Department of Pharmacy, Tufts Medical Center, Boston, MA, USA.
Ann Pharmacother. 2013 Jul-Aug;47(7-8):e34. doi: 10.1345/aph.1R784. Epub 2013 May 28.
To report a case of tremors and agitation associated with the administration of low doses of intravenous hydromorphone in a patient with acute kidney injury in the setting of chronic kidney disease.
A 91-year-old man was admitted for a left intertrochanteric hip fracture. On hospital days 1 and 2, the patient received hydromorphone 1 mg intravenously for pain. By hospital day 3, the patient had received a total of 3.5 mg of hydromorphone. He then became tremulous and agitated, which worsened as the dose was increased. During hospital day 4, the hydromorphone dosage was increased to 0.5 mg intravenously every 4 hours for what was perceived to be inadequate pain control, manifesting as tremors and agitation. On hospital day 5, hydromorphone, now considered a potential cause of the tremors and agitation, was discontinued. The total amount of hydromorphone administered was 8 mg over 5 days. By hospital day 6, the tremors and agitation had decreased in severity and had resolved by hospital day 7.
Previous reports suggest that hydromorphone-induced neurotoxicity is more likely to occur following high doses over extended periods, especially in patients with kidney dysfunction. There is a paucity of evidence suggesting that neurotoxicity can occur following low doses for short periods of time. Morphine-3-glucuronide has neuroexcitatory properties including myoclonus, allodynia, agitation, or tremors. Structural similarities between morphine-3-glucuronide and hydromorphone-3-glucuronide suggest that neuroexcitatory effects with hydromorphone are feasible. The Naranjo probability scale indicated that hydromorphone-induced tremors were possible. Our case is distinct because the patient received low doses of hydromorphone over a short period.
Neurotoxicity can occur in patients with kidney dysfunction while they receive low doses of intravenous hydromorphone over short periods. Diligent monitoring and reporting of such effects are necessary to better understand risk factors and a mechanism.
报告一例慢性肾脏病合并急性肾损伤患者静脉注射低剂量氢吗啡酮引起震颤和激越的病例。
一名 91 岁男性因左侧股骨转子间骨折入院。在入院第 1 天和第 2 天，患者接受氢吗啡酮 1 毫克静脉注射以缓解疼痛。入院第 3 天，患者总共接受了 3.5 毫克氢吗啡酮。此后，他出现震颤和激越，随着剂量增加而加重。入院第 4 天，氢吗啡酮剂量增加至 0.5 毫克，每 4 小时静脉注射一次，因为认为疼痛控制不足，表现为震颤和激越。入院第 5 天，由于怀疑氢吗啡酮是震颤和激越的潜在原因，停止使用该药物。在 5 天内共给予氢吗啡酮 8 毫克。入院第 6 天，震颤和激越的严重程度有所减轻，入院第 7 天已缓解。
先前的报告表明，氢吗啡酮引起的神经毒性更可能发生在高剂量长时间使用后，特别是在肾功能不全的患者中。目前的证据表明，低剂量短时间使用也可能导致神经毒性。吗啡-3-葡萄糖醛酸具有神经兴奋作用，包括肌阵挛、感觉异常、激越或震颤。吗啡-3-葡萄糖醛酸和氢吗啡酮-3-葡萄糖醛酸之间的结构相似性表明，氢吗啡酮具有神经兴奋作用是可行的。Naranjo 概率量表表明，氢吗啡酮引起的震颤是可能的。我们的病例是独特的，因为患者在短时间内接受了低剂量的氢吗啡酮。
肾功能不全患者在短时间内接受低剂量静脉注射氢吗啡酮时可能会发生神经毒性。需要仔细监测和报告此类影响，以更好地了解风险因素和发病机制。
