A 35-year-old lady was referred by surgeons for a gastroenterology-nutrition opinion. At 18 years old, while living in social care, she had received a diagnosis of irritable bowel syndrome that had settled after self-management. In her mid-20s she had a miscarriage and developed recurrent severe abdominal pains. She attended gynaecology and was told she had “blocked tubes”, leading to a total abdominal hysterectomy and bilateral salpingo-oophrectomy. Abdominal pains had worsened post-operatively and she had undergone recurrent laparoscopic adhesiolysis. She was given increasing doses of opioids, including a fentanyl patch and lozenges for breakthrough pain. She suffered with severe constipation and bloating and eating worsened the pains. A gastrostomy feeding tube was put in, but because of the pain she was intolerant of even a small volume by drip feeding. She and the surgeons decided to request parenteral nutrition. Her body mass index was above the normal range and no clinically assisted nutrition or hydration was indicated. Cross-sectional imaging and barium follow through showed no adhesional obstruction or structural pathology. Light finger-tip brush strokes over the area of maximum pain elicited patient-reported severe pain and nausea.
Centrally mediated abdominal pain syndrome (CAPS) and narcotic bowel syndrome (NBS) are now recognised as being related to each other, but are distinct from more common disorders, such as irritable bowel syndrome (IBS) . These disorders have estimated prevalence of 0.5–2.0% that peaks in the mid-30–40s, and they are more common in women than in men.
Both conditions are thought to arise from abnormal processing of pain signals within the central nervous system and, therefore, are centrally mediated. They share some clinical features of neuropathic pain, including a combination of constant and spontaneous pain, allodynia (non-painful stimuli perceived as painful) and hyperalgesia (painful stimuli perceived as being more painful) [2,3].
Opioid-induced hyperalgesia is a counterintuitive concept whereby opioids alter pain-processing neurobiology in sensitised nerves via multiple molecular mechanisms. Pain, therefore, is enhanced. Carefully withdrawing the opioids can result in an overall reduction of the pain levels .
Dr Peter Paine is a consultant gastroenterologist and clinical lead at Salford Royal Foundation Trust. His doctoral research explored psychophysiological mechanisms in visceral and somatic pain. He runs a tertiary regional functional gut disorder clinic with a particular interest in chronic abdominal pain. He is currently the Chair of the Neurogastroenterology and Motility section of the BSG.
Keefer L, Drossman DA, Guthrie E et al. Centrally mediated disorders of gastrointestinal pain. Gastroenterology 2016;150:1408–1419.
Searle RD, Howell SJ, Bennett MI. Diagnosing postoperative neuropathic pain: a Delphi survey. Br J Anaesth 2012;109:240–244.
Kilgallon E, Vasant DH, Green D et al. Chronic continuous abdominal pain: evaluation of diagnostic features, iatrogenesis and drug treatments. Aliment Pharmacol Ther2019;49(10):1282–1292.
Szigethy E, Knisely M, Drossman D. Opioid misuse in gastroenterology and non-opioid management of abdominal pain. Nat Rev Gastroenterol Hepatol 2018;15:168–180.
Drossman DA. Functional abdominal pain syndrome. Clin Gastroenterol and Hepatol 2004;2:353–365.
Keefer L, Mandal S. The potential role of behavioral therapies in the management of centrally mediated abdominal pain. Neurogastroenterol Motil 2015;27:313–323.
Public Health England. Opioids Aware: a resource for patients and healthcare professionals to support prescribing of opioid medicines for pain. www.rcoa.ac.uk/faculty-of-pain-medicine/opioids-aware (accessed May 5, 2019).
Drossman DA, Tack J, Ford AC et al. Neuromodulators for functional gastrointestinal disorders (disorders of gut-brain interaction): a Rome Foundation Working Team report. Gastroenterology 2018;154:1140–1171.