Successful treatment of erythromelalgia with intrathecal hydromorphone and clonidine.

OBJECTIVE: The objective of this study was to determine if intractable pain from erythromelalgia could be successfully treated with intrathecal hydromorphone and clonidine. DESIGN: A single case of pain from erythromelalgia refractory to multiple treatment modalities was examined and treated. SETTING: The setting is an outpatient pain clinic at a major university teaching hospital. PATIENT: Our patient is an 82-year-old woman with hypertension and peripheral vascular disease. INTERVENTION: Intrathecal opioid and an alpha2-agonist were administered. OUTCOME MEASURES: Outcome was determined by means of patient self-report during office follow-up visits. RESULTS AND CONCLUSIONS: Administration of intrathecal opioid and an alpha2-agonist can be effective in the treatment of the pain of erythromelalgia and offers an alternative pain treatment modality for patients with unremitting pain refractory to more conservative therapy.

Neuromuscular blocking action of suxamethonium after antagonism of vecuronium by edrophonium, pyridostigmine or neostigmine.

The reported effects of edrophonium on a subsequent dose of suxamethonium are variable and the effects of pyridostigmine have not been evaluated extensively. We have studied this interaction in patients anaesthetized with propofol and sufentanil. After recovery from an initial bolus (1 mg kg-1) of suxamethonium, vecuronium was infused to produce 75% block. After 30 min, the infusion was discontinued and saline 5 ml, edrophonium 0.75 mg kg-1, pyridostigmine 0.24 mg kg-1 or neostigmine 0.05 mg kg-1 was given. Fifteen minutes later the mean durations of a second bolus of suxamethonium were: 10.5 (SD 3.9) min (saline), 10.9 (3.7) min (edrophonium), 18.7 (5.4) min (pyridostigmine) and 23.8 (7.4) min (neostigmine). Corresponding plasma cholinesterase activities (percentage of baseline) were: 91 (18), 87 (9), 21 (10) and 52 (26). When both treatment groups and individual patients were compared, the changes in duration of action did not correlate with changes in cholinesterase activity. These data suggest that other mechanisms in addition to cholinesterase inhibition may contribute to this drug interaction.