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Sedation caused by clonidine in patients with spinal cord injury

2003; Elsevier BV; Volume: 90; Issue: 6 Linguagem: Inglês

10.1093/bja/aeg134

1471-6771

Jean‐Marc Malinovsky, M. Malinge, J. Lepage, M. Pinaud,

Anesthesia and Pain Management

BackgroundIn patients with spinal cord injury, cephalad spread of intrathecal (i.t.) medication could be delayed.MethodsWe used bispectral index and an observer scale to assess sedation after two different doses of i.t. clonidine in patients with or without spinal cord injury. Twelve patients with neurological deficit caused by trauma (Spinal Cord Injury, SCI) were compared with patients without neurological disease. They received 10 mg of i.t. bupivacaine with clonidine, with either 50 µg (low dose, n=6) or 150 µg (high dose, n=6) at L2–L3. A further 12 patients, six with spinal trauma lesion and six healthy, received i.t. bupivacaine and 150 µg of i.m. clonidine.ResultsSedation and a decrease in BIS occurred only in patients receiving 150 µg of clonidine. Onset of sedation and the decrease in BIS was delayed in most spinal cord injured patients whatever the route of administration (P<0.001). Duration of sedation was not different between the groups. Delayed sedation and decrease of BIS after i.t. clonidine in patients with spinal cord injury are similar than those observed after i.m. clonidine.ConclusionA systemic effect is likely to be the main reason for sedation. In patients with spinal cord injury, cephalad spread of intrathecal (i.t.) medication could be delayed. We used bispectral index and an observer scale to assess sedation after two different doses of i.t. clonidine in patients with or without spinal cord injury. Twelve patients with neurological deficit caused by trauma (Spinal Cord Injury, SCI) were compared with patients without neurological disease. They received 10 mg of i.t. bupivacaine with clonidine, with either 50 µg (low dose, n=6) or 150 µg (high dose, n=6) at L2–L3. A further 12 patients, six with spinal trauma lesion and six healthy, received i.t. bupivacaine and 150 µg of i.m. clonidine. Sedation and a decrease in BIS occurred only in patients receiving 150 µg of clonidine. Onset of sedation and the decrease in BIS was delayed in most spinal cord injured patients whatever the route of administration (P<0.001). Duration of sedation was not different between the groups. Delayed sedation and decrease of BIS after i.t. clonidine in patients with spinal cord injury are similar than those observed after i.m. clonidine. A systemic effect is likely to be the main reason for sedation.