Peripheral Nerve Compression Associated with Low-Voltage Electrical Injury without Associated Significant Cutaneous Burn

Author(s): Smith MA, Muehlberger T, Dellon AL

Source: Plastic & Reconstructive Surgery 109: 137-143, 2002


Three patients with low-voltage (<1000 V) electrical burns of the extremities are presented.  Voltages varied between 110-480 V A.C.  None of the patients had pre-existing symptoms or risk factors consistent with peripheral neuropathy or nerve compression.  All three patients developed immediate and progressive neuropathy of the upper and lower extremities following electrical injury, despite little or no cutaneous morbidity.  All three patients were eventually treated with decompression of the affected nerves in the primarily injured extremity.  Two of three patients required delayed decompression of the nerves in the non-primary extremities for treatment of delayed progressive neuropathy.  All of the decompressions were performed several months after electrical injury (range 7-36 months) and were preceded by pressure threshold measurements and static two-point discrimination measurements.  These same studies were performed to monitor the recovery of the decompressed nerves and compared with patient norms for age.  Histologic epineural and synovial specimens were obtained in one patient at the time of decompression, 3 years after injury.

All patients reported subjective improvements in sensation following surgery.  However, none recovered normal pressure threshold or two-point distance sensitivity.  Thus, there are limitations of sensory testing as a determinant for nerve decompression or as a monitor of nerve recovery in these cases.  It appears that the patients’ clinical symptoms guided surgical treatment, and their subjective recovery was reportedly appropriate despite persistent objective abnormalities on nerve testing.  Histologic specimens from the one patient sampled 3 years after injury showed dense epineural fibrosis.  Importantly, the authors do an excellent job of outlining the clinical course of progressive compressive neuropathy following low-voltage electrical injury. They hypothesize three possible mechanisms of neurologic dysfunction:  delayed-reversible neuropathy as a result of perineural injury; immediate-transient neuropathy as a result of intraneural electrical conduction; and immediate-irreversible neuropathy caused by direct intraneural thermal injury. The inclusion of standard electrophysiologic data would have been interesting.  Nonetheless, this paper reminds us of the insidious nature of electrical injuries and the need for careful assessment over time to identify and treat neurologic consequences, even in the absence of visible cutaneous injuries. 


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