Use of Lidocaine for Analgesia in Children and Adolescents
Lidocaine is contraindicated in patients with a known hypersensitivity. Allergic reactions to lidocaine appear to be rare, but cases of angioedema, laryngospasm, bronchospasm, pruritus, urticaria, anaphylactoid reactions, and shock have been reported. There appears to be minimal cross sensitivity to lidocaine in patients allergic to para-aminobenzoic acid derivatives such as procaine, tetracaine, or benzocaine. Lidocaine should not be used as an analgesic in patients with second or third-degree heart block, or severe sinoatrial block without a pacemaker. Lidocaine analgesia should be considered only in patients with stable cardiovascular and hemodynamic parameters.
Early symptoms of lidocaine toxicity include central nervous system (CNS) excitation, with nervousness, lightheadedness or dizziness, anxiety, confusion, tinnitus, blurred or double vision, a sensation of heat, cold, or numbness, twitching, tremor, and vomiting. The period of CNS excitation may be brief in some patients, while others may not exhibit this phase and will present with symptoms of CNS depression. Patients may also exhibit tachypnea, tachycardia, fever, and metabolic acidosis. At higher concentrations (> 5 mcg/mL), symptoms may progress to tonic-clonic seizures, blood pressure and heart rate lability, respiratory depression, and cardiovascular collapse. Patients exhibiting early signs of toxicity should have their infusion decreased and a lidocaine level obtained. If symptoms do not resolve, the infusion should be discontinued. In patients with signs of severe toxicity, lidocaine should be discontinued and supportive therapy initiated.
Intravenous lipid emulsion has been shown to be an effective tool for reducing lidocaine concentrations. The American Society of Regional Anesthesia and Pain Medicine (ASRA) recommends that lipid emulsion be considered in patients with systemic local anesthetic toxicity following airway management, administration of benzodiazepines for seizures, and control of cardiac arrhythmias. The ASRA guidelines recommend a bolus of 1.5 mL/kg 20% lipid emulsion followed by a 0.25 mL/kg/min infusion with adjustment based on patient response. The mechanism for the beneficial effect of lipid emulsion is not clearly understood. It has been suggested that fat emulsion serves as a "lipid sink" in the systemic circulation, facilitating dissolution of lidocaine into the lipid micelles of the emulsion which are then cleared by the liver. Administration of lipid emulsion also provides free fatty acids to meet the increased metabolic demands occurring as the result of a lidocaine overdose.
Contraindications and Warnings
Lidocaine is contraindicated in patients with a known hypersensitivity. Allergic reactions to lidocaine appear to be rare, but cases of angioedema, laryngospasm, bronchospasm, pruritus, urticaria, anaphylactoid reactions, and shock have been reported. There appears to be minimal cross sensitivity to lidocaine in patients allergic to para-aminobenzoic acid derivatives such as procaine, tetracaine, or benzocaine. Lidocaine should not be used as an analgesic in patients with second or third-degree heart block, or severe sinoatrial block without a pacemaker. Lidocaine analgesia should be considered only in patients with stable cardiovascular and hemodynamic parameters.
Early symptoms of lidocaine toxicity include central nervous system (CNS) excitation, with nervousness, lightheadedness or dizziness, anxiety, confusion, tinnitus, blurred or double vision, a sensation of heat, cold, or numbness, twitching, tremor, and vomiting. The period of CNS excitation may be brief in some patients, while others may not exhibit this phase and will present with symptoms of CNS depression. Patients may also exhibit tachypnea, tachycardia, fever, and metabolic acidosis. At higher concentrations (> 5 mcg/mL), symptoms may progress to tonic-clonic seizures, blood pressure and heart rate lability, respiratory depression, and cardiovascular collapse. Patients exhibiting early signs of toxicity should have their infusion decreased and a lidocaine level obtained. If symptoms do not resolve, the infusion should be discontinued. In patients with signs of severe toxicity, lidocaine should be discontinued and supportive therapy initiated.
Intravenous lipid emulsion has been shown to be an effective tool for reducing lidocaine concentrations. The American Society of Regional Anesthesia and Pain Medicine (ASRA) recommends that lipid emulsion be considered in patients with systemic local anesthetic toxicity following airway management, administration of benzodiazepines for seizures, and control of cardiac arrhythmias. The ASRA guidelines recommend a bolus of 1.5 mL/kg 20% lipid emulsion followed by a 0.25 mL/kg/min infusion with adjustment based on patient response. The mechanism for the beneficial effect of lipid emulsion is not clearly understood. It has been suggested that fat emulsion serves as a "lipid sink" in the systemic circulation, facilitating dissolution of lidocaine into the lipid micelles of the emulsion which are then cleared by the liver. Administration of lipid emulsion also provides free fatty acids to meet the increased metabolic demands occurring as the result of a lidocaine overdose.
SHARE
