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Local anesthetic systemic toxicity ( LAST) Dr. S. Parthasarathy MD, DA, DNB, Dip Diab.MD ,DCA, Dip software based statistics, PhD (physiology) FICA What is it ?? • Allergic reactions • Tissue toxicity – TNS, lignocaine spinal • Probably blockade of calcium channels ---• LAST – systemic Allergy • True immunologic reactions to LAs are generally rare. • True allergic reactions to preservative-free amide-type local anesthetics are so rare. • True anaphylaxis appears more common with ester LAs that are metabolized directly to PABA • Accidental intravenous injections are often misdiagnosed as allergic reactions. • Some patients may react to preservatives, such as methylparaben, included with LAs. History • 1880 = cocaine invented and toxicity described • 1960 = bupivacaine discovered = • Later levo bupi and ropi invented • Lipid emulsion for LAST ( 0.1 in 1000) Mechanisms • Cardiovascular effects are caused by blockade of cardiac VASCs and K+ channels. Levobupivacaine and ropivacaine are thought less likely to interact with cardiac VASCs. • Possible calcium channel block • Mitochondrial dysfunction • Convulsions may be caused by the blockade of GABA A receptors in the CNS • Fast in fast out -- lignocaine • Fast in slow out --- bupivacaine • ( dissociation constant – more with bupi ) Order of toxicity • • • • • Intercostal Caudal Epidural Brachial plexus Sciatic IVRA Why difference • • • • • • • Age – extremes Additive Speed Which drug Concurrent illness Concurrent drugs Site • Bupi – 2-3 mg / kg • Ligno – 4-5 mg/kg • Ligno with adrenaline 7 mg / kg • But beware of combinations – additive toxicity Toxicity • • • • • • • • • Cocaine Tetracaine Bupivacaine L. bupi Ropi Mepi Ligno Prilo 2– chlorprocaine worst least Moving towards safer molecules ? Pick up here Starts from to • (auditory changes, circum oral numbness, metallic taste, and agitation), • central nervous system (CNS) findings (seizure, coma, respiratory arrest) • Inhibitory neurons first !!- so seizures • cardiovascular events (hypertension, hypotension, tachycardia, bradycardia, ventricular arrhythmias, cardiac arrest) • Injection of lignocaine in the brain induced arrhythmias • Cause – for cardiac effects – CNS depression hypotension and rhythm disturbances . • Hypercarbia , acidosis enhance CNS toxicity Differential diagnosis • • • • • Vasovagal High spinal Total spinal Concomitant disease High epinephrine dosage Management Prevention is the essence • • • • • • • • USG Check dose of local and epinephrine Effective dose in increments – catheters ?? Aspirate frequently Negative aspiration not foolproof because probe will compress the vein Discard bloody locals Monitor CVS and IV access Hepatic or Talk with the patient renal disease Stop injecting (CC:CNS ratio 2 : 7.1 for the two LA) lignocaine Convulsion Lethality 22 mg/kg 76mg/kg Bupivacaine 5mg/kg 20mg/kg Are they clinically relevant ?? • the reduced toxic potential of the two pure leftisomers supports their use in those clinical situations in which the risk of systemic toxicity related to either overdosing or unwanted intravascular injection is high, such as during epidural or peripheral nerve blocks. Treatment • Convulsions • • • • Thiopentone 1-3 mg/kg Diazepam - 0.15 mg/kg Midazolam – 0.1 mg / kg Less doses – because thio itself is myocardial depressant .propofol may cause more hypotension • Benzodiazepines also decrease arrhythmias Arrhythmias • • • • Better to use calcium channel blockers Valproate ( fits and rhythm disturbances ) Phenytoin Bretylium • NO XYLOCAINE Resuscitation • • • • • • • • Airway- breathing- circulation Oxygen - 100 % Ventilation Special Vasopressin ? CPB ? GIK Amiodarone if preliminary resuscitation fails ---- Lipid emulsion • Bolus of intralipid – 20 % - 1.5 ml/kg – 1 minute • Infusion – 0.25 ml /kg/minute • Chest compressions – lipid should circulate • Can increase to 0.5 ml/kg/min • Maximum of 8 ml/kg - 12 ml /kg – guidelines vary Mechanism • Direct • Sink theory – sticks to lipid soluble LA and get rid of the drug out of the tissue • Indirect • Overrides mitochondrial translocase from the LA • Predominant CNS changes – anticonvulsants • Predominant CVS changes – Go for intra lipid early Prilocaine • More than 600 mg • Associated with – o toluidine and methemoglobinemia • IV methylene blue is the treatment Summary • • • • • • • Intercostal , IVRA Toxic doses Which local anesthetic Symptoms and DD Prevention Treatment Lipid emulsion or anticonvulsants - Thank you all