Dexamethasone 4 mg, Lidocaine 30 mg, Vitamin B1 50 mg, Vitamin B12 250 mcg, Vitamin B6 50 mg Liquid injectables

Lidocaine hydrochloride stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action.

Systemic plasma levels of lidocaine following Lidocaine Hydrochloride Injection do not correlate with local efficacy.

Absorption — Information derived from diverse formulations, concentrations and usages reveals that lidocaine hydrochloride 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.

Distribution — The plasma binding of lidocaine hydrochloride 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 hydrochloride is protein bound. Binding is also dependent on the plasma concentration of the alpha-1‑acid glycoprotein.

Lidocaine hydrochloride crosses the blood-brain and placental barriers, presumably by passive diffusion.

Elimination — The elimination half-life of lidocaine hydrochloride following an intravenous bolus injection is typically 1.5 to 2 hours.

Metabolism — Lidocaine hydrochloride is metabolized rapidly by the liver, and 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 hydrochloride.

Excretion — Approximately 90% of lidocaine hydrochloride administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged by the kidneys. The primary metabolite in urine is a conjugate of 4‑hydroxy-2,6-dimethylaniline.

Patients with Hepatic Impairment — Because of the rapid rate at which lidocaine hydrochloride is metabolized, any condition that affects liver function may alter lidocaine hydrochloride kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction.

Patients with Renal Impairment — Renal dysfunction does not affect lidocaine hydrochloride kinetics but may increase the accumulation of metabolites.

Naturally occurring glucocorticoids (hydrocortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.

Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli.