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Nerve injury is a potentially serious complication of peripheral nerve (PN) blocks, which can lead to permanent disability. Fortunately, many neurologic deficits are reversible. This chapter will outline mechanisms, clinical course, and treatment of patients with neurologic injury after nerve blocks.
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CLASSIFICATION AND MECHANISMS OF INJURY
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Perhaps the most practical classification of neurologic injury is that of Seddon. The classification proposes three types of PN injury, ranging from mild to severe (Figure 10-1).
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Neuropraxia: The mildest of the three types, it consists of damage to the myelin sheath. A common clinical example is transient nerve dysfunction that may occur after nerve stretching or its compression. With this injury, axons and supporting connective tissue of importance to the nerve function (i.e., endoneurium, perineurium, and epineurium) remain intact. The prognosis is favorable, with complete recovery of nerve function in a few weeks to months.
Axonotmesis: Axonal injury associated with fascicular disruption, crush, or toxic injury. Damage to the endoneurium and perineurium occurs. Recovery may be prolonged and incomplete, depending on the extent (partial or complete) of perineurium disruption.
Neurotmesis: The complete transection of the nerve. These injuries typically require surgical intervention and the prognosis is poorer.
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Most nerve injuries are mixed, with different fascicles exhibiting different degrees of injuries. Often all three different degrees of injury will be present in different fascicles.
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The mechanisms of PN block-related injury fall into one of four broad categories:
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Mechanical or traumatic injury: Includes compression, stretching, laceration, or injection injury. The leading cause of block-related nerve injury is an injection into a fascicle, causing a direct needle and injection trauma, rupture of the perineurium, and loss of the protective environment within the fascicle with consequent myelin and axonal degeneration.
Vascular injury: Damage to the nerve vasculature during nerve blocks can result in local or diffuse ischemia. It occurs when there is direct vascular injury, acute occlusion of the arteries, or hemorrhage within a nerve sheath.
Chemical injury: Results from tissue toxicity of injected solution (e.g., local anesthetic [LA], alcohol, or phenol) or its additives. The toxic solution may be injected directly into the nerve or adjacent tissues, which causes an acute inflammatory reaction or chronic fibrosis that indirectly involves the nerve.
Inflammatory injury: Nonspecific inflammatory responses targeting PNs can occur either remote from the site of the surgery or within the operative area. Distinguishing inflammation from other causes of PN injury may be difficult.
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The etiology of PN injury is difficult to discern in many instances. The injury is often multifactorial. Possible etiologies include mechanical needle-nerve trauma, intraneural hematoma, perineural and intraneural inflammation, and neurotoxicity of the injectate ...