Consumer medicine information

Lignocaine Hydrochloride Injection MIN-I-JET

Lidocaine (lignocaine) hydrochloride

BRAND INFORMATION

Brand name

Min-I-Jet Lignocaine Hydrochloride Injection

Active ingredient

Lidocaine (lignocaine) hydrochloride

Schedule

S4

 

Consumer medicine information (CMI) leaflet

Please read this leaflet carefully before you start using Lignocaine Hydrochloride Injection MIN-I-JET.

WHAT IS IN THIS LEAFLET?

This leaflet contains information about Lignocaine Hydrochloride Injection MIN-I-JET. Please read it carefully and keep it for future reference. The information in this leaflet is only a summary and is not intended to replace advice from your doctor.

Please consult your doctor or pharmacist if you have any comments or questions.

WHAT IS LIGNOCAINE?

Lignocaine is a local anaesthetic. It stops all pain and feeling in the area around where it is injected.

WHEN IS LIGNOCAINE USED?

Lignocaine allows doctors to sew up cuts in the skin and to undertake operations without any pain even though the patient is awake. Lignocaine can also be used in certain emergency situations where the heart beat is abnormal.

As lignocaine is often used in medical emergencies, the injection may be given by paramedical personnel such as ambulance or nursing staff.

WHO SHOULD NOT HAVE LIGNOCAINE INJECTIONS?

Lignocaine should not be given if you:

  • are allergic to it
  • have had a previous severe reaction to it
  • have had a previous severe reaction to any other local anaesthetic or other drug.

In certain emergency situations lignocaine should not be given to you if you have a particular heart condition.

BEFORE YOU HAVE A LIGNOCAINE INJECTION

Before you receive a lignocaine injection you should tell your doctor if you:

  • have had an allergic reaction to lignocaine
  • have had any previous unpleasant reactions to lignocaine
  • have had any previous unpleasant reactions to any other local anaesthetic or drug
  • have any heart complaint
  • have epilepsy or liver disease
  • have kidney disease
  • have malignant hypothermia
  • have blood poisoning
  • are breast feeding
  • are suffering from any illness
  • are pregnant
  • are taking any medicines and what they are, especially drugs for epilepsy, heart rhythm disorders, propranolol or cimetidine.

SIDE EFFECTS OF LIGNOCAINE

As with any medicine, some side effects may occur.

When lignocaine is used to numb the skin for operations, side effects are very rare unless a large dose is used or several injections are given. Patients who are allergic to lignocaine may develop a rash and some patients may become drowsy, apprehensive or excited. Blurred vision, ringing in the ears, disorientation and nausea may also occur.

More severe reactions can follow if lignocaine is injected into the blood for the treatment of emergency heart conditions. In this situation lignocaine can cause convulsions and severe heart and breathing problems.

Always tell your doctor if you have any unpleasant effects after receiving Lignocaine Hydrochloride Injection MIN-I-JET.

THE DOSE OF LIGNOCAINE

The dose of lignocaine will vary depending on the reason for which it is used.

The amount used to numb the skin will depend on how big the operation is. The maximum dose in adults is 200 mg and in children it is 3 mg per kilogram of weight.

The doses for treating heart conditions are similar but are injected into a vein. Elderly people may need a smaller dose.

OVERDOSE

An overdose of lignocaine can upset the brain causing unconsciousness and convulsions and can also cause breathing and heart problems leading to death in extreme cases.

There is no specific treatment for an overdose of lignocaine. Basic resuscitation measures should be instituted to make sure that the patient can breathe and has a heartbeat.

WHAT DO Lignocaine Hydrochloride Injection MIN-I-JET CONTAIN?

Lignocaine Hydrochloride Injection MIN-I-JET:

Australian Registration Number Lignocaine 2% (100 mg in 5 mL)
AUST R 29041

Each Lignocaine Hydrochloride Injection MIN-I-JET also contains sodium chloride and water.

HOW TO STORE Lignocaine Hydrochloride Injection MIN-I-JET

Lignocaine Hydrochloride Injection MIN-I-JET should be stored below 25°C (room temperature). It should not be used after the expiry date on the package.

WHERE CAN I GET MORE INFORMATION?

You can get more information from your doctor or pharmacist.

Lignocaine Hydrochloride Injection MIN-I-JET are manufactured by:
International Medication Systems Ltd
1886 Santa Anita Avenue, South El Monte 91733, California USA

and distributed by:
CSL Limited, ABN 99 051 588 348
45 Poplar Road, Parkville, Victoria 3052 Australia

Date of Information: June 1996
Date of Amendment: April 2008

Published by MIMS July 2008

BRAND INFORMATION

Brand name

Min-I-Jet Lignocaine Hydrochloride Injection

Active ingredient

Lidocaine (lignocaine) hydrochloride

Schedule

S4

 

Name of the medicine

Lignocaine hydrochloride.

Excipients

Water for injections; sodium chloride.

Description

Chemical name: 2-diethylaminoaceto-2',6'-xylidide. Molecular formula: C14H22N2O. CAS: 6108-05-0. It is a stable, colourless, crystalline solid whose hydrochloride salt is readily soluble in water.

Pharmacology

Lignocaine stabilises the neuronal membrane and prevents the initiation and transmission of nerve impulses, thereby affecting local anaesthetic action. The onset of action is rapid and the blockade may last from 60 to 90 minutes.
In the heart, lignocaine reduces automaticity by decreasing the rate of diastolic (phase 4) depolarisation. Lignocaine is considered to be a class I (membrane stabilising) antiarrhythmic agent. The duration of the action potential is decreased due to blockade of the sodium channel and the refractory period is shortened.

Pharmacokinetics

Lignocaine is rapidly distributed to all body tissues; about 65% is protein bound. Lignocaine crosses the placenta. The half-life is 1.6 hours. About 80% of the dose is metabolised in the liver; less than 10% is excreted unchanged in the urine.

Indications

For local or regional anaesthesia by infiltration; for regional intravenous anaesthesia and nerve blocks such as major plexus blocks and epidural anaesthesia.
Treatment or prophylaxis of life threatening ventricular arrhythmias, including those associated with myocardial infarction, general anaesthesia in patients predisposed to ventricular arrhythmias, digitalis intoxication, or following resuscitation from cardiac arrest.

Contraindications

Known history of allergy or hypersensitivity to lignocaine or other amide type local anaesthetics such as prilocaine, mepivacaine or bupivacaine. See also Interactions.
Stokes-Adams syndrome or severe degrees of sinoatrial, atrioventricular or intraventricular block.
Lignocaine suppresses ventricular pacemaker activity and the result may be ventricular arrhythmias, including in those undergoing epidural anaesthesia.
Serious disease of the central nervous system or the spinal cord, e.g. meningitis, spinal fluid block, cranial or spinal haemorrhage, tumours, poliomyelitis, syphilis, tuberculosis or metastatic lesions of the spinal cord.
Myasthenia gravis, severe shock or impaired cardiac conduction.
Local anaesthetic techniques must not be used when there is inflammation and/or sepsis in the region of the proposed injection and in the presence of septicaemia.
Epidural and spinal anaesthesia in patients with uncorrected hypotension and in patients with coagulation disorders or receiving anticoagulation treatment.

Precautions

Resuscitative equipment and medicines, including oxygen, should be immediately available when lignocaine is used to manage possible lignocaine induced reactions involving the cardiovascular, respiratory or central nervous system effects (see Adverse Reactions).
Constant electrocardiograph (ECG) monitoring is essential for the proper IV administration of lignocaine. Signs of excessive depression of cardiac conductivity, such as prolongation of PR interval and QRS complex should be followed by prompt cessation of the IV infusion.
In emergency situations, when a ventricular rhythm disorder is suspected, and ECG equipment is not available, a single dose may be administered when the doctor in attendance has determined that the potential benefit outweighs the risks.
Mortality. In the Cardiac Arrhythmia Suppression Trial (CAST), a long-term multicentred randomised double blind study in patients with asymptomatic nonlife-threatening ventricular arrhythmia, who had myocardial infarction more than six days but less than two years previously, an excess mortality and nonfatal cardiac arrest rate was seen in patients treated with encainide or flecainide (56/730), compared with that seen in patients assigned to matched placebo treated groups (22/725). The average duration of treatment with encainide or flecainide in this study was ten months.
While there are no comparable mortality trial data for other class I antiarrhythmic agents postmyocardial infarction or in other clinical settings, meta-analyses of small scale clinical trials of these agents in similar populations suggest a trend towards increased mortality compared to placebo and no evidence of benefit.
All class I antiarrhythmic agents share the capacity to produce slowing of conduction velocity which can promote tachycardias via re-entry mechanisms. Therefore, the prophylactic use of class I antiarrhythmic drugs following myocardial infarction is potentially hazardous. Indeed the use of these agents for other than life threatening arrhythmias or severe symptoms due to arrhythmias is not recommended.
Lignocaine should be used with caution in patients with severe shock, bradycardia, hypokalaemia, cardiac conduction disturbances (see Contraindications), severe digitalis intoxication. In the case of bradycardia complicated by ventricular tachyarrythmia, lignocaine might be combined with atropine or an atropine-like medicine or pacemaker treatment.
Since antiarrhythmic medicines may be ineffective in patients with hypokalaemia, serum potassium levels should be normalised prior to lignocaine administration. Hypoxia and acid/ base disturbances should also be corrected as these factors may potentiate ventricular arrhythmias.
The IV dose of lignocaine should not exceed 100 mg in a single injection, and no more than 200 to 300 mg in a one hour period (see Dosasge and Administration) as a hypotensive response is sometimes observed with IV administration of lignocaine.
Patients with reduced hepatic blood flow or function, and those on prolonged infusions of lignocaine, have a longer lignocaine half-life and lower clearance resulting in accumulation of lignocaine. Patients with congestive cardiac failure have a reduced clearance. In patients with renal failure, accumulation of lignocaine and its metabolites may develop during prolonged or repeated administration. These patients may, therefore, require a reduction in dosage.
Patients with a chronic elevation in cardiac output or a drug induced induction of hepatic microsomal enzymes will have a reduced elimination half-life of lignocaine and may therefore require a higher dosage.
Debilitated, elderly or acutely ill patients should be given reduced doses commensurate with their age and physical status.
Dosage reduction may be required during concomitant use with propranolol, metoprolol or cimetidine as there is a possibility of reduced elimination of lignocaine.
Use with caution in patients with genetic predisposition to malignant hyperthermia as the safety of amide local anaesthetic agents in these patients has not been fully assessed.
Blood lignocaine concentrations should be measured in patients in shock who may have markedly reduced lignocaine clearance, on prolonged infusions of greater than 24 hours duration especially in patients with cardiac or hepatic failure, those who are refractory to the usual dosage given, and in the presence of ambiguous signs and symptoms of lignocaine toxicity. Severe reactions are often preceded by somnolence and paraesthesia, therefore, these symptoms should not be dismissed.
Caution should be observed in patients with cardiac decompensation and hypotension or posterior diaphragmal infarction with a tendency towards development of heart block.
When high doses are used and the patient's myocardial function is impaired, combination with other medicines which reduce the excitability of cardiac muscle requires caution.
Theoretical evidence suggests that lignocaine may have porphyrogenic properties. The clinical significance of this is unknown. Caution should be exercised if intravenous lignocaine is administered to patients with acute porphyria.
The lignocaine is in a single use Min-I-Jet prefilled syringe. Once the unit is assembled and used, any remaining portion of the solution must be discarded with the entire unit.

Impaired renal function

Impairment of renal function is unlikely to affect lignocaine clearance in the short term (24 hours). However, toxicity due to accumulation of lignocaine and its metabolites may develop with prolonged or repeated administration.

Impaired hepatic function

Patients with reduced hepatic blood flow or function, and those on prolonged infusions of lignocaine, have a longer lignocaine half-life and lower clearance and may, therefore, require a reduction in dosage. To lessen the risk of acute toxicity, a regimen with boluses 10 to 30 minutes apart followed by an infusion is preferable to a single bolus followed by infusion.

Use in the elderly

A reduction in dosage may be necessary for elderly patients with compromised cardiovascular and/or hepatic function and/or prolonged infusions.

Carcinogenesis, mutagenesis, impairment of fertility

A metabolite of lignocaine, 2,6-dimethylamiline (2,6-xylidine), has tumorigenic potential in humans.
A two year old toxicity study of 2,6-xylidine, a metabolite of lignocaine, 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 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.

Use in pregnancy.

(Category A)
Although lignocaine has been used extensively for surgical procedures during pregnancy with no reports of ill effects to the mother or fetus, there are no adequate or well controlled studies in pregnant women of the effect of lignocaine on the developing fetus.
The safe use of lignocaine during pregnancy has not been established with respect to possible adverse effects upon fetal development. Therefore, lignocaine should only be used in pregnancy if the expected medical benefits outweigh any potential risk.
Fetal bradycardia frequently follows paracervical block and may be associated with fetal acidosis. Fetal heart rate should always be monitored during paracervical anaesthesia. When the recommended dose is exceeded, the incidence of fetal bradycardia increases.

Use in lactation.

The amount of lignocaine appearing in breast milk from a breastfeeding mother receiving parenteral lignocaine is unlikely to lead to a significant accumulation of the parent drug in the breastfed infant. The remote possibility of an idiosyncratic or allergic reaction in the breastfed infant from lignocaine remains to be determined.
Lignocaine is excreted in breast milk. The clinical significance of this is unknown.

Use in children

The safety of lignocaine in the treatment of arrhythmias in children has not been established. Through their lower enzyme capacity, neonates are at risk of methaemoglobinaemia which can become clinically overt (cyanosis).

Interactions

Antiarrhythmic medicines.

Local anaesthetics of the amide type, such as lignocaine, should be used with caution in patients receiving antiarrhythmic medicines (e.g. disopyramide, procainamide, mexilitene), since potentiation of cardiac effects may occur.

Amiodarone.

Amiodarone has been reported to reduce the clearance of lignocaine in two case reports, although a small prospective study of combined therapy on lignocaine pharmacokinetics found no change in clearance or other pharmacokinetic factor. This combination has been reported to precipitate seizures and lead to severe bradycardia and a long sinoatrial arrest. Until more experience with concurrent use of lignocaine and amiodarone becomes available, patients receiving the combination should be monitored carefully.

Beta-adrenoreceptor antagonists.

Propranolol, nadolol and metoprolol reduce the metabolism of IV administered lignocaine and the possibility of this effect with other β-adrenergic blockers should be kept in mind. If these medicines are administered concurrently, the patient should be closely observed for signs of lignocaine toxicity and serum lignocaine concentrations should be carefully monitored.

Cimetidine.

Cimetidine reduces the clearance of IV administered lignocaine and toxic effects due to high serum lignocaine levels have been reported when these two medicines have been administered concurrently.

Anticonvulsive agents.

Phenytoin and other antiepileptic drugs such as phenobarbitone, primidone and carbamazepine appear to enhance the metabolism of lignocaine but the significance of this effect is not known. Phenytoin and lignocaine have additive cardiac depressant effects.

Fluvoxamine.

Coadministration of fluvoxamine drastically reduces the elimination of lignocaine.

Inhalation anaesthetics.

Lignocaine decreases the minimum effective concentration of inhalation anaesthetics, e.g. nitrous oxide.

Skeletal muscle relaxants.

Lignocaine and skeletal muscle relaxants, e.g. suxamethonium, lead to excessive neuromuscular blockade; therefore, this combination must be used with caution.

Alcohol.

There have been no reports of direct interaction between alcohol and lignocaine. However, acute severe alcohol intoxication can centrally depress the cardiovascular system and may thereby prolong lignocaine elimination half-life.

Potential for influence of lignocaine on the plasma levels/ effects of other medicines.

Lignocaine is metabolised by CYP1A2 and CYP3A4 and thus has the potential to inhibit the metabolism of medicines metabolised by these isoenzymes, thus increasing their plasma levels; however, this effect has so far not been reported.

Potential for influence of other medicines on the plasma levels/ effect of lignocaine.

Concomitant treatment with medicines that are substrates, inhibitors or inducers of CYP1A2 or CYP3A4 has the potential to influence the metabolism and hence the plasma levels and effect of lignocaine.

Effect on laboratory tests

Creatinine.

Creatinine measurements in patients with therapeutic plasma levels of lignocaine are about 15 to 35% higher when measured by an enzymatic method versus the Jaffe method. This appears to be due to assay interference from N-ethylglycine, a metabolite of lignocaine.

Adverse Effects

Reactions to lignocaine hydrochloride are similar in character to those observed with other local anaesthetics.
Adverse experiences are, in general, dose related and may result from high plasma levels or from a hypersensitivity, idiosyncrasy or diminished tolerance.
Serious adverse events are generally systemic in nature; the following types are those more commonly reported.

Central nervous system.

CNS manifestations are excitatory and/or depressant and may be characterised by lightheadedness, nervousness, apprehension, euphoria, confusion, dizziness, drowsiness, disorientation, tinnitus, double or blurred vision, vomiting, sensations of heat, cold or numbness, paraesthesia, twitching, tremors, convulsions, unconciousness, psychosis, dyspnoea, respiratory depression and/or arrest, agitation, difficulty swallowing and slurred speech.
The excitatory manifestations may be very brief or may not occur at all, in which case the first manifestations of toxicity may be drowsiness merging into unconciousness and respiratory arrest. Drowsiness following administration of lignocaine is usually an early sign of a high blood level of the drug and may occur as a result 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 medicines available to manage such patients (see Overdosage, Treatment).

Cardiovascular.

Cardiovascular manifestations are usually depressant and are characterised by bradycardia, hypotension and cardiovascular collapse, which may lead to cardiac arrest. Methaemoglobinaemia can occur following IV administration, particularly in neonates. Arrhythmias, including ventricular tachycardia/ ventricular fibrillation.

Allergic.

Allergic reactions are characterised by cutaneous lesions, urticaria, oedema or anaphylactoid reactions. Allergy to amide type local anaesthetics is very rare.

Dosage and Administration

Local anaesthesia.

The dose varies depending upon the area to be anaesthetised, the vascularity of the tissues, the number of neuronal segments to be blocked, individual tolerance and the anaesthetic technique. The lowest dose needed to provide effective anaesthesia should be used.
Injection should be made slowly and with frequent aspiration to guard against intravascular injection, which may produce toxic effects. Care should be taken in performing epidural anaesthesia to prevent intravascular or subarachnoid injection of the large dose of anaesthetic.
For continuous epidural or caudal anaesthesia and paracervical block for obstetric analgesia the maximum dose should not be repeated at intervals of less than 90 minutes.
During spinal anaesthesia the positioning of the patient is very important (see Precautions) and the patient's pulse and blood pressure should be monitored.
Adults. The dose should not exceed 200 mg. For spinal anaesthesia, the dose should not exceed 100 mg.
Children. The dose should not exceed 3 mg/kg.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.

Intravenous use in cardiac arrhythmias.

Patients with congestive heart failure or cardiogenic shock may require smaller bolus doses.
Adults. The usual dose is lignocaine 50 to 100 mg administered intravenously under ECG monitoring. The dose may be injected at a rate of approximately 25 to 50 mg (2.5 to 5.0 mL of the lignocaine 1% solution or 1.25 to 2.5 mL of the 2% solution) per minute. A sufficient period of time should be allowed to enable a slow circulation to carry the drug to the site of action. If the initial dose of 50 to 100 mg does not produce the desired response, a second dose may be given after five minutes. No more than 200 to 300 mg of lignocaine should be administered during a one hour period.
Following a single injection in those patients in whom arrhythmia tends to recur and who are incapable of receiving oral antiarrhythmic therapy, intravenous infusions of lignocaine may be administered at a rate of 1 to 4 mg/minute (20 to 50 mcg/kg/minute). Intravenous infusions must be given under ECG monitoring to avoid potential overdosage and toxicity. The infusion should be reassessed as soon as the patient's cardiac rhythm appears to be stable or at the earliest signs of toxicity. It should rarely be necessary to continue intravenous infusions of Min-I-Jet Lignocaine for prolonged periods. As soon as possible, patients should be changed to an oral antiarrhythmic agent for maintenance therapy.
Children. Experience with lignocaine is limited. A suggested paediatric dose is a loading dose of lignocaine 0.5 to 1 mg/kg repeated if necessary up to 3 to 5 mg/kg, followed by continuous infusions of 10 to 50 microgram/kg/minute.
Elderly. The dose may need to be reduced depending on age and physical state.

Overdosage

Symptoms.

Reactions due to overdose with lignocaine are systemic and involve the central nervous, respiratory and cardiovascular systems. Effects include medullary depression, tonic and clonic convulsions and cardiovascular collapse (see Adverse Reactions).
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.

Cardiovascular toxicity.

In anaesthetised or unconscious patients, signs of CNS toxicity may not be apparent. Thus, cardiovascular toxicity, (especially cardiovascular depression) may be the first indication of lignocaine toxicity in these patients.
In rare cases, cardiac arrest has occurred without prodromal CNS effects.

Treatment.

Institute emergency resuscitative procedures and administer the drugs necessary to counteract each appropriate abnormality. For severe convulsions, small increments of diazepam or an ultra-short acting barbiturate (thiopentone) should be given. If the patient is anaesthetised, a short acting muscle relaxant may be given intravenously. Patency of the airway and adequacy of ventilation must be assured. Should circulatory depression occur, vasopressors such as metaraminol may be used.
Contact the Poisons Information Centre on 131 126 for advice on the management of overdosage.

Presentation

Injection (Min-I-Jet: single use prefilled syringe), 2% (20 mg/mL): 5 mL.

Storage

Store below 25°C.

Poison Schedule

S4.