Xylocaine W/ Adrenaline Drug Interactions

Antiarrhythmic Drugs: Local anaesthetics of the amide-type eg, lignocaine, should be used with caution in patients receiving other local anaesthetics or agents structurally related to amide-type local anaesthetics eg, certain antiarrhythmic drugs eg, disopyramide, procainamide, mexiletine since potentiation of cardiac effects may occur. Specific interaction studies with lignocaine and antiarrhythmic 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 lignocaine in 2 case reports, although a small prospective study of combined therapy on lignocaine pharmacokinetics found no changes in clearance or other pharmacokinetic factor. This combination has been reported to precipitate seizures and lead to severe sinus 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 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 drugs are administered concurrently, the patient should be closely observed for signs of lignocaine toxicity.
Cimetidine: Cimetidine reduces the clearance of IV administered lignocaine and toxic effects due to high serum lignocaine levels have been reported when these 2 drugs have been administered concurrently.
Anticonvulsive Agents: Phenytoin and other antiepileptic drugs eg, 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.
Inhalational Anaesthetics: Lignocaine decreases the minimum effective concentration of inhalational anaesthetics eg, nitrous oxide.
Skeletal Muscle Relaxants: Lignocaine and skeletal muscle relaxants eg, suxamethonium, lead to excessive neuromuscular blockade; therefore, this combination must be used with caution.
Structurally-Related Local Anaesthetics: Lignocaine should be used with caution in patients receiving agents structurally related to local anaesthetics.
In addition, the following interactions may occur with solutions with adrenaline:
CNS-Acting Drugs: Solutions with adrenaline should be used with extreme caution in patients receiving monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants as severe sustained hypertension may result. The effects of adrenaline may be potentiated by some antihistamines and thyroid hormones (see Precautions). Phenothiazines and butyrophenones may reduce or reverse the pressor effects of adrenaline which may lead to a hypotensive response and tachycardia.
Oxytocic Drugs of the Ergot-Type: Solutions with adrenaline should not be used in the presence of oxytocic drugs of the ergot-type as they are known to interact to produce severe, persistent hypertension and its subsequent sequelae.
Adrenergic Neuron-Blocking Agents: Solutions with adrenaline should be used with extreme caution in the presence of adrenergic neuron-blocking agents (eg, guanethidine, debrisoquine, bethanidine).
Inhalation Anaesthetics: Serious cardiac arrhythmias and acute pulmonary oedema if hypoxia is present may occur if preparations containing adrenaline are employed in patients during or following the administration of chloroform, halothane, cyclopropane, trichloroethylene, or other halogenated compounds.
Cardiac Glycosides: Solutions with adrenaline may interact with cardiac glycosides resulting in cardiac arrhythmias.
Beta-Blockers: Non-cardioselective β-blockers eg, propranolol enhance the pressor effects of adrenaline which may lead to severe hypertension and bradycardia.
Quinidine: Solutions with adrenaline may interact with quinidine resulting in cardiac arrhythmias.
Hypoglycaemics: Adrenaline-induced hyperglycaemia may lead to loss of blood sugar control in diabetic patients treated with hypoglycaemic agents.
Alkaline Solutions: The solubility of lignocaine is limited at pH values >7. This must be taken into consideration if adding an alkaline solution since precipitation might occur at higher pH values.
Laboratory Test Effects: Creatinine: Creatinine measurements in patients with therapeutic plasma levels of lignocaine are about 15-35% 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.
Creatine Kinase: The IM injection of lignocaine may result in an increase in creatine kinase levels for up to 48 hrs. This may interfere with the diagnosis of myocardial infarction.