Practice Essentials A must read till end, to all surgeons TOXICITY OF LIGNOCAINE While generally safe, local anesthetic agents can be toxic if administered inappropriately, and in some cases may cause unintended reactions even when properly administered. The toxicity of local and infiltration anesthetics can be local or systemic. Systemic toxicity of anesthetics most often involves the central nervous system (CNS) or the cardiovascular system. Signs and symptoms Manifestations of local anesthetic toxicity typically appear 1 to 5 minutes after the injection, but onset may range from 30 seconds to as long as 60 minute Toxicity manifestations can be categorized as follows: CNS Cardiovascular Hematologic Allergic Local tissue CNS manifestations Classically, systemic toxicity begins with excitement, psychosis Circumoral and/or tongue numbness Metallic taste Lightheadedness Dizziness Visual and auditory disturbances (difficulty focusing and tinnitus) Disorientation Drowsiness With higher doses, initial CNS excitation is often followed by a rapid CNS depression, with the following features: Muscle twitching Convulsions Unconsciousness Coma Respiratory depression and arrest Cardiovascular depression and collapse Cardiovascular manifestations Chest pain Shortness of breath Palpitations Lightheadedness Diaphoresis Hypotension Syncope Hematologic manifestations Methemoglobinemia has been frequently reported in association with benzocaine use; however, lidocaine and prilocaine have also been implicated. At low levels (1-3%), methemoglobinemia can be asymptomatic, but higher levels (10-40%) may be accompanied by any of the following complaints: Cyanosis Cutaneous discoloration (gray) Tachypnea Dyspnea Exercise intolerance Fatigue Dizziness and syncope Weakness Allergic manifestations Rash Urticaria Anaphylaxis is rare. Imaging studies are determined by the overall clinical picture. For example, if the patient has a seizure and the etiology of the seizure is not apparent, consider a head computed tomography scan. See Workup for more detail. Management Attention to impending airway compromise, significant hypotension, dysrhythmias, and seizures takes precedence. Once other possible etiologies of the patient's new symptoms have been excluded, management of the specific symptoms can begin. Treatment of local anesthetic toxicity may include the following : Airway management Seizure suppression (benzodiazepines preferred) Management of cardiac dysrhythmias Lipid emulsion therapy Adverse effects are usually caused by high plasma concentrations of the agent, which may result from one of the following: Inadvertent intravascular injection Excessive dose or rate of injection Delayed drug clearance Administration into vascular tissue Patient factors can also affect toxicity. For example, because lidocaine is hepatically metabolized, liver dysfunction increases the risk of toxicity. Because lidocaine is also protein bound, low protein states may also increase risk. Acidosis increases the risk because it favors dissociation of lidocaine from plasma proteins. Interactions with other drugs (eg, cimetidine, beta-blockers) can also affect lidocaine drug levels. See Etiology. The toxicity of local and infiltration anesthetics can be localized or systemic. The localized adverse effects of anesthetic agents include neurovascular manifestations such as prolonged anesthesia and paresthesias, which may become irreversible. Systemic toxicity of anesthetics most often involves the central nervous system (CNS) or the cardiovascular system. Concurrent administration of other drugs, such as benzodiazepines, may mask the development of CNS symptoms but not cardiovascular symptoms. Relatively rarely (<1%), local anesthetic agents can affect the immune system, producing an immunoglobulin E (IgE)–mediated allergic reaction. Most cases are associated with the use of amino esters. Some anesthetics, particularly benzocaine, are associated with hematologic effects, namely methemoglobinemia. CNS toxicity is biphasic. The earlier manifestations are due to CNS excitation, with problems such as seizures. Subsequent manifestations include CNS depression with a cessation of convulsions and the onset of unconsciousness and respiratory depression or arrest. Cardiovascular effects occur at higher serum concentrations of local anesthetics. These effects may include reentrant arrhythmias. Acceleration of the ventricular rate has been reported in patients with atrial arrhythmias. See Presentation. Treatment of local anesthetic toxicity may include the following : Airway management Seizure suppression Management of cardiac arrhythmias Lipid emulsion therapy Most local anesthetic solutions that contain premixed epinephrine contain preservatives; in these solutions, the pH is adjusted lower to maintain the stability of epinephrine and antioxidants The following factors influence duration of action: Addition of epinephrine to local anesthetic solutions prolongs duration of action by causing vasoconstriction and decreasing systemic absorption Degree of protein binding primarily determines duration of action; high protein binding increases duration Increasing pH (using sodium bicarbonate) also prolongs duration of action Anesthetic concentration and dilution CNS toxicity from local anesthetics manifests initially as CNS excitation, followed by CNS depression. This biphasic effect occurs because local anesthetics first block inhibitory CNS pathways (resulting in stimulation) and then eventually block both inhibitory and excitatory pathways (resulting in overall CNS inhibition). Cardiovascular effects occur because these agents block sodium channels through a fast-in, slow-out mechanism that affects impulse conduction through the heart and nerve tissue. In the heart, this depresses Vmax (ie, the rate of depolarization during phase 0 of the cardiac action potential) and may lead to reentrant arrhythmias. Additionally, conduction through the sinus and atrioventricular nodes is suppressed. avoid rapid injection. The occurrence of numerous fatalities associated with the cardiovascular toxicity of bupivacaine prompted a search for less toxic long-acting local anesthetic agents. The minimum doses of anesthetics in which adverse reactions have occurred are listed in Table 3, below. Table 3. Minimum Intravenous Toxic Dose of Local Anesthetic in Humans . Agent Minimum Toxic Dose (mg/kg) Procaine 19.2 Tetracaine 2.5 Chloroprocaine 22.8 Lidocaine 6.4 Mepivacaine 9.8 Bupivacaine 1.6 Etidocaine 3.4 In addition to high doses, high injection rates also increase the risk of adverse reactions to local anesthetics. Patient factors that increase risk include the following: Renal or hepatic compromise Metabolic or respiratory acidosis Preexisting heart block or heart conditions Pregnancy Extremes of age Hypoxia Epidemiology The frequency of local anesthetic toxicity is difficult to determine because these agents are used widely in a variety of settings, and most reactions are not reported. Systemic toxicity from local anesthetics may occur in as many as 1:1000 peripheral nerve blocks; however, most of these probably involve only minor subjective symptoms. Without treatment, local anesthetic toxicity can result in seizures, respiratory depression or arrest, hypotension, cardiovascular collapse or cardiac arrest, and death. Patient Education Advise patients with adverse reactions to a specific anesthetic agent to avoid that specific anesthetic agent in the future and to alert medical personnel of the reaction. If a patient has experienced an adverse reaction to one class of anesthetic (ester or amide), risk for adverse reactions is higher for all agents in that class. However, if the episode involved seizures, the patient should be reassured that this does not indicate an increased risk for the development of a seizure disorder in the future.

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