Electrophysiologic testing for the diagnosis of peripheral nerve injuries.

ANESTHESIOLOGISTS have an important role in preventing perioperative nerve injury, monitoring nerve function to minimize damage, and diagnosing peripheral nerve lesions at an early stage to optimize their management. The purpose of the current article is therefore to clarify the use and limitations of electrophysiologic testing in the diagnosis and management of anesthesiarelated nerve injuries. The occurrence of perioperative nerve injuries is well described. In the American Society of Anesthesiologists Closed Claims Database (a standardized collection of case summaries from the closed malpractice claims of a number of insurance companies), 16% of the 4,183 claims have been for anesthesia-related nerve injury. Regional nerve block may lead to a focal nerve deficit. During surgery itself, direct injury or tourniquet compression to insure a bloodless field may be responsible. In rare instances, the compression is seemingly innocuous, as from a blood pressure cuff that inflates automatically at periodic intervals. Malpositioning of patients during surgery may lead to compression or entrapment neuropathies, especially in the upper limbs and involving particularly the ulnar or radial nerve; less commonly, the median, musculocutaneous, axillary, or other nerves are affected. In the legs, peroneal or sciatic neuropathy may lead to foot drop, which may mistakenly be attributed to a radiculopathy; an obturator or lateral femoral cutaneous neuropathy may also occur, sometimes in relation to a prolonged period in the lithotomy position. In other instances, the mechanism of nerve injury is not apparent, and symptoms of nerve involvement may not develop until several days after anesthesia. In such circumstances, the etiology may be multifactorial, relating, for example, to minor degrees of compression in conjunction with a preexisting subclinical lesion, metabolic derangements, or an increased susceptibility to damage, or injury may have occurred after the patient has left the operating room. Regardless of the underlying mechanism, anesthesia-related nerve injury most commonly involves the ulnar nerve (28% of nerve-injury cases in the Closed Claims Database) or brachial plexus (20%). Mechanical stretch or elongation is probably the most common cause of anesthesia-related brachial plexopathy. In all these various circumstances, electrophysiologic testing is important in defining the neurogenic basis of weakness and localizing the site of the lesion. It is also of help in determining the severity of injury and thus in guiding prognostication. Electrodiagnostic testing does not, however, indicate the etiology of the neuropathy. For example, it may confirm the presence of an ulnar neuropathy, localize the lesion to the elbow, suggest whether it is new or of long standing, and indicate its severity, but it does not indicate its cause, which must be inferred on clinical grounds. The precise mechanism of perioperative ulnar neuropathy may not be obvious, but location at the elbow provides some support for a compressive basis, perhaps related to malpositioning. With mild injuries, any clinical deficit relates primarily to a block in the conduction of nerve impulses through the affected segment of nerve (neurapraxia), with preserved conduction in neighboring segments. When the offending cause has been removed, recovery occurs over a variable time that may be as long as several weeks if the injury was severe enough to cause structural changes of the myelin sheath encasing axons. Complete recovery, however, can generally be anticipated. By contrast, severe nerve injuries lead to axonal degeneration, in which case recovery does not occur except by axonal regeneration or sprouting from surviving neighboring axons and is likely to be prolonged and incomplete. The prognosis is influenced particularly by the integrity of the supporting structures in the nerve. Axonotmesis is the term used to designate such an injury when axons are disrupted, but the epineurium (and usually the perineurium) remains intact. More severe injury, in which the epineurium is disrupted, is designated neurotmesis, and recovery does not occur without surgical repair; even then, it is usually incomplete.