Symptoms of acute systemic toxicity:
Central nervous system toxicity presents with symptoms of increasing severity. Patients may present initially with circumoral Paraesthesia, numbness of the tongue, light-headedness, hyperacusis and tinnitus. Visual disturbances and muscular tremors or muscle twitching 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 usually follow, which may last from a few second to several minutes. Hypoxia and hypercapnia occur rapidly following convulsions due to increase 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.
Effects on the cardiovascular system may be seen in severe cases. Hypotension, bradycardia, arrhythmia and cardiac arrest may occur as a result of high systemic concentrations, with potentially fatal outcome.
Recovery occurs as a consequence of redistribution of the local anaesthetic drug from the central nervous system, and metabolism and may be rapid unless large amounts of the drug have been injected.
Treatment of acute toxicity:
If signs of acute systemic toxicity appear, injection of the anaesthetic should be stopped immediately.
Treatment will be required if convulsions and CNS depression occurs. The objectives of treatment are to maintain oxygenation, stop the convulsions and support the circulation. A patent airway should be established and oxygen should be administered, together with assisted ventilation (mask and bag) if necessary.
The circulation should be maintained with infusions of plasma or intravenous fluids. Where further supportive treatment of circulatory depression is required, use of a vasopressor agent may be considered although this involves a risk of CNS excitation. If convulsion do not stop spontaneously in 15-20 seconds, they may be controlled by the intravenous administration of Diazepam or Thiopentone Sodium, bearing in mind that anti-convulsant drugs may also depress respiration and the circulation. Prolonged convulsions may jeopardize the patient's ventilation and oxygenation and early endotracheal intubation should be considered. If cardiac arrest should occur, standard cardiopulmonary resuscitation procedures should be instituted. Continual optimal oxygenation and ventilation and circulatory support as well as treatment of acidosis are of vital importance.
Dialysis is of negligible value in the treatment of acute overdosage with lidocaine.
3 years (36 months).
Known hypersensitivity to anaesthetics of the amide type; hypovolemia; complete heart block.
Solutions containing adrenaline (epinephrine) should not be used in areas of the body supplied by end arteries or otherwise having a compromised blood supply such as digits, nose, ear or penis. Solutions containing adrenaline (epinephrine) should not be given intravenously.
Lidocaine caused precipitation of amphotericin, methohexital sodium and sulfadiazine sodium in glucose injection. It is recommended that admixtures of lidocaine and glyceryltrinitrate should be avoided.
Sodium Chloride
Sodium Hydroxide
Hydrochloric Acid
Water for Injections
Solution for injection.
In common with other local anaesthetics, adverse reactions to lidocaine are rare and are usually the result of raised plasma concentrations due to accidental intravascular injection, excessive dosage or rapid absorption from highly vascular areas, or may result from a hypersensitivity, idiosyncrasy or diminished tolerance on the part of the patient.).
Immune system disorders
Hypersensitivity reactions (allergic or anaphylactoid reactions, anaphylactic shock) see also Skin & subcutaneous tissue disorders.
Skin testing for allergy to Lidocaine is not considered to be reliable.
Nervous & Psychiatric disorders
Neurological signs of systemic toxicity include dizziness or light-headedness, nervousness, tremor, circumoral paraesthesia, tongue numbness, drowsiness, convulsions, coma.
Nervous system reactions may be excitatory and or depressant.).
Ear and labyrinth disorders
Tinnitus, hyperacusis.
Cardiac and vascular disorders
Cardiovascular reactions are depressant and may manifest as hypotension, bradycardia, myocardial depression, cardiac arrhythmias and possibly cardiac arrest or circulatory collapse.
Hypotension may accompany spinal and epidural anaesthesia. Isolated cases of bradycardia and cardiac arrest have also been reported.
Respiratory, thoracic or mediastinal disorders
Dyspnoea, bronchospasm, respiratory depression, respiratory arrest.
Gastrointestinal
Nausea, vomiting.
Skin & subcutaneous tissue disorders
Rash, urticaria, angioedema, face oedema.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard. By reporting side effects you can help provide more information on the safety of this medicine.
No further relevant information other than that which is included in other sections of the Summary of Product Characteristics.
Lidocaine is a local anaesthetic of the amide group. Lidocaine Hydrochloride Injection BP is for use in infiltration anaesthesia, intravenous regional anaesthesia and nerve blocks.
Lidocaine is a local anaesthetic of the amide type. It is used to provide local anaesthesia at various sites in the body and it acts by inhibiting the ionic refluxes required for the initiation and conduction of impulses, thereby stabilising the neuronal membrane. In addition to blocking conduction in nerve axons in the peripheral nervous system, lidocaine has important effects on the central nervous system and cardiovascular system. After absorption, lidocaine may cause stimulation of the CNS followed by depression and in the cardiovascular system, it acts primarily on the myocardium where it may produce decreases in electrical excitability, conduction rate and force of contraction.
Lidocaine is absorbed from injection sites including muscle and its rate of absorption is determined by factors such as the site of administration and the tissue vascularity. Except for intravascular administration, the highest blood levels occur following intercostal nerve block and the lowest after subcutaneous administration. Lidocaine is bound to plasma proteins, including alpha-1-acid-glycoprotein. The drug crosses the blood-brain and placental barriers.
Lidocaine is metabolised in the liver and about 90% of a given dose undergoes N-dealkylation to form monoethylglycinexylidide and glycinexylidide, both of which may contribute to the therapeutic and toxic effects of lidocaine. Further metabolism occurs and metabolites are excreted in the urine with less than 10% as unchanged lidocaine. The elimination half-life of lidocaine following an intravenous bolus injection is one to two hours, but this may be prolonged in patients with hepatic dysfunction.
6 December 2013
Lidocaine Hydrochloride Injection BP 2% w/v.
Mercury Pharma International Ltd
4045, Kingswood Road,
City West Business Park,
Co Dublin, Ireland
Do not store above 25°C.
2ml, 5ml, 10ml & 20ml translucent plastic ampoules, polypropylene Ph. Eur., packed in cardboard cartons to contain 10, 20, 50 and 100 ampoules.
PL 02848/0177
Each 1ml of solution contains 20mg of Lidocaine Hydrochloride.
Lidocaine should only be used by people with skills in resuscitation.
Facilities and equipment for resuscitation should be available when administering local anaesthetics.
As with other local anaesthetics, lidocaine should be used with caution in patients with epilepsy, myasthenia gravis, congestive cardiac failure, bradycardia or respiratory depression, including where agents are known to interact with Lidocaine either to increase its availability or additive effects e.g. phenytoin or prolong its elimination e.g. hepatic or end renal insufficiency where the metabolites of Lidocaine may accumulate.
The effect of local anaesthetics may be reduced if the injection is made into an inflamed or infected area.
Intramuscular Lidocaine may increase creatinine phosphokinase concentrations which can interfere with the diagnosis of acute myocardial infarction. Lidocaine has been shown to be porphyrinogenic in animals and should be avoided in persons suffering from porphyria.
Hypokalaemia, hypoxia and disorder of acid-base balance should be corrected before treatment with intravenous lidocaine begins.
Certain local anaesthetic procedures may be associated with serious adverse reactions, regardless of local anaesthetic drug used.
Central nerve blocks may cause cardiovascular depression, especially in the presence of hypovolaemia, and therefore epidural anaesthesia should be used with caution in patients with impaired cardiovascular function.
Epidural anaesthesia may lead to hypotension and bradycardia. This risk can be reduced by preloading the circulation with crystalloidal or colloidal solutions. Hypotension should be treated promptly.
Paracervical block can sometimes cause foetal bradycardia or tachycardia and careful monitoring of foetal heart rate is necessary.
Injections in the head and neck region may be made inadvertently into an artery causing cerebral symptoms even at low doses.
Retrobulbar injections may rarely reach the cranial subarachnoid space, causing serious/severe reactions including cardiovascular collapse, apnoea, convulsions and temporary blindness.
Retro- and peribulbar injections of local anaesthetics carry a low risk of persistent ocular motor dysfunction. The primary causes include trauma and/or local toxic effects on muscles and/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 local anaesthetic. For this reason, as with all local anaesthetic, the lowest effective concentration and dose of local anaesthetic should be used.
Lidocaine Injection is not recommended for use in neonates. The optimum serum concentration of lidocaine required to avoid toxicity, such as convulsions and cardiac arrhythmias, in this age group is not known.
Where outpatient anaesthesia affects areas of the body involved in driving or operating machinery, patients should be advised to avoid these activities until normal function is fully restored.
The method of administration of lidocaine varies according to the procedure (infiltration anaesthesia, intravenous regional anaesthesia or nerve block).
The dosage should be adjusted according to the response of the patient and the site of administration. The lowest concentration and smallest dose producing the required effect should be given.
The maximum dose for healthy adults should not exceed 200 mg [or 500mg if given in solutions containing adrenaline (epinephrine)].
Children and elderly or debilitated patients require smaller doses, commensurate with age & physical status.
If only part used, discard the remaining solution.
22/03/2006
