Regression of sensory analgesia with lumbar epidural catheters.

TO the Editor-I read with interest the study by Boylan et al.' comparing epidural bupivacaine-morphine analgesia with patient-controlled analgesia after abdominal aortic surgery. However, I have a major concern. After a loading dose of 1 0 ml of 2% lidocaine followed by 15 ml of 0.25%) bupivacaine via a lumbar epidural catheter, sensory block in the epidural group was probably at an adequate thoracic level for upper abdominal surgery. Forty-eighthour postoperative analgesia was provided by epidural infusion of morphine combined with 0.125%) bupivacaine at a mean infusion rate of 4.3 ml/h and a few 5-ml bolus injections of 0.25% bupivacaine in some patients. This dose of bupivacaine is too low to prevent regression of sensory analgesia below the level of surgery. This would have been noticed if not only visual analog pain scores but also levels of sensory analgesia had been obtained, as in any other study investigating the analgesic effects of neuraxial local anesthetics. Nonlipophilic opioids such as morphine slow the regression of sensory analgesia, as was demonstrated by Hjortscn et al.' Using a lumbar epidural catheter, they maintained a thoracic level of sensory analgesia for 16 h by adding 0.5 mg/h of morphine to 8 ml/h of 0.5% bupivacaine (nearly eight times more bupivacaine than that used by Boylan et a/. I ) .