Introduction

Crohn’s disease (CD) and ulcerative colitis (UC) are the two premier forms of inflammatory bowel disease (IBD). In the Montreal Classification System, CD was divided into non-stricturing/non-penetrating (B1), stricturing (B2), and penetrating (B3), based on clinical behavior. Stricturing disease is believed to result from persistent inflammation. CD-related strictures often lead to significant morbidities such as bowel obstruction and the development of fistula and abscess. In contrast, UC is characterized by the extent of colonic involvement with categories including extensive colitis, left-sided colitis, and proctitis. Despite being a “mucosal disease,” long-term UC can also cause strictures due to cancer, muscularis mucosae hyperplasia, and submucosal fibrosis possibly related to inflammatory cells. The inflammatory component of stricture may respond to corticosteroids or anti-tumor necrosis factor (TNF) therapy. On the other hand, there has been a concern that rapid tissue healing from anti-TNF therapy may result in or promote the formation of stricture.

CD-associated primary strictures have traditionally been treated with surgery, with bowel resection, stricturoplasty, or bypass. However, surgical therapies for both CD and UC are often associated with subsequent strictures at anastomosis sites. A Belgium team of investigators reported that strictures occurred at the surgical anastomosis or neoterminal ileum in 46% of patients after surgical intervention for CD. In patients with UC who underwent ileal pouch-anal anastomosis (IPAA), anastomotic strictures have been reported as occurring in 10%–40% of patients. The purported causes of anastomotic strictures included surgery-related ischemia, bacterial stasis, and high pressures within the intestine. Anastomotic strictures tend to recur, even after surgical resection and reanastomosis, and stricturoplasty.

The disease process of IBD is complex, which is further complicated by the use of medications and surgery-altered anatomy, the strictures in IBD patients represent a wide spectrum of phenotypes. Diagnosis and classification are important for proper management and improvement of short and long outcomes.

Definition and Source of Stricture

Intestinal stricture is defined as abnormal narrowing of bowel lumen. The term of stricture has been used interchangeable with stenosis. A stricture can lead to a spectrum of narrowing, from subtle to complete obstruction. In patients with IBD, either CD or UC, stricture may result from disease process (ranging from inflammation and fibrosis to malignancy) in the mucosa, muscularis mucosae, submucosa, or muscularis propria, or combination ( intrinsic stricture ). Other extraintestinal disease process can also cause bowel stricture or obstruction ( extrinsic stricture ), such as abscess, adhesion, compression of benign or malignant mass.

In addition to the presence of narrowing of bowel, multiple other factors may determine whether the patient presents bowel-obstructive symptoms, including degree of stricture, general medical conditions, pain tolerance, and psychological conditioning and deconditioning. Therefore, stricture can be divided into symptomatic stricture and asymptomatic ones ( Table 8.1 ).

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Classification and Reclassification of Inflammatory Bowel Diseases: From Clinical Perspective Principles of Endoscopic Therapy in Inflammatory Bowel Diseases Endoscopic Evaluation of Surgically Altered Bowel in Patients With Inflammatory Bowel Diseases Endoscopic Management of Hepatobiliary Complications of Inflammatory Bowel Disease Fecal Microbiota Transplantation as Therapy for Inflammatory Bowel Disease Common Complications of Surgery for Crohn’s Disease and Ulcerative Colitis

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