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• W2134572471 abstract "To the Editor: The pain of chronic pancreatitis (CP) is often severe and difficult to manage. Treatment options, including surgery, neural blocks and opioid drugs, have mixed results. Part of the difficulty in management is that the pathogenesis of the condition is not fully understood.1.AGA Technical Review: Treatment of pain in chronic pancreatitis.Gastroenterology. 1998; 115: 765-776Abstract Full Text Full Text PDF PubMed Scopus (270) Google Scholar There is established evidence that chronic pain perception is mediated via the N-methyl-D-aspartate (NMDA) receptor. Activation of this receptor leads to the phenomenon of “wind up” and central sensitization. Ketamine hydrochloride acts as a non-competitive antagonist at the NMDA receptor and has been demonstrated to be beneficial in chronic pain states, including chronic neuropathic and nociceptive pain.2.Eide P.K. Stubhaug A. Brevik H. Oye I. Ketamine: relief from chronic pain through the actions at the NMDA receptor.Pain. 1997; 72: 289-291PubMed Google Scholar, 3.Clark J.L. Kalan G.E. Effective treatment of severe cancer pain of the head using low-dose ketamine in an opioid-tolerant patient.J Pain Symptom Manage. 1995; 10: 310-314Abstract Full Text PDF PubMed Scopus (87) Google Scholar We describe a successful case of ketamine therapy in the pain management of a patient who presented with intractable pain secondary to chronic pancreatitis (CP). We have been unable to find any previous reports of ketamine use for this condition. A 65-year-old man was admitted with severe pain secondary to alcoholic CP. He had been diagnosed nine months prior. His pain was progressive with minimal relief from increasing opioid medication. There was no surgically amenable pathology and celiac plexus neuroablation was deferred due to difficulties with anticoagulation (the patient was receiving warfarin following aortic valve replacement five years previously). On admission, he described his pain as severe. His pain score was 4/4 using a verbal numeric scale. Pain was constant in the epigastric region, with radiation through to his back. He also described “darting” or “stabbing” sensations superimposed on this background pain. Prior to transfer to our unit, he had received morphine 20 mg intramuscularly. Regular analgesic requirements were controlled-release oral morphine 80 mg twice daily, naproxen 500 mg twice daily, and acetaminophen (paracetamol) 1g four times daily, which were continued as background analgesia. Other symptoms included disturbed sleep despite hypnotics, depressed mood, anorexia, constipation, and inability to care for himself independently. Ketamine hydrochloride (Ketalar, Parke-Davis, Hampshire, UK) 100 mg over 24 hours via continuous subcutaneous (SC) infusion was commenced. The following day, his pain score was 1/4 and he had slept well for the first time in nine months. Mood and appetite had improved. His ketamine infusion was increased initially every 48 hours due to continuing pain. Pain scores ranged from 1 to 4/4 in the first twelve days, with average scores of 2. However, he was sleeping well and began to shave and dress himself. Increasing the dose of ketamine to 0.3 mg/kg/hr on day 13 resulted in much reduced pain scores and rescue analgesic requirements. Pain scores ranged from 0 to 2 (average 0.5) and he was pain free for the majority of the time. Average daily rescue morphine requirements were 10.8 mg for the first 12 days and 3.3 mg for the last 12 days. Ketamine infusion was well tolerated; the only adverse effect was inflammation at the site of infusion, which necessitated regular re-siting of the butterfly needle. Due to the improvements in symptoms, arrangements were made for his discharge home. Unfortunately, on Day 25 of his care he developed a fatal Pseudomonas pneumonia. Management of chronic pancreatic pain is difficult due to the range of pathology (alcohol, tumors, hypercalcemia, hyperlipidemia), and also because its pathogenesis is not fully understood.1.AGA Technical Review: Treatment of pain in chronic pancreatitis.Gastroenterology. 1998; 115: 765-776Abstract Full Text Full Text PDF PubMed Scopus (270) Google Scholar Various mechanisms, such as ischemia, necrosis, perineural infiltration, ductal distension and pseudocyst formation, have been postulated but the condition may be multifactorial.4.Pitchumoni C.S. Chronic pancreatitis: pathogenesis and management of pain.J Clin Gastroenterol. 1998; 27: 101-107Crossref PubMed Scopus (35) Google Scholar Recent guidelines for the management of pain secondary to CP may help but stress that there is no established standard of care.5.American Gastroenterological Association Medical Position Statement: Treatment of pain in chronic pancreatitis.Gastroenterol. 1998; 115: 763-764Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar Surgery is reserved for macropathology or for denervation procedures but has a success rate of only 68%.6.McHale A. Buechter K.J. Cohn Jr., I. O'Leary J.P. Surgical management of chronic pain from chronic pancreatitis.Am Surg. 1997; 63: 1119-1123PubMed Google Scholar Celiac plexus neuroablation is disappointing and the long-term use of opioids raises concerns about adverse consequences.1.AGA Technical Review: Treatment of pain in chronic pancreatitis.Gastroenterology. 1998; 115: 765-776Abstract Full Text Full Text PDF PubMed Scopus (270) Google Scholar Ketamine, which has been shown to block activation of the NMDA receptor experimentally, can produce clinical benefit.2.Eide P.K. Stubhaug A. Brevik H. Oye I. Ketamine: relief from chronic pain through the actions at the NMDA receptor.Pain. 1997; 72: 289-291PubMed Google Scholar Successful use of ketamine has been reported in chronic pain states, such as postherpetic neuralgia, phantom pain,7.Reich D.L. Silvay G. Ketamine: an update on the first twenty- five years of clinical experience.Can J Anaesth. 1989; 36: 186-197Crossref PubMed Scopus (574) Google Scholar and cancer pain.8.Mercadante S. Lodi F. Sapio M. Calligara M. Serretta R. Long-term ketamine subcutaneous continous infusion in neuropathic cancer pain.J Pain Symptom Manage. 1995; 10: 564-568Abstract Full Text PDF PubMed Scopus (98) Google Scholar Our patient exhibited elements of both nociceptive and neuropathic pain. Ketamine may be given intravenously, intramuscularly, orally and intrathecally but is usually given SC for ease of administration.7.Reich D.L. Silvay G. Ketamine: an update on the first twenty- five years of clinical experience.Can J Anaesth. 1989; 36: 186-197Crossref PubMed Scopus (574) Google Scholar Doses for SC infusion are empirical and range from 0.2 mg/kg/hr to 1.5 mg/kg/hr.8.Mercadante S. Lodi F. Sapio M. Calligara M. Serretta R. Long-term ketamine subcutaneous continous infusion in neuropathic cancer pain.J Pain Symptom Manage. 1995; 10: 564-568Abstract Full Text PDF PubMed Scopus (98) Google Scholar In our patient, the initial dose was 0.08 mg/kg/hr and may explain the delay in full pain control. Increasing the dose to 0.3 mg/kg/hr achieved complete pain relief. Ketamine may cause adverse effects, most notably psychotomimetic disturbances but also nausea, dizziness, fatigue, and inflammation at infusion sites.7.Reich D.L. Silvay G. Ketamine: an update on the first twenty- five years of clinical experience.Can J Anaesth. 1989; 36: 186-197Crossref PubMed Scopus (574) Google Scholar Our patient only experienced site inflammation. In conclusion, we found ketamine offered an effective and well-tolerated means of pain control in severe pain secondary to chronic pancreatitis." @default.
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• W2134572471 title "Ketamine in the management of chronic pancreatic pain" @default.
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