Xylotin

Lidocaine HCl Injections are sterile, nonpyrogenic, aqueous solutions that contain a local anesthetic agent with or without epinephrine and are administered parenterally by injection.
XYLOTIN (50 mg/5 mL (1%) Solution): Each mL contains: Lidocaine Hydrochloride USP 10 mg.
XYLOTIN (300 mg/30 mL (1%) Solution): Each mL contains: Lidocaine Hydrochloride USP 10 mg.
Lidocaine HCl: C₁₄H₂₂N₂O.HCl.H₂O.
Excipients/Inactive Ingredients: Sodium chloride, Sodium Hydroxide and Hydrochloric acid.
Preservative-free.

Pharmacology: Mechanism of Action: Lidocaine HCl stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action.
Pharmacodynamics: 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, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system, and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.
Pharmacokinetics: Information derived from diverse formulations, concentrations and usages reveals that lidocaine HCl 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 HCl 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 HCl is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein.
Lidocaine HCl crosses the blood-brain and placental barriers, presumably by passive diffusion.
Lidocaine HCl 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 HCl. Approximately 90% of lidocaine HCl 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 HCl following an intravenous bolus injection is typically 1.5 to 2.0 hours. Because of the rapid rate at which lidocaine HCl is metabolized, any condition that affects liver function may alter lidocaine HCl kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine HCl 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 HCl required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6.0 μg free base per mL. In the rhesus monkey arterial blood levels of 18-21 μg/mL have been shown to be threshold for convulsive activity.

Xylotin injections are indicated for the production of local or regional anaesthesia by the following techniques: infiltration; intravenous regional anaesthesia-excluding solutions with adrenaline; peripheral nerve block such as intercostal block; major plexus block such as brachial plexus block; epidural block; subarachnoid block.

Adult: Recommended dosages for XYLOTIN solutions for various anaesthetic procedures in the average, healthy, 70 kg adult patient: See table.

Click on icon to see table/diagram/image

Recommended doses: The previously suggested concentrations and volumes serve only as a guide. Toxic doses vary widely between patients and toxic effects may occur after any local anaesthetic procedure.
Careful observation of the patient must therefore be maintained. It is recommended that the dose of lidocaine at any one time should not exceed 3 mg/kg . However, the dose administered must be tailored to the individual patient and procedure, and the maximum doses here quoted should be used as a guide only.
Hypotension: During thoracic, lumbar and caudal epidural anaesthesia, a marked fall in blood pressure and/or intercostal paralysis may be seen, possibly due to the use of excessive doses, improper positioning of the patient or accidental disposition of the anaesthetic within the subarachnoid space. Hypotension and bradycardia may occur as a result of sympathetic blockade.
Test dose: For epidural anaesthesia, a 3-5 mL test dose of a local anaesthetic solution preferably containing up to 15 micrograms of adrenaline should be administered.
Verbal contact and repeated monitoring of heart rate and blood pressure should be maintained for 5 minutes after the test dose after which, in the absence of signs of subarachnoid or intravascular injection, the main dose may be administered.
Use of a test dose containing adrenaline may have further advantages in that an intravascular injection of adrenaline will be quickly recognised by an increase in heart rate, usually within about 40 seconds. To detect this, the heart rate and rhythm should be monitored with an electrocardiogram.
Prior to administration of the total dose, aspiration should be repeated. The main dose should be injected slowly, with continual assessment of the patient. If toxic symptoms or signs occur, the injection should be stopped immediately.

Acute emergencies from local anesthetics are generally related to high plasma levels encountered during therapeutic use of local anesthetics or to unintended subarachnoid injection of local anesthetic solution (see Adverse Reactions, Warnings, and Precautions).
With accidental intravascular injections, the toxic effect will be obvious within 1-3 min. With overdosage, peak plasma concentrations may not be reached for 20-30 min depending on the site of injection and toxic signs will be delayed. Toxic reactions mainly involve the central nervous and cardiovascular systems.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.
Symptoms of acute toxicity: Central nervous system toxicity is a graded response with symptoms and signs of escalating severity. The first symptoms are circumoral paraesthesia, numbness of the tongue, lightheadedness, hyperacusis and tinnitus. Visual disturbance and muscular tremors are more serious and precede the onset of generalised convulsions. These signs must not be mistaken for neurotic behaviour.
Unconsciousness and grand mal convulsions may follow. These may last from a few seconds to several minutes. Hypoxia and hypercarbia occur rapidly following convulsions due to the increased muscular activity, together with the interference with normal respiration and loss of the airway. In severe cases, apnoea may occur. Acidosis increases the toxic effects of local anaesthetics.
Recovery is due to redistribution of the local anaesthetic drug from the central nervous system and metabolism. Recovery may be rapid unless large amounts of the drug have been injected.
Cardiovascular toxicity indicates a more severe situation. Hypotension, bradycardia, decreased cardiac output, heart block, arrhythmia and even ventricular arrhythmias, ventricular fibrillation and cardiac arrest may occur as a result of huge systemic concentrations of local anaesthetics.
Cardiovascular toxic effects are generally preceded by signs of toxicity in the central nervous system, unless the patient is receiving a general anaesthetic or is heavily sedated with drugs such as a benzodiazepine or a barbiturate. In rare cases, cardiac arrest has occurred without prodromal CNS effects.
Treatment of overdosage: If signs of acute systemic toxicity appear injection of the local anaesthetic should be stopped immediately. If convulsions occur then immediate attention is required for the maintenance of a patent airway and assisted or controlled ventilation with oxygen, via a positive airway pressure delivery system mask. Adequacy of the circulation should then be evaluated, bearing in mind that drugs used to treat convulsions depress the circulation when administered intravenously.
Should convulsions persist despite adequate respiratory support, and if the status of the circulation permits, appropriate anticonvulsant medication such as an ultra-short acting barbiturate (e.g. thiopentone) or a benzodiazepine (e.g. diazepam) may be administered IV. The clinician should be familiar with these anticonvulsant drugs prior to use of local anaesthetics.
Suxamethonium will stop the muscle convulsions rapidly but will require tracheal intubation and controlled ventilation, and should only be used by those familiar with these procedures.
If ventricular fibrillation or cardiac arrest occurs, effective cardiovascular resuscitation treatment must be instituted and maintained for a prolonged period if necessary. Optimal oxygenation and ventilation, and circulatory support as well as treatment of acidosis are of vital importance.
If cardiovascular depression occurs (hypotension, bradycardia), appropriate treatment with intravenous fluids, vasopressor, chronotropic and or inotropic agents should be considered.
Children should be given doses commensurate with age and weight.
Dialysis is of negligible value in the treatment of acute overdosage with lidocaine.

Allergy or hypersensitivity to amide type local anaesthetics or to any excipients. Detection of suspected hypersensitivity by skin testing is of limited value.
Local anaesthetics are contraindicated for epidural and spinal anaesthesia in patients with uncorrected hypotension or coagulation disorders or in patients receiving anti-coagulation treatment.
Local anaesthetic techniques must not be used when there is inflammation and/or sepsis in the region of the proposed injection and/or in the presence of septicaemia.
Xylotin should not be used in patients with Stokes-Adam syndrome, Wolff-Parkinson-White syndrome, or with severe degrees of sinoatrial, atrioventricular, or intraventricular block in the absence of an artificial pacemaker.
General contraindications related to epidural anaesthesia, regardless of the local anaesthetic used, should be taken into account.

Lidocaine injections for infiltration and nerve block 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 the block to be employed 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.
Methaemoglobinaemia: Cases of methaemoglobinaemia have been reported in association with local anaesthetic use. Although all patients are at risk for methaemoglobinaemia, patients with glucose-6-phosphate dehydrogenase deficiency, congenital or idiopathic methaemoglobinaemia, 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 anaesthetics must be used in these patients, close monitoring for symptoms and signs of methaemoglobinaemia is recommended.
Signs and symptoms of methaemoglobinaemia may occur immediately or may be delayed some hours after exposure, and are characterized by a cyanotic skin discoloration and abnormal coloration of the blood. Methaemoglobin 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 Xylotin and any other oxidizing agents. Depending on the severity of the symptoms, patients may respond to supportive care, i.e., oxygen therapy, hydration. More severe symptoms 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.

General: The safety and effectiveness of lidocaine HCl depend on proper dosage, correct technique, adequate precautions, and readiness for emergencies. Standard textbooks should be consulted for specific techniques and precautions for various regional anesthetic procedures.
Resuscitative equipment, oxygen, and other resuscitative drugs should be available for immediate use. (See Warnings and Adverse Reactions.) The lowest dosage that results in effective anesthesia should be used to avoid high plasma levels and serious adverse effects. Syringe aspirations should also be performed before and during each supplemental injection when using indwelling catheter techniques. During the administration of epidural anesthesia, it is recommended that a test dose be administered initially and that the patient be monitored for central nervous system toxicity and cardiovascular toxicity, as well as for signs of unintended intrathecal administration, before proceeding. When clinical conditions permit, consideration should be given to employing local anesthetic solutions that contain epinephrine for the test dose because circulatory changes compatible with epinephrine may also serve as a warning sign of unintended intravascular injection. An intravascular injection is still possible even if aspirations for blood are negative. Repeated doses of lidocaine HCl may cause significant increases in blood levels with each repeated dose because of slow accumulation of the drug or its metabolites. Tolerance to elevated blood levels varies with the status of the patient. Debilitated, elderly patients, acutely ill patients, and children should be given reduced doses commensurate with their age and physical condition. Lidocaine HCl should also be used with caution in patients with severe shock or heart block.
Lumbar and caudal epidural anesthesia should be used with extreme caution in persons with the following conditions: existing neurological disease, spinal deformities, and severe hypertension.
Careful and constant monitoring of cardiovascular and respiratory (adequacy of ventilation) vital signs and the patient's state of should be accomplished after each local anesthetic injection. It should be kept in mind at such times that restlessness, anxiety, tinnitus, dizziness, blurred vision, tremors, depression or drowsiness may be early warning signs of central nervous system toxicity.
Since amide-type local anesthetics are metabolized by the liver, Lidocaine Injection should be used with caution in patients with hepatic disease. Patients with severe hepatic disease, because of their inability to metabolize local anesthetics normally, are at greater risk of developing toxic plasma concentrations. Lidocaine Injection should also be used with caution in patients with impaired cardiovascular function since they may be less able to compensate for functional changes associated with the prolongation of A-V conduction produced by these drugs.
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 the management of malignant hyperthermia 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).
Proper tourniquet technique, as described in publications and standard textbooks, is essential in the performance of intravenous regional anesthesia. Solutions containing epinephrine or other vasoconstrictors should not be used for this technique.
Lidocaine HCl should be used with caution in persons with known drug sensitivities. Patients allergic to para-aminobenzoic acid derivatives (procaine, tetracaine, benzocaine, etc) have not shown cross-sensitivity to lidocaine HCl.
Lidocaine should be given with great caution to patients with epilepsy, impaired cardiac conduction, bradycardia, severe shock or digitalis intoxication. Lidocaine should also be administered with great caution to patients with impaired cardiovascular function as they may be less able to compensate for functional changes associated with the prolongation of AV conduction produced by these drugs. In patients with Stokes-Adams syndrome or Wolff-Parkinson-White syndrome extreme care should be taken to avoid accidental arterio-venous injection.
Central nerve blocks may cause cardiovascular depression, especially in the presence of hypovolaemia. Epidural anaesthesia should be used with caution in patients with impaired cardiovascular function. Epidural anaesthesia may lead to hypotension and bradycardia. Hypotension should be treated promptly with a sympathomimetic intravenously and repeated as necessary.
Local anaesthetics should be given with great caution (if at all) to patients with pre-existing abnormal neurological pathology, e.g. myasthenia gravis. Use with extreme caution in epidural, caudal and spinal anaesthesia when there are serious diseases of the CNS or of the spinal cord, e.g. meningitis, spinal fluid block, cranial or spinal haemorrhage, tumours, poliomyelitis, syphilis, tuberculosis or metastatic lesions of the spinal cord.
Inadvertent intravascular or subarachnoid injection of small doses of local anaesthetics injected into the head and neck area, including retrobulbar, dental and stellate ganglion blocks, may produce adverse reactions similar to systemic toxicity seen with unintentional intravascular injections of larger doses.
Clinicians who perform retrobulbar blocks should be aware that there have been reports of cardiovascular collapse and apnoea following the use of local anaesthetic injections for retrobulbar block. Prior to retrobulbar block, necessary equipment, drugs and personnel should be immediately available as with all other regional procedures. Retrobulbar injections may very occasionally reach the subarachnoid space, causing temporary blindness, cardiovascular collapse, apnoea, convulsions etc. These must be diagnosed and treated promptly.
Retro- and peribulbar injections of local anaesthetics carry a low risk of persistent ocular muscle dysfunction. The primary causes include trauma and/or local toxic effects on muscles or nerves. The severity of such tissue reactions is related to the degree of trauma, the concentration of the local anaesthetic and the duration of exposure of the tissue to the local anaesthetic. For this reason, as with all local anaesthetics, the lowest effective concentration and dose of local anaesthetic should be used. Vasoconstrictors may aggravate tissue reactions and should be used only when indicated.
Patients being treated with anti-arrhythmic drugs class III (e.g. amiodarone) should be under close surveillance and ECG monitoring since cardiac effects may be additive.
Xylotin should only be prescribed to patients with acute porphyria on strong or urgent indications. Appropriate precautions should be taken for all porphyric patients.
Carcinogenesis, Mutagenesis, Impairment of Fertility: A two-year oral toxicity study of 2,6-xylidine, a metabolite of lidocaine, has shown that in both male and female rats, 2-6-xylidine in daily doses of 900 mg/m2 (150 mg/kg) resulted in carcinomas and adenomas of the nasal cavity. No nasal tumours were observed in the low dose (15 mg/kg or control animals). In addition, the compound also caused subcutaneous fibromas and or fibrosarcomas in male and female rats (significant at 150 mg/kg).The genotoxic potential of 2,6-xylidine has been studied with mixed results: Positive results were reported in assays for gene mutations (weakly positive in the Ames test with metabolic activation and in the mouse lymphoma assay) and chromosomal damage (chromosomal aberrations in Chinese hamster ovary cells at concentrations at which the drug precipitated from solution). No evidence of genotoxicity was found in in vivo assays for chromosomal damage (micronucleus assay) and DNA damage (unscheduled DNA synthesis). Covalent binding studies of DNA from liver and ethmoid turbinates in rats indicate that 2,6-xylidine may be genotoxic under certain conditions in vivo.

Pregnancy: Teratogenic Effects - Pregnancy Category B: Reproduction studies have been performed in rats at doses up to 6.6 times the human dose and have revealed no evidence of harm to the fetus caused by lidocaine HCl. There are, however, no adequate and well-controlled studies in pregnant women. Animal reproduction studies are not always predictive of human response. General consideration should be given to this fact before administering lidocaine HCl to women of childbearing potential, especially during early pregnancy when maximum organogenesis takes place.
Labor and Delivery: Local anesthetics rapidly cross the placenta and when used for epidural, paracervical, pudendal or caudal block anesthesia, can cause varying degrees of maternal, fetal and neonatal toxicity. (See Pharmacology: Pharmacokinetics under Actions.) The potential for toxicity depends upon the procedure performed, the type and amount of drug used, and the technique of drug administration. Adverse reactions in the parturient, fetus and neonate involve alterations of the central nervous system, peripheral vascular tone and cardiac function.
Maternal hypotension has resulted from regional anesthesia. Local anesthetics produce vasodilation by blocking sympathetic nerves. Elevating the patient's legs and positioning her on her left side will help prevent decreases in blood pressure.
The fetal heart rate also should be monitored continuously, and electronic fetal monitoring is highly advisable.
Epidural, spinal, paracervical, or pudendal anesthesia may alter the forces of parturition through changes in uterine contractility or maternal expulsive efforts. In one study, paracervical block anesthesia was associated with a decrease in the mean duration of first stage labor and facilitation of cervical dilation. However, spinal and epidural anesthesia have also been reported to prolong the second stage of labor by removing the parturient's interfering with motor function. The use of obstetrical anesthesia may increase the need for forceps assistance.
The use of some local anesthetic drug products during labor and delivery may be followed by diminished muscle strength and tone for the first day or two of life. The long-term significance of these observations is unknown. Fetal bradycardia may occur in 20 to 30 percent of patients receiving paracervical nerve block anesthesia with the amide-type local anesthetics and may be associated with fetal acidosis. Fetal heartrate should always be monitored during paracervical anesthesia. The physician should weigh the possible advantages against risks when considering a paracervical block in prematurity, toxemia of pregnancy, and fetal distress. Careful adherence to recommended dosage is of the utmost importance in obstetrical paracervical block. Failure to achieve adequate analgesia with recommended doses should arouse suspicion of intravascular or fetal intracranial injection. Cases compatible with unintended fetal intracranial injection of local anesthetic solution have been reported following intended paracervical or pudendal block or both. Babies so affected present with unexplained neonatal depression at birth, which correlates with high local anesthetic serum levels, and often manifest seizures within six hours. Prompt use of supportive measures combined with forced urinary excretion of the local anesthetic has been used successfully to manage this complication.
Case reports of maternal convulsions and cardiovascular collapse following use of some local anesthetics for paracervical block in early pregnancy (as anesthesia for elective abortion) suggest that systemic absorption under these circumstances may be rapid. The recommended maximum dose of each drug should not be exceeded. Injection should be made slowly and with frequent aspiration. Allow a 5-minute interval between sides.
Nursing Mothers: Lidocaine passes into breast milk. The amount of lidocaine appearing in breast milk from a nursing mother receiving parenteral lidocaine is unlikely to lead to a significant accumulation of the parent drug in the breast-fed infant. The remote possibility of an idiosyncratic or allergic reaction in the breast-fed infant from lidocaine remains to be determined.

Systemic: Adverse experiences following the administration of lidocaine HCl are similar in nature to those observed with other amide local anesthetic agents. These adverse experiences are, in general, dose-related and may result from high plasma levels caused by excessive dosage, rapid absorption or inadvertent intravascular injection, or may result from a hypersensitivity, idiosyncrasy or diminished tolerance on the part of the patient. Serious adverse experiences are generally systemic in nature. The following types are those most commonly reported: Central Nervous System: CNS manifestations are excitatory and/or depressant and may be characterized by lightheadedness, nervousness, apprehension, euphoria, confusion, dizziness, drowsiness, tinnitus, hyperacusis, blurred or double vision, vomiting, sensations of heat, cold or numbness, twitching, tremors, convulsions, unconsciousness, respiratory depression and arrest, agitation, difficulty swallowing, paraesthesia circumoral, numbness of the tongue and slurred speech.
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 HCl is usually an early sign of a high blood level of the drug and may occur as a consequence of rapid absorption. In unconscious patients, circulatory collapse should be watched for as CNS effects may not be apparent, as an early manifestation of toxicity may in some cases progress to frank convulsions and ultimately lead to respiratory depression and/or arrest. It is crucial to have resuscitative equipment and anticonvulsant drugs available to manage such patients (see Treatment of overdosage under Overdosage).
Cardiovascular System: Cardiovascular manifestations are usually depressant and are characterized by bradycardia, hypotension, and cardiovascular collapse, which may lead to cardiac arrest.
Cardiac arrhythmias and hypertension have also been observed.
Methaemoglobinaemia can occur following IV administration.
Cardiovascular toxic effects are generally preceded by signs of toxicity in the central nervous system, unless the patient is receiving a general anaesthetics or is heavily sedated with drugs such as a benzodiazepine or a barbiturate. In rare cases, cardiac arrest has occurred without prodromal CNS effects.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.
Haemodynamic: Regional anaesthesia may lead to maternal hypotension.
Allergic: Allergic reactions are characterized by cutaneous lesions, urticaria, edema or anaphylactoid reactions. Allergic reactions may occur as a result of sensitivity either to local anesthetic agents or to the methylparaben used as a preservative in the multiple dose vials. Allergic reactions as result of sensitivity to lidocaine HCl are extremely rare and, if they occur, should be managed by conventional means. The detection of sensitivity by skin testing is of doubtful value.
Neurologic: The incidences of adverse reactions associated with the use of local anesthetics may be related to the total dose of local anesthetic administered and are also dependent upon the particular drug used, the route of administration and the physical status of the patient.
Neurological reactions following regional nerve blocks have included persistent numbness, paraethesia and other sensory disturbances.
In a prospective review of 10,440 patients who received lidocaine HCl for spinal anesthesia, the incidences of adverse reactions were reported to be about 3 percent each for positional headaches, hypotension and backache; 2 percent for shivering; and less than 1 percent each for peripheral nerve symptoms, nausea, respiratory inadequacy and double vision. Many of these observations may be related to local anesthetic techniques, with or without a contribution from the local anesthetic.
In the practice of caudal or lumbar epidural block, occasional unintentional penetration of the subarachnoid space by the catheter may occur. Subsequent adverse effects may depend partially on the amount of drug administered subdurally. These may include spinal block of varying magnitude (including total spinal block), hypotension secondary to spinal block, loss of bladder and bowel control, and loss of perineal sensation and sexual function. Persistent motor, sensory and/or autonomic (sphincter control) deficit of some lower spinal segments with slow recovery (several months) or incomplete recovery have been reported in rare instances when caudal or lumbar epidural block has been attempted. Backache and headache have also been noted following use of these anesthetic procedures.
There have been reported cases of permanent injury to extraocular muscles requiring surgical repair following retrobulbar administration.
Peripheral nerve injury and arachnoiditis have been observed.

Anti-arrhythmic drugs: Local anaesthetics of the amide type, such as lidocaine, should be used with caution in patients receiving other local anaesthetics or agents structurally related to amide type local anaesthetics e.g. certain anti-arrhythmic drugs such as disopyramide, procainamide, mexilitene since potentiation of cardiac effects may occur. Specific interaction studies with lidocaine and anti-arrhythmic drugs class III (eg. amiodarone) have not been performed, but caution should be advised (see Precautions).
Amiodarone: Amiodarone has been reported to reduce the clearance of lidocaine in two case reports, although a small prospective study of combined therapy on lidocaine pharmacokinetics found no change in clearance or other pharmacokinetic factor. This combination has been reported to precipitate seizures and to lead to severe sinus bradycardia and a long sinoatrial arrest. Until more experience with concurrent use of lidocaine and amiodarone becomes available, patients receiving the combination should be monitored carefully.
Beta-adrenoreceptor antagonists: Propranolol and metoprolol reduce the metabolism of IV administered lidocaine and the possibility of this effect with other beta-adrenergic blockers should be kept in mind. If these drugs are administered concurrently, the patient should be closely observed for signs of lidocaine toxicity.
Cimetidine: Cimetidine reduces the clearance of IV administered lidocaine and toxic effects due to high serum lidocaine levels have been reported when these two drugs have been administered concurrently.
Anticonvulsive agents: Phenytoin and other antiepileptic drugs such as phenobarbitone, primidone and carbamazepine appear to enhance the metabolism of lidocaine but the significance of this effect is not known. Phenytoin and lidocaine have additive cardiac depressant effects.
Inhalational anaesthetics: Lidocaine decreases the minimum effective concentration of inhalational anaesthetics, e.g. nitrous oxide.
Skeletal muscle relaxants: Lidocaine and skeletal muscle relaxants, e.g. suxamethonium, lead to excessive neuromuscular blockade; therefore this combination must be used with caution.
Structurally related local anaesthetics: Lidocaine should be used with caution in patients receiving agents structurally related to local anaesthetics.
Patients that are administered local anaesthetics may be at increased risk of developing methaemoglobinaemia when concurrently exposed to the following oxidizing agents: Nitrates/Nitrites (eg. nitroglycerin, nitroprusside, nitric oxide, nitrous oxide); Local anaesthetics (eg. lidocaine, bupivacaine, mepivacaine, tetracaine, prilocaine, procaine, articaine); Antineoplastic agents (eg. cyclophosphamide, flutamide, rasburicase, isofamide, hydroxyurea); Antibiotics (eg. dapsone, sulphonamides, nitrofurantoin, para-aminosalicylic acid); Antimalarials (eg. chloroquine, primaquine); Anticonvulsants (eg. phenytoin, sodium valproate, phenobarbital); Other drugs (eg. acetaminophen, metoclopramide, sulfa drugs [i.e. sulfasalazine], quinine).
Laboratory effects: Creatinine: Creatinine measurements in patients with therapeutic plasma levels of lidocaine are about 15-35% higher when measured by an enzymatic method versus the Jaffé method. This appears to be due to assay interference from N-ethylglycine, a metabolite of lidocaine.
Creatine kinase: The intramuscular injection of lidocaine may result in an increase in creatine kinase levels for up to 48 hrs. This may interfere with the diagnosis of myocardial infarction.

Store at temperatures not exceeding 30°C and protect from light.

Anaesthetics - Local & General

N01BB02 - lidocaine ; Belongs to the class of amides. Used as local anesthetics.

POM