MON 2011 - Slide 32 - D. Schrijvers - Pain control
1. Palliative care Pain in cancer patients D. Schrijvers, MD, PhD Department Medical Oncology Ziekenhuisnetwerk Antwerpen(ZNA)-Middelheim Antwerp Belgium
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3. Prevalence Patients (%) after curative treatment Patients (%) during anticancer treatment van den Beuken-van Everdingen et al. Ann Oncol 2007 33% ( 95%CI 21 - 46%) 59% (95%CI 44-73%) % Study % Study
4. Prevalence Patients (%) with advanced, metastatic or terminal disease All disease stages (%) van den Beuken-van Everdingen et al. Ann Oncol 2007 64% (95%CI 58-69%) % Study 53% (95%CI 43-63%) % Study
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10. Classification: relation to duration Schrijvers D. Ann Oncol 2007 Type pain Acute Chronic Breakthrough Duration Short Long Short Cause Identifiable Difficult to Sometimes identify identifiable Function Protection None None Aim treatment Treatment/ Prevention Prevention/ Prevention Treatment Side effects Acceptable Not acceptable not acceptable
46. Undertreatment of cancer pain Deandrea et al. Ann Oncol 2008 Author Year N° patients % negative Pain Management Index (95% CI) Cleeland 1994 597 42 (38–46) Larue 1995 270 51 (45–57) Elliott 1997 314 16b, 41b Trowbridge 1997 320 38 (31–46), 35 (28–42) Saxena 1999 200 79 (73–85) de Wit 1999 313 49 (43–55) Mystakidou 2001 220 76 (70–82) Sabatowski 2001 905 13 (11–15) Beck 2001 426 31 (27–35) Shvartzman 2003 218 75 (69–81) Hyun 2003 508 41 (37–45) Di Maio 2004 752 82 (79–85) Russell 2006 864 7 (3–11), 9 (7–11) Enting 2007 244 65 (59–71)
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Editor's Notes
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van den Beuken-van Everdingen MH,
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Neuropathic pain arises following nerve injury or dysfunction. A: After nerve damage, transcription and axonal trafficking of sodium channels to the site of injury is increased, with concomitant attenuation of potassium channels. The altered expression of ion channels results in neurons becoming hyperexcitable and generating ectopic activity, which is thought to lead to the genesis of spontaneous and paroxysmal pain. B: At the cell body of primary afferent neurons within the dorsal root ganglia (DRG), sympathetic neuronal sprouting occurs and may account for sympathetically maintained pain. C: Peripheral nerve injury causes a multitude of changes in gene transcription and activation of various kinases and proteins, including enhanced N-methyl-D-aspartate (NMDA) receptor activity. However, nerve injury also elicits hypertrophy and activation of glial cells, including microglia within the grey matter of the spinal cord. Microglia express P2X4 purinergic receptors, allowing them to be activated by adenosine triphosphate (ATP). Following activation, microglia release various pronociceptive cytokines, such as interleukin-1 (IL-1), tumour necrosis factor alpha (TNF- ) and neurotrophins, including brain-derived neurotrophic factor, which in turn exacerbates nociceptive transmission and contributes to the sensitization and maintenance of neuropathic pain. Note: Aß = A beta neuron, A = A delta neuron, C = C nociceptor, 5HT = serotonin, KCC2 = chloride transporter, NA = noradrenaline, Nav = sodium channel, NO = nitric oxide, Kv = potassium channel, PGs = prostaglandins, PKs = protein kinases, P2X4 = purinergic receptor. 04/14/11
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