bupivacaine/clonidine

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Reactions 1007 - 26 Jun 2004 S Bupivacaine/clonidine First report of spinal cord disorder: case report A 45-year-old man developed a spinal cord lesion after long- term continuous intrathecal infusion of bupivacaine and clonidine for refractory pain in his right leg. The man initially received a single intrathecal bupivacaine 2mg injection at the L3–L4 level, which significantly reduced his pain; a programmable pump was subsequently implanted to deliver a continuous intrathecal infusion of 4% bupivacaine. His bupivacaine dose was quickly increased, and maintained between 24 and 26.6 mg/day. After 13 months, clonidine 200 µg/day was added due to decreasing efficacy and episodes of orthostatic hypotension associated with the bupivacaine infusion. He received bupivacaine 20 mg/day and clonidine 200 µg/day over the next 600 days, with good pain relief. Approximately 3 years after pump implantation, the man presented with lower back pain with anterior belt-like irradiation, paraesthesia and weakness in his left leg, and urinary and faecal retention. An examination revealed gait ataxia with impaired proprioception in his left leg, abolished vibration sensation up to his left knee, and a left foot drop. Three days later he lost proprioception up to the level of Th11 bilaterally, and developed left leg hyper-reflexia, extensor left plantar reflex and bilateral hypoaesthesia of all sacral segments. A spinal MRI revealed a round 3mm cavity within the spinal cord at the level of Th9–11, and oedema extending from the level of Th5 to the conus medullaris. The intrathecal pump was stopped, with the catheter left in place, and the man was treated with oral prednisolone. Over the next 3 months his symptoms improved, but his proprioception was only partially recovered and mild gait ataxia persisted. MRIs 1 and 3 months later showed a hyper- intense posterolateral lesion at the Th10–11 level on the left side, a centromedullary lesion at Th9, and resolution of the oedema. Author comment: "Although the precise cause of the lesion remains unknown, we have considered the possibility of a direct trauma as well as a drug related neurotoxic effect. Direct injury cannot be excluded." Perren F, et al. Spinal cord lesion after long-term intrathecal clonidine and bupivacaine treatment for the management of intractable pain. Pain 109: 189-194, No. 1-2, May 2004 - Switzerland 800977374 » Editorial comment: A search of AdisBase and Medline did not reveal any previous case reports of spinal cord disorder associated with bupivacaine or clonidine. The WHO Adverse Drug Reactions database contained one report of spinal cord compression, but no reports of spinal cord injury associated with clonidine, and no reports of spinal cord compression or injury associated with bupivacaine. 1 Reactions 26 Jun 2004 No. 1007 0114-9954/10/1007-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

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Page 1: Bupivacaine/clonidine

Reactions 1007 - 26 Jun 2004

★ SBupivacaine/clonidine

First report of spinal cord disorder: case reportA 45-year-old man developed a spinal cord lesion after long-

term continuous intrathecal infusion of bupivacaine andclonidine for refractory pain in his right leg.

The man initially received a single intrathecal bupivacaine2mg injection at the L3–L4 level, which significantly reducedhis pain; a programmable pump was subsequently implantedto deliver a continuous intrathecal infusion of 4% bupivacaine.His bupivacaine dose was quickly increased, and maintainedbetween 24 and 26.6 mg/day. After 13 months, clonidine200 µg/day was added due to decreasing efficacy and episodesof orthostatic hypotension associated with the bupivacaineinfusion. He received bupivacaine 20 mg/day and clonidine200 µg/day over the next 600 days, with good pain relief.Approximately 3 years after pump implantation, the manpresented with lower back pain with anterior belt-likeirradiation, paraesthesia and weakness in his left leg, andurinary and faecal retention. An examination revealed gaitataxia with impaired proprioception in his left leg, abolishedvibration sensation up to his left knee, and a left foot drop.Three days later he lost proprioception up to the level of Th11bilaterally, and developed left leg hyper-reflexia, extensor leftplantar reflex and bilateral hypoaesthesia of all sacralsegments. A spinal MRI revealed a round 3mm cavity withinthe spinal cord at the level of Th9–11, and oedema extendingfrom the level of Th5 to the conus medullaris.

The intrathecal pump was stopped, with the catheter left inplace, and the man was treated with oral prednisolone. Overthe next 3 months his symptoms improved, but hisproprioception was only partially recovered and mild gaitataxia persisted. MRIs 1 and 3 months later showed a hyper-intense posterolateral lesion at the Th10–11 level on the leftside, a centromedullary lesion at Th9, and resolution of theoedema.

Author comment: "Although the precise cause of thelesion remains unknown, we have considered the possibilityof a direct trauma as well as a drug related neurotoxic effect.Direct injury cannot be excluded."Perren F, et al. Spinal cord lesion after long-term intrathecal clonidine andbupivacaine treatment for the management of intractable pain. Pain 109: 189-194,No. 1-2, May 2004 - Switzerland 800977374

» Editorial comment: A search of AdisBase and Medline didnot reveal any previous case reports of spinal cord disorderassociated with bupivacaine or clonidine. The WHO AdverseDrug Reactions database contained one report of spinal cordcompression, but no reports of spinal cord injury associatedwith clonidine, and no reports of spinal cord compression orinjury associated with bupivacaine.

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Reactions 26 Jun 2004 No. 10070114-9954/10/1007-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved