|LETTER TO EDITOR
|Year : 2015 | Volume
| Issue : 12 | Page : 822-823
Ultrasound guided brachial block in a case of brachial plexus hypertrophy
John George Karippacheril1, Shetty Nanda2
1 Department of Anaesthesiology, Universal Hospital, Abu Dhabi, United Arab Emirates
2 Department of Anaesthesiology, Corniche Hospital, Abu Dhabi, United Arab Emirates
|Date of Web Publication||11-Dec-2015|
John George Karippacheril
Department of Anaesthesiology, Universal Hospital, P. O. Box: 5056, Abu Dhabi
United Arab Emirates
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Karippacheril JG, Nanda S. Ultrasound guided brachial block in a case of brachial plexus hypertrophy. Indian J Anaesth 2015;59:822-3
A 38-year-old man with machine-related crush injury of the left hand was scheduled for emergent debridement of the injured limb. In view of his inadequate fasting and relative asymptomatic presentation, an ultrasound-guided brachial block was planned after discussion of the risks. A sonographic scout examination done at the supraclavicular level revealed hypertrophic brachial plexus bilaterally [Figure 1]. The individual trunks of the plexus were nearly equal in diameter to the size of the visualised subclavian artery in cross section, measured to be about 4.1 mm [Figure 1]. A colour Doppler interrogation did not reveal any colour flow over the area of apparent plexus hypertrophy. Due to the association of such plexus hypertrophy with demyelinating disease, the history was obtained again. The patient denied any history of weakness in the upper limbs, except for occasional tingling sensation after heavy work. He also denied any onset of muscle weakness after an episode of fever or any breathing difficulty in the past. He had no history of comorbid disease and laboratory tests were unremarkable. He had grade 5/5 power in his right upper limb with no sensory deficits or hyporeflexia in either limb. Supraclavicular brachial block was performed with 20 ml of 2% lignocaine with 1:200,000 adrenaline and 20 ml of 0.5% bupivacaine. Adequate surgical condition was achieved in approximately 30 min.
|Figure 1: Sonogram of the left (a) and right (c) brachial plexus at supraclavicular level showing hypertrophy of trunks lateral (L) to subclavian artery (SCA) in cross section. Colour Doppler of the left (b) and right (d) brachial plexus at supraclavicular level showing absent colour flow and hypertrophy of trunks lateral (L) to subclavian artery in cross section. Sonogram of the left (e) and right (f) brachial plexus at supraclavicular level showing measurements of individual trunks lateral (L) to subclavian artery in cross section|
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The rest of the anaesthetic management was uneventful. The regression of brachial block was assessed hourly. After approximately 8 h, the patient was able to lift the upper limb against gravity. He did not complain of any paraesthesias or pain. A neurology consult was obtained the following day, motor and sensory nerve conduction velocity (NCV) tests were performed in the right upper limb and both lower limbs. As the NCV test was reported normal, no further management was advised except follow-up.
Myriad conditions such as Charcot-Marie-Tooth disease formerly called hereditary motor and sensory neuropathy, chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), neoplasms and leprosy, have been reported causes for brachial plexus hypertrophy.  Its occurrence is rare and very few cases have been reported.  Repeated episodes of demyelination and remyelination produce a proliferation of multiple layers of Schwann cells around the axon, termed an onion bulb. Acquired demyelination (i.e., inflammatory demyelination) but not hereditary myelinopathies produce a conduction block, resulting in loss of the ability of the nerve action potential to reach the muscle, thereby producing weakness. Demyelination is present if motor and sensory NCVs are reduced to <70% of the lower limits of normal. In CIDP, patients typically present with proximal limb weakness for at least 2 months duration, significant hyporeflexia or areflexia, with reduced NCV and nerve biopsy features of demyelination.
Biopsy of sural nerve tissue in our case was not done (due to patient reluctance) but could have shown the confirmatory microscopic features of demyelinating disease. Magnetic resonance imaging has been suggested to obtain detailed views and three-dimensional reconstruction.  Literature is unable to definitively support or refute the use of regional anaesthesia in patients with pre-existing peripheral neuropathy. , However, in our case, history and NCV testing seems to suggest this finding of hypertrophy to be either a hereditary variant or an early stage of the disease. Focal neoplasms of the plexus may produce a similar appearance, however, in our case it was seen bilaterally. There are reports of prolonged conduction blockade with the use of local anaesthetics in demyelinating disease, postoperative monitoring in our case, however, showed a normal duration of recovery.  Although caution is advised in performing nerve block on cases detected to have brachial plexus hypertrophy, we report a case that did not have prolonged conduction block.
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