OCTOCAINE 50 — lidocaine hydrochloride and epinephrine bitartrate injection, solution
Solutions for local anesthesia in Dentistry
Octocaine (Lidocaine Hydrochloride and Epinephrine, USP) is a sterile isotonic solution containing a local anesthetic agent, Lidocaine Hydrochloride, and a vasoconstrictor, Epinephrine (as bitartrate) and are administered parenterally by injection. Both solutions are available in single dose cartridges of 1.7 mL (See INDICATIONS AND USAGE for specific uses). The solutions contain lidocaine hydrochloride which is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl)-monohydrochloride, and has the following structural formula :
C14 H22 N2 0•HCl• H2 0 M.W. 288.8
Epinephrine is ( — )-3,4-Dihydroxy- -[(Methylamino) methyl] benzyl alcohol and has the following structural formula :
C9 H13 NO3 •C4 H6 06 M.W. 333.3
|SINGLE DOSE CARTRIDGE|
(as the bitartrate)
|Sodium Chloride||Potassium metabisulfite||Edetate Disodium|
|The pH of all solutions are adjusted to USP limits with sodium hydroxide.|
Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of nerve impulses, thereby effecting local anesthetic action.
When used for infiltration anesthesia in dental patients, the time of onset averages less than two minutes for Octocaine Injections. Octocaine Injections provide an average pulp anesthesia of at least 60 minutes with an average duration of soft tissue anesthesia of approximately 2.5 hours.When used for nerve blocks in dental patients, the time of onset for both forms of Octocaine (Lidocaine and Epinephrine) injections averages 2-4 minutes. Octocaine injections provide pulp anesthesia averaging at least 90 minutes with an average duration of soft tissue anesthesia of 3 to 3.25 hours.
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 and/or the beta-adrenergic receptor stimulating action of epinephrine when present.
Information derived from diverse formulations, concentrations and usages reveals that lidocaine is completely absorbed following parenteral administration, its rate of absorption depending, for example, upon various factors such as the site of administration and the presence or absence of a vasoconstrictor agent. Except for intravascular administration, the highest blood levels are obtained following intercostal nerve block and the lowest after subcutaneous administration.
The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentratlon. At concentration 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-l-acid glycoprotein.
Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.
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 of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent is typically 1.5 to 2.0 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 6.0 μg free base per mL. In the rhesus monkey, arterial blood levels of 18-21 μg/mL have been shown to be the threshold for convulsive activity.
Octocaine (Lidocaine and Epinephrine Injection, USP) is indicated for the production of local anesthesia for dental procedures by nerve block or infiltration techniques.
Only accepted procedures for these techniques as described in standard textbooks are recommended.
Lidocaine and Epinephrine Injection is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type or to any components of the injectable formulations.
DENTAL PRACTITIONERS WHO EMPLOY LOCAL ANESTHETIC AGENTS SHOULD BE WELL VERSED IN DIAGNOSIS AND MANAGEMENT OF EMERGENCIES WHICH MAY ARISE FROM THEIR USE. RESUSCITATIVE EQUIPMENT, OXYGEN AND OTHER RESUSCITATIVE DRUGS SHOULD BE AVAILABLE FOR IMMEDIATE USE.
To minimize the likelihood of intravascular injection, aspiration should be performed before the local anesthetic solution is injected. If blood is aspirated, the needle must be repositioned until no return of blood can be elicited by aspiration. Note, however, that the absence of blood in the syringe does not assure that intravascular injection will be avoided.
Local anesthetic procedures should be used with caution when there is inflammation and/or sepsis in the region of the proposed injection.
Octocaine Injections contain potassium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people.
OCTOCAINE, along with other local anesthetics, is capable of producing methemoglobinemia. The clinical signs of methemoglobinemia are cyanosis of the nail beds and lips, fatigue and weakness. If methemoglobinemia does not respond to administration of oxygen, administration of methylene blue intravenously 1-2 mg/kg body weight over a 5 minute period is recommended.
The American Heart Association has made the following recommendations regarding the use of local anesthetics with vasoconstrictors in patients with ischemic heart disease: “Vasoconstrictor agents should be used in local anesthesia solutions during dental practice only when it is clear that the procedure will be shortened or the analgesia rendered more profound. When a vasoconstrictor is indicated, extreme care should be taken to avoid intravascular injection. The minimum possible amount of vasoconstrictor should be used.” (Kaplan, EL, editor: Cardiovascular disease in dental practice, Dallas 1986, American Heart Association.)
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