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Modern medicine can trace the use of local anesthetics back to the year 1884, when the Austrian Physician Karl Koller first used topical cocaine to assist with an ophthalmological operation.1 The following year, the premier Surgeon William Halstead first used injected cocaine to generate the intentional blockade of nerve transmission.2 Unfortunately for Halsted, his experiments with cocaine soon led to a concurrent dependency.3 The emerging illicit market for this compound soon prompted the search for a less toxic agent.3 Procaine, more commonly known by its trade name Novocain, was the first synthetic local anesthetic. It is a benzoic acid ester derivative developed by the German chemist Alfred Einhorn in 1904. Although it had less drawbacks than its cocaine predecessor, it was far from the ideal agent. Lidocaine was the first amide local anesthetic agent and was first produced in 1945. The market for more effective agents continued to blossom. Over the following decades, no less than 20 additional agents were developed for use as a local anesthetic agent, each possessing unique pharmacokinetic properties to tailor its utility to specific clinical applications. They are all synthetic derivatives of cocaine.
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Parallel to this proliferation in pharmacologic development, the clinical utilization of these agents has become widespread throughout all medical specialties. The daily practice of Emergency Medicine presents multiple scenarios that necessitate their use. The Emergency Physician must maintain a familiarity with the local anesthetic agents available and their unique characteristics, have an expertise in their delivery, be knowledgeable of the potential side effects, and know how to avoid and treat adverse reactions to ensure the safest and most optimal pain relief.
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At a cellular level, nerve cell function and signal conduction are dependent upon a resting negative intracellular electrical potential (approximately −70 mV) as compared to the surrounding extracellular environment. This polarity results from the abundance of sodium (Na+) cations found within the extracellular space. Membrane-based sodium–potassium (Na+/K+) pumps establish this sodium gradient. Adjacent voltage-gated sodium channels maintain the gradient by inhibiting the concentration mediated and electrically driven sodium influx that would invariably result. Upon the stimulation of an idle neuron, a small intracellular sodium influx ensues. This sodium influx results in a slight depolarization of the resting membrane potential. When a critical threshold of sodium influx is met, the voltage-gated sodium channels reflexively open. This results in a massive sodium ion influx and widespread membrane depolarization.4–6 Impulse transmission proceeds as this membrane depolarization is propagated down the entire length of the nerve fiber.7
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Local anesthetic agents function by reversibly binding to membrane-based sodium channels, thereby inhibiting the initial sodium influx that results upon the stimulation of an idle neuron.4–9 If a significant number of these channels are blocked, the critical threshold of sodium influx required for the voltage-gated sodium channel opening cannot be met, widespread membrane depolarization cannot occur and nerve ...