Lidocaine 1% is a widely utilized local anesthetic belonging to the amide class, often recognized commercially as Xylocaine. This medication temporarily eliminates the sensation of pain in a localized area. While lidocaine is frequently combined with a vasoconstrictor like epinephrine, this article addresses the applications and properties of the formulation without epinephrine, commonly referred to as “plain” lidocaine. Understanding this preparation is important for its correct and safe use.
The Mechanism of Local Anesthesia
The sensation of pain requires a signal, or action potential, to be transmitted along nerve fibers to the brain. This electrical signal relies on the movement of ions across the nerve cell membrane, particularly the rapid influx of sodium ions. Voltage-gated sodium channels are the specialized protein structures controlling this sodium flow.
Lidocaine molecules exert their effect by physically interacting with these sodium channels. After injection, the drug diffuses into the nerve and binds to the channels, essentially blocking the pore. This blockage prevents the rapid flow of sodium ions into the cell, which is necessary for the nerve to depolarize and generate an action potential.
By inhibiting this step, the transmission of pain signals is halted, resulting in localized numbness and a loss of sensation. This cellular action is reversible; as the drug concentration decreases, the sodium channels are freed, and normal nerve function returns. Lidocaine is an amide-type anesthetic, known for its stability and predictable action.
Clinical Applications of the Plain Formulation
The key difference between plain lidocaine and its counterpart is the absence of epinephrine, a potent vasoconstrictor that restricts local blood flow. Epinephrine is typically added to lengthen the duration of action and reduce the amount of drug that quickly enters the systemic circulation. However, the lack of vasoconstriction makes the plain formulation the preferred choice in specific situations.
One application is in procedures involving anatomical areas with limited collateral blood supply, such as the fingers, toes, nose, ears, and penis. Using a vasoconstrictor in these “end-artery” areas carries a theoretical risk of causing prolonged lack of blood flow, or ischemia, which can lead to tissue damage. Although modern data suggests this risk is lower than historically believed, the plain formulation remains the standard of care for digital blocks to avoid this complication.
The plain formulation is also mandated for patients with specific health conditions or drug regimens. Patients with severe cardiovascular disease, poorly controlled hypertension, or certain heart arrhythmias may be overly sensitive to the systemic effects of absorbed epinephrine. The plain formulation is also selected for patients taking medications like monoamine oxidase (MAO) inhibitors or tricyclic antidepressants, as these drugs can interact dangerously and amplify epinephrine’s cardiovascular effects. It is also used for intravenous regional anesthesia, often called a Bier block, where the anesthetic is injected into a limb isolated by a tourniquet; a vasoconstrictor is never used in this scenario.
Pharmacokinetics: Onset, Duration, and Metabolism
The pharmacokinetics of plain lidocaine determine its onset, duration, and metabolism. When injected, lidocaine 1% typically has a rapid onset of action, often providing localized numbness within two to five minutes. This fast onset allows procedures to begin quickly.
The absence of epinephrine means the drug is absorbed into the surrounding bloodstream more quickly from the injection site. This rapid absorption significantly shortens the duration of the anesthetic effect compared to formulations containing a vasoconstrictor. For simple infiltration, the duration of plain lidocaine action is generally 30 to 60 minutes, though this varies depending on the injection site’s vascularity.
Lidocaine undergoes metabolism primarily in the liver. The drug is broken down by the cytochrome P450 enzyme system, specifically involving CYP3A4, into various metabolites. These metabolites, including monoethylglycinexylidide and xylidide, are then primarily excreted through the kidneys. Liver dysfunction can prolong the half-life of lidocaine, meaning the drug stays in the body longer.
Monitoring and Systemic Reactions
The rapid absorption of plain lidocaine means the drug enters the systemic circulation quickly. This speed of entry increases the risk of local anesthetic systemic toxicity (LAST), especially if a large volume is injected or if the drug is accidentally delivered directly into a blood vessel. Therefore, careful monitoring and technique are necessary to keep the drug concentration below toxic levels.
Before injection, the clinician should aspirate (pull back on the syringe plunger) to ensure the needle tip is not inside a blood vessel. The maximum recommended dose for lidocaine without epinephrine is 4.5 milligrams per kilogram of body weight, up to a total of 300 milligrams. This limit should not be exceeded, as staying below this maximum dose is a safety measure to prevent toxicity.
Systemic toxicity manifests in two main categories, with central nervous system (CNS) symptoms typically appearing first. Early CNS signs include a metallic taste, numbness around the lips (perioral numbness), ringing in the ears (tinnitus), and dizziness. If drug levels continue to rise, more severe symptoms like muscle twitching, agitation, and seizures can occur. Cardiovascular effects, generally seen at higher blood concentrations, include a drop in blood pressure (hypotension) and a slow heart rate (bradycardia) that can progress to serious heart arrhythmias.