PG PPT LOCAL ANESTHESIA_011219.pptx for science

Local anesthesia

1. L OCAL ANESTHESIA PRESENTED BY- DR.ALISHA MEHER GUIDED BY- DR.PROF. CHINMAYA BHAWANI PRASAD (HOD SHALYA TANTRA)

2. EVERYTHING TO KNOW ABOUT LOCAL ANESTHESIA: INTRODUCTION TO ANESTHESIA DEFINATION HISTORY NEURON AND NERVE MECHANISM OF NERVE CONDUCTION PHARMACODYNAMICS AND PHARMACOKINETICS OF LA NEED OF LA COMPOSITION IDEAL LA CLASSIFICATION LA AGENTS PRE-ANESTHETIC TEST SELECTION OF LA FACTORS AFFECTING LA ACTIVITY SYSTEMIC EFFECTS OF LA CONTRAINDICATIONS COMPICATIONS TOXICITY ANAPHYLATIC REACTION OF LA AND ITS MANAGEMENT PRECAUTION TAKEN FOR LA

3. ANESTHESIA : Greek word: “an” = without ; “ aisthesia ”= sensation Loss of sensation in all or particular part of body with or without loss of consciousness CARDINAL FEATURES :

4. WHAT IS LOCAL ANESTHESIA ? Local anaesthetics (Las) are drugs which upon topical application or local injection cause reversible loss of sensory perception, especially of pain, in a restricted area of the body. They block generation and conduction of nerve impulse at any part of the neuron with which they come in contact, without causing any structural damage . REVERSIBLE ,RECEPTOR BLOCK SKIN(APPLIED AREA) BRAIN NERVE IMPULSE

5. WHAT ACHARYAS DESCRIBE ABOUT SAGYAHARANA:

6. Cocaine(COCA PLANT; Erythroxylaceae , Erythroxylum gracilipes ) is a naturally occurring compound
It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic. Dr.Carl Koller,an austrian opthalmologist in 1884 demostrated that dropping a soluction of cocaine into eyes of frogs and guniea pigs produced a local anesthetic effect ;also he works on use of cocaine in catract extraction and iridectomy . Procaine , the first synthetic derivative of cocaine, was developed in 1904 by Alfred Einhorn . Later, Nils Lofgren,a swedish chemist later developed lidocaine (under the name XYLOCAINE). HISTORY OF LOCAL ANESTHESIA:

7. SIGNIFICANT PERSONS IN THE FIELD OF ANESTHESIA:

8. INTRODUCTION TO NEURON: A Neuron is an electically excitable cell that Processes & transmits information through electrical & chemical signals . NERVE:- A whitish fibre or bundle of fibres in the body that trasmits impulses of sensation to brain or spinal cord and impulse from these to muscles and organs

9. 3)Depending upon types of axons 2)Depending upon structure Transmission of impulse from nerve to CNS differs depending on whether a nerve is myelinated or unmyelinated . 1)Depending upon No. of Poles 4)Depending upon Function

10. MECHANISM OF NERVE CONDUCTION Resting Member Potential (-70mV) Threshold (-55mV ) ELECTRICAL + CHEMICAL Action Potential = DEPOLARISATION+REPOLARIZATION Rising Phase +40mV . Absolute refractory 2) Falling phage . Relative refractory 3) Hyperpolarisation Impulse transmission through axons

11. HOW LOCAL ANAESTHESIA WORKS ( pharmacodynamics ): Acetylcholine theory: Local anesthesia prevents acetylcholine at the synapse to alter the cell permeability,Thus prevents depolarization. This theory is less accepted as acetylcholine is not always present at the synapse . Calcium displacement theory: Local anesthesia blocks calcium channels and prevents the displacement of calcium needed for depolarization . Surface charge theory: local anesthesia is positively charged and it binds to outer surface of nerve membrane,thus hindering the depolarization process. Membrane expansion theory: local anesthesia is hydrophillic and it easily diffuses into the nerve membrane,thus altering the nerve membrane permeability. Specific receptor theory: local anesthesia soluction attaches itself to specific receptors present at the external or internal surface of nerve membrane and generally near the Na+ channel.this blocks the sodium channel and inhibits depolarization.

12. PHARMACOKINETICS: ABSORPTION: Depanding upon the vascularity of the area .it depands whether the drug will absorb into systemic circulation or not. DISTRIBUTION: Depands upon the degree of tissue and plasma protein binding the drug. More the protein bound the agent,the longer the duration of action as free drug is more slowly made available for metabolism. METABOLISM: ESTERS: breakdown rapidly by plasma esterases to inactive compounds having a short t1\2 . Cocaine hydrolize in liver AMIDES: Metabolize in liver by amidases.its a slow process hence its t1\2 is longer .so if given in repeated dose of by infusion. EXCREATION: BOTH ESTERS AND AMIDES ARE EXCREATED BY KIDNEYS AS XYLIDINES(amine).

13. NEED OF LOCAL ANESTHESIA: USE TO TREAT PAINFUL CONDITION E.g. mouth ulcer while taking meal PREVENT PAIN DURING A PROCEDURE OR OPERATION OF A PARTICULAR AREA OPERATED (for Dx and Rx) biopsy

14. LOCAL ANESTHESIA CAN APPLIED AS IN FORM OF- OINTMENTS=2% JELLY(CATHETER,SKIN GRAFTS)=2% SPRAY=4% CREAMS 0VER SUPERFICIAL SKIN (TOPICAL)=2% INJECTABLES OVER SUB MUCOSA,MUCOSA,MUSCULAR AREA,INTRAVENOUS (INFILTRATIONS= 0.5-2%) VISCOUS MINOR NERVE BLOCKER= NOT EXCEED 2% SPINAL= 0.5-5% EPIDURAL=0.25-2%

15. COMPOSITION OF LOCAL ANASTHESIA: LOCAL ANESTHETIC AGENT : lignocaine hydrochloride 2%(20mg\ml) VASOCONSTRICTOR : Adrenaline – 1:80,000 to 1:2,00,000 REDUCING AGENT(ANTIOXIDENT ): Sodium metabisulphite-0.5mg\ml This agent reacts with oxygen before it destroys the vasoconstrictor concentration. PRESERVATIVE : Methyl paraben - 0.1 mg\ml This agent is added to the soluction to give a shelf life of 2yrs or more It can cause allergic reactions. SALT: Sodium chloride -0.9 %- this is added to make the soluction isotonic. DISTILLED WATER OR RINGER LACTATE SOLUCTION : Added to give volume to the soluction and acts as a vehicle. FUNGICIDE : Thymol - it is added to provide antifungal properties.

16. LOCAL ANESTHESIA CONSIST OF HYDROPHILLIC TERTIARY AMINE GROUP LINKED WITH LIPOPHILLIC AROMATIC GROUP local anesthesia are alkaloid bases that are combined with acids,usually hydrochloride ,to form water soluable salts. SO IT MAKES LOCAL ANESTHETIC DRUG TO GET EASILY ABSORBE AND DISTRIBUTED IN THE APPLIED AREA the salt are used because they are stable and soulable in water ,water solubility is necessary for their diffusion through interstitial fluids to the nerve fibers. some local anesthesia having 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. Ex- bupivacaine , highly lipid soluble,is approximately 4 times more potent than lidocaine. local anesthesia block nerve fiber conduction by acting on nerve membrane: inhibit Na ions activity BLOCKS DEPOLARIZATION blocks nerve conduction LA blocks conduction in the following order: Small myelinated axons non myelinated axons Large myelinated axons Thus, a differential block can be achieved .i.e. pain sesation is blocked more readily than other sensory modalities. thus the loss of nerve function proceed as- Loss of pain Temperature Touch Proprioception Skeletal muscle tone Thus is why people may still feel touch but not pain when using local anesthesia.

17. IDEAL LOCAL ANESTHESIA: RAPID ONSET OF ACTION LONG ACTING LOCAL CONSTRICTOR EFFECT NO LOCAL\SYSTEMIC TOXICITY NO ALLERGIC REACTION ECONOMICAL REVERSIABLE ACTION SAFE COMPATABLE ph TO LOCAL TISSUES(BASE\ALKALOID) EASY STERLIZABLE WITHOUT LOOSING ITS POTENCY AND SHELF LIFE

18. CLASSIFICATION OF LOCAL ANASTHESIA AGENTS: BASED ON CHEMICAL STRUCTURE: ESTERS: ESTERS OF BENZOIC ACID: - Butacaine -Cocaine - hexylcaine Piperacaine Tetracaine Benzocaine 2) ESTERS OF PARA AMINO BENZOIC ACID: CHLOROPROCAINE PROPOXYCAINE AMIDES: BASED ON SOLUBILITY(DURATION OF ACTION AND POTENCY): INJECTABLES: LOW POTENCY,SHORT DURATION OF ACTION: E.g. procaine,chloroprocaine INTERMIDIATE POTENCY AND INTERMEDIATE ACTION: E.g. lidocaine,prilocaine HIGH POTENCY AND LONG DURATION ACTION: E.g. bupivacaine,tetracaine,debucaine,ropivacaine SURFACE ANESTHESIA: SOLUBLE: E.g cocaine,lidocaine,tetracaine INSOLUABLE: .E.g. benzocaine,oxethazine BUPIVACAINE LIDOCAINE PRILOCAINE QUINOLONES: centbucridine

19. LOCAL ANESTHETIC AGENTS: LIDOCAINE HYDROCHLORIDE : Introduced in 1950s. Excellent efficacy and safe 0.25-5% concentration available 4mg\kg lasts for 90min. Used with or without adrenaline.with adrenaline has longer.CI : End atreries e.g. glans penis,ear loubles , tips of nose,fingers and toes. Topical=2%,epidural=1.5-2 %, spinal=5 %, infiltration=0.5-1.5 % 2% with1:1000000 epinephrine or 1:2000000 epinephrineor 4%. Due due water solubality chances of toxicity is more. So, lowest dose which provides anasthesia should be used. Water soulability provides more tissue penetration than lidocaine base. 2% viscous-oral rinse in dental procedure Cotton applicators or packs- 1 to 5ml(40-200mg)or 0.6 to 3mg\kg.

20. 2) BUPIVACAINE( marcaine ): LONG ACTING Mostly used in post operative mangement Provides 4-5hrs after infiltration and 8hrs after nerve block. With epineprine 7hrs anesthesia. Available = 0.5%,0.5% with 1:2000000 epinephrine or 3% mepivacaine Dose=3mg\kg , epidural=0.25%-0.5%,spinal=0.5% in 3ml

21. SELECTION OF LOCAL ANESTHESIA :

22. FACTORS AFFECTING LA ACTIVITY : LIPID SOLUABILTY: higher the lipid solubility higher the ability of penetration to lipoprotein membrane and therefore greater the potency. pH:Anesthesia is decreased by the acidification of tissues.e.g inflammatory condition. (acidosis decrease the portion of nonionization of drug, reduce the ability to cross the membrane) VASODILATORS:LA with a vasodilator is more effective than the same agent without vasodilator. alkalization of LA increases the effectiveness and speed of action only LA without a vasoconstrictor are vasodilators thereby increasing the chances of its toxicity. PROTEIN BINDING: the greater the degree of membrane protein binding, longer is the duration of action. pKa : Acid dissociation constant

23. SAFTY LEVEL OF LA: WITHOUT VASOCONSTRICTORS: 3-4mg\kg WITH VASOCONSTRICTORS: 7mg\kg

24. SYSTEMIC ACTION OF LOCAL ANESTHESIA: CNS- Readily cross BBB. causes depression On therapeautic dose,no CNS effects of clinical significance. anticonvulsant propertiese ( lidocaine,procaine,etc ) while some causes seizures.

25. CARDIOVASCULAR SYSTEM: Direct action on myocardium: LA MODIFY ELECTROPHYSIOLOGICAL CHANGES IN THE MYOCARDIUM. LA PRODUCES MYOCARDIAL DEPRESSION DECREASE CONDUCTION RATE,FORCE OF CONTRACTION Direct action on periperal vasculature: cocaine, periferal cutaneous vasoconstriction others , vasodilation .though relaxation of smooth muscle in wall of blood vessels. On B.P.: Hypotension, by direct decreasing the myocardium and smooth muscle relaxation in the vessel wall. RESPIRATORY SYSTEM : In therapeutic dose,relaxant of bronchial smooth muscle In overdose, produces respiratory arrest due to generalized CNS DEPRESSION. MALIGNANT HYPERTHERMIA: SYMPTOMS: TACHYCARDIA,RIGID MUSCLE SPASM,UNSTABLE B.P. ,CYANOSIS,RESPIRATORY ACIDOSIS,MAY LEAD TO DEATH Amide group of LA are capable to provoke MH

26. Alcohol and smoking Steriod use (.2yrs) ALLERGY TO LA BISULFIDE ALLERGY MI within 6months UNSTABLE ANGINA PECTORIS CARDIAC DYSRTHYRMIAS CEREBRAL STOKE WITHIN 6MONTHS SEVERE RENAL DYSFUNCTION D.M Recent hepatitis A and hepatitis B Jaundice Local infection and sepsis Chronic renal failure Hyperthyroidsm \THYROTOXICOSIS Pregnency during 1 st trimenster Hypertension MH Congenital methemoglobinemia . AND OTHER CONGENITAL LIVER DYSFUNCTIONS CONDITIONS -increased H.R. , tremor, increased basal metabolic rate, irritability, increase B.P , increase body temp. MEDICATIONS - anti depresents,beta blockers,etc BODY PARTS - END ARTERIES E.g. digits of hands and feets,ears,nose,penis . CONTRAINDICATION:

27. SYSTEMIC COMPLICATION: Toxicity Syncope Allergic reaction Nausea and vomiting LOCAL COMPLICATIONS: Hematoma pain Slurred speech Blurred vision Headache Dizziness Edema - Paresthesia (trauma to the nerve) Trismus \muscle twitching Soft tissue injury COMPLICATION:

28. MENIFECTATION OF TOXICITY- -visual and auditory distrubances , light headedness,numbness of tongue Muscular twitching Unconciousness Convulsion CNS depression Coma Cardiac depression Toxicity of local anesthesia depands upon various factors- Amount of drug injected site of injection- vasularity Addition of vasodilators Nature of drug given Presence of associated conditions such as low cardiac output , renal failure, liver diseases ,etc adverse effects are usually caused due to high plasma concentration , resulting from: intravasular injection Excessive dose or rate of inj. Delayed drug clearance Administration into vascular tissue LA TOXIC EFFECTS- CNS: seizures,CNS depression including respiratory arrest CARDIOVASCULAR: depresses heart result in bradycardia,hypotension , cardiovascular collaspe,cardiac arrest LA TOXICITY:

29. Maintain ‘ABC’. O2 mask Ventilation if apnea occurs Convulsion- i.v . dizapam,thiopentone in incremental dose Cardiovasular collaspe - ephedrine,CPR as needed MANAGEMENT OF LA TOXICITY:

30. ALLERGIC SHOCK\ANAPHYLATIC SHOCK DUE TO LA: Esters are highly allergics , so pre anesthetic test needed. Pt may develop allergy only to bisulfide preservative used to stabilize the vasoconstriction. SIGN AND SYMPTOMS: Generalized body rash or skin redness Urticaria Swelling of throat Bronchospasm Asthama - Abdominal cramping - Irregular heartbeat - Hypotension Angioneurotics edema(swelling of face and lips)

31. Pharmacological management of anaphylatic shock : EPINEPHRIN- ADRENALIN:1:1000 SC INJ. Dose= 1mg T.D.S 5min apart Opens bronchioles allowing free breathing,increase B.P , intensify heartrate Its effect is drastic, but short lived. BENEDRYL(DIPHENHYDRAMINE) : 25-50mg sc inj Pills are available to prevent serious severe allergic reaction ,given a hour before the procedure. AMINOPHYLLINE: opens blocked breathing passage HYDROCORTISONE: iv inj Reduces generalize allergic inflammatory reactions on long term basis MEPHETERMINE SULFATE: iv inj Counteract hypotension on a prolonged basis.

32. PRE ANESTHETIC TEST: SKIN PRICK TEST\SENSITIVITY TEST REQUIREMENTS- Cotton 1-3ml syringe 26-30 gauze needle Surgical spirit Pen INTRADERMAL INJECTION WAIT FOR 20-30 MIN FOR ANY ANAPHYLATIC REACTION

33. Slow atraumatic insertion. Sharpe needle(1\3 rd part should be seen from outside) PROPER STERELIZATION Injecjected in proper anatomical land mark. pre anesthetic test must be done before injection of any Las. inject LA slowly, not exceding max. safe dose,espicially in children. avoid injecting large bolus at once. Small boluses,given slowly to achieve the desires effect are safer. adrenalin(vasoconstrictor) containing LA CI in pt having any type of cardiac issues,hyrotoxicosis , uncontrolled hypertension, pt receiving betablockers , tricyclic antidrepresants Propanonol ( betablocker )reduces metabolism of amides group of LA reducing hepatic blood flow. PRECAUSIONS: