![]() Pain relief (in anal fissures, haemorrhoids, pruritus ani, pruritus vulvae, herpes zoster, or herpes labialis): 1–2 g applied when necessary avoid long-term use.ĭental practice: rub gently into dry gum. The lowest dosage necessary to produce adequate anesthesia should be used. Lidocaine 5% ointment is used for anesthesia of skin and mucous membranes mouth and perianal area.ĭosage of Lidocaine 5% ointment depends on the indications and the area of surface to be anesthetized, tissue vascularity and individual patient tolerance. Lidocaine crosses the placenta and blood-brain barrier it is distributed into breast milk. Renal impairment does not affect the clearance of lidocaine but accumulation of its active metabolites can occur. Concomitant therapy with drugs that alter hepatic blood flow or induce drug-metabolising microsomal enzymes can also affect the clearance of lidocaine. Reduced clearance of lidocaine has been found in patients with heart failure, alcoholic liver disease, or chronic or viral hepatitis. Further metabolism occurs and metabolites are excreted in the urine with less than 10% of unchanged lidocaine. Both of these metabolites may contribute to the therapeutic and toxic effects of lidocaine and since their half-lives are longer than that of lidocaine, accumulation, particularly of glycinexylidide, may occur during prolonged infusions. Metabolism in the liver is rapid and about 90% of a given dose is dealkylated to form monoethylglycinexylidide and glycinexylidide. Lidocaine is largely metabolised in the liver and any alteration in liver function or hepatic blood flow can have a significant effect on its pharmacokinetics and dosage requirements. ![]() the elimination half-life is 1 to 2 hours but may be prolonged if infusions are given for longer than 24 hours or if hepatic blood flow is reduced. Any alteration in the concentration of AAG can greatly affect plasma concentrations of lidocaine. Plasma protein binding of lidocaine depends in part on the concentrations of both lidocaine and AAG. The extent of binding is variable but is about 60-80%. Lidocaine is bound to plasma proteins, including α1-acid glycoprotein (AAG). Lidocaine is widely distributed into highly perfused tissues followed by redistribution into skeletal muscle and adipose tissue. Perfusion rate in the mucous membranes influences on the absorption. ![]() The rate and extent of absorption depends upon concentration and total dose administered, the specific site of application and duration of exposure. Lidocaine is readily absorbed from mucous membranes. In general, autonomic activity is affected first, followed by loss of pain and other sensory functions, and finally, loss of motor activity regression of anesthesia usually occurs in the order. Small nerve fibers are generally more susceptible to the effects of Lidocaine than are large ones. A current theory is that Lidocaine reduces nerve cell membrane permeability by competing with calcium for the membrane binding sites that control membrane permeability to sodium. ![]() Lidocaine appears to block conduction of nerve impulses bу decreasing permeability of the nerve cell membrane to sodium ions, thereby decreasing the rate of depolarization of the nerve membrane, increasing threshold for electrical excitability, and preventing propagation of the potential. Lidocaine blocks the generation and conduction of impulses through all nerve fibers-sensory, motor, and autonomic. Lidocaine is a useful surface anesthetic but it may be rapidly and extensively absorbed following topical application to mucous membranes, and systemic effects may occur. Lidocaine is a local anesthetic of the amide type with actions. ![]()
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