Pain Management in Patients with IBD: Individualizing Treatment Approaches

Patients with inflammatory bowel disease (IBD) commonly suffer from debilitating abdominal pain, even in the absence of disease activity.¹ Once regarded as attributable to inflammation, new research suggests “multifactorial etiology and overlapping contributing factors” that contribute to pain perception in IBD patients.¹ Traditional analgesic and anti-inflammatory drugs are limited in their effectiveness because abdominal pain is not a monolithic entity and therefore a “one size fits all” approach will not be effective in many situations. A recent article by Srinath et al reviews the approaches to abdominal pain in IBD.

What is Pain?

Pain is a perceptual experience resulting from the subjective interpretations of signals from the body as “painful.”¹ Functional abdominal pain is different from somatization disorder. The former is a hypersensitivity disorder, while the latter is a brain disorder in which the brain misinterprets visceral signals.¹ Often there is a psychological process of expectation that adds complexity to the patient’s experience of pain.

Types of Abdominal Pain

The authors identify three types of abdominal pain:

• Visceral pain, mediated by nociceptors in the intestinal mucosal layers, is a response to stretching caused by intestinal distension and forceful muscular contractions. It is often gradual in onset, as compared to somatic pain, which is transmitted through faster myelinated fibers.¹
• Somatic-parietal pain: Somatic pain originates from the skin or muscles overlying the abdominal tract. Parietal pain originates from the outer membrane covering the peritoneum. It is intense and easier to localize than visceral pain.¹
• Referred abdominal pain is most often directly referred to the corresponding area of the abdominal wall.²

Factors that Influence Pain Perception in IBD

There are peripheral (body), central (brain), and environmental (stress) factors that can influence pain perception in IBD:

Inflammation: Certain inflammatory mediators sensitize afferent nerve endings, resulting in a lower threshold for activation, while others are involved in the induction and/or maintenance of pathological pain.^3,4 Previous inflammatory episode(s) may have lasting effects on pain signaling in the periphery and/or pain processing in the central nervous system.¹ A “robust visceral hypersensitivity” exists even in remission, suggesting neurobiological substrates of persistent pain in those with IBD.¹

Additional physiological factors include strictures and adhesions, small intestinal bacterial overgrowth, and dysmotility.¹

Psychological and neurobiological underpinnings of abdominal pain overlap.⁵ Depression and anxiety are extremely common in IBD patients (roughly 30% during remission; and during flares, 80% and 60% for anxiety and depression respectively).^5,6 These states may affect sensory processing by amplifying symptom severity.¹ Additionally, a depressive coping style and catastrophic thinking negatively affect pain perception.⁷

Psychosocial stressors, including early abuse and daily life stressors, may impact psychological function and may influence pain perception.¹

Sleep disturbances, also common in IBD, may influence pain perception. Disease activity, IBD-related medications, subclinical inflammation, and psychological dysfunction all impact sleep disturbance1

Medications used in the treatment of IBD, including aminosalicylates, thiopurines, enteral iron formulations, and (paradoxically) opioid analgesics may contribute to abdominal pain.¹

Genetic contributors are complex. Research is underway to identify genetic factors that contribute to disease susceptibility.