Allodynia in bilateral lower limbs after epidural catheter insertion.

Sir,

Neurological complications after regional anaesthesia are rare, ranging from 1:1000 to 1:100,000.[1] Allodynia is an even rarer complication of central neuraxial blockade, with only a few case reports in the literature. Here, we report a case of a patient who experienced allodynia in both the lower limbs after epidural catheter insertion.

A 23-year-old male patient with end-stage renal disease, scheduled for renal transplantation, was planned under general anaesthesia (GA) with epidural analgesia. Before proceeding for epidural catheter insertion, while infiltrating local anaesthetic (LA), 2% lignocaine with a 1.5” long 26-gauge needle in the T11-12 inter-vertebral space, the patient complained of a current-like sensation in both his lower limbs. This sensation resolved immediately upon withdrawal of the needle. Lignocaine was infiltrated after repositioning. After confirming the loss of resistance, a 20-gauge epidural catheter was inserted and fixed at 7 cm. However, administering a test dose of 3 ml of 1.5% lignocaine with 1:200,000, adrenaline led to paraesthesia in both the lower limbs. The catheter was left in situ and charged with a subarachnoid dose of morphine (200 μg). Another epidural catheter was sited in L2-L3 intervertebral space and fixed at 8 cm. It was decided to test and charge it after the surgery. Subsequent induction of GA and surgical intervention was uneventful.

After the patient was extubated at the end of the surgery, he complained of a burning sensation in both the lower limbs. The local examination was insignificant. Within 1 h, his discomfort progressed to tactile allodynia in both feet and calves, without any motor weakness. He writhed in pain even with a little tactile stimulation. As per neurological consultation, both the epidural catheters were removed to eliminate any source of neural irritation, and tablet gabapentin 300 mg loading followed by 100 mg thrice a day was started. He was already receiving steroids for immunosuppression. Since there was no motor weakness, imaging or nerve conduction study was not advised; instead hourly neurological examination was done. Over the next 3 days, allodynia transformed into paraesthesia and its intensity lessened. It persisted in the distal half of the medial aspect of calves and the dorsomedial aspect of both feet. After 2 weeks, the zone of paraesthesia had shrunk to the distal half of the dorsomedial aspect of the foot, which too eventually disappeared over the next 3 months. Gabapentin was stopped while steroids continued as a part of the immunosuppression regime.

Allodynia, or pain as a result of a stimulus that does not normally provoke pain, is a type of neuropathic pain with unknown exact aetiology.[2] It is believed to occur due to loss of inhibition over Aβ fibres.[2] Mechanical or chemical neuronal injury may cause either spontaneous firing of Aβ neurons or loss of inhibition on them at the dorsal horn which leads to exaggerated depolarisations. The latter is perceived as painful stimuli.

Ramos[3] and Morkane[4] reported a similar incidence; however, in their case, the dermatomes of allodynia corresponded well with the site of epidural insertion and injection. Choi[5] reported a case of allodynia after spinal anaesthesia. Handa[6] reported a case where pre-existing allodynia due to spinal cord injury at the C5 level improved after epidural analgesia at the L1-L2 level way beyond the intended analgesic effect spread. Similar to our case, the dermatomal spread did not match. There is evidence of upregulation of voltage-gated sodium (Na) channels (NaV1.7) in the spinal cord at the dorsal horn, which may be blocked by LAs.

Allodynia, epidural and LA share a complex, less understood relationship. We hypothesise that allodynia in our case might have occurred due to nerve root irritation. The latter could have resulted from direct needle trauma, impingement by an epidural catheter or direct LA toxicity. However, all three mechanisms seem inadequate to explain the allodynia. Direct LA toxicity is unlikely due to the dose, concentration and the site of injection of the test dose, which was the only LA given in epidural/subarachnoid space. Moreover, the dermatomal distribution of allodynia was L4-S1. The first sited catheter was at T11-12 while the second was at L2-3. These levels do not correspond with dermatomes of allodynia.

We conclude that even though rare, once this complication is encountered, irrespective of the cause, it needs to be treated aggressively with steroids, antiepileptics and antidepressants to prevent any long-term sequelae, coupled with counselling.[3]

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Conflicts of interest

There are no conflicts of interest.