2. Stable in light.

3. Liquid and vapourisable at room temperature i.e. low latent heat of vaporization.

5. Stable with soda lime, as well as plastics and metals

6. Environmentally friendly – no ozone depletion

7. Cheap and easy to manufacture

Biological properties 

  1. Pleasant to inhale, non-irritant, induces bronchodilatation
  2. Low blood: gas solubility – i.e. fast onset
  3. High oil: water solubility – i.e. high potency
  4. Minimal effects on other systems – e.g. cardiovascular, respiratory, hepatic, renal or endocrine
  5. No biotransformation – should be excreted ideally via the lungs, unchanged
  6. Non-toxic to operating theatre personnel

The use of reversible local anesthetic chemical agents is the most common method to achieve pain control in dental practice. Some ideal properties of local anesthetics are as follows:

  • Specific action
  • Reversible action
  • Rapid onset of action
  • Suitable duration of action
  • Active whether applied topically or injected
  • Nonirritant
  • Causes no permanent damage
  • No systemic toxicity
  • High therapeutic ratio
  • Chemically stable and a long shelf life
  • Ability to combine with other agents without loss of properties
  • Sterilizable without loss of properties
  • Non-allerenic
  • Non-addictive

Where do Local Anesthesia Act ?­

where does local anesthesia work

L.A can interfere with excitation process in nerve membrane in one or more of the following ways:­

  1. Altering the basic resting potential of nerve membrane.
  2. Altering the threshold potential
  3. Decrease rate of depolarization
  4. Increase prolonging rate repolarization.

Theories of Local Anesthesia

  1. Acetylcholine theory        acetylcholine theory
  2. Calcium gate theory calcium gate theory
  3. Surface charge theory surface charge theory
  4. Membrane expansion membrane expansion theory
  5. Specific receptor theory specific receptor theory


Local anesthesia can be used by itself or it can be combined with other types of anesthesia such as spinal or epidural anesthesia.

This is done to reduce the stress associated with surgery, and to provide pain relief after surgery.

More commonly, it is used for pain caused by hemorrhoids, fissure, insect bite, and minor burns. It is applied topically.

It is also indicated for vaginal, rectal and otological examination, cystoscopy, catheterization, urethral operations, and endotracheal intubation.

Indications of local anesthesia in various field of dentistry


  1. To make needle insertion painless
  2. Extraction of teeth and fractured roots
  3. Odentectomy
  4. Treatment of alveolgia
  5. Alvelectomy
  6. Apicectomy
  7. Incision and drainage of localized abscess
  8. Removal of cyst ;residual infection, hpertrophic scar and neoplastic growth , ranula and salivary calculi
  9. In the treatment of tic doulorex by producing prolonged anesthesia  with a combination of local anesthetic agent and alcohol injection ,for blocking the involved nerve
  10. A therapeutic test to localize the source of vague pain about the face.


The following operative and restorative procedures

  1. Cavity preparation
  2. Crown and bridge abutment preparation
  3. Pulpotomy or pulpectomy


  1. Surgical treatment of periodontal tissue
  2. Deep scaling and prophylaxis treatment
  3. Mucogingival surgical procedures


  1. Giving denture patients relief from sore spots which are painful even though denture have been relieved


1. Separation of teeth


1To prevent gagging and retching caused by the contact of the film with palatal tissues and posterior part of the oral cavity .These tissues or the areas are anesthetized before placing the film in these cases usually surface anesthesia is used.


These can be divided into two groups:

1 Absolute contraindications

2 Relative contraindications

Absolute contraindications

History of allergy to local anesthetic agents

Local anesthetic agents belonging to the same chemical group should not be used. However, local anesthetic agents in the different chemical group can be used .In case, a patient gives history of allergy to an amide local anesthetic agent, an ester local anesthetic agent can be used.


1. Fear and apprehension

2. Presence of acute inflammation or suppurative infection at the site of insertion of the needle

3. infants or small children

4. mentally retarded patients

5. restricted mouth opening

6. patient with significant medical diseases :, cardiovascular diseases , hepatic dysfunction, renal dysfunction ,clinical hyperthyroidism

a. patient with significant cardiovascular diseases ;all local anesthetic solution containing high concentration of vasoconstrictors ,such as epinephrine as in gingival retraction  cord should be avoided .local anesthetic agents containing higher dilution of epinephrine ,such as 1.10000000 or 3%  mepivacaine or 4 % prilocaine can be used

b. patient with hepatic dysfunction : all local anesthetics agents belonging to amide group undergo biotransformation in the liver

c.  patient with significant renal dysfunction: all amides and esters should be avoided  however these can be used judiciously .

d.  patient with clinical hyperthyroidism: high conc. of vasoconstrictor as in epinephrine should be avoided .local anesthetic agents containing higher dilutions of epinephrine such as 1.1000 or 1 ;200000 or 3% mepivacaine or 4 % prilocaine can be used

7. Major surgical procedures

8. presence of certain anamolies or developmental defects

9. presence of congenital methemoglobinemia

10. presence of atypical plasma cholinesterase


1. Patient remains awake and cooperative

2. little distortion of normal physiology ,therefore can be used in poor risk patients

3. Low incidence of morbidity

4. additional trained personally not required

5. Technique not difficult to master

6. Percentage of failure is small

7. no additional expenses to the patient

8. patient need not miss the previous meal .in fact ,should have one ,patient should not come on empty stomach


                   No true disadvantages to the use of regional analgesia, when the patient is mentally prepared and when there are no contraindications .in every instance ,when satisfactory anesthesia can be achieved and the patient is cooperative ,regional analgesia is the method  of choice.


All local anesthetics are membrane stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors). Though many other drugs also have membrane stabilizing properties, not all are used as local anesthetics (propranolol, for example). Local anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Local anesthetic 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.

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 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”. In the protonated form, the molecule binds to the local anesthetic binding site on the inside of the ion channel near the cytoplasmic end.


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.

All nerve fibers are sensitive to local anesthetics, but generally, those with a smaller diameter tend to be more sensitive than larger fibers. 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).


Displacement of Ca++ from sodium channel receptor site

Binding of LA molecule to this site

Blockade of sodium channel

Decrease in sodium conductance

Failure to achieve threshold potential level lack of development of

propagated action potential


A) Complications arising from drugs or chemicals used for local anesthesia

1. Soft tissues injurySOFT TISSUE INJURY FROM L.A

2. Sloughing of tissues ( Tissues ischemia and necrosis)

B) Complications arising from injection techniques

I. Breakage of anesthetic cartridge

2. Breakage of needle NEEDLE BREAKAGE

3.. Needle-stick injuries


5. Failure to obtain local anesthesia

C) Complications arising from both

1. Pain on injection

2. Burning on injection

3. Infection

4. Trismus  TRISMUS

5. Edema EDEMA

6. Mucosal Blanching

7. Persistent aesthesia or anesthesia

8. Persistent or prolonged pain pain

9. Post-injection herpetic lesions or post-anesthetic intraoral lesions

10. Bizarre neurological complications

a) Facial nerve paresis or paralysis facial nerve paralysis

b) Visual disturbances

1. Diploma or double vision

many fingers seen on single hand isolated on white

many fingers seen on single hand isolated on white

2. Amaurosis or temporary blindness

3. Permanent blindness.

Local anesthetics complication are broadly classified in two parts.

A) localized complication

B) Systemic complication  localized complication:-

The localized adverse effects :-

• The local adverse effects of anesthetic agents include

• neurovascular manifestations such as prolonged anesthesia (numbness) and paresthesia ( tingling, feeling of “pins and needles”. or strange sensations ). These are symptoms of localized nerve impairment or nerve damage.

 Causes of localized symptoms include:

1. Neurotoxicity due to allergic reaction,

2. Excessive fluid pressure in a confined space,

3. Severing of nerve fibers or support tissue with the needle/catheter,

4. Injection-site hematoma that puts pressure on the nerve, or

5. Injection-site infection that produce inflammatory pressure on the nerve and/or necrosis.

Systemic complication :-

General systemic adverse effects are due to the pharmacological effects of the anesthetic agents used. The conduction of electric impulses follows a similar mechanism in peripheral nerves, the central nervous system, and the heart. The effects of local anesthetics are therefore not specific for the signal conduction in peripheral nerves.

A) Neurological complication of local anesthesia:- 

  • Local anesthetics may cause adverse effects either by action on the nerves  and muscles or neurotoxicity following systemic absorption.
  • Injection injury of neural structures may result from the procedure.
  • Seizures are a frequent adverse effect of local anesthetics, and principal of management are those applicable to drug- induced seizures.
  • Careful selection of the anesthetic agent and meticulous procedure for local anesthesia are important preventive measures.

Clinical manifestations

CNS excitation manifested by:

  • Restlessness
  • Tremors
  • Light-headedness
  • Syncope – Tinnitus
  • Nausea and vomiting
  • Slurring of speech
  • Irrational conversation

Seizures that may be followed by CNS depression.

CNS depression manifested by:

  • Drowsiness
  • Respiratory arrest – Coma respiratory arrest

• Complications related to peripheral and cranial nerves: –

  1. Irritation of spinal nerve roots
  2. Complications of leakage of cerebrospinal fluid
  3. Cauda equine syndrome
  4. Paraplegia due to toxic or ischemic myelopathy
  5. Meningitis
  6. Epidural hematoma

Effect on muscles:

  1. myonecrosis following local injection into muscles

Neurophthalmologic complications:

  1. Reduction of visual acuity following retro bulbar anesthesia
  2. Homer syndrome
  3. Extra ocular muscle palsies
  4. Neurologic manifestations of systemic toxicity of local anesthetics: Numbness of the tongue and perioral region

Cardiovascular system

The conductive system of the heart is quite sensitive to the action of local r anesthetic. Cardiovascular manifestation are usually depressant and are  characterized by bradycardia, hypotension, and cardiovascular collapse, which  may lead to cardiac arrest.


Allergic reactions are characterized by cutaneous lesions, urticaria, edema or anaphylactoid reactions. Allergic reactions may occur as a result of sensitivity either to local anesthetic agents or to the methylparaben used as a preservative in the multiple does vials. Allergic reactions as a result of sensitivity to lidocaine are extremely rare and, if they occur, should be managed by conventional means. The detection of sensitivity by skin testing is of doubtful value.


Adverse reactions to local anesthetics (especially the esters) are not uncommon, but true allergy is very rare Allergic reactions to the esters is usually due to a sensitivity to their metabolite, para-aminobenzoic acid (PABA), and does not result in cross-allergy to amides. Therefore, amides can be used as alternatives in those patients. Nonallergic reactions may resemble allergy in their manifestations. In some cases, skin tests and provocative challenge may be  necessary to establish a diagnosis of allergy. There are also cases of allergy to paraben derivatives, which are often added as preservatives to local anesthetic solutions.


  1.  Amourosis
  2. Mydriasis mydriasis
  3. Ptosis         ptosis
  4. Diplopiamany fingers seen on single hand isolated on white


This theory suggests that after inadvertent administration into the inferior alveolar vein following an inferior alveolar nerve block, the pressurized injection and diffusion will allow the flow of anesthetic into the pterygold venous plexus and consequently into the cavernous sinus through emissary veins that traverse the bony foramina. Once the anesthetic is positioned within the cavernous sinus, the abducens nerve would be more vulnerable to the effect of the anesthetic because of its immediacy within the sinus

Myofascial planes

Often considered a cause of anesthetic failure, myofascial plane orientation may create a path of least resistance where the anesthetic solution flows away from the nerve and toward the orbital area. Studies radiopaque dyes combined with local anesthetics have demonstrated that an injection can be made within the direct area of nerve without producing an effect, whereas in supplementary illustrations, the solution was administered more than 2 cm away but still generated excellent anesthesia. In the formal case, the anesthetic spreads over the path of least resistance away from the nerve; in the latter case, it is directed toward the nerve.

Sympathetic ganglion anesthesia

Campbell and the conjunctive a case with a Horner-like syndrome with ptosis, vascular dilatation of the conjunctiva miosis, horseness in vocalization, and  wide-spread rash over the ipsilateral upper body. In their report, it was suggested that the local anesthetic administration resulted in a stellate ganglion block, which may explain the patient’s hoarseness of voice. Proposed Causes of Occular Complications with maxillary injections


As opposed to mandibular injections for which the injection site is further   away from the orbit, maxillary injections have an increased opportunity of diffusion carrying the local anesthetic solution into the orbital area. It is  oik proposed that simple diffusion from the pterygomaxillary fossa to the orbit (through defects in the bone or via the vascular, lymphatic and venous networks that link these spaces results in ocular consequences.


Inadvertent intra-arterial injection into the superior alveolar artery, with retrograde flow to the internal maxillary artery and then to the middle meningeal artery, serves as the basis for this theory. A middle meningeal branch occasionally penetrates the superior orbital fissure and anastomoses with the lacrimal branch of the ophthalmic artery the risk of an ocular complication occurring as proposed by this theory would be increased when the solution is injected rapidly and under pressure.

This hypothesis proposes an inadvertent venous injection in to the pterygoid venous plexus to explain a possible cause of ocular complication.   The theory proposes that the anesthetic solution would reach the orbit through the canvernous sinus, which recives drainage from the pterygoid venous plexus via the inferior and superior ophthalmic veins, which could communicate with the various musculature associated with the eye.



The factors which can precipitate vasodepressor syncope may be divided into two group:

1. Psychogenic factors, and

2. Non-psychogenic factors

Psychogenic factors

  • Fright and anxiety
  • Emotional stress
  • Receipt of unwelcomeness
  • Pain of sudden and unexpected nature
  • Sight of blood or of surgical or other dental instruments, such as local anesthetic syringe, injection needle etc.

In dental surgery set-up the psycologenic factors are the most common precipitating factors. These factors lead to fight-or-flight response; and in the absence of muscular activity, manifest as loss of consciousness, termed as vasodepressor syncope.

Non-psychogenic Factors

  • Sitting in upright position or standing for prolonged period. It leads to 4.4 pooling of blood in periphery thereby decreasing cerebral blood flow.
  • Hunger or starvation.
  • Exhaustion.
  • Poor physical condition boo
  • Hot, humid and crowded environment.
  • The above mentioned condition and contribute to a situation resulting in syncope.
  • Injection of a local anesthetic agent with or without a vasoconstrictor in to an it artery.

 Clinical Manifestations

The clinical manifestations develop rapidly. However the actual loss of mtr consciousness occurs after a period of time. The clinical features of vasodepressor syncope may be grouped into three definite phases:

i) Presyncope

ii) Syncope

iii) Postsyncope


Local anesthetic agents are relatively safe and free of side effects provided they are administered in an appropriate dosage and in an appropriate anatomical location. The ester group of drugs is more toxic than the amide group. The adverse drug reactions include:

1) Allergic reactions,

2) Anaphylactic reactions,

3) Toxic reactions (overdose),

4) idiosyncratic reactions.

The causes, signs and symptoms, prevention of these reactions are mentioned. The management procedures are common to all the reactions.

These include the following:

1. Stop the dental procedure.

2. Place the patient in supine position (legs slightly elevated).

3. Call medical assistance.

4. Institute the prelim nary medical care.

5. Keep the airway patent.

6. Administer

7. Monitor the vital signs.

8. Transfer the patient to a general hospital in the vicinity having ICU facility.

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