LIDOCAINE HYDROCHLORIDE AND DEXTROSE- lidocaine hydrochloride and dextrose monohydrate injection, solution
5% Lidocaine Hydrochloride and 7.5% Dextrose Injection, USP is a sterile, nonpyrogenic, hyperbaric solution for use in spinal anesthesia.
5% Lidocaine Hydrochloride and 7.5% Dextrose Injection, USP contains lidocaine HCl, which is chemically designated as 2-(diethylamino)-N-(2,6-dimethylphenyl)-acetamide monohydrochloride, monohydrate and Dextrose (D-Glucose monohydrate) which have the following structural formulas:
Lidocaine Hydrochloride (monohydrate)
5% Lidocaine Hydrochloride and 7.5% Dextrose Injection, USP contains 50 mg/mL of lidocaine hydrochloride, anhydrous with 75 mg/mL of dextrose, hydrous in water for injection. May contain sodium hydroxide and/or hydrochloric acid for pH adjustment. pH 6.5 (6.0 to 7.0). The osmolar concentration is 0.75 mOsmol/mL (calc.). The specific gravity is 1.030 to 1.035.
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. The duration of perineal anesthesia provided by 1 mL (50 mg) 5% Lidocaine Hydrochloride and 7.5% Dextrose Injection, USP averages 100 minutes, with analgesia continuing for an additional 40 minutes. The duration of surgical anesthesia provided by 1.5 to 2 mL (75 to 100 mg) of this agent is approximately two hours.
Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to block of autonomic fibers, or 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
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 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 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.
The elimination half-life of lidocaine following an intravenous bolus injection 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 6.0 mcg free base per mL. In the rhesus monkey arterial blood levels of 18 to 21 mcg/mL have been shown to be threshold for convulsive activity.
Lidocaine Hydrochloride and Dextrose Indications and Usage
5% Lidocaine Hydrochloride and 7.5% Dextrose Injection, USP is indicated for the production of spinal anesthesia when the accepted procedures for this technique as described in standard textbooks are observed.
Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type.
The following conditions preclude the use of spinal anesthesia:
- Severe hemorrhage, shock or heart block
- Local infection at the site of proposed puncture
- Known sensitivity to the local anesthetic agent.
5% LIDOCAINE HYDROCHLORIDE AND 7.5% DEXTROSE INJECTION, USP FOR SPINAL ANESTHESIA SHOULD BE EMPLOYED ONLY BY CLINICIANS WHO ARE WELL VERSED IN DIAGNOSIS AND MANAGEMENT OF DOSE-RELATED TOXICITY AND OTHER ACUTE EMERGENCIES THAT MIGHT ARISE FROM SPINAL ANESTHESIA AND THEN ONLY AFTER ENSURING THE IMMEDIATE AVAILABILITY OF OXYGEN, OTHER RESUSCITATIVE DRUGS, CARDIOPULMONARY EQUIPMENT, AND THE PERSONNEL NEEDED FOR PROPER MANAGEMENT OF TOXIC REACTIONS AND RELATED EMERGENCIES (see also ADVERSE REACTIONS and PRECAUTIONS). DELAY IN PROPER MANAGEMENT OF DOSE-RELATED TOXICITY, UNDERVENTILATION FROM ANY CAUSE AND/OR ALTERED SENSITIVITY MAY LEAD TO THE DEVELOPMENT OF ACIDOSIS, CARDIAC ARREST AND, POSSIBLY, DEATH.
Cases of methemoglobinemia have been reported in association with local anesthetic use. Although all patients are at risk for methemoglobinemia, patients with glucose-6-phosphate dehydrogenase deficiency, congenital or idiopathic methemoglobinemia, cardiac or pulmonary compromise, infants under 6 months of age, and concurrent exposure to oxidizing agents or their metabolites are more susceptible to developing clinical manifestations of the condition. If local anesthetics must be used in these patients, close monitoring for symptoms and signs of methemoglobinemia is recommended.
Signs of methemoglobinemia may occur immediately or may be delayed some hours after exposure, and are characterized by a cyanotic skin discoloration and/or abnormal coloration of the blood. Methemoglobin levels may continue to rise; therefore, immediate treatment is required to avert more serious CNS and cardiovascular adverse effects, including seizures, coma, arrhythmias, and death. Discontinue 5% Lidocaine Hydrochloride and 7.5% Dextrose Injection and any other oxidizing agents. Depending on the severity of the signs and symptoms, patients may respond to supportive care, i.e., oxygen therapy, hydration. A more severe clinical presentation may require treatment with methylene blue, exchange transfusion, or hyperbaric oxygen.
Intra-articular infusions of local anesthetics following arthroscopic and other surgical procedures is an unapproved use, and there have been post-marketing reports of chondrolysis in patients receiving such infusions. The majority of reported cases of chondrolysis have involved the shoulder joint; cases of gleno-humeral chondrolysis have been described in pediatric and adult patients following intra-articular infusions of local anesthetics with and without epinephrine for periods of 48 to 72 hours. There is insufficient information to determine whether shorter infusion periods are not associated with these findings. The time of onset of symptoms, such as joint pain, stiffness and loss of motion can be variable, but may begin as early as the 2nd month after surgery. Currently, there is no effective treatment for chondrolysis; patients who experienced chondrolysis have required additional diagnostic and therapeutic procedures and some required arthroplasty or shoulder replacement.
To avoid intravascular injection, aspiration should be performed before the local anesthetic solution is injected. 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 guarantee that intravascular injection has been avoided.
Spinal anesthetics should not be injected during uterine contractions since spinal fluid current may carry the drug farther cephalad than desired.
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