Intestinal stricture, defined as abnormal narrowing of the bowel lumen, has also been termed stenosis. The common modalities for diagnosing intestinal strictures are computed tomography (CT), magnetic resonance imaging (MRI), contrasted abdominal series or enema, and endoscopy ( Fig. 5.1 ). Emerging diagnostic tools also include intestinal ultrasound (see Chapter 40 ) and endoluminal functional lumen imaging ( Fig. 5.2 ) . The definitions from endoscopists’ or radiologists’ perspectives are different. The luminal narrowing that prevents the typically nonresistant passage of an endoscope indicates a clinically significant stricture . Radiologists define stricture as a bowel segment with luminal narrowing and unequivocal dilation (≥ 3 cm) of the upstream bowel segment. The luminal narrowing is defined as a luminal diameter reduction of at least 50% compared with that of a normal adjacent bowel loop .

Common modalities for diagnosing strictures in Crohn’s disease. (A) Magnetic resonance enterography; (B) computed tomography enterography; (C) contrasted enema; (D) thin or ultrathin endoscope.

Diagnosis and measurement of stricture using an endoluminal functional lumen imaging probe. (A) A severe, fibrotic ileal pouch inlet stricture (green arrow); (B) introduction of the balloon catheter through the stricture; (C) water-filled balloon; (D) image showing the length and diameter of the stricture.

A stricture can lead to a spectrum of narrowing from subtle to complete obstruction. In patients with inflammatory bowel disease (IBD), either Crohn’s disease (CD) or ulcerative colitis (UC), intrinsic stricture may result from disease processes ranging from inflammation and fibrosis to malignancy in the mucosa, muscularis mucosae, submucosa, muscularis propria, or a combination. Extraluminal disease process can also cause bowel stricture or obstruction (extrinsic stricture), such as abscess, adhesion, and compression from the benign or malignant mass. Bowel obstruction in CD is also categorized into intraluminal (such as prolapse and inflammatory polyps), intramural, or extraluminal (such as pulling from adhesions and compression from masses or lymphadenopathy) causes [ ] ( Figs. 5.3 and 5.4 ). Small or large bowel strictures should be biopsied at the index colonoscopy and yearly endoscopy afterward to rule out malignancy ( Fig. 5.5 ).

Macroscopic features of strictures in Crohn’s disease. (A) Intraluminal—caused by large inflammatory polyps in the lumen; (B) Intramural—caused by fibrosis, muscular hyperplasia, and neuronal hyperplasia; (C) Extrinsic—luminal angulation from adhesions.

Intraluminal obstruction in Crohn’s disease by pedunculated inflammatory polyps. (A and B) Endoscopic removal of the lumen-blocking polyps with a hot snare; (C) the inflammatory polyps on computed tomography (green line area).

Malignant stricture in a patient with long-standing Crohn’s disease and history of ileocolonic resection and ileocolonic anastomosis (ICA). (A) A tight stricture at the ICA; (B) attempt to perform endoscopic stricturotomy with an insulated-tip knife; (C) endoscopic biopsy of the ICA stricture showed adenocarcinoma that was confirmed by subsequent surgical pathology of resection.

Histology photo: Courtesy HB Mabel Ko, MD, Columbia University Irving Medical Center.

In the Montreal classification system CD is divided into nonstricturing/nonpenetrating (B1), stricturing (B2), and penetrating (B3), based on clinical behavior, as shown in Chapter 4 ( Table 4.1 ) . Intrinsic stricturing disease results from persistent inflammation (B1) and fibrosis. On the contrary, stricture is a major contributing factor to the formation of fistula (B3) and abscess. Strictures often lead to significant morbidities, particularly bowel obstruction. The main treatment strategies for stricture are the early, timely, adequate control of mucosal and transmural inflammation with medical therapy and relief of obstruction with mechanical force, such as endoscopic balloon dilation (EBD), endoscopic stricturotomy (ESt), endoscopic strictureplasty, endoscopic stricturectomy, bowel resection, stricturoplasty, and fecal diversion with construction of a stoma .

The distinction between inflammatory and fibrotic strictures is important, which helps to guide the need and timing of medical, endoscopic, or surgical therapy. However, the distinction has been difficult in clinical practice, despite advances in abdominal imaging. From an endoscopy perspective, inflammatory strictures are characterized by edema, erythema, friability or contact bleeding, or ulcers on the surface of the stricture, and mucosal scars at adjacent bowel ( Fig. 5.6 ). Fibrotic strictures are featured with a hard-to-touch surface and a pink or whitish color ( Fig. 5.6 ). There are also mixed strictures ( Table 5.1 ).

Endoscopic distinction between inflammatory and fibrotic strictures. (A and B) Mild inflammatory stricture at the terminal ileum with erythema and friable overlying mucosa in a patient with Crohn’s disease; (C and D) a fibrotic, hard-to-touch stricture at the ileocecal valve (C) in a separate patient with mucosal scars in the adjacent cecum (D).

Stricture in CD represents a spectrum of clinical phenotypes, underlying disease processes, and prognosis. A classification of IBD-related stricture has been proposed ( Table 5.1 ) . In the classification system IBD-related strictures are categorized based on the source, clinical presentation, underlying disease, the presence of prior surgery, malignant potentials, degree, location, number, length, and associated disease conditions ( Figs. 5.7–5.9 ). Proper diagnosis and classification of stricture will guide monitoring of disease progression and medical, endoscopic, and surgical therapy and improve quality of life and long-term outcomes. For example, the treatment approach and outcome for the primary (or disease-related) and secondary (surgery or medicine-related) strictures are different.

Patterns of strictures in Crohn’s disease. (A) Subtle, web-like stricture in the terminal ileum; (B) web-like strictures from the use of nonsteroidal antiinflammatory drugs; (C) subtle stricture at the end-to-side ileocolonic anastomosis with a scope trauma; (D) small bowel narrowing from adhesions.

Patterns of strictures in Crohn’s disease. (A) Ulcerated colonic stricture; (B) angulated, ulcerated stricture in the terminal ileum; (C) severe, nonulcerated fibrotic stricture in the colon; (D) spindle-shaped, ulcerated stricture in the terminal ileum.

Severity or degree of strictures in Crohn’s disease. (A) Mild stricture at the terminal ileum resistant to the pediatric colonoscope; (B) moderate resistance; (C) severe-marked resistance; (D) pinhole, nontraversable to a regular endoscope.

Endoscopy plays a key role in the assessment of degree, number, length, and associated mucosal inflammation as well as delivery of therapy (such as balloon dilation and ESt) in patients with strictures ( Fig. 5.9 and 5.10 ).

Esophageal stricture from iron deficiency (Plummer–Vinson syndrome) in a patient with severe small bowel Crohn’s disease. (A and B) Web-like tight strictures undergoing endoscopic balloon dilation; (C) multiple esophageal strictures in barium esophagram.

Isolated involvement of the esophagus CD is rare. Often esophageal strictures in patients with CD result from the use of medications (such as nonsteroidal antiinflammatory drugs [NSAIDs] and potassium tablets) or metabolic complications (such as iron deficiency [ Fig. 5.4 ]). Superimposed viral, bacterial, or fungal infections in the esophagus may manifest as esophageal ulcers but rarely as strictures. Concurrent immune-mediated disorders, such as eosinophilic esophagitis ( Fig. 5.11 A and B) and pemphigus vulgaris ( Fig. 5.11 C and D), can cause multiple, recurrent esophageal strictures in patients with CD.

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