Local Anaesthetic solution in dental treatment

drazadsami 14 views 96 slides Mar 01, 2025
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About This Presentation

It is used in the field of dentistry


Slide Content

Local Anesthetics

Local Anaesthetics Local anesthetics are the drugs or the agents which are used to produce transient & reversible loss of sensation in a circumscribed area of the body without affecting the degree of consciousness.

Local anaesthesia Local anaesthesia is a transient and reversible condition of loss of sensation in a circumscribed area of the body without imparing the degree of consciousness . or LA is defined as a loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves.

Properties of an ideal anaesthetic Following properties are most desirable for a local anesthetic : Have a specific and reversible action . Be non-irritant to the tissue to which it is applied. Should not cause any permanent alteration of nerve structure. It’s systemic toxicity should be low. It must be effective regardless of whether it is injected into the tissue/ is applied locally to mucous membranes .

Cont,d … Be active topically and by injection Have a r apid action. The time of onset of anesthesia should be as short as possible. The duration of action must be long enough to permit completion of the procedure. Be chemically stable and sterilizable . Be able to administered with other agents e.g vasoconstrictors without loss of properties.

Composition of local anaesthetics A local anesthetic agent: Lignocaine, prilocaine . A reducing agent- (e.g. S odium metabisulphate) to enhance the stability of added vasoconstrictors. A preservative - ( Capryl-hydro-cuprieno-toxin is added as preservatives to maintain the sterility of L.A solution , increase the shelf life of the solution.) Fungicide- It prevents the solution to become cloudy due to the proliferation of fung i (e.g thymol is added as fungicidal)

Cont … Vasoconstrictor- Most local anaesthetics produce some degee of vasoldilation, and they may be rapidly absorbed after local injection. Consequently vasoconstrictors are frequently added Adrenaline, Nor –adrenaline, Felypressin The vehicle: The anesthetic agent & the additives are dissolve in modified Ringer’s solution.

Advantages of Vasoconstrictors Vasoconstrictor are drugs that constricts blood vessels & thereby control tissue perfusion. They are added to local anesthetic solution to oppose the vasodilatory actions of the local anesthetics. These vasoconstrictors provide by: Constricting blood vessels ,vasoconstrictor decrease blood flow to the site of administration. P rolong their duration of action & depth by localizing them in tissues D ecrease the systemic toxicity and increase the safety margin of local anaesthetics by reducing their rate of absorption P roduces a relatively bloodless field during surgical procedures

Classification according to nature of source The local anaesthetic can be classified into four groups: A. Natural: Cocaine B. Synthetic 1. Nitrogenous compound Aminoesters of PABA(Para Amino Benzoic Acid) e.g procaine Alkyl Esters of PABA e.g Benzocaine D erivatives of acetanilide:Lidocaine Derivatives of acridine:Bucricaine. 2. Synthetic non-nitrogenous compound e.g Benzyl Alcohol C. Miscellaneous Drugs with local action e.g clove oil, Phenol oil ,Chlorpromazine.

Classification of Local anaesthetics based on route of administration Surface / topical anaesthetics- Aerosol: 10% ethyl chloride spray. Gel:5% lignocaine. Emulsion: Tetracaine, Benzocaine. Injectable: Infiltration: Injected in to the tissue( Sub mucous injection, sub periostial injection,intraseptal injection etc. ) Block: Field block (Terminal nerve) Nerve block (main nerve trunk nerve block) Intra- ligamentary injection. Intra-pulpal injection. Spinal anaesthesia Epidural anaesthesia Intravenous Regional Anaesthesia

infiltration Field block Nerve block

Classification according to duration of action

Classification according to the basis of chemical structure: Esters Amide Quinolone 1.Esters of benzoic acid : cocaine, Benzocaine B utacaine Tetracaine Hexylcaine Piperocaine . 2. Ester of PABA : Chloroprocaine Procaine Propoxycaine Lidocaine Prilocaine Mepivacaine Bupivacaine Etidocaine Dibucaine Ropivacaine Articaine Centbucridine

Difference between esters and amides Amide Amides can be stored for long period. Amide anaesthetics are heat-stable & can therefore be autoclaved. Amides are metabolized principally in the liver. Amides, very rarely cause allergic phenomena. For these reasons amides are now more commonly used than esters. Ester The ester linkage is more easily broken than the amide bond so the ester drugs are less stable in solution & cannot be stored for as long as amides. Esters cannot. Esters are metabolized rapidly by plasma enzymes The metabolism of most esters results in the production of para-amino benzo ic acid (PABA) which is associated with allergic reaction.

Type Example Class A: Agent acting on the receptor site on external surface of nerve membrane. Biotoxinse e.g. tetrodotoxin , Saxitoxin . Class B: Agent acting at the receptor site on internal surface of nerve membrane. Quaternary ammonium analogues of lidocaine. Class C : Agent acting by a receptor independent physio-chemical mechanism. Benzocaine Class D: Agent acting by combination of receptor & receptor independent mechanism. Most clinically useful anesthetic agents e.g. articaine , lidocaine, mepivacaine , prilocaine . According to the biological site

Theories of Local Anesthetics Acetylcholine Theory Calcium Displacement Theory Surface Charge Theory Specific receptor Theory Membrane Expansion Theory

Cont … Specific Receptor Theory (Most accepted): This theory proposed that LA act by binding to the specific receptors on sodium channel. The action of the drug is direct , not mediated by some change in general properties of cell membrane. Biochemical & electrophysiological studies have indicated that specific receptor sites of LA agents exists in sodium channel either on it’s external surface or its internal surfaces. Once the LA has gained access to receptors, permeability of sodium ion is decreased or eliminated & nerve conduction is interrupted.

Bio-transformation/Absorption & Excretion of LA 01. Ester type: site of application Systemic absorption Plasma bound Metabolized by plasma cholinesterase enzyme 5% unchanged Excreted through kidney

Absorption & Excretion of LA 02. Amide type: Site of application Systemic absorption Metabolized by microsomal enzyme cytochrome P450 Excreted through kidney

Chemistry of LA Local anesthetic drugs are weak organic bases and are insoluble in water & unstable. Their pka value range from 7.5 to 10. In this form they have little value or no clinical value. However they readily mixed with acid & can be converted into soluble salts by hydrochloride . The salt , both water soluble & stable, is dissolved in either sterile water or saline.

Structure Activity Relationship of LA Li pophilic part ester/ amide group Hydrophilic part intermediate chain Lipophilic part: Largest portion/ essential for local anesthetic . Aromatic in structure. It is derived from benzoic or thiophene . Intermediate chain: This chain includes the ester or amide group & the bridge. The anesthetic structure is completed by an intermediate hydrocarbon chain containing an ester or an amide linkage. Hydrophilic part: is an amino derivatives of ethyl alcohol or acetic acid. LA without a hydrophilic part are not suited for injection but are good topical anesthetics.

Chemical structure of LA A; Ester Type B; Amide Type

Cont …

Cont …

Action Potential Resting membrane potential: The constant electrical potential difference across the cell membrane with the inside negative relative to the outside of the cell at rest. Action Potential: The rapid changes in the membrane potential that begins with a sudden change from the normal resting negative membrane potential to positive potential & then ends with in an almost equally rapid change back to the negative.

Cont …. Depolarization: The rapid rise of the membrane potential in the positive direction due to rapid influx of Na+ channels. Repolarization: Immediately after depolarization, the membrane potential reverse & fall rapidly towards the normal negative resting potential due to rapid efflux of K+ through voltage gated K+ channels.

Mechanism of action L.A Local Anesth e tics agent compete with Ca++ for phospholipid receptor in the nerve cell membrane LA agent displace Ca++ from the sodium channel receptor site Binding of local anesthetic molecule to this receptor site D isrupt voltage gated sodium channel which prevents inwards passage Na+ ions . Block the Na+ influx Block depolarization Fail to initiate at propagation of action potential Block the impulse conduction no pain sensation

Dissociation of Local Anesthetics Injectable LA are weak bases, equilibrates into two form: ionized form & non- ionized form. The LA salt, both water soluble & stable, is dissolve in sterile water & saline. It exists simultaneously as uncharged molecule( RN), also called the base, & as positively charged molecules (RNH+) called cation. The non- ionized/ uncharged, lipid soluble, free base form is able to cross the cell membrane. RNH+ ⇌ RN + H The relative proportion of each ionic form in the solution varies with the PH of the solution or surrounding tissue. In the presence of a high concentration of hydrogen ions ( low PH) , the equilibrium shift to the left & most of the anesthetic solution exist in cationic form: RNH+ > RN + H

Cont …. As hydrogen ion concentration decreases (higher PH), the equilibrium shifts towards the free base form. RNH+ < RN + H

Cont …. The relative proportion of ionic forms also depends on the pKa or dissociation constant, of the specific LA. The pKa is the measure of the affinity of a molecule for hydrogen ion. When the pH of the solution has the same value as the pKa of the LA , exactly 50% of the drug exists in the RNH+ form & 50% in the RN form. The percentage of drug existing in either form can be determined from Henderson- Hasselbalch equation. pH= pKa + log10 Base/Acid (Determines how much of a LA will be in a non-ionized vs ionized form. Based on tissue pH & anesthetic pka .)

Actions on nerve membrane 2 factors involved in the action of LA are: Diffusion of the drug through the nerve sheath Binding at the receptor site in the ion channel. The uncharged ,lipid soluble, free base form are the anesthetics is responsible for diffusion through the nerve sheath. The process is explained in the following example: One thousand molecule of LA with a pKa of 7.9 are injected into the tissue outside of a nerve. The tissue pH is normal 7.4. From the dissociation constant & Henderson-Hasselbalch equation, it can be determined that at normal tissue pH 75% of LA molecules are present in the cationic form(RNH+) & 25% in the free base form.

Conti…. 3. In the theory then, all 250 lipophilic RN molecules will diffuse through the nerve sheath to reach the axoplasm of the neuron. 4.When this happens the extracellular equilibrium between RNH⇌ RN has been disrupted by the passages of the free base form into the neuron .the remaining 750 extracellular RNH+ molecules will now reequilibrate according to the tissue pH & the pKa of the drugs: RNH+ (570) RN(180) + H

Cont …. pH 7.5 Extracellular 250 RNH+ 750 RN 250 Nerve sheath intracellular pH 7.4 RN RNH+ 250 RNH+ (180) RN(70)

Agent pKa % base(RN) At pH 7.4 Onset of action , min Benzocaine 3.5 100 _ Mepivacaine 7.7 33 2-4 Lidocaine 7.7 29 2-4 Prilocaine 7.7 25 2-4 Articaine 7.8 29 2-4 Etidocaine 7.9 25 2-4 Ropivacaine 8.1 17 2-4 Bupivacaine 8.1 17 5-8 Tetracaine 8.6 7 10-15 Cocaine 8.6 7 _ Procaine 9.1 2 14-18

Cont..... The 180 newly created lipophilic RN molecules diffuse into the cell, starting the entire process again. Theoretically this will continue until a LA molecules diffuses into the axoplasm . The inside of the nerve should be viewed next. After penetration of the nerve sheath & entry into the axoplasm by the lipophilic RN form of the anesthetic, reequilibration take place inside the nerve, because a LA cannot exists in only the RN form at an intracellular pH of 7.4. 75% of those RN molecules present within the axoplasm revert into the RNH+ form, the remaining 25% of molecules remain in the uncharged RN form.

From the axoplasmic side the RNH+ enter into the sodium channel, bind to the channel receptor site, & Ultimately are responsible for the conduction blocked.

How does pH affect Local Anesthetics Differences in extracellular & intracellular pH are highly significant in pain control when inflammation or infection is present. During infection tissue pH is low. LA are injected in their acid –salt form & the plain LA is approximately 6.5 where vasoconstrictor containing LA is 3.5, the more acidic the solution , the greater number of H+ ions available & the greater the percentage of RNH+ found in solution. The lower the pH of the anesthetic solution & the tissue into which it is injected the lower is the percentage of RN form.

(At this low pH approximately 99% of LA molecules are present in the charge cationic form, with 1% approximately in the lipophilic base form.) So adequate blocked of the nerve is more difficult to achieve in inflamed or infected tissues because local anesthetics exist in both an ionized & un-ionized form . Infected tissue has a more acidic pH due to inflammatory mediators, neutralizing the un- ionized form. since less concentration of base forms of molecules able to cross the nerve sheath & increased absorption of remaining anesthetic molecules into dilated blood vessels in this region. The slower is onset & the less profound is the resultant anesthesia.

Pharmacological action of LA. 1.Reversible block of conduction in nerve endings and nerve trunks 2 .On smooth muscle: Direct relaxation of vascular smooth muscle cause vasodilatation. 3. On CVS : produce myocardial depression decrease conduction rate decrease force of contraction. The primary effect of LA on blood pressure is hypotension except cocaine. 4. On CNS: depression of central nervous system. 5. On Respiratory system: usually unaffected.

Factors affecting the Local Anesthetic solution 1. The agents pKa : The lower the pKa value & faster the onset of action. 2. Lipid solubility: More lipid soluble higher the potency, faster the onset of action. 3. Protein binding : Increased the protein binding capacity , increased duration of action. 4. Vasodilatory effect: Greater vasodilator activity decreased potency & slower the onset of action. 5. Tissue pH: Low pH of the solution, irritate the tissue.

Calculation of maximum dosage & Number of cartridge 2% Lidocaine anesthetic HCL + Epinephrine 1:100,000 Lidocaine 2% 2 gm LA in 100ml of solution or 2000mg LA in 100ml of solution. In 100ml of solution have 2000mg of LA So 1 “ “ “ “ =20 mg of LA 1.8 “ “ “ “ = 20 1.8 =36mg So, 1.8= 36 mg Maximum dosage with adrenaline = 7mg x kg( 50 kg patient) =(7 x 5o) mg = 350 mg Number of Cartridge: 350/36 = 9.7

Cont … Maximum Adrenaline in 1 day = 0.2 mg 1gm:100000ml 1ooomg:100000ml =1000/100000 = 0.01 mg/ml adrenaline in 2% lidocaine.

Drug Clinical percent mg/ml mg/cartridge 1.8 ml recommended mg/kg Absolute Maximum mg Articaine 4%, 40mg/ml 72 7.0 Not listed Lidocaine 2%, 20 mg/ml 36 4.4 300 Mepivacaine 2%, 20mg/ml 36 4.4 300 Mepivacaine 3%, 30mg/ml 54 4.4 300 Prilocaine 4%, 40mg/ml 72 6.0 400 Bupivacaine 0.5%, 5 mg/ml 9 1.3 90 Maximum recommended dosages of local anesthetic

Effect of over dosages of local anesthetics minimal to moderate overdose level signs Talkativeness Excitability Slurred speech Generalized muscular twitching Euphoria Dysarthria Nystagmus Sweating Vomiting Failure to follow the commands Elevated BP, heart rate, respiratory rate symptoms Lightheadedness, dizziness Restlessness Nervousness Numbness Sensation of twitching Metallic taste Visual disturbance Auditory disturbance Drowsiness & disorientation Loss of consciousness

Moderate to high overdose level Sign: Tonic- clonic seizure activity followed by Generalized CNS depression Depressed BP, heart rate, respiratory rate

Indications of Local Anesthesia In Oral Surgery : To make needle insertion painless. Extraction of teeth & fractured roots Odontectomy Treatment of alveolalgia . Removal of cyst, hypertropic tissue, ranula salivary calculi. To reduce hemorrhage. A therapeutic diagnosis test to localized the source of pain about the face.

B. In conservative dentistry: Cavity preparation Pulpotomy or pulpectomy Apisectomy Crown , bridge preparation C. In periodontology : Surgical treatment of periodontal disease Deep scaling Mucogingival surgical procedures.

Contraindication of LA with adrenaline Absolute contraindication : History of allergy to local anesthetic agents or, H istory of any unstable angina , congestive heart failure, Recent MI ( less than 6 months) Cardiac dysrhythmia. Uncontrolled hypertension Uncontrolled hyperthyroidism Epilepsy

Contraindication 2. Relative contraindication: Fear & apprehension when patient uncooperative for regional anesthesia Chronic renal failure. Taking long term steroid In trismus/lock jaw or ankylosis of T.M. joint Presence of acute inflammation or supporative infection at the site of insertion of needle. Mentally retarded patient who are unable to cooperate. Presence of atypical plasma cholinesterase.

Differences between G.A and L.A Points L.A G.A Site of action M/A 3.Pt’sconsciousness 4.Pain sensation and all reflexes 5.Pre-an e sthetic medication L ocal nerve fibres Blocks conduction of nerve impulse 3. Present 4.Locally lost reversibly 5.Not needed C.N.S Directly depress the C.N.S 3.Reversible loss of consciousness 4.All lost reversibly 5.Needed

Cont …. 7.Toxicities 8.Use in non-co-operative patient 9. Muscle relaxation 10 .Use 7.Less, so safer 8.Not possibl e 9. Local 10 .During minor operations 7.More ,so dangerous 8.Possible 9. Generalized 10 .During major operation s

General Anesthesia : Indications in Dentistry In small children, when removal of teeth in different quadrant of mouth is planned. In adults when multiple extractions are to be done on a single occa s ion. Following failed of l ocal a nesthes ia. Open reduction of fracture of maxilla and mandible. Surgery of tumour.

Advantages of L.A.: Patient remains awake and co-operative. No special preparation of the patient is needed. No need of complicated appartus. Little distortion of normal physiology. Additional trained person not required. Easy administration . Per-operative & post operative care is not needed. . Percentage of failure is less .

Lidocaine HCL Classification: amide Chemical formula: 2-diethylamino-2’ ,6- acetoxylidide hydrochloride. pKa : 7.9 pH of plain solution: 6.5 pH of vasoconstrictor containing solution: 3.5 Onset of action : Rapid ( 3 to 5 min) Effective dental concentration: 2% For surface application: 2 % lidocaine HCL gel 10% topical spray. 2.5% & 5% ointment.

Cont.. For parenteral administration: 2% lidocaine without a vasoconstrictor 2% lidocaine with epinephrine 1:50000 2% lidocaine with epinephrine 1: 100,000. 5% lidocaine with epinephrine 1: 80,000 Pregnancy classification: B Safety during lactation: S

Definition: Topica l an e sthesia / Surface : is obtained by the application of a suitable anasthetic agent to an area of skin/mucous membrane which it penetrates to anesthetize superficial nerve-endings. Infiltration: Anest hetic solution deposited near the terminal nerve of any nerve will infiltrate through tissues to reach the main nerve- trunk and thus produce anaesthesia of the localised area served by them.

Cont … Nerve block anesthesia: When anaesthetic solution is given near to a nerve trunk, the area supplied by that nerve is anesthetized, by blocking all impulses, this is known as regional or block anaesthesia.

Mandibular teeth anesthesia

Maxillary teeth anesthesia

Name of some vasoconstrictors: Adrenaline, Nor-adrenaline, Levonordefrin, Isoproteren o l, Phenylephrine, Felypressin.

Vasoconstrictor(Adrenaline) In the usual concentration of 1: 80000 adrenaline reliably prolongs the effect of a local analgesic & by slowing absorption makes it possible to increased the amount of local analgesic that can be safely given. Systemic action: it may causes myocardial excitability ( Increased the rate & force of contraction of heart, cardiac output). It raises the systolic pressure transiently but tends to decreased the diastolic pressure.

C ont. . Felypressin is a synthetical produced of polypeptide. I n dentistry in a dilution of 0.03 IU/ml with 3% prilocaine is used. Indication: It can be used safely in patients with M ild to moderate cardio-vascular diseases, like hypertension, In hyperthyriodisim. 2. Can be used in patient taking antidepressant drugs such as- tricyclic antidepressant or, mono-amine-oxidase inhibitors.

Pharmacological effects of Adrenaline Cardiac effects: beta1 receptor: contractility, heart rate, cardiac output, oxygen consumption. Vascular effects: alfa receptor: vasoconstriction of skin, mucous membrane ,vascular smooth muscle, heart . Beta 2 receptor: vasodilatation of skeletal muscle ( small dose)& coronary vessels. But at larger dose produce vasoconstriction because alfa receptor are stimulated.

Blood pressure Systolic blood pressure is increased. Diastolic blood pressure decreased. ( small dose) Respiratory: B2 : Dilatation of bronchial smooth muscle.

Pharmacological action of nor epinephrine Vascular effect: alfa1 receptor: vasoconstriction of cutaneous blood vessels. Blood pressure: Alfa receptor: peripheral vasoconstriction & increase peripheral vascular resistance. Increased Systolic & Diastolic BP. Heart rate: B1 : Decreased heart rate.

Partition Co efficient of local anesthetics Pco of an agent is the ratio of solubility of that agent to lipid & water solution. The higher the ratio , they more soluble to lipid solution, but less soluble to water solution.. For LA it is desirable to have higher Pco ( that is higher lipid solubility). So that the lipophilic part of LA can easily diffuse through lipid barrier & cell membrane. But too high lipid solubility or high Pco means low water solubility. That means the hydrophilic part of LA won’t be able to work inside cell.

Predisposing factors for local anesthetics overdose: Patients general health, age, weight. Dysfunction of the liver & kidneys which increased the level of local anesthetics in the blood stream. Rapidity of infection. Route of administration. Amout of local anesthetics administered.

C omplication s of Local Anesthetics & their Management local / Late complication 1. Trism u s: inability to open the mouth . Trism u s or lock jaw- due to misplace injection of L.A into pterigoid muscle causes muscle spasm and patient will not be able to open the mouth. Hematoma formation. Management: Apply moist heat( towels ) to the site for 20mins every hour. Analgesics should be given. Muscle relaxant. Advice the patient to open and close the mouth as means of physiotherapy.

2.Haematoma formation: The point of a venous plexus or artery during the administration of either an inferior dental or an infraorbital injection may cause hematoma formation. There is bleeding into tissues cause swelling and discoloration of the overlying skin within 24-28 hours. Management: Cold compression If infected : Antibiotic, Drainage.

3. Facial nerve paralysis Peripheral nerves of facial nerve maybe anesthetized if needle puncture parotid g l and capsule and cause a transient, uniletaral paralysis of muscles of chin, lower lip, cheek and eye. The term bell’s palsy was commonly used. Management: a Reassure the patient, explain that the situation is transient, will last for few hours & resolve without residual effect. An eye patch should be applied to the affected eye until muscle tone return.

Cont …. 5.Blanching effect: causes: Excessive pressure during injection Management: Hot compression 4. Soft tissue injury: Analgesic for pain if necessary. Antibiotic Petrolium jelly or other lubricant to cover a lip lesion & to minimize irritation.

Cont … 6.Prolong anesthesia or paresthesia due to trauma to nerve, neurolytic injection. Mx : Reassuring Explain to the patient that paresthesia persists for at least 2 month. Tincture of time is the recommended treatment. Dental treatment may continue, but avoid re administering LA into the region of the previously traumatized nerve. Use alternate LA technique.

In those few situations in which post injection discomfort, oedema, becomes evident management of the specific problem is indicated. 7.Odema Mx : it resolves in several days without formal therapy. If pain persists prescribe analgesics. 8.Sloughing of the soft tissue due to topical anesthetic, prolong ischemia. Mx : Reassure the patient. Management will be symptomatic. For pain prescribe analgesic & topically applied ointment. It resolves within a few week.

09.Post anesthetic intraoral lesion. Mx : Primary management is symptomatic. Reassure the patient. if the pain causes the patient to complain topical anesthetic solutions may be applied as needed to the painful areas. Orabase a protective paste without kenalog can provide a degree of pain relief. The lesion usually resolves within 7 to 10 days.

Immediate Complication due to faulty technique: 1. Pain at the site of Injection: Injection of L.A may be accompained by pain or a burning sensation. Causes: 1. Multiple needle prick. 2.Non sterile solution. 3. Cold solution 4.rapid injection of LA solution. 5. Non isotonic solution. 6. Dull needles. Prevention: Inject slowly’ try to take atleast 1 min to admister 1 cartridge. Store cartridge at room temprature. Do not store L.A cartridge in disinfection solutions.

Prevention: Inject slowly’ try to take atleast 1 min to admister 1 cartridge. Store cartridge at room temprature. Do not store L.A cartridge in disinfection solutions.

2. Needle breakage: The unexpected movement of the patient is the primary cause. Smaller diameter needles (ie,30 gauges) are more likely to break than the larger diameter (ie,25 gauge) Bent needles Defective needles Prevention: Don’t insert a needle into tissue in it’s hub, always leave a portion exposed. Use needle more than 18 mm. Use larger diameter needles for block technique. Do not apply excessive force on the needle once it is inserted into the tissue.

Management: Remain calm. A sk the patient to remain still keep the mouth open. If a portion of the needle is visible, remove it with a haemostate. If needle is not visible; Inform the patient. Record the events in patient’s chart. Detect the location of broken part with CT scan with 3D reconstruction. Then removal of the needle under GA.

Systemic complication/ immediate A ) Syncope or fainting : Syncope is due to sudden fall of cerebral circulation and is accompanied by restlessness, pale & cold skin, sweating, nausea, decreased blood pressure, tachycardia etc. Management : 1) Stop the procedure 2) Placement of the patient in the dental chair in supine position with legs slightly elevated.(10 degree Trendelenburg position).

3)Loosen the tight clothes. 4) Inhalation of aromatic spirit of ammonia to stimulate CNS. 5) Administration of O2 with full mask 6) Monitoring vital signs- heart rate and blood pressure 7) Water spray on the mouth. 8)Glucose intake

B) Hypersensitivity : Hypersensitivity or allergic reaction because, ester type of L.A are metabolized to PABA derivatives for example procaine are more likely to produce allergic reaction (para amino benzoic acid) Allergy may also due to preservative methyl paraben used in local anesthesia. Anaphylactic shock : Anaphylactic shock is an immediate (Type-I) hypersensitivity reaction cause the release of histamine following exposure to an allergen in a previously sensitized ind i vidual .

Symptoms are- Initial facial flushing, itching, paresthesia, cold extremities. Facial edema Rapid, weak or impalpable pulse. Deep fall in blood pressure. asthma Rhinitis Urticaria Angio-oedema . Laryngeal oedema

Treatment : 1) Placement of the patient in dental chair in supine position with legs slightly elevated. 2) Administration of O2 with full face mask 3) 0.3 ml of 1: 1000 epinephrine if less than 30 kg, 0.15 ml if more than 30 kg adrenaline solution should be injected intramuscularly. Repeat every 15 min if necessary, until the patient respond. 4) Hydrocortisone 200 mg I/V is given 5) Antihistamine- chlorpheniramine 10mg I/M is given.

Prevention of local anesthetics complication Fainting :elimination of the predisposing factors like stress, anxiety, sight of blood or dental instrument, standing for prolonged period, starvation, hot weather etc. medical history Proper positioning of the patient Take light meal prior to treatment Proper injection technique Use of anti anxiety drugs

Cont’d Pain on injection: follow the technique local anesthesia properly. Use sharp needle Sterile local anesthetics with normal temperature . Inject slowly. Needle breakage: Check the needle before use. Use larger gauge & long needle Do not insert a needle into tissues to its hub. Do not redirect a needle once it is inserted into tissues.

Cont’d Trismus: Use sharp, sterile, disposable needle with aseptic technique. Avoid repeated injection & multiple injection into same area. Use minimum effective volume of LA. Soft tissue injury: a cotton roll can be placed between the lip & teeth if they are still anesthetized. Warn the patient against eating, drinking & biting on the lip. Proper handle of needle.

Cont,d Hematoma: Proper injection technique & anatomical landmark. Avoid relocating the needle to different sites inside the tissue. Infection: Use sterile disposable needle. Proper handle of needle to avoid its contact with non sterile surface.

Causes of failure of Local anaesthesia Technical fault Inadequate dose N ot to push in the correct place Wrong selection of local anesthetic solution. Inadequate anaesthesia is obtained if L.A solution is injected in purulent pus forming infection. Anatomical variation with accessory innervation. If the agent is used after expir ed date. Anxiety of the patient. Injection into blood vessel.

How to overcome the failure Adequate amount should be given just at the correct place. Check anatomical landmarks. Pus forming area should be avoided . Proper selection of LA. Local anaesthetic solution should be used before expire date. If necessary, individual dose should be measured for different person.
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