Editor—Sickle cell disease (SCD) is a common form of clinically significant haemoglobinopathy.1 Although subclinical peripheral nerve involvement may be observed in SCD,2 no peripheral neurological impairment has been reported after nerve block in patients with SCD. Only one case of peripheral neuropathy has been reported after spinal anaesthesia.3 We report a case of peripheral neuropathy after a popliteal sciatic nerve block in a patient with SCD.

A 54-yr-old woman presented for right foot surgery. Her medical history included severe SCD (haemoglobin S-C). The results of clinical preoperative neurological examination were normal and a popliteal sciatic nerve block was planned for surgery.

By mistake, a left popliteal ultrasound-guided block was performed. Ninety-five milligrams of ropivacaine with 75 µg of clonidine were injected incrementally, without report of pain or paraesthesia and no intraneural injection was detected. The patient was informed of this side error and a new block was administered on the right limb after the same protocol without any problem. Surgery was performed without tourniquet and intraoperative and immediate postoperative courses were uneventful.

On Day 1 after surgery, the patient reported persistence of sensory and motor block in the sciatic nerve area on both sides. She was discharged home at Day 4, without improvement at neurological examination. At Day 30, paraesthesia and weakness in both legs and feet persisted. At Day 40, electroneuromyography showed decreased bilateral amplitudes of potentially prolonged distal latencies, and slowing conduction velocities in the sciatic nerves at sensory and motor investigations (Fig. 1), consistent with a diagnosis of axonal loss and demyelinating neuropathy. At 10 weeks, electroneuromyography showed a significant improvement in these parameters, suggesting a diagnosis of moderate acute polyradiculoneuropathy, which was spontaneously regressive (Fig. 1). At 6 months, clinical examination showed significant improvement and 2 yr after surgery, neurological examination was almost normal.

Fig 1

Needle electromyography of the right interosseous muscle (a), and the left extensor digitorum brevis muscle at 5 (b) and 10 weeks (c). The y-axis indicates the voltage in 500 µV per division. The x-axis indicates the time in 500 ms per division.

Fig 1

Needle electromyography of the right interosseous muscle (a), and the left extensor digitorum brevis muscle at 5 (b) and 10 weeks (c). The y-axis indicates the voltage in 500 µV per division. The x-axis indicates the time in 500 ms per division.

Several mechanisms may explain the occurrence of neuropathy after single-shot peripheral nerve blocks. Intraneural injection of local anaesthetic, direct needle trauma, and tourniquet are the main factors.4,5 In our patient, bilateral intraneural injection, direct nerve injuries, or both during the procedures seem unlikely. Indeed, pre-existing subclinical polyneuropathy has been reported as playing a role in the development of postoperative nerve injury.6,7

To date, SCD has not been reported as a predisposing condition for neuropathy after peripheral nerve block. If central neuropathy is a common complication of SCD, symptomatic peripheral nerve damage is, in contrast, extremely rare. Neuropathy resulting from peripheral nerve infarction, such as complications of sickle cell vaso-occlusive crisis, seems uncommon. Recently, Okuyucu and colleagues conducted an electromyographic study in asymptomatic patients with the most severe form of SCD (SCD HbS/HbS). They found abnormalities in 19.6% of patients, with demyelination and axonopathy. It is possible that the severity of the vaso-occlusive crisis, associated with other factors such as hypoxaemia, acidosis, and dehydration, may play a role in the occurrence of peripheral neuropathy.8 In our patient, the presence of latent preoperative neuropathy related to SCD may be hypothesized. A study in a rat model demonstrated that extraneural injection of ropivacaine in the nerve area results in substantial histological evidence of nerve injury with demyelination and wallerian degeneration, with short-term regeneration.9 In our patient, injection of ropivacaine in close contact with popliteal nerves may therefore be responsible for the post-block demyelinating neuropathy.

In clinical practice, identifying undetected pre-existing subclinical neuropathy before peripheral nerve block administration in patients with SCD is mandatory. Thorough and well-documented preoperative neurological examination will help to define optimal anaesthetic protocol.

Declaration of interest

None declared.

Acknowledgement

We are grateful to Nikki Sabourin-Gibbs, Rouen University Hospital, for her help in editing the manuscript.

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