DrugLib.com — Drug Information Portal

Rx drug information, pharmaceutical research, clinical trials, news, and more

Laryng-O-Jet (Lidocaine Hydrochloride Topical) - Description and Clinical Pharmacology

 
 



Rx Only

DESCRIPTION

Lidocaine HCI Topical Solution USP, 4% is a sterile, aqueous solution containing a local anesthetic agent and is administered topically.
    Lidocaine hydrochloride is designated chemically as acetamide, 2-(diethylamino)-N-(2, 6-dimethylphenyl)-monohydrochloride, with the following structural formula:

Composition of Lidocaine HCI 4% Topical Solution: Each mL of aqueous solution contains lidocaine HCI, 40 mg, and sodium hydroxide and/or hydrochloric acid to adjust pH to 5.0 to 7.0. No preservative is added since all or part of the contents of the syringe unit is administered as a single dose and the unit should not be re-used.

CLINICAL PHARMACOLOGY


Mechaninsm of Action:

Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action. The onset of action is rapid.

Hemodynamics:

Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. These changes may be attributable to a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.

Pharmacokinetics and Metabolism:

Lidocaine may be absorbed following topical administration to mucous membranes, its rate and extent of absorption depending upon concentration and total dose administered, the specific site of application, and duration of exposure. 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 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 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.
    Studies have shown that peak blood levels of lidocaine may occur as early as 5 and as late as 30 minutes after endotracheal administration of a 4% lidocaine HCI solution.
    The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 μg 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 plasmalevels above 6 μg free base per mL. In the rhesus monkey arterial blood levels of 18-21μg/mL have been shown to be threshold for convulsive activity.

-- advertisement -- The American Red Cross
 
Home | About Us | Contact Us | Site usage policy | Privacy policy

All Rights reserved - Copyright DrugLib.com, 2006-2017