s in which this residue has caused the lumen to occlude (see adverse reactions and dosage and administration ) methemoglobinemia 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 central nervous system and cardiovascular adverse effects, including seizures, coma, arrhythmias, and death. discontinue lidocaine hydrochloride jelly usp, 2% 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.

n cross sensitivity to lidocaine. many drugs used during the conduct of anesthesia are considered potential triggering agents for familial malignant hyperthermia. since it is not known whether amide-type local anesthetics may trigger this reaction and since the need for supplemental general anesthesia cannot be predicted in advance, it is suggested that a standard protocol for management should be available. early unexplained signs of tachycardia, tachypnea, labile blood pressure and metabolic acidosis may precede temperature elevation. successful outcome is dependent on early diagnosis, prompt discontinuance of the suspect triggering agent(s) and institution of treatment, including oxygen therapy, indicated supportive measures and dantrolene (consult dantrolene sodium intravenous package insert before using).

n applied for several minutes at the corona. an additional dose of not more than 15 ml (300 mg) can be instilled for adequate anesthesia. prior to sounding or cystoscopy, a penile clamp should be applied for 5 to 10 minutes to obtain adequate anesthesia. a total dose of 30 ml (600 mg) is usually required to fill and dilate the male urethra. prior to catheterization, smaller volumes of 5 to 10 ml (100 to 200 mg) are usually adequate for lubrication. for surface anesthesia of the female adult urethra slowly instill 3 to 5 ml (60 to 100 mg of lidocaine hcl) of the jelly into the urethra. if desired, some jelly may be deposited on a cotton swab and introduced into the urethra. in order to obtain adequate anesthesia, several minutes should be allowed prior to performing urological procedures. lubrication for endotracheal intubation apply a moderate amount of jelly to the external surface of the endotracheal tube shortly before use. care should be taken to avoid introducing the product into the lumen of the tube. do not use the jelly to lubricate endotracheal stylettes (see warnings and adverse reactions ) concerning rare reports of inner lumen occlusion. it is also recommended that use of endotracheal tubes with dried jelly on the external surface be avoided for lack of lubricating effect. maximum dosage: no more than 600 mg of lidocaine hcl should be given in any 12 hour period. children it is difficult to recommend a maximum dose of any drug for children since this varies as a function of age and weight. for children less than ten years who have a normal lean body mass and a normal lean body development, the maximum dose may be determined by the application of one of the standard pediatric drug formulas (e.g., clark's rule). for example, in a child of five years weighing 50 lbs., the dose of lidocaine hydrochloride should not exceed 75–100 mg when calculated according to clark's rule. in any case, the maximum amount of lidocaine administered should not exceed 4.5 mg/kg (2 mg/lb) of body weight.

hing, tremors, convulsions, unconsciousness, respiratory depression and arrest. the excitatory manifestations may be very brief or may not occur at all, in which case the first manifestation of toxicity may be drowsiness merging into unconsciousness and respiratory arrest. drowsiness following the administration of lidocaine is usually an early sign of a high blood level of the drug and may occur as a consequence of rapid absorption. cardiovascular system cardiovascular manifestations are usually depressant and are characterized by bradycardia, hypotension, and cardiovascular collapse, which may lead to cardiac arrest. allergic allergic reactions are characterized by cutaneous lesions, urticaria, edema or anaphylactoid reactions. allergic reactions may occur as a result of sensitivity either to the local anesthetic agent or to other components in the formulation. allergic reactions as a result of sensitivity to lidocaine are extremely rare and, if they occur, should be managed by conventional means. the detection of sensitivity by skin testing is of doubtful value.

inistration. lidocaine is also well-absorbed from the gastrointestinal tract, but little intact drug may appear in the circulation because of biotransformation in the liver. 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 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-i-acid glycoprotein. lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion. studies of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent 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 twofold 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 mcg free base per ml. in the rhesus monkey arterial blood levels of 18 to 21 mcg/ml have been shown to be the threshold for convulsive activity.

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 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-i-acid glycoprotein. lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion. studies of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent 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 twofold 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 mcg free base per ml. in the rhesus monkey arterial blood levels of 18 to 21 mcg/ml have been shown to be the threshold for convulsive activity.