Electrodiagnostic Assessment of Peri-Procedural Iatrogenic Peripheral Nerve Injuries and Rehabilitation

Abstract

Iatrogenic nerve injuries are a significant concern for medical professionals and the patients affected. Peri-procedural nerve injuries result in functional deficits associated with pain and disability. The exact pathophysiology and etiology of peri-procedural nerve injuries are complex and often elude providers. The rates of injury to specific nerves are unclear and relate to both procedural and patient specific risk factors. Initial classification of the nerve injury into neurapraxia, axonotmesis, mixed nerve injury, or possible complete transection (neurotmesis) guides rehabilitation and management. Electrodiagnostic medical consultation at least four weeks post-injury, supplemented with nerve imaging (ultrasound and magnetic resonance imaging), can allow for accurate nerve injury classification. Supplemented with nerve imaging and detailed clinical evaluation, treatment, recovery and rehabilitation can be maximized. Recognizing nerves at risk associated with medical and surgical procedures can facilitate injury avoidance and early diagnosis. If a nerve injury is incomplete, in an optimized physiologic milieu (good glucose control, smoking cessation, etc.), there is a good potential for spontaneous (total or partial) improvement over time. Surgical referral should be considered for severe nerve injuries within 6 months, especially if there is concern for neurotmesis, and/or deteriorating nerve function. This review gives guidance for approaching peri-procedural peripheral nerve injuries, including the timing and the role of electrodiagnostic medical consultation including serial electrodiagnostic studies in management and rehabilitation.

Keywords: electrodiagnosis; electromyogram; iatrogenic peripheral nerve injury; nerve rehabilitation; perioperative peripheral nerve injury.

FIGURE 1

Timeline for electrodiagnostic studies in suspected peri‐procedural iatrogenic peripheral nerve injury: An early indication of SNAP propagation failure has been described as early as 7–9 days and is considered complete by day 10 [78, 80, 81, 83, 84]. Alpha‐motor neuron axon damage results in neuromuscular junction transmission failure in 6 days and Wallerian degeneration is detectable in motor nerve axons by day 11 post‐injury [78, 80, 81, 83]. Wallerian degeneration can be observed in muscle fibers demonstrating FP immediately distal to the lesion within 7 days, mid‐distance muscle fibers after 14 days, and in all distally innervated muscle fibers by 28 days. CMAP‐compound muscle action potential; EMG‐electromyography; FP‐fibrillation potentials/positive sharp waves; MUAP‐motor unit action potential; SNAP‐sensory nerve action potential; Wallerian degeneration (WD).

FIGURE 2

Approach to peri‐procedural iatrogenic peripheral nerve injury evaluation. When a potential PPNI is identified, patients benefit from risk factor modification and early referral to EMS. When patients undergo post‐procedural therapies, determining if recovery fits the expected trajectory can be difficult. Serial clinical evaluations can assist in trajectory determination. If trajectory is unclear, EDX testing may provide useful information in medical decision‐making. It can become difficult for patients and clinicians to remain confident and persistent in their rehabilitation program while nerve regrowth slowly progresses. If recovery regresses (red flags, e.g., potential hematoma, infection, more weakness, or sensory loss), then ongoing nerve damage due to scarring or another etiology, should be seriously considered. Repeat EDX testing, namely new fibrillation potentials or smaller CMAPs and SNAPs, may suggest deterioration. Surgical evaluation can and should be considered even years after the original nerve insult for possible hardware removal, painful neuroma, or tendon transfer to improve function [78]. Repeat EDX testing can also determine nerve recovery and customize the rehabilitation program to match the recovery pattern. CMAPs‐compound muscle action potentials; EDX‐electrodiagnostic; EMS‐ electrodiagnostic medicine specialist; PNI‐peripheral nerve injury; PPNI‐peri‐procedural peripheral nerve injury; SNAPs‐sensory nerve action potentials.

FIGURE 3

Using electrodiagnosis to determine possible neurotmesis in the acute setting. This figure tries to simplify the process for determining possible neurotmesis. Trying to determine if there are viable axons across the zone of injury is often difficult. Anatomic anomalies (e.g., MGA, RCA, or accessory fibular nerve that might bypass the injury) must be considered. Technical difficulties—namely insertion of needle into unintended muscles leading to inaccurate muscle (and nerve) identification, must also be considered. For example, misinterpreting motor unit potentials as coming from the infraspinatus (suprascapular nerve) rather than teres minor (axillary nerve) may misidentify neurotmesis. Volume conducted distant motor unit potentials in a stressful and painful testing situation can be mistaken for motor unit potentials within the muscle being directly evaluated (e.g., the muscle with the electromyography needle in it). *Denotes that the presence or absence of FP can be irrelevant in this decision, but may be important for other reasons. For example, if there are FP at 0–7 days, that strongly suggests the presence of an older lesion (more than 14–28 days). EDX‐electrodiagnostic; EMG‐electromyography; FP‐ fibrillation potentials/positive sharp waves; MUAP‐motor unit action potential; MGA‐Martin‐Gruber anastomosis; NCS‐nerve conduction studies; RCA‐Riche‐Canneau anastomosis.