Improved Opioid Analgesic Effect Following Opioid Dose Reduction

Department of Anesthesiology, Pain Medicine Division, Penn State Milton S Hershey Medical Center, Penn State College of Medicine, Hershey, Pennsylvania 17033-0850, USA.
Pain Medicine (Impact Factor: 2.3). 10/2008; 9(6):724-7. DOI: 10.1111/j.1526-4637.2008.00501.x
Source: PubMed


Traditionally, opioids have been the cornerstone of therapy for patients suffering from cancer pain, regardless of the potential to develop opioid tolerance. In chronic pain patients who experience worsening pain despite increasing doses of opioids, the clinical role of opioid-induced hyperalgesia is gaining more recognition.
Presented here is the case of a 56-year-old man with recurrent squamous cell lung carcinoma and spinal metastases, suffering with intractable 8/10 pain on the visual analog scale in his chest, lower thoracic spine, and upper lumbar spine. He was admitted five times for pain control. In spite of escalating doses of oxycodone, morphine, and hydromorphone, the patient continued to experience severe pain. Also, he endured undesirable sedation, fatigue, and generalized weakness. The clinical picture suggested the possibility of opioid-induced hyperalgesia. We decreased the hydromorphone dose by 40-50% and started methadone. The patient's pain level dropped to a more acceptable 3/10. He was more alert, and his pain was tolerable until his death.
Opioid-induced hyperalgesia might be considered in a patient who has no evidence of disease progression, who is on clinically reasonable doses of opioids, and whose pain escalates as opioid doses are increased. A reduction of opioids and the addition of a low-dose N-methyl-D-aspartate receptor antagonist may provide a favorable clinical outcome in those patients who have failed to benefit from opioid rotation and other adjunctive pain treatments.

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    • "This NMDAR increase leads in turn to an upregulation of the NO synthase cascade and negative functional regulation of morphine algesia, as well as to protein kinase C-mediated phosphorylation of opioid receptors (Koppert and Schmelz, 2007; da Cunha Leal et al., 2010; Rodríguez-Muñoz et al., 2012). Increased NMDAR activation may also downregulate glutamate reuptake mechanisms, leading to central sensitization (Vorobeychik et al., 2008; da Cunha Leal et al., 2010; Lenz et al., 2011; Tompkins and Campbell, 2011; Wilson et al., 2011; Holtman and Jellish, 2012; Juba et al., 2013). Patients receiving NMDA receptor antagonists including ketamine (da Cunha Leal et al., 2010) and MgSO 4 alongside opioids have exhibited recovery of opioid analgesic effect, further substantiating these proposed mechanisms (Figure 1) (Daeninck and Bruera, 1999; Gupta et al., 2011; Colvin and Fallon, 2010; Pasero and McCaffery, 2012; Lee et al., 2013a). "
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