Local anesthetics completely abolish neuronal signal transmission by binding reversibly within sodium channels on neuronal membranes. They produce dense sensory blockade in the region injected when infiltrated into the skin and subcutaneous tissues, or within the territory of the specific nerve when injected around a major peripheral nerve. When local anesthetics are injected along the neuraxis, they produce segmental anesthesia in a dermatomal distribution when placed in the epidural space, and profound sensory and motor block of the trunk and lower extremities when placed within the thecal sac. When large doses of local anesthetic are placed within the lumbar thecal sac or any local anesthetic is placed intrathecally at higher thoracic or cervical spinal levels, total spinal anesthesia can occur, heralded by sudden loss of consciousness, bradycardia, and hypotension.

Local anesthetics have three basic building blocks: a lipophilic aromatic end (benzene ring), a hydrophilic tertiary amine end, and an intermediate chain connecting the two ends. The chemical connection between the intermediate chain and the aromatic end allows us to classify local anesthetics as either “esters” or “amides.” Figure 4-1 illustrates these basic chemical building blocks. Amino amides are chemically more stable and have less potential for allergic reactions than the esters. The properties of amide and ester local anesthetics are compared in Table 4-1. The two most common agents used for image-guided injection are the amide local anesthetics, lidocaine and bupivacaine. Ropivacaine is another amino amide local anesthetic with a potency and duration similar to that of bupivacaine; preclinical data suggest that ropivacaine has significantly less cardiotoxicity when compared to racemic bupivacaine, but this has not translated into any measurable clinical difference in the safety of these two agents. The onset and duration of the common local anesthetics are illustrated in Figure 4-2.

The doses and expected distribution of neural blockade of local anesthetics are second nature to the anesthesiologist. Those with less experience using local anesthetics must gain some familiarity with their dosing and potential toxicities before attempting to use these drugs during image-guided injection. The typical doses of lidocaine and bupivacaine used to produce local anesthesia, peripheral nerve block, and epidural or spinal anesthesia are compared in Table 4-2.

Local anesthetics have low allergic potential. The majority of “allergic reactions” reported by patients are misinterpretations of the cause of symptoms following local anesthetic injection. A frequent scenario reported by patients as “an allergy to local anesthetic” arises from use of local anesthetics in dental practice. On close questioning, the symptoms are usually attributable to intravascular injection of local anesthetic containing epinephrine as a vasoconstrictor (e.g., racing of the heart, palpitations, even a feeling of doom). Rarely are actual allergic manifestations (e.g., urticaria, bronchospasm, anaphylaxis) part of the history.

The American Society of Regional Anesthesia and Pain Medicine published a Practice Advisory on the treatment of local anesthetic systemic toxicity in 2010 (Table 4-4). This group of experts emphasizes the need to seek additional help and institute basic life support measures immediately upon any suspicion of local anesthetic systemic toxicity. Once the ventilation with 100% oxygen has been established, immediate cessation of seizure activity with a small dose of benzodiazepine should follow. Cardiac toxicity can rapidly lead to cardiac arrest, and cardiopulmonary resuscitation (CPR) must be initiated immediately; prolonged use of CPR is both necessary and warranted, given the time needed for metabolism and elimination of these agents. In recent years, remarkable reductions in systemic toxicity have been demonstrated in experimental animals that have been given infusions of lipid emulsion following cardiac arrest induced by systemic administration of local anesthetics, a practice termed “lipid rescue”. Based on the improvement in survival demonstrated in animal studies and the lack of major adverse effects associated with intravenous administration of lipid emulsion, the use of lipid rescue has been rapidly moved to use in emergent treatment of local anesthetic toxicity (Table 4-4). Finally, a number of case reports detail successful resuscitation and full recovery when cardiopulmonary bypass is instituted soon after cardiac arrest caused by local anesthetic systemic toxicity.