Local anaesthesia

• 1. Local Anaesthesia DEFINITION: Local anaesthesia is drug-induced reversiblelocal blockade of nerve conduction in a specific part ofthe body that does not alter consciousness.

2. Prosperities 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 3. structural classification of localanaestheticsExamples ofamides includelidocaine,bupivacaine andprilocaine.Examples of estersinclude cocaine,procaine andamethocaine. 4. Esters vs Amides The ester linkage is more easily broken so the ester drugsare less stable in solution and cannot be stored for as longas amides. Amide anaesthetics are also heat-stable. The metabolism of most esters results in the productionof para-aminobenzoate (PABA) which is associated withallergic reaction. Amides, in contrast, very rarely cause allergicphenomena. For these reasons amides are now morecommonly used than esters. 5. The mechanism of action of local anaesthetics Disruption of ionchannel function viaspecific binding tosodium channels,holding them in aninactive state. Disruption of ionchannel function bythe incorporation oflocal anaestheticmolecules into the cellmembrane . 6. Demonstrating video 7. 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. 8. LA and pH All local anaesthetic agents are weak bases, meaning thatthey exist in two forms: unionised (B) and ionised (BH+). The pKa of a weak base defines the pH at which bothforms exist in equal amounts. As the pH of the tissues differs from the pKa of thespecific drug, more of the drug exists either in its chargedor uncharged form. 9. Local anaesthetics and infection The relevant feature of infected tissue isthat it tends to be a more acidicenvironment than usual. As the pH is reduced the fraction ofunionised local anaesthetic is reducedand consequently the effect is delayedand reduced. Infected tissue may also have anincreased blood supply and hence moreanaesthetic may be removed from thearea before it can affect the neurone. 10. Physicochemical characteristics ofa local anaesthetic affect itsfunction The aromatic ring structure and hydrocarbon chain lengthdetermine the lipid solubility of the drug. The more lipid soluble drug penetrates the cellmembrane more easily to exert its effect. Thus bupivacaine which is highly lipid soluble isapproximately four times more potent than lidocaine. 11. The duration of action The duration of action of the drug is also related to thelength of the intermediate chain joining the aromatic andamine groups. Protein binding , Procaine is only 6% protein bound andhas a very short duration of action, wherease bupivacaineis 95% protein bound. bupivacaine have a longer durationof action . 12. Absorption and distribution Some of the drug will be absorbed into the systemiccirculation: how much will depend on the vascularity ofthe area to which the drug has been applied. The distribution of the drug is influenced by the degree oftissue and plasma protein binding of the drug. the moreprotein bound the agent, the longer the duration ofaction as free drug is more slowly made available formetabolism. 13. Metabolism and excretion Esters (except cocaine) are broken down rapidly byplasma esterases to inactive compounds andconsequently have a short half life. Cocaine is hydrolysedin the liver. Ester metabolite excretion is renal. Amides are metabolised hepatically by amidases. This is aslower process, hence their half-life is longer and they canaccumulate if given in repeated doses or by infusion. 14. Adverse Effects CNS: excitation followed by depression(drowsiness to unconsciousness anddeath due to respiratory depression. Cardiovascular System: bradycardia,heart block, vasodilation (hypotension) Allergic reactions: allergic dermatitis toanaphylaxis (rare, but occur most oftenby ester-type drugs). 15. MechanismBlock nerve conduction reversibly. Two groups amideProcaine,chloroprocaine,tetracaineLidocaine,prillocaine,mepivocaine,bubivacaine,ropivacaineLess common More commonPlasma cholinestraseMetabolized at liverMore side effectless 16. Uses: Local anesthesia. Ventricular arrhythmia. Decrease haemodynamic response to tracheal intubationalso decrease cough. Treatment of epileptic fits. 17. Advantage of using adrenaline:Epinephrine vasoconstricts arteries reducing bleeding and also delays theresorption of lidocaine, almost doubling the duration of anaesthesia.Bupivacaine has caused several deaths when the epidural anaesthetichas been administered intravenously accidentally. 18. Treatment of overdose: lipid rescue There is animal evidence that Intralipid, a commonlyavailable intravenous lipid emulsion, can be effective intreating severe cardiotoxicity secondary to localanaesthetic overdose. 19. Contraindications Heart block, second or third degree (without pacemaker) Severe sinoatrial block (without pacemaker). Serious adverse drug reaction to lidocaine or amide localanaesthetics. Concurrent treatment with quinidine, flecainide,disopyramide, procainamide (Class I antiarrhythmicagents). Prior use of Amiodarone hydrochloride. 20. Hypotension not due to Arrhythmia. Bradycardia. Accelerated idioventricular rhythm. 21. Six Placement SitesSurface/topical Local infiltration Peripheral nerveanesthesiablock Bier block (IV Epidural Spinal anesthesia regionalanesthesia anesthesia) 22. Topical/Surface anesthesiaFor 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: produceslocalized vasoconstriction as well asanesthesia.Localized vasoconstriction: less bleeding. improved surgical field visualization. 23. 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. 24. Nebulized lidocaine (Xylocaine)--surface anesthesia Upper & lower respiratory tractprior to bronchoscopy or fiber-optic Laryngoscope. Treatment for intractable cough. Normal subjects: No effect onairflow resistance (they producesome bronchodilation). Patients with asthma: nebulizedlidocaine (Xylocaine) may increaseairflow resistance(bronchoconstriction)-- concern ifbronchoscopy is intended for thispatient group. 25. 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. 26. Skin Surface ApplicationBarrier: keratinized skin layer Higher local anestheticconcentrations required:o5% lidocaine (Xylocaine)-prilocaine (Citanest) cream{2.5% lidocaine (Xylocaine)& 2.5% prilocaine(Citanest)} no local irritation. even absorption. no systemic toxicity. 27. Combination of local anesthetic:Definition: eutectic mixture of local anesthetics (EMLA) .General definition: eutectic--said of a mixture which has the lowest meltingpoint which it is possible to obtain by the combination of the givencomponents.Melting point of combined drug is lower then either lidocaine (Xylocaine) orprilocaine (Citanest) alone. 28. Clinical uses of EMLA applications-- pain relief for: Venipuncture Lumbar puncture Arterial cannulation 29. Special uses In combination with nitroglycerin ointment -- makes venous cannulation easier by causing vasodilation. EMLA use in blood sampling: no effect on blood analysis.Factors affecting EMLA analgesia time to onset, duration of action, & efficacy Skin blood flow. Epidermal/girl thickness. Application duration. Presence of pathology. 30. Contraindications/Concerns EMLA cream not recommended for mucosal application due to faster lidocaine (Xylocaine)/prilocaine (Citanest) absorption. EMLA cream not recommended for application to skin wounds (wound infection risk, increased) EMLA cream: contraindicated in patients are allergic to amide local anesthetics 31. Local Infiltration Definition: Extravascular placement of the local anesthetic in the region tobe 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), 32. Duration of action: Duration extended by 2x using 1:200,000 epinephrine. Caution: Epinephrine-containing local anesthetic solution should not beinjected intracutaneously (intradermal) or into tissues supplied by"end-arteries" such as ears, nose, fingers because vasoconstriction maybe sufficiently severe to produce tissue ischemia and gangrene. 33. Peripheral Nerve Block Procedure: local anesthetic injection into tissues around individual nervesor nerve plexuses (e.g. brachial plexus). Mechanism: Local anesthetic diffusion path: nerve outer surface (mantle) to the nerve core [driving force: concentration gradient]. Anesthetized first: mantle fibers (innervating more proximal structures). Anesthetized last: core fibers (innervating more distal anatomy) Explanation of why anesthesia develops proximately first. Recovery in the opposite direction (sensation returns proximally first;lastly the distal anatomy). 34. The median nerve is blockedby inserting the needlebetween the tendons of thepalmaris longus and flexorcarpi radialis. The needle isinserted until it pierces thedeep fascia. Three to 5 mL oflocal anesthetic is injected.Although the piercing of thedeep fascia has been describedto result in a fascial "click", it ismore reliable to simply insertthe needle until it contacts thebone. The needle is thenwithdrawn 2-3 mm and thelocal anesthetic is injected. 35. Mixed peripheral nerves: (motor/sensory) Sequence of onset & recovery (motor anesthesia first or sensory anesthesia first): dependent on anatomical locations within the nerve fiber. Not recommended: Tetracaine (pontocaine): slow onset & more likely tocause systemic toxicity; not recommended for peripheral nerve block or forlocal infiltration. 36. Duration of action-dependencies Prolongation of drug effect:safer with added vasoconstrictor (e.g. epinephrine) thanby increasing local anesthetic dose. Example: bupivacaine (Marcaine) + epinephrine:peripheral nerve block may last 14 hours (in somereports). 37. Intravenous Regional Anesthesia(Bier Block)Procedure: Local anesthetic injection into anextremity isolated by tourniquet. Result: rapid anesthesia onset; skeletalmuscle relaxation.Duration of anesthetic action: Dependent on how long the tourniquetis kept inflated. Following tourniquet deflation: rapidrecovery as blood dilutes localanesthetic concentration.Probable Mechanism: Drug action on nerve endings & nervetrunks. 38. Lidocaine PrilocaineHigherlower plasma prilocaine (Citanest) concentrationsfollowing tourniquet deflation, compared tolidocaine LessSaferAgents not recommended: Chloroprocaine (Nesacaine) -- High incidence of thrombophlebitis.Bupivacaine (Marcaine) -- More likely than other local anesthetic tocause cardiotoxicity upon tourniquet deflation.Ropivacaine (Naropin)-Might also cause cardiotoxicity upontourniquet deflation (less likely than with bupivacaine (Marcaine)). 39. Indications for local anesthesia Most frequent use: regional anesthesia. Analgesic espescially post operative pain. Lidocaine (Xylocaine) also reduces blood pressure response to directlaryngoscopic tracheal intubation, an effect probably secondary togeneralized cardiovascular depression. Treatment of intractable cough. 40. 1-Causes.2-Factors reducing toxicity.3-Signs and symptoms.4-Treatment of toxicity. 41. Causes : Accidental rapidintravenous injection Rapid absorption, such asfrom a very vascular siteie mucous membranes. Overdose . 42. Factors reducing toxicity: Decide on the concentration of the local anaesthetic thatis required for the block to be performed. Calculate thetotal volume of drug that is allowed according to thetable below 43. Use the least toxic drug available Use lower doses in frail patients or at the extremes ofages Always inject the drug slowly (slower than 10ml /minute)and aspirate regularly looking for blood to indicate anaccidental intravenous injection Injection of a test dose of 2-3ml of local anaestheticcontaining adrenaline will often (but not always) cause asignificant tachycardia if accidental intravenous injectionoccurs 44. Add adrenaline (epinephrine) to reduce the speed ofabsorption. The addition of adrenaline will reduce themaximum blood concentration by about 50%. Usuallyadrenaline is added in a concentration of 1:200,000, witha maximum dose of 200 micrograms. Make sure that the patient is monitored closely by theanaesthetist or a trained nurse during the administrationof the local anaesthetic and the following surgery. 45. Signs and Symptoms of Local Anaesthetic Toxicity:1-CNS toxicity : Early or mild toxicity: light-headedness, dizziness,tinnitus, circumoral numbness, abnormal taste, confusionand drowsiness. Severe toxicity: tonic-clonic convulsion leading toprogressive loss of consciousness, coma, respiratorydepression, and respiratory arrest. 46. 2-CVS toxicity: Early or mild toxicity: tachycardia and rise in bloodpressure. This will usually only occur if there is adrenalinein the local anaesthetic. If no adrenaline is added thenbradycardia with hypotension will occur. Severe toxicity: Usually about 4 - 7 times the convulsantdose needs to be injected before cardiovascular collapseoccurs. Collapse is due to the depressant effect of thelocal anaesthetic acting directly on the myocardium. 47. Essential Precautions: Secure intravenous access before injection of any dosethat may cause toxic effects Always have adequate resuscitation equipment and drugsavailable before starting to inject. 48. Treatment of Toxicity:Treatment is based on the A B C D of Basic Life Support : A. Ensure an adequate airway, give oxygen in highconcentration if available B.Ensure that the patient is breathing adequately.Ventilate the patient with a self inflating bag if there isinadequate spontaneous respiration. Intubation may berequired if the patient is unconscious and unable tomaintain an airway. 49. CTreat circulatory failure with intravenous fluids and vasopressors such as ephedrine (10mg boluses) if hypotension occurs. Adrenaline may be used cautiously intravenously in boluses of 0.5 - 1ml of 1:10,000 (1mg in 10ml) if ephedrine is either not available or not effective in correcting the hypotension. Treat arrhythmias 50. D Drugs to stop fitting such as Diazepam 0.2-0.4mg/kgintravenously slowly over 5 minutes repeated after 10minutes if required, or 2.5mg - 10 mg rectally.Thiopentone 1-4 mg/kg intravenously may also be used intheatre Treatment of local anaesthetic toxicity is likely to have agood outcome if toxicity is recognised and basicresuscitation is started early. Monitor patients closelywhen using local anaesthetics. If a reaction occurs. 51. Advantages of local anaesthesia Non inflammable. Excellent muscle relaxant effect. During local anesthesia the patient remains conscious. It requires less skilled nursing care as compared to otheranesthesia like general anesthesia. Maintains his own airway. 52. Less pulmonary complication.s 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. 53. Suitable for patients who recently ingested food or fluids. Local anesthesia is useful for ambulatory patients havingminor procedures. Ideal for procedures in which it is desirable to have the patientawake and cooperative. Less bleeding. Expenses are less. 54. Disadvantages of local anaesthesia There are individual variations in response to local anestheticdrugs. Rapid absorption of the drug into the bloodstream can causesevere, potentially fatal reactions. Apprehension may be increased by the patients ability to seeand hear. Some patients prefer to be unconscious andunaware. 55. Direct damage of nerve. Post-dural headache from CSF leak. Hypotension and bradycardia through blockade of thesympathetic nervous system. Not suitable for extremes of ages. Multiple needle bricks may be needed. 56. Introduction Spinal anesthesia alsocalled spinal analgesia orsub-arachnoid block (SAB),is a form of regionalanesthesia involvinginjection of a localanesthetic into thesubarachnoid space,generally through a fineneedle. 57. Difference from epidural anesthesia Epidural anesthesia is a technique whereby a localanesthetic drug is injected through a catheter placed intothe epidural space. This technique has some similarity tospinal anesthesia, and the two techniques may be easilyconfused with each other. 58. Differences include: The involved space is larger for an epidural, andconsequently the injected dose is larger, being about 1020 mL in epidural anesthesia compared to 1.53.5 mL in aspinal. In an epidural, an indwelling catheter may be placed thatavails for additional injections later, while a spinal isalmost always a one-shot only. The onset of analgesia is approximately 1530 minutes inan epidural, while it is approximately 5 minutes in aspinal. 59. Injected substances Bupivacaine (Marcaine) is the local anaesthetic mostcommonly used, although lignocaine (lidocaine),tetracaine, procaine, ropivacaine, levobupivicaine andcinchocaine may also be used. Sometimes a vasoconstrictor such as epinephrine isadded to the local anaesthetic to prolong its duration. 60. Mechanism Regardless of the anesthetic agent (drug) used, thedesired effect is to block the transmission of afferentnerve signals from peripheral nociceptors. Sensory signals from the site are blocked, therebyeliminating pain. The degree of neuronal blockade depends on the amountand concentration of local anesthetic used and theproperties of the axon. 61. Limitations Spinal anesthetics are typically limited to proceduresinvolving most structures below the upper abdomen. To administer a spinal anesthetic to higher levels mayaffect the ability to breathe by paralyzing the intercostalrespiratory muscles, or even the diaphragm in extremecases (called a "high spinal", or a "total spinal", withwhich consciousness is lost). 62. Indications This technique is very useful in patients having an irritableairway (bronchial asthma or allergic bronchitis),anatomical abnormalities which make endotrachealintubation very difficult (micrognathia), borderlinehypertensives where administration of general anesthesiaor endotracheal intubation can further elevate the bloodpressure, procedures in geriatric patients. 63. Contraindications Non-availability of patients consent, local infection orsepsis at the site of lumbar puncture, bleeding disorders,space occupying lesions of the brain, disorders of thespine and maternal hypotension. 64. OperationsAll surgical interventions below the umbilicus, is the generalguiding principle: Abdominal & vaginal hysterectomies Laparoscopy Assisted Vaginal Hysterectomies (LAVH)combined with general anesthesia Caesarean sections Hernia (inguinal or epigastric) Piles fistulae & fissures orthopaedic surgeries on the pelvis, femur, tibia and the ankle nephrectomy 65. ComplicationsCan be broadly classified as immediate (on the operatingtable) or late (in the ward or in the P.A.C.U. post-anesthesiacare unit): Spinal shock. Cauda equina injury. Cardiac arrest. Hypothermia. Broken needle. Bleeding resulting in hematoma, with or without subsequent neurologicalsequelae due to compression of the spinal nerves. 66. Infection: immediate within six hours of the spinal anestheticmanifesting as meningism or meningitis or late, at the site ofinjection, in the form of pus discharge, due to impropersterilization of the LP set. PDPH: Post dural puncture head ache or post spinal head ache. 67. Epidural anesthesia 68. Mechanism Direct action on nerveroots and spinal cordfollowing local anestheticdiffusion across the dura. Diffusion of localanesthetic intoparavertebral region. 69. Onset of action:15-30minute delay . Choice of local anesthetics: Lidocaine (Xylocaine): frequently used; diffuses well for tissues. Bupivacaine (Marcaine) & Ropivacaine (Naropin) (0.5%-0.75%). 70. Epidural anathesiaSpinal anathesiaSite of injectionIn the epidural space Subarachnoid spaceOnset and duration Slow onset and continous duration Rapid onset and limited (use catheter)durationadvantages Can be used in analgesiaNot usedNeedle Curved,longand blunt (touhy)Small and sharpdose 10_30ml 1_4mlspaceAny space usually lumberlumberQuality of sensory lessMore liableand motor nerveblocktoxicity Hypotention gradual Sudden total spinal ++++ systemic toxicity +++ + 71. Indications:1-Pain relief:a)Post operativeb)Labour painc)Cancer2-Operations in perineum lower limblower abdomen.3-Expected difficult intubation. An epidural injection may beperformed anywhere along thevertebral column (cervical, thoracic,lumbar, or sacral). 72. Contra indications: A)absolute: 1-Hypovolemia. 2-Refusal of patient. 3-Coagulopathy. 4-Local and systemic sepsis. B)relative: - Increase intra cranial pressure deformity of vertebral column. 73. ComplicationsA)during operation: 1)Hypotension 2)Bradycardia 3)Cardiac arrest 4)Nausea ,vomiting 5)Failed spinal 6)Total spinal 7)Broken needle 8)Hypothermia 74. B)Post operative:1)Post dural punctureheadache.2)Back pain.3)Meningitis andneurological sequalae.4)Haematoma.5)Urine retention.