Akten Gel

Akten® is indicated for ocular surface anesthesia during ophthalmologic procedures.

The recommended dose of Akten® is 2 drops applied to the ocular surface in the area of the planned procedure. Akten® may be reapplied to maintain anesthetic effect.

Akten® Ophthalmic Gel, 3.5% contains 35 mg per mL of lidocaine hydrochloride for topical ophthalmic administration.

None

Pregnancy. Pregnancy Category B.

Reproduction studies for lidocaine have been performed in both rats and rabbits. There was no evidence of harm to the fetus at subcutaneous doses up to 50 mg/kg lidocaine (more than 800 fold greater than the human dose on a body weight basis) in the rat model. There are however, no adequate and well controlled studies in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used in pregnancy only if clearly needed.

Nursing Mothers

Lidocaine is secreted in human milk. The clinical significance of this observation is unknown. Although no systemic exposure is expected with administration of Akten®, caution should be exercised when Akten® is administered to a nursing woman.

Pediatric Use

Safety and efficacy in pediatric patients have been extrapolated from studies in older subjects and studies in pediatric patients using different formulations of lidocaine.

Geriatric Use

No overall clinical differences in safety or effectiveness were observed between the elderly and other adult patients.

Mechanism of Action

Akten® is a local anesthetic agent that stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action. Anesthesia generally occurs between 20 seconds to 1 minute and persists for 5 to 30 minutes.

Pharmacokinetics

Lidocaine may be absorbed following topical administration to mucous membranes. Its rate and extent of absorption depend upon various factors such as concentration, the specific site of application, viscosity of the agent, and duration of exposure.

The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 mcg 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 is metabolized rapidly by the liver, and metabolites and unchanged drug 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 pharmacologic/toxicologic 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.

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 rate at which lidocaine is metabolized, any condition that affects liver function may alter lidocaine kinetics. The half-life may be prolonged twofold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites.