Journal: Reg Anesth Pain Med 33(5):435-441, 2008. 64 References
Reprint: Department of Anesthesiology, Medical College of Wisconsin, 8701 Watertown Plank Road, MEB, Room 462C, Milwaukee, WI 53226-0509 (QH Hogan, MD)
Faculty Disclosure: Abstracted by J. Joyce, who has nothing to disclose.
Although the great majority of peripheral nerve block anesthetics are followed by complete return to normal nerve activity, a small number result in persistent deficits of motor or sensory performance, or in the generation of pain. Local anesthetics are drugs with diverse actions, and are applied in formidable concentrations during nerve blocks. Anesthesia providers direct sharp devices into close proximity with the nerves in order to deliver these drugs, thereby risking mechanical injury.
Local anesthetics produce a variety of cytotoxic effects in cell cultures, including inhibition of cell growth, motility, and survival, and may also produce morphologic changes. The extent of these effects is proportionate to the local anesthetic solution. High concentrations of extrafascicular anesthetics produce axonal injury independent of edema formation and elevated endoneurial fluid pressure. The duration of exposure and concentration of local anesthetic determines the degree and incidence of local anesthetic-induced residual paralysis.
Injection of local anesthetic into a nerve fascicle is clearly neurotoxic. Ester local anesthetics and carbonated lidocaine produce widespread and severe damage of the nerve fibers and the blood-nerve barriers when injected within the fascicles. Together, these various observations lead to the conclusion that the surrounding perineurium plays an important role in protecting the fascicular contents from the cytotoxic effects of local anesthetics.
Interruption of the perineural tissue around the nerve fascicles breaches the blood-nerve barrier and produces edema of the nerve and herniation of the endoneural contents through the rent. A fascicular injury is more likely to result from nerve contact with a sharp beveled needle than with a blunt beveled needle, but if penetration of a fascicle is achieved, a sharp beveled needle causes greater damage. While it is clear that needle trauma can result in nerve damage, it is uncertain whether block techniques that seek to elicit mechanical contact paresthesias during block needle insertion increase the risk of lasting injury.
Failure of blood flow to the primary afferent neuron results in metabolic stress. The earliest response to the peripheral sensory neuron to ischemia is depolarization and generation of spontaneous activity, perceived by the subject as paresthesias. It is likely that the combined effects of several mechanisms increase the probability of injury. Further uncertainty in discerning the roles of these factors in any particular case is introduced by the growing recognition of genetic variability in sensitivity of subjects to pharmacologic traumatic processes. |
