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Inflammatory bowel disease–like conditions: ischemic bowel diseases and vasculitides


Abbreviations

ANCA

antineutrophil cytoplasmic antibody

BD

Behçet disease

CD

Crohn’s disease CT computed tomography

EGPA

eosinophilic granulomatosis with polyangiitis

IBD

inflammatory bowel disease

GI

gastrointestinal Ig immunoglobulin

PAN

polyarteritis nodosa

SLE

systemic lupus erythematosus

UC

ulcerative colitis

Introduction

Diagnosis and differential diagnosis of inflammatory bowel disease (IBD) are important for the management and prognosis. Among mimics of IBD a group of diseases with underlying ischemia, vasculitis, or vasculopathy share similar clinical presentations and abdominal imaging with that of IBD. Treatment strategies of ischemic bowel disease are different from that of IBD. Even the management plan of immune-mediated vasculitis is not necessarily the same to that for Crohn’s disease (CD) or ulcerative colitis (UC). Underlying disease processes in ischemic bowel disease and systemic vasculitides, such as tissue ischemia, tissue hypoxia, hypercoagulability, and vascular inflammation, may also contribute to the etiopathogenesis and disease exacerbation or progression of IBD . On the other hand, granulomatous inflammation may be present in vasculitis-associated gastrointestinal (GI) disorders, such as Behçet disease (BD) . Patients with IBD carry a high risk for concurrent vasculitis . It is speculated that these immune-mediated GI diseases may represent phenotypes of a wide spectrum of IBD ( Chapter 1 : Introduction and classification of inflammatory bowel diseases).

Endoscopic evaluation with tissue biopsy plays a key role in the diagnosis and differential diagnosis. A combined assessment of clinical, endoscopic, histologic, serological, and radiographic features is needed. Endoscopic evaluation should include documentation of disease distribution and severity and features of inflammation and ulcerations. It should be pointed out that endoscopy should be performed with caution, due to the increased risk for perforation, in a patient with suspected GI involvement from an acute flare of ischemic colitis or vasculitis ( Chapter 2 : Setup and principle of endoscopy in inflammatory bowel disease).

Ischemic bowel diseases

Intestinal ischemia can result from acute arterial embolic or thrombotic occlusion, venous thrombosis, or hypoperfusion of the mesenteric vasculature. Colonic ischemia is the most common form.

Colonic ischemia

The etiology of colonic ischemia includes nonocclusive colonic ischemia, embolic and thrombotic arterial occlusion, and Mesenteric vein thrombosis. It can present with acute or chronic forms. Nonocclusive colonic ischemia predominantly affects watershed areas, such as the splenic flexure and rectosigmoid junction. Segmental distribution is one of the hallmarks of colonic ischemia. Colonic ischemia can present with acute or chronic forms. Endoscopic features of acute colonic ischemia are edematous, erythema, friable mucosa, spontaneous bleeding, erosions, ulcers, and in severe cases, necrosis and perforation ( Figs. 28.1–28.4 ). Patients with colonic ischemia may have mucosal scars, mucosal bridges, pseudopolyps, and ulcerated or nonulcerated strictures on endoscopy ( Figs. 28.5 and 28.6 ). These endoscopic features overlap with some of CD and UC.

Figure 28.1, Acute ischemic colitis with edema and erythema. (A) Diffuse severe edema of the transverse colon, (B) mucosal edema and patchy erythema, and (C) thumb printing of the ascending and transverse colon and hepatic flexure on contrasted enemas.

Figure 28.2, Patterns of acute colonic ischemia. (A) Patchy erythema of mucosa at the rectosigmoid junction; (B) discrete deep ulcers at the splenic flexure; (C) small ulcer with stigmata of bleeding at the splenic flexure; and (D) diffuse mucosal edema, erythema, and bleeding at the hepatic flexure.

Figure 28.3, Ulcer patterns in duodenal and colonic ischemia. (A) Series of ischemic ulcers covered with black plaques in the folds of the second part of the duodenum; (B and C) discrete, large, clean-based ulcers in the right colon; and (D) anastomotic ulcers with a leak at the colo-colonic anastomosis after left partial colectomy for ischemic colitis.

Figure 28.4, Marked ulcers with necrosis in acute bowel ischemia, the pattern is rare in Crohn’s disease or ulcerative colitis. (A) Large ischemic ulcer with superficial necrosis at the transverse colon; (B) deep ischemic ulcer with necrosis at the duodenum bulb resulting from angiogram embolization of prior duodenum ulcer; (C) circumferential deep ulcers with nodularity of the surround sigmoid colon mucosa; and (D) deep, large ischemic ulcer with necrosis in the cecum, with a high risk of bowel perforation.

Figure 28.5, Mucosal patterns of chronic colonic ischemia. (A and B) Linear, longitudinal mucosal scars in the hepatic flexure; (C) long mucosal bridge at the splenic flexure; and (D) inflammatory polyp at the rectal sigmoid junction. These patterns are also commonly seen in ulcerative colitis or Crohn’s colitis with mucosal healing.

Figure 28.6, Colonic strictures in the ischemic colon. (A and B) Ulcerated strictures at the splenic flexure; (C and D) nonulcerated strictures in the rectosigmoid junction. The splenic flexure and rectosigmoid colon are common locations for nonocclusive colonic ischemia.

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