In the acute care setting, providers of care for inflammatory bowel disease (IBD) patients are often faced with the dilemma of providing effective abdominal pain management in a population that has worse outcomes with both opioid and NSAID therapy. There is increased mortality associated with opioid use and risk of disease relapse with NSAID use in IBD patients.1,2 Due to this, patients often feel that their pain is inadequately addressed.3,4 There are multiple sources of abdominal pain in IBD, and understanding the mechanisms and presentations can help identify effective treatments. We will review pharmacologic and supportive therapies to optimize pain management in IBD.
Common pain presentations in IBD
Visceral pain is a dull, poorly localized, cramping pain from intestinal distension. It is associated with inflammation, dysmotility, obstruction, and visceral hypersensitivity. Somatic and parietal pain is sharp, intense, and often localizable. Somatic pain originates from surrounding skin or muscles, and parietal pain arises from irritation of the peritoneum.5 We will review two common pain presentations in IBD.
Case 1: Mr. A is a 32-year-old male with stricturing small bowel Crohn’s disease s/p small bowel resection, who presents to the ED with 3 days of abdominal pain, nausea, and vomiting. C-reactive protein is elevated to 6.8 mg/dL (normal 0.0 – 0.6 mg/dL), and CT is consistent with active small bowel inflammation, intraabdominal abscess at the anastomosis, and associated partial small bowel obstruction. He describes a sharp, intense abdominal pain with cramping. His exam is significant for diffuse abdominal tenderness and distension.
Case 2: Ms. B is a 28-year-old female with ulcerative colitis on mesalamine monotherapy who presents to the hospital for rectal bleeding and cramping abdominal pain. After 3 days of IV steroids her rectal bleeding has resolved, and CRP has normalized. However, she continues to have dull, cramping abdominal pain. Ibuprofen has improved this pain in the past.
Mr. A is having somatic pain from inflammation, abscess, and partial bowel obstruction. He also has visceral pain from luminal distension proximal to the obstruction. Ms. B is having visceral pain despite resolution of inflammation, which may be from postinflammatory visceral hypersensitivity.
Etiologies of pain
It’s best to group pain etiologies into inflammatory and noninflammatory causes. Inflammatory pain can be secondary to infection, such as abscess or enteric infection, active bowel inflammation, or disease complications (that is, enteric fistula). It is important to recognize that patients with active inflammation may also have noninflammatory pain. These include small bowel obstruction, strictures, adhesions, narcotic bowel syndrome, bacterial overgrowth, and visceral hypersensitivity. See figure 1.
The brain-gut connection matters
Abdominal pain in IBD patients starts from painful stimuli in the gut. In addition to direct pain pathways, multiple areas of the brain modulate perception of pain.6 Patients with psychiatric comorbidities have increased perception of abdominal pain.7 In fact, high perceived stress is associated with disease relapse.8 Treatment of psychiatric disorders improves these symptoms with lasting effects.9 Addressing psychological and psychosocial needs is essential to successful pain management with long-term effect on quality of life and pain perception in IBD patients.