ADr. Amit T.

Suryawanshi Literature

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Dr. Amit T. Suryawanshi

(MDS)

Facial Cosmetic SurgeonOral & Maxillofacial SurgeonDental Surgeon & ImplantologistHair Transplant Surgeon (Germany)

Consulting Surgeon in Kolhapur, Sangli, Pune & Mumbai (India) & founder of Face Art International Super specialityat Kolhapur

Cell Phone no. +91 9405622455 Clinic Landline - +91 7758976097 Email–

Pharmacokinetics and Metabolism ofDental Injectable (Lidocaine)

Lidocaine (Lignocaine, Xylocaine) is widely used as a local anaesthetic and antiarrhythmic drug and in patients with acute myocardial infarction as prophylaxis for ventricular fibrillation. Pharmacokinetic studies in man show wide variability in drug disposition between patients. Lidocaine is rapidly metabolized by the liver and less than 10% of a dose is excreted unchanged in the urine. Oxidative N-dealkylation, a major pathway of metabolism, results in the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological activities of these metabolites are similar to but less potent than Lidocaine. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline.The elimination half-life of Lidocaine following an intravenous bolus injection is typically 1.5 to 2 hours. Oral absorption of Lignocaine is found to be 97% . Volume of distribution is found to be 1.3 l/kg. Therapeutic effects of Lidocaine are generally associated with plasma levels of 1.5 to 6 mcg/mL. The blood to plasma distribution ratio is approximately 0.84. Objective adverse manifestations become increasingly apparent with increasing plasma levels above 6 mcg/mL.The plasma protein binding of Lidocaine is dependent on drug concentration and decreases with increasing concentration. At concentrations of 1 to 4 mcg/mL, 60 to 80 percent of Lidocaine is protein bound. Because of the rapid rate at which Lidocaine is metabolized, any condition that alters liver function, including changes in liver blood flow, which could result from severe congestive heart failure or shock may alter Lidocaine kinetics. The half-life may be two-fold or more greater in patients with liver dysfunction due to decreased volumes of distribution and clearance. so

lignocaine concentration may continue to rise for 24 to 48 hours so require reduction in loading and maintenance doses. Renal dysfunction does not affect Lidocaine kinetics, but may increase the accumulation of metabolites.Lidocaine readily crosses the placental and blood-brain barriers. Dialysis has negligible effects on the kinetics of Lidocaine.Toxicity, sometimes with serious clinical consequence, is uncommon and is usually related to over dosage.