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Opioid-induced hyperalgesia: case report A 48-year-old man developed hyperalgesia during treatment with hydromorphone and morphine for analgesia. The man with rectal cancer presented for a laparoscopic-assisted abdominoperineal resection (APR). He had managed his pain by consuming illicit opioids including morphine, hydromorphone [hydromorph contin] and oxycodone for approximately 4 months. During current presentation, in the operation room, he received pre-induction thoracic epidural at level T8. Induction of the anaesthesia was uneventful. For the maintenance, he received ketamine (volatile anesthetic) along with thoracic epidural infusion of hydromorphone 10 µg/mL, bupivacaine 0.125% and epinephrine. Two hours later, the surgeon converted the procedure to an open technique with a mid-line laparotomy incision. He received hydromorphone 0.5mg boluses for a total dose of 4.5mg over a period of 5.5 hours. The surgical resection was successful and uneventful. His postoperative analgesia was managed by acute pain service (APS). His epidural was continued with IV patient-controlled analgesia (PCA) with solution containing hydromorphone 0.5 mg/mL and ketamine with settings of a bolus of 0.5 mg hydromorphone with a 6 minute lockout to a maximum dose of hydromorphone 5 mg/hour and ketamine. His surgeon requested strict nothing per rectum and nil per os (NPO), which limited the adjuncts available for pain control. In the morning of the postoperative day (POD) 1, he reported of pain as 9/10 on the numeric rating scale (NRS). He described pain as a a deep abdominal burning sensation. The level of sensory blockade was T6–L1 bilaterally. He had received a total of 10.5mg of hydromorphone along with ketamine as PCA solution with 18 denied attempts over the night. Further, his epidural was bolused at 5mL and the basal rate was increased to 20 mL/hour. After bolus, his NRS was 8 with some pain relief. Reassessment of the epidural block level showed no change in the coverage. A basal rate of 0.5 mg/hour of hydromorphone along with ketamine was added to his PCA and remaining PCA settings were left unchanged. In the morning of POD 2, his NRS was again 9. His epidural was changed to a more concentrated solution containing hydromorphone 10 µg/mL along bupivacaine and epinephrine. He received 5mL epidural bolus, which was maintained at 20 mL/hour. In the afternoon, his NRS was 7 with little change in PCA usage. Thereafter, he received epidural bolus of preservative-free morphine 5mg. In the morning of POD 3, his NRS was 8, indicative of small reduction of pain over the night. He started refusing to ambulate due to discomfort. The refractory pain was thought to be due to opioid-induced hyperalgesia [time to reaction onset not stated]. Hence, dexmedetomidine 1 µg/mL (off-label use) was added to the man’s epidural solution. He received 5mL epidural bolus at basal rate of 20 mL/hour. In the afternoon, his NRS was 7, following which a decrease in number of denied attempts in his PCA was observed. Between POD 4 and POD 7, a significant