Lidocaine Hcl

INDICATIONS: For temporary relief of pain and itching associated with minor burns, sunburn, minor cuts, scrapes, insect bites, and minor skin irritation.

DOSAGE AND ADMINISTRATION: Apply a thin film to the affected area two or three times daily or as directed by a physician.

ADVERSE REACTIONS: During or immediately after treatment, the skin at the site of treatment may develop erythema or edema or may be the locus of abnormal sensation.

PHARMACOKINETICS: Lidocaine may be absorbed following topical administration to mucous membranes, its rate and extent of absorption depending upon the specific site of application, duration of exposure, concentration, and total dosage. In general, the rate of absorption of local anesthetic agents following topical application occurs most rapidly after intratracheal administration. Lidocaine is also well-absorbed from the gastrointestinal tract, but little intact drug appears in the circulation because of biotransformation in the liver. Lidocaine is metabolized rapidly by the liver and metabolites and unchanged drugs are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to but less potent than, those of Lidocaine. Approximately 90% of Lidocaine administered is excreted in the form of various metabolites and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline. The plasma binding of Lidocaine is dependent on drug concentration and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 g of free base per mL, 60 to 80 percent of Lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein. Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion. Studies of Lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent is typically 1.5 to 2 hours. Because of the rapid rate at which Lidocaine is metabolized, any condition that affects liver function may alter Lidocaine kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect Lidocaine kinetics but may increase the accumulation of metabolites. Factors such as acidosis and the use of CNS stimulants and depressants affect the CNS levels of Lidocaine required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6 g free base per mL. In the rhesus monkey, arterial blood levels of 18-21 g/mL have been shown to be threshold for convulsive activity.