Management of local anesthetic toxicity and importance of lipid infusion

Abstract

Local anesthetics (LA) are one of the groups that block the transmission of sensory, motor and autonomic nerve impulses commonly used in clinical anesthesia. All local anesthetic molecules in clinical use consist of three parts: a lipophilic (aromatic) end, a hydrophilic (amine) end, and a chain that provides the connection between the ends. Physicochemical properties determine the clinical efficacy of local anaesthetics The part that determines the lipid solubility of local anesthetics is the aromatic ring. A higher dose of local anesthetics is required for cardiovascular system (CVS) toxicity. Hypertension, tachycardia and ventricular arrhythmia are the first of the diseases of CVS. Hypotension, arrhythmia, bradycardia and cardiac arrest develop as local anesthetics increase in blood. The symptoms of central nervous system (CNS) toxicity associated with LA are related to the plasma levels of drugs. Initially, there are drowsiness, dizziness, sedation, disorientation, tinnitus, nystagmus, metallic taste, nausea and vomiting. Then, restlessness, irritability, tremors and muscle twitches occur. After this, the tonic-clonic seizure and loss of consciousness develops, finally, apnea, cardiovascular collapse and coma. In the treatment of local anesthetic toxicity, it is recommended to provide airway, avoid the propofol if seizure occurs and treat with benzodiazepine. If cardiac arrest develops, it is recommended to switch to advanced life support, to reduce the given dose of adrenaline, to administer lipid emulsion (20%) and to respond to treatment if cardiopulmonary bypass is not provided.