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Local Anesthetic Toxicity: Prevention and Treatment

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Local Anesthetic Toxicity: Prevention and Treatment Local Anesthetic Toxicity: Prevention and Treatment John W. Wolfe, M.D. Staff Anesthesiologist Indiana University School of Medicine Indianapolis, Indiana John F. Butterworth, M.D. Chairman, Department of Anesthesia Indiana University School of Medicine Indianapolis, Indiana LESSON OBJECTIVES dine, and the site of injection on peak Upon completion of this lesson, the reader local anesthetic concentrations in blood. should be able to: 6. Describe the mechanism of local anes- 1. List the signs and symptoms of local thetic central nervous system toxicity. anesthetic toxicity. 7. Identify the risk factors for local anes- 2. Discuss the concept of "maximum safe thetic toxicity. doses of a local anesthetic." 8. Plan the treatment of local anesthetic- 3. Describe methods for reducing the risk of induced cardiac arrhythmias and cardiac local anesthetic toxicity. arrest. 4. Explain the treatment of local anes- 9. Describe the mechanism of local anes- thetic-related neurologic symptoms and thetic cardiovascular toxicity. toxic side effects. 10. Explain the dosage and proposed mech- 5. Discuss the effects of epinephrine, cloni- anism of lipid emulsion therapy. Current Reviews for Nurse Anesthetists designates this lesson for 1 CE contact hour in Clinical pharmacology/therapeutics. Introduction Mechanism of Cardiac and central nervous system (CNS) toxic Local Anesthetic Toxicity side effects of local anesthetics are relatively rare but potentially catastrophic complications of local and Local anesthetics normally produce their desired regional anesthesia. Fortunately, the likelihood of a effects on peripheral nerves by binding and inhibit- local anesthetic toxic event can be reduced by ad- ing voltage-gated sodium channels in neural cell herence to good technique. These reactions are in membranes. When a sufficient fraction of these most cases readily treatable. This lesson will review sodium channels are inhibited, the neuron cannot the pharmacology, risk factors, presentation, and depolarize and cannot generate or conduct action treatment of local anesthetic toxicity. potentials. Curr Rev Nurs Anesth 34(2):13-24, 2011 15 Local anesthetic molecules are weak bases. At these effects likely varies among local anesthetic physiologic pH, they exist in solution as a mixture of agents. Lidocaine tends to produce vasodilation and neutral, more lipid-soluble molecules and protonated, negative inotropy while rarely producing arrhyth- relatively lipid-insoluble molecules. In order to mias. In contrast, bupivacaine has a greater ten- approach the local anesthetic binding site on Na dency to produce ventricular arrhythmias in addition channels, local anesthetic molecules must penetrate to vasodilation and negative inotropy. to the inner surface of the plasmalemma. The For purposes of this lesson, we have made no uncharged fraction of a local anesthetic molecule mix assumptions as to the mechanism by which local is therefore considered to be the fraction that most anesthetics actually produce either CNS or cardio- readily produces both desired and undesired drug vascular toxicity. It is possible that these toxic side actions. Curiously, once the molecule gains entry effects occur through binding to sodium channels; it into the cytoplasm, it is the charged form that has is equally possible that another mechanism is oper- greater potency. The different properties of the lipid- ative. soluble and lipid-insoluble fractions are important when one considers treatments for local anesthetic toxicity. Routes for Entry of Local Anesthetic into the There are three principal routes for entry Systemic Circulation of local anesthetic into the plasma: direct There are three principal routes for entry of local injection into an artery or vein, absorption anesthetic into the blood: direct injection into an from a depot dose in other tissues, and artery or vein, absorption from a depot dose in other transcutaneous or transmucosal absorp- tissues, and transcutaneous or transmucosal absorp- tion. tion. In the plasma, all local anesthetics are bound to Intravascular Injection proteins to varying degrees, primarily to aracid Intravascular injection of local anesthetic agents glycoprotein (AAG) and albumin. Plasma protein is possible with most regional anesthetic techniques levels are affected by disease states and age. The due to the proximity of vascular structures to ner- long-duration local anesthetics (bupivacaine and vous tissue. For example, accidental injection of ropivacaine) are bound by plasma proteins to a local anesthetic into the epidural venous plexus can greater extent than the less potent, shorter duration occur when dosing an epidural catheter, and injec- local anesthetics. Bupivacaine is approximately 95% tion into the femoral artery or vein can occur during protein-bound. Intermediate-duration local anes- an attempted femoral nerve block. thetics (lidocaine and mepivacaine) have a smaller Injection into an artery feeding the brain must protein-bound fraction (60-70%). Protein binding be considered when performing regional anesthetics helps to reduce the likelihood that local anesthetics in the neck, such as interscalene brachial plexus in blood will enter brain or cardiac tissue causing blocks. With accidental injection of local anesthetic either CNS or cardiac toxicity. into a carotid or vertebral artery, a bolus dose of local Local anesthetics may bind a wide variety of anesthetic at a relatively high plasma concentra- channels and enzymes in cardiac muscle and in the tion is delivered directly to the brain. In this case, CNS, and increased blood concentrations of local one should expect rapid onset of CNS toxic side anesthetics can cause toxic effects in these tissues. effects, with rapid onset of seizures after even a very Possible mechanisms by which local anesthetics can small intravascular injection. Fortunately, due to produce cardiovascular collapse include depression of the typically small dose of local anesthetic injected, cardiac contractility, potentiation of cardiac arrhyth- these seizures are generally short-lived and usually mias, and peripheral vasodilation. The balance of not accompanied by cardiac toxicity. Slower Absorption Faster Absorption Subcutaneous Sciatic Brachial plexus Epidural Caudal Intercostal Trachea! Intravenous Figure 1. Relative Absorption Rates of Local Anesthetic at Various Locations 16 Current Reviews for Nurse Anesthetists Table 1 Risk Factors for Local Factors Increasing Risk Anesthetic Toxicity of Local Anesthetic Toxicity (see Table 1) Administration in a site with rapid Route of Administration absorption The location of local anesthetic injection affects Young age its absorption rate and peak plasma concentration. Large total dose of local anesthetic The local anesthetic dose may need to be reduced Renal dysfunction when it is placed into an area with especially rapid Hepatic dysfunction absorption, such as the airway or in intercostal nerve Heart failure blocks, as compared to sites with relatively slow Pregnancy absorption, such as subcutaneous injections or sciatic nerve blocks. Young Age Infants, particularly those aged 0-3 months, Absorption from Tissues have reduced concentrations of plasma proteins to When local anesthetic is injected into perineural which local anesthetics bind, such as AAG. This connective tissue (as in a peripheral nerve block) or leads to greater peak levels of free (unbound) local the epidural space, the nerve-blocking action is anesthetic after single injections, such as caudal epi- terminated by gradual absorption from the nerve dural blocks. The unbound form is largely respon- into the systemic circulation. Local anesthetic sible for toxic side effects. Infants also have a re- metabolism has almost no effect on the duration of duced capacity to metabolize local anesthetic drugs, nerve blocks. Injecting a given dose of local anes- with lower plasma clearance rates than adults This thetic into highly vascular tissue will lead to greater may lead to greater plasma levels when continuous plasma drug concentrations than placing the same infusions of local anesthetics are given. Due to these dose of local anesthetic into a poorly vascularized factors, both bolus doses and infusion rates of local site. Epinephrine is effective in retarding the rate of anesthetics should be reduced in infants. absorption of local anesthetic and reducing peak plasma levels of local anesthetic. The effect of Local anesthetic toxicity symptoms are clonidine is less clear, with some studies showing caused by the free fraction of the local increased plasma local anesthetic concentrations anesthetic drug (the fraction not bound to when clonidine is included in local anesthetic plasma proteins). Any condition that re- solutions. Figure 1 shows the relative absorption duces plasma protein levels may increase rates for local anesthetics after injection into various a patient's risk of local anesthetic toxicity. sites. Tumescent liposuction techniques present a scenario in which large amounts of local anesthetic Total Dose of Local Anesthetic Administered solution may be absorbed into the systemic circu- All other factors being equal, administering lar- lation in an unpredictable manner. Typically, dilute ger doses of local anesthetic will lead to increased lidocaine with epinephrine is injected through the plasma concentrations. Patient size should be con- liposuction cannula. Dangerously elevated plasma sidered when determining a local anesthetic dose. Of lidocaine levels have been reported when large
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