Local anesthesia can be produced with the direct administration of any of the following agents: 1.0% lidocaine (Xylocaine, AstraZeneca Pharmaceuticals), 0.25% bupi-vacaine (Marcaine, AstraZeneca Pharmaceuticals, and Sen-sorcaine, AstraZeneca Pharmaceuticals), 0.5% ropivacaine (Naropin, AstraZeneca Pharmaceuticals), and 1.0% mepi-vacaine (Carbocaine, Sanofi-Winthrop Pharmaceuticals). The administration of these agents into the epidural space or perineural space is capable of producing adequate sensory block of the adjacent nerve roots or ganglia. With increasing drug concentrations, the onset of action shortens dramatically and the degree of motor block increases. Systemic drug absorption decreases with the coadministration of epinephrine, which also slightly prolongs the duration of action (32). On average, a total of 5-10 mL of any one of the aforementioned medications is sufficient in the adult patient population for most pain management applications (33). The operator needs to ensure that any agent administered into the epidural route has been appropriately formulated for epidural use (34).
For diagnostic and prognostic purposes, a short-acting agent such as 1.0% preservative-free lidocaine is most appropriate (33). For therapeutic purposes, longer acting regimens such as 0.25% preservative-free bupivacaine or 0.5% ropivacaine in combination with a long-acting steroid such as 80 mg of depot methylprednisolone (Depo-Medrol, Pharmacia & Upjohn) are more appropriate (33).
The frequency of administration is variable between institutions and specific patient requirements. Acute painful conditions may require daily lumbar epidural nerve blocks with both local anesthetics and steroids (35). Lumbar radiculopathy and diabetic neuropathy are examples of chronic pain syndromes treated on various schedules, from every other day, to once a week, to every few weeks, and are dictated by the results and the patient's clinical status.
Mechanism of Action Local anesthetics completely block electrical impulse conduction in excitable neural tissues such as peripheral nerves, spinal roots, and auto-nomic ganglia when applied locally in appropriate concentrations. By blocking sodium channels, electrical impulses are halted both proximally (pain) and distally (motor). The resulting effect is the particular nerve, whether it has a sensory, motor, or autonomic function, is blocked. The concomitant pain sensation, muscle contraction or autonomic effect is interrupted in the area exposed to the local anesthetic as well as the tissues innervated distal to the site of application. Unlike the effects of neurolytic agents, the impulse conduction block produced by local anesthetics is painless and completely reversible. The nerve block dissipates as the drug is released from its bonds to the sodium channel receptors (36). The unique effect of a local anesthetic block is provision of a transient neural quiescence. This transient period of relaxation is frequently sufficient to allow spontaneously discharging hyperactive neurons to decrease gradually their level of activity, and thereby produce pain relief that extends far beyond the few hours duration of the local anesthetics' pharmacologic blocking action.
The thin lipoprotein nerve membrane contains voltage-responsive ion transmitting channels that render the membrane excitable, and therefore capable of generating and
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