Consider Lipid Emulsion Rescue for Local Anesthetic Overdose
Heath A. Fallin MD
David A. Burns MD
Regional anesthesia—the injection of local anesthetics to block or treat pain—continues to grow in popularity. Regional techniques can provide complete nerve blockade, leading to superior analgesia with relatively few side effects. In rare cases, however, use of regional techniques leads to an overdose of local anesthetic through unintentional intravascular injection of anesthetic or through systemic absorption following local anesthetic infiltration. Systemic overdose is a potentially devastating complication characterized by seizures, cardiovascular collapse, and, possibly, death. Until recently, the standard treatment available to treat local anesthetic overdose was the standard advanced cardiac life support (ACLS) protocol for cardiopulmonary resuscitation (CPR) and, especially in the case of bupivacaine toxicity, these measures were often not enough and cardiopulmonary bypass was necessary. Now, however, new evidence supports using lipid infusion to treat local anesthetic overdose.
BACKGROUND
Local anesthetics produce their effects by blocking sodium channels. The effect is desirable during regional anesthesia when local anesthetics are infiltrated around nerves to provide analgesia and, if desired, motor blockade. If a local anesthetic is absorbed intravenously, however, the same sodiumchannel blockade can occur in all tissues, including the brain and the heart, producing similar dose-dependent attenuation of action potentials throughout these structures.
In the central nervous system (CNS), local anesthetics first depress the inhibitory pathways in the amygdala and hypocampus. Symptoms of such depression begin with visual, auditory, or sensory hallucinations (including circumoral numbness, metallic taste, and tinnitus); progress to irritability, lightheadedness, tremors and muscle twitching; and finally culminate in generalized tonic-clonic seizures. As blood levels increase, the excitatory pathways are also suppressed, leading to loss of consciousness, coma, and eventual respiratory arrest. In general, CNS changes are an early indicator of local anesthetic toxicity and are seen before cardiac toxicity develops.
Local anesthetics also cause direct vasodilation and cardiac depression. The cardiac tissue response to local anesthetics is similar to the nerve tissue
response: Blockade of sodium channels inhibits the cardiac action potential, leading to myocardial depression. Lidocaine is frequently used to decrease myocardial irritability through this mechanism. More potent anesthetics, such as bupivacaine and etidocaine, however, can actually act as proarrhythmic agents, since these anesthetics bind to sodium channels in a statedependent fashion, leading to bradycardia and conduction delay through the myocardium, thereby allowing re-entrant arrhythmias, ventricular fibrillation, or asystole. These cardiac complications resist normal resuscitative measures, and multiple deaths from systemic local anesthetic toxicity, especially with bupivacaine, have been reported.
response: Blockade of sodium channels inhibits the cardiac action potential, leading to myocardial depression. Lidocaine is frequently used to decrease myocardial irritability through this mechanism. More potent anesthetics, such as bupivacaine and etidocaine, however, can actually act as proarrhythmic agents, since these anesthetics bind to sodium channels in a statedependent fashion, leading to bradycardia and conduction delay through the myocardium, thereby allowing re-entrant arrhythmias, ventricular fibrillation, or asystole. These cardiac complications resist normal resuscitative measures, and multiple deaths from systemic local anesthetic toxicity, especially with bupivacaine, have been reported.
PREVENTION/PREVENTION
So how do we treat local anesthetic overdose? The primary method of treatment is prevention. Use the least potent and least toxic drug available to achieve the desired affect, and alter the dose based on patient age, weight, and comorbidities to prevent systemic toxicity. Bupivacaine is very cardiotoxic, and the dextro enatiomer seems to possess the most potent effects. This is why the levobupivacaine enatiomer was developed as a separate preparation. Bupivicaine, particularly in high doses or high concentrations, should be avoided. Premedication of patients with benzodiazepines, such as midazolam or lorazepam, may facilitate patient cooperation and can raise the seizure threshold and the level of local anesthetic required to cause CNS symptoms. Remember, however, that these symptoms usually occur early with local anesthetic toxicity and benzodiazepine use may mask these early warning signs without raising the cardiac toxicity threshold.
Before administering local anesthetic, ensure adequate intravenous (IV) access is available, standard monitors are in place, and resuscitative drugs and equipment are readily available. Airway equipment must also be readily available in the event of an overdose, as rapid intubation may be required.
Consider using the following techniques while placing a block to prevent overdose. Avoid transvascular approaches, if possible, and use ultrasound imaging, if available, to confirm needle position before injection. Aspirate before injection and frequently during block placement, and remember to allow adequate time for blood to become visible in the hub of the needle or catheter. Inject a small test dose after aspiration, and evaluate the patient for symptoms before giving the full dose to the patient. Fractionation, the splitting of the total dose into smaller aliquots with aspiration between them, helps ensure that the needle or catheter has not migrated into a nearby vessel during the block placement. Finally, monitor the patient throughout the block, and maintain verbal communication, if possible, to ascertain early signs of intravascular injection (tinnitus, metallic taste in mouth, anxiety or faintness).
To prevent systemic absorption, you may mix a vasoconstrictor with the anesthetic to slow systemic absorption. Epinephrine is a popular choice, although other vasoactive medications are also used. Epinephrine has the added advantage of causing a rapid increase in heart rate during test-dose administration if it is absorbed systemically.
TREATMENT
Despite the best techniques, however, systemic injection or toxic absorption of local anesthetics still occurs, perhaps in as many as 20 of every 10,000 peripheral nerve blocks. In the case of overdose, treatment measures are largely supportive and follow established treatment protocols for the symptoms experienced. First and foremost, evaluate the airway: Apply supplemental oxygen, ventilatory support, or intubation, if necessary. Ventilate the seizing patient to limit acidosis and to ensure adequate tissue oxygenation. Treat seizures with thiopental, 50 mg IV, or midazolam, 2 mg IV, and titrate up, as necessary, until seizures cease. Succinylcholine may help relax the seizing patient, but remember that muscle blockade only stops the muscular symptoms of seizures; the CNS will have continued seizure activity along with increased metabolic and oxygen demands.
If cardiovascular symptoms occur, begin CPR and ACLS resuscitation measures immediately. Local anesthetic overdose may lead to refractory cardiovascular symptoms, and prolonged CPR may be necessary—CPR of 1 hour or more may be required until clearance of the anesthetic occurs and the heart can begin to beat again; do not give up too quickly! Use a cardioverter to treat malignant ventricular arrhythmias, as required, and provide pharmacological support as necessary: Atropine for bradycardia; ephedrine for hypotension; and epinephrine, as required, for cardiovascular collapse. Multiple doses of these drugs may be required and are indicated in local anesthetic overdose. If available, consider instituting cardiac bypass to allow the patient time to clear the drug from the circulatory system and regain normal cardiac function.
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