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• W2024074967 abstract "Pain is the most devastating complication that occurs in cancer patients. Over 90% of patients in the advanced stage of their disease report uncontrolled pain.1Fine P.G. The evolving and important role of anesthesiology in palliative care.Anesth Analg. 2005; 100: 183-188Crossref PubMed Scopus (50) Google Scholar Cancer pain may be managed by following the World Health Organization “analgesic ladder” approach, which, when followed, can provide adequate pain relief in greater than 80% of the cases.2Mercadante S. Fulfaro F. World Health Organization guidelines for cancer pain: a reappraisal.Ann Oncol. 2005; 16: iv132-iv135PubMed Scopus (92) Google Scholar The incidence of intractable cancer pain that cannot be controlled by traditional methods is estimated to be around 2% in those with advanced disease.3Zech D.F.J. Grond S. Lynch J. Hertel D. Lehmann K.A. Validation of World Health Organization guidelines for cancer pain relief: a 10-years prospective study.Pain. 1995; 63: 65-76Abstract Full Text PDF PubMed Scopus (894) Google Scholar Inadequate pain control could be due to opioid tolerance, dose-limiting side effects, and progression of disease.4Mercadante S. Portenoy R. Opioid poorly-responsive cancer pain. Part 1: clinical considerations.J Pain Symptom Manage. 2001; 21: 144-149Abstract Full Text Full Text PDF PubMed Scopus (117) Google Scholar Several studies in recent years have demonstrated ketamine as a coanalgesic for intractable cancer pain. Subanesthetic doses of ketamine have been shown to be effective as an adjuvant analgesic in decreasing opioid requirements.5Mercadante S. Arcuri E. Terelli W. Casuccio A. Analgesic effect of intravenous ketamine in cancer patients on morphine therapy: a randomized, controlled, double-blind, crossover, double-dose study.J Pain Symptom Manage. 2000; 20: 246-252Abstract Full Text Full Text PDF PubMed Scopus (212) Google Scholar An advantage of using a subanesthetic dose of ketamine is the lower risk of side effects, including delirium, hallucinations, nightmares, and dysphoria. We report a case in which an intravenous ketamine infusion was used successfully to obtain adequate pain relief in an outpatient with intractable cancer pain. The patient was a 31-year-old, 55 kg female with a medical history of adenocarcinoma of the colon. At age 28, she underwent colon resection and several courses of chemotherapy. Two years later, she underwent exploratory laparotomy with sigmoid resection and bilateral salpingo-oophorectomy secondary to metastasis. She was admitted for pain management due to extensive metastases to the liver, pelvis, lungs, and bone. Despite escalating doses of intravenous opioids, her pain remained 10/10 on the visual analog scale (VAS). Two weeks prior to her last admission to our hospital, she sustained a fracture to her left mid-femoral diaphysis and underwent placement of an intramedullary rod. She complained of pain in the left hip with left sciatic pain distribution, as well as pain over the quadriceps femoris. A consultation was requested from the Chronic Pain Service for management of pain and reduction of sedation to allow discharge to home. After admission, the patient was treated with morphine patient-controlled analgesia (PCA) infusion therapy (basal 0.36 mg/kg/h, 10 mg every 5 min bolus, maximum 12 doses per hour), extended-release oxycodone 240 mg twice daily, and gabapentin 300 mg four times daily. Rapid titration of morphine to 0.91 mg/kg/h failed to provide adequate relief and resulted in excessive sedation. Neuraxial analgesia was contraindicated secondary to the anticoagulant therapy for her cancer-associated hypercoagulable state. An intravenous infusion of ketamine was initiated after the patient was transferred to the intensive care unit. Ketamine infusion was started at 0.2 mg/kg/h and slowly titrated to 0.3–0.4 mg/kg/h over the next 4 hours in conjunction with the morphine PCA (basal 0.36 mg/kg/h, 10 mg every 5 min bolus). In the next couple of days, ketamine was further increased to 0.6 mg/kg/h and the morphine basal infusion was decreased to 0.2 mg/kg/h to obtain a VAS of 2/10 before hospital discharge. Other pain medications to be continued at home included extended-release oxycodone 80 mg three times daily, hydromorphone 8 mg twice daily, and gabapentin 300 mg four times daily. Our goal was to titrate the morphine dose down while concurrently increasing the ketamine dose. The infusion rates for ketamine and morphine were adjusted based on daily clinical assessment for pain and side effects by a visiting nurse and consultation with the Chronic Pain Management Service. Fig. 1 shows a decreasing morphine infusion rate as the ketamine dosage was increased in an outpatient setting beginning on Day 4. Throughout the month-long infusion, the patient denied any side effects (hallucinations, evoked nystagmus, vertigo, dizziness, speech difficulties, and altered mental status) that could be induced by ketamine administration. Within 8 days of the start of ketamine infusion, we were able to decrease the morphine by half while keeping ketamine at 0.62 mg/kg/h. During the next 21 days, morphine was kept at approximately 0.09 mg/kg/h as ketamine was titrated down from a maximum of 0.65 mg/kg/h. As the patient's pain was getting under control with ketamine and morphine, she received another round of chemotherapy with mitomycin and 5FU/leucovorin on Days 20 and 23. Intravenous access became a concern due to the need for continuous infusion of chemotherapy. It was decided to stop the ketamine infusion in the hope that the N-methyl-D-aspartate (NMDA) receptors had been reset to allow the antinocioceptive effects to persist. On Day 27, ketamine was eventually titrated off for 5 days, with a constant basal morphine infusion of 0.09 mg/kg/h. The patient experienced excruciating pain secondary to tumor progression on Day 32, requiring rapid escalation of the morphine basal infusion to 21.8 mg/kg/h (not shown in Fig. 1). Chemotherapy was discontinued and palliative care reinstituted, with ketamine infusion restarted at 0.29 mg/kg/h. The patient expired on Day 33. Ketamine is commercially available as a racemic mixture of R(−) and S(+) enantiomers. It has a relatively short half-life. The alpha-elimination phase lasts a few minutes and its beta-elimination half-life is 2–3 hours. It is metabolized by the hepatic cytochrome p450 system. Ketamine interacts with numerous receptors, including NMDA and nonNMDA glutamate receptors, nicotinic and muscarinic cholinergic receptors, and monoaminergic and opioid receptors.6Kohrs R. Durieux M. Ketamine: teaching an old drug new tricks.Anesth Analg. 1998; 87: 1186-1193PubMed Google Scholar Ketamine is a noncompetitive NMDA receptor antagonist that can inhibit the “wind up” phenomenon in spinal cord neurons.7Woolf C.J. Thompson S.W. The induction and maintenance of central sensitization is dependent on N-methyl-D-aspartic acid receptor activation: implications for the treatment of post-injury pain hypersensitivity states.Pain. 1991; 44: 293-299Abstract Full Text PDF PubMed Scopus (1664) Google Scholar It is this antagonistic effect that accounts for most of the analgesic, amnestic, pyschotomimetic, and neuroprotective effects.9Houghton A.K. Parsons C.G. Headley P.M. Mrz 2/579, a fast kinetic NMDA channel blocker, reduces the development of morphine tolerance in awake rats.Pain. 2001; 91: 201-207Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar Woolf and Mannion (1999)8Woolf C.J. Mannion R.J. Neuropathic pain: aetiology, symptoms, mechanisms, and management.Lancet. 1999; 353: 1959-1964Abstract Full Text Full Text PDF PubMed Scopus (1770) Google Scholar demonstrated that blocking central sensitization with NMDA antagonists can abolish pain hypersensitivity in patients with neuropathic pain. Our patient received a ketamine infusion varying between 0.09 mg/kg/h to 0.65 mg/kg/h. The subanesthetic ketamine doses were effective in controlling pain without inducing significant side effects. The possible side effects of ketamine include somnolence, vertigo, hallucinations, increased salivation, evoked nystagmus, and altered mental status. Satisfactory analgesia was achieved without exceeding 0.65 mg/kg/h ketamine. Progressive reduction in morphine dose was not associated with opioid withdrawal. Eventually ketamine was titrated off on Day 27, which was the 10th day on a constant morphine PCA rate of 0.09 mg/kg/h. The discontinuation of ketamine was short-lived, lasting only 5 days before it was restarted at 0.29 mg/kg/h on Day 32 when the basal morphine PCA infusion reached 21.8 mg/kg/h. The increased pain one day prior to her death may have been related to tumor progression or to the possibility that ketamine had an additive or a synergistic effect on morphine. As shown in Fig. 1, morphine had to be increased from 0.09 mg/kg/h to 0.18 mg/kg/h, then to 0.36 mg/kg/h when ketamine was terminated on Days 26 through 31. Animal studies have shown that the concomitant administration of an NMDA antagonist and an opioid may result in a synergistic or additive analgesic effect.9Houghton A.K. Parsons C.G. Headley P.M. Mrz 2/579, a fast kinetic NMDA channel blocker, reduces the development of morphine tolerance in awake rats.Pain. 2001; 91: 201-207Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar With the use of ketamine <0.65 mg/kg/h, morphine was decreased by fourfold. We believe this decrease was attributed to the reduction in opioid tolerance. A study by Tiseo and Inturrisi10Tiseo P.J. Inturrisi C.E. Attenuation and reversal of morphine tolerance by the competitive N-methyl-D-aspartate receptor antagonist, LY274614.J Pharmacol Exp Ther. 1993; 264: 1090-1096PubMed Google Scholar demonstrated that mu opioid tolerance is mediated by NMDA receptors and the nitric oxide system. The NMDA receptor also plays a role in chronic pain development via central sensitization. A persistent noxious stimulus to the dorsal horn can lead to activation of NMDA receptors as well as activation of wide dynamic range neurons, resulting in the expansion of receptive fields and an increase in the magnitude and duration of response.11Woolf C.J. Chong M.S. Pre-emptive analgesia treating postoperative pain by preventing the establishment of central sensitization.Anesth Analg. 1993; 77: 362-379Crossref PubMed Scopus (1382) Google Scholar Lossignol et al.12Lossignol D.A. Obiols-Portis M. Body J.J. Successful use of ketamine for intractable cancer pain.Support Care Cancer. 2005; 13: 188-193Crossref PubMed Scopus (47) Google Scholar reported the successful use of ketamine in the treatment of intractable cancer pain, but their patient required escalating doses of morphine despite the coadministration of ketamine. Walker et al.13Walker S.M. Cousins M.J. Reduction in hyperalgesia and intrathecal morphine requirements by low-dose ketamine infusion.J Pain Symptom Manage. 1997; 14: 129-132Abstract Full Text PDF PubMed Scopus (16) Google Scholar reported a case in which a continuous low dose intravenous ketamine infusion was successful in producing a rapid reduction in intrathecal morphine dosage and hyperalgesia. We report a case of successful use of ketamine infusion for the treatment of intractable cancer pain in an outpatient for greater than 30 days. Our patient was able to spend quality time with her son, husband, and other family members without sedation and other side effects, which limited opioid dosage, and remain in the comfort of her home. A reliable visiting nurse service, with the involvement of a chronic pain specialist, was critical in the success of this treatment option for our patient, who did not wish to be placed in a hospice. She underwent chemotherapy on Days 20 and 23, as her pain was getting under control with ketamine, in the hope for a chance of longer survival. In conclusion, patients with intractable cancer pain may benefit from the use of intravenous ketamine infusion to obtain adequate pain relief. Our patient was effectively managed as an outpatient with both ketamine and morphine via continuous infusion. This technique of outpatient infusion therapy hopefully will allow palliative treatment of the dying in the dignity of the home." @default.
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