Nerve injury following peripheral nerve blockade (PNB) is a potentially devastating complication that can result in permanent disability.1 Data from a recent review of published studies suggest that the incidence of neurologic symptoms following PNB varies depending on the anatomic location, ranging from 0.03% for supraclavicular blocks to 0.3% for femoral blocks to up to 3% for interscalene blocks.2 Fortunately, the vast majority of these neuropathies appear to be temporary rather than permanent neuropathy and resolve over weeks to months.
The exact etiology of neurologic injury related to PNB remains unclear in many instances. Suggested etiologies include mechanical trauma from the needle, nerve edema and/or hematoma, pressure effects of the local anesthetic injectate, and neurotoxicity of the injected solutions (both local anesthetics and adjuvants, e.g., epinephrine).3 Confounding factors that may play a role in nerve injury include preexisting neuropathies (e.g., diabetes mellitus), surgical manipulation, prolonged tourniquet pressure, or compression from postoperative casting.4
It is well-established that direct injection into peripheral nerves (i.e., accidentally during intramuscular administration) can result in nerve injury.5 This is one of the reasons why intraneural injections are avoided during peripheral nerve blockade. More recent data however, suggest that intraneural injections are not always associated with nerve injury. This chapter summarizes the clinically relevant considerations regarding the etiology of nerve injury during peripheral nerve blockade.
Knowledge of the functional histology of nerves is essential to understanding the consequences of intraneural injection. Nerves are made up of fascicles supported and enveloped by perineurium and a loose collection of collagen fibers termed the epineurium. The epineurium is easy permeable and carries the nutritive vessels of larger nerves. Each fascicle is made up of bundles of nerve fibers (axons) and their associated Schwann cells held together by a tough squamous epithelial sheath called the perineurium, which acts as a semipermeable barrier to local anesthetics. The nerve fibers are supported within the perineurium by a delicate connective tissue matrix called the endoneurium, which contains capillaries that arise from the larger epineurial vessels. Figure 10-1 features normal anatomy of a mixed peripheral nerve and relationship of the epineurium and perineurium.
Anatomy of the peripheral nerve as seen on an electron microscopy image. 1-Epineurium, 2-Fascicle, 3-Fascicular bundles (several fascicles bound together), Arrows-perineurium.
Peripheral nerve lesions can be classified in terms of their degree of functional disruption.6Neurapraxia refers to a mild insult in which the axons and connective tissue structures supporting them remain intact. This type of injury is often associated with focal demyelination and generally reversible over the course of weeks to several months. Axonal interruption with conservation of the neural connective tissues is termed axonotmesis. Regeneration at a rate of 1 to 2 mm/day occurs, and recovery is generally favorable although not always complete. Neurotmesis represents complete fascicular interruption, including the ...