KEY WORDS
Brachial plexopathy - brachial plexus injury - electrical injury
INTRODUCTION
Electrical injuries account for approximately 3% of burn injuries.[1] Various neurological syndromes have been described after electrical injuries.[2] The brain, spinal cord and nerves may be involved.[3] Involvement of peripheral nerves is well recognised in the form of multiple mononeuropathies
which are transient and reversible in most cases.[4] However, brachial plexopathy due to electrical injury is rare.[5]
CASE REPORT
A 17-year-old male sustained high-voltage electrical injury to his left forearm due
to contact with a live wire hanging from a generator van. He also sustained a laceration
over the site of contact of the wire while untangling the wire. He gave no history
of head injury or fall. No entry or exit wound was found. On exploration of the forearm
laceration, soft tissue structures were normal. A distal third minimally displaced
radius fracture was noted and fixed by percutaneous nailing. No other proximal fractures
were found. The patient complained of loss of shoulder abduction, elbow flexion and
extension and inability to extend his wrist and use his fingers, suggestive of a brachial
plexopathy. Conservative management with rest to the affected shoulder and arm was
instituted and patient followed up at 1 month. No corticosteroids were given. Physiotherapy
was initiated and an electromyography was done which was suggestive of axonal degeneration
involving median, axillary, musculocutaneous and radial nerves. Serial electromyography
was performed at 8 weeks which reported no axonal regeneration. However, the patient
had started regaining partial shoulder abduction, ulnar deviation of wrist and finger
flexion at approximately 4 months after injury. He was posted for brachial plexus
exploration at 6 months as his elbow flexion did not recover. On exploration, there
was extensive damage with multiple thickened lobulations to long sections of median,
musculocutaneous and radial nerves extending from their origins at the cords up to
mid arm [Figure 1]. Rest of the plexus exploration was unremarkable [Figure 2]. No perineural fibrosis was noted. The surrounding tissue was surprisingly well
preserved. Histopathology of the affected nerve segments showed fibrous tissue.
Figure 1: Intra-operative findings on exploration. Thickened lateral and posterior cords
Figure 2: Intact normal C7 seen intraoperatively
Long Sural nerve cable grafts were harvested. A single 13 cm long nerve graft was
placed between anterior division of C7 root and radial nerve at the cranial end of
sternal head of pectoralis major [Figure 3]. Lateral cord to musculocutaneous and median nerve reconstruction was performed
using 12 and 26 cm single long nerve grafts, respectively [Figure 4].
Figure 3: C7 to Radial nerve reconstructed with 13 cm long cable graft
Figure 4: Long nerve grafts from lateral cord to musculocutaneous and median nerves
After post-operative immobilisation for 4 weeks, gradual physiotherapy was initiated.
The patient was followed up with clinical examination regularly. At 8 months after
surgery, the patient has MRC grade 3+ elbow flexion and 2+ elbow extension and 3+
ulnar finger flexion with almost no recovery of median supplied muscles. At 1-year
follow-up, there is MRC grade 3+ power in pronator of the wrist and MRC grade 3 power
of the finger flexors except the index finger. Extension at wrist and fingers is absent
for which wrist fusion and tendon transfer are planned.
DISCUSSION
Electric current can damage nerve tissue by direct effect or Joule heating. Joule
heating causes protein denaturation leading to burns.[6]
[7] However, no cutaneous burns were noted in this case. Direct effect of current is
more complex and leads to disruption of the lipid bilayer of cell membrane which is
electric field driven, leading to loss of integrity of cell membrane and hence cellular
lysis.[8] Nervous tissue has lower resistance to electricity compared to other tissues. This
explains the high incidence of neurological findings in electric injuries.[9] Direct current in addition to causing myelin degeneration also causes microvascular
damage and thrombosis to vasa nervosa, resulting in intraneural fibrosis as seen in
our case.[10] The most common neurological feature following high-voltage electric trauma is unconsciousness
which is seen in 21%–67% of patients. Peripheral neuropathies are also common, seen
in approximately 17% of patients.
However, brachial plexopathy is extremely rare, reported in less than a handful of
cases.[5] Recovery of neurological deficits is reversible in most cases, rarely progressive
and permanent. Recovery is hypothesised to occur by a process of lateral collateralisation.
However, in our case, although complete recovery occurred in the ulnar nerve and axillary
nerve; no recovery was noted in the musculocutaneous, median and radial nerves;, Hence
surgical intervention was warranted. Another interesting point is that despite usage
of long nerve grafts in excess of 10 cm for intraplexal reconstruction, we achieved
reasonably good function of musculocutaneous and radial nerves. Contrary to all, evidence
including patient's deposition regarding his modality of injury the possibility of
a strong mechanical force causing infraclavicular brachial plexus injury and fracture
of the radius cannot be ruled out.
CONCLUSION
High-voltage electrical injury can have a wide variety of early and late neurological
presentations including brachial plexus palsy rarely. In our case which presented
with a global palsy initially, partial recovery was seen within 3 months as described
in literature; however, part of the deficit remained and required surgical intervention.
Long nerve grafts used for reconstruction of damaged brachial plexus can give reasonable
results.
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