Ischemic strictures occur in the small bowel or colon. The causes are small mesenteric vessel emboli, trauma, and the sequelae of hernia or bands. This may be the result of a slowly developing chronic ischemic process corresponding to the clinical state of intestinal angina. Partial vascular occlusion and emboli can sometimes be found. Recurrent abdominal pain and weight loss are the two primary characteristic symptoms [1].

Ischemic strictures are concentric, and can be short or long, single or multiple. They produce signs and symptoms of intestinal obstruction. CT depicts concentric strictures with marked wall thickness accompanied by proximal intestinal dilation. Enteroscopy (Fig. 12.2a) and fluoroscopic enteroclysis (Fig. 12.2b) reveal concentric ulcerous stenosis, sometimes leading to longitudinal ulceration.

Angiodysplasia has been claimed to be one of the most common causes of small-bowel bleeding, and sometimes acute upper GI and colonic bleeding in the elderly [17]. The tortuously ectatic mucosal capillaries communicate with the enlarged submucosal veins and venules. The lesions are common in the jejunum, the ileum, and the right colon. They are believed to result from chronic low-grade obstruction of the submucosal veins where they traverse the muscularis propria. The resulting back-pressure causes further dilation of the mucosal vessels draining into the veins [1]. Angiodysplasia are often multiple and restricted to the mucosa and submucosa, unlike the lesions of hereditary hemorrhagic telangiectasia (HHT), which occurs in all layers of the bowel wall [18]. Histologically, angiodysplasia consists of dilated, distorted, tortuous, and thin-walled vessels lined by endothelium with little or no smooth muscle and no inflammation, fibrosis, or atherosclerosis. Initially, only submucosal veins are dilated, but in older lesions, mucosal veins and capillaries and even arteries become dilated. Congenital arteriovenous malformations that have thick-walled arteries, much larger than angiodysplasia and visible from the serosal side, also cause GI bleeding [19].

Gastrointestinal telangiectasia, which appears nearly identical to angiodysplasia, is associated with HHT, scleroderma, CREST syndrome, and possibly Turner syndrome. HHT is a genetic vascular disorder caused by mutation of the endoglin (ENG) gene and (type I HHT) or of the activin A receptor type II-like 1 (ACVRL1) gene (type II HHT) [20]. These mutations impair blood vessel growth and repair, resulting in irregular, tortuous blood spaces line by a single thin layer of endothelial cells. These mutations produce a syndrome of multiple orocutaneous telangiectasias. The nasal and gastrointestinal lesions frequently bleed significantly and repeatedly [21]. This bleeding tendency is explained by the thin and fragile vascular wall that lacks an elastic lamina or muscle layer and perhaps intralesional venous hypertension due to arterial shunting of blood.

Endoscopy is the diagnostic procedure of choice. Angiodysplasia appears as a dense macular and reticular network of vessels, which is typically 2–8 mm wide, and intensely red because of the high oxygen content in erythrocytes within vessels supplied by arteries without intervening capillaries (Fig. 12.3a). A pale anemic mucosal halo surrounding angiodysplasia can be observed due to shunting of blood (vascular steal) from surrounding tissue by the low-resistance angiodysplastic shunt [22]. Telangiectasias in HHT are generally redder than angiodysplasias. Arteriovenous malformation is a submucosal mass covered by blueish mucosa where dilated vessels are seen through. It is sometimes pulsating and has ulceration or scarring on its surface. In patients with HHT, endoscopy shows multiple telangiectasias are visible besides gastrointestinal tract (e.g., oral cavity, pharynx, larynx; see Fig. 12.3b).

The majority of patients with duodenal varices visualized on endoscopy have extrahepatic portal hypertension. In contrast to duodenal varices, it appears that most cases of varices in other portions of the small intestine and colonic varices are seen in patients with intrahepatic portal hypertension who have previously undergone abdominal surgery [23]. Although ectopic varices can occur at several sites, bleeding ectopic varices are most commonly found in the duodenum and at sites of previous bowel surgery including stomas. In a review of 169 cases of bleeding ectopic varices, 17% occurred in the duodenum, 17% in the jejunum or ileum, 14% in the colon, 8% in the rectum, and 9% in the peritoneum [24].

Contrast-enhanced CT are used to diagnose intestinal varices. Angiography provides the necessary information about the location and extent of the varices. Endoscopy reveals serpiginous vessels projecting into the lumen (Fig. 12.4).

Ischemic colitis is the most common form of ischemic injury to the gut, and occurs more frequently in elderly people. The disease can result from either occlusive or nonocclusive events, mainly in the territory of the inferior mesenteric artery, in colonic branches of the superior mesenteric artery, and in the superior and inferior mesenteric veins. Large arterial vessel occlusion may be caused by thrombi or atheromatous lesions. Aortic surgery can cause ischemic colitis because of unnoticed ligation of the IMA, the occurrence of intraoperative hypoperfusion, or embolization of atheromatous debris. It has also been reported in long-distance runners. Ischemic colitis is predominantly seen in the left colon [2]. The splenic flexure and rectosigmoid junction, where low perfusion exists (watershed areas), are commonly affected, while the rectum is not usually compromised because of excellent collateral perfusion. Right colon ischemic colitis is rare, but is associated with poor prognosis. A wide spectrum of manifestations can be seen: acute transient type (reversible colopathy characterized by mucosal and submucosal hemorrhage, acute fulminant type (irreversible colopathy characterized by transmural and progression to necrosis), and chronic stenosing type (partially reversible vascular disease usually manifested by late colonic stenosis).

Mesenteric phlebosclerosis is a rare disease, characterized by thickening of the wall of the right hemicolon with calcification of mesenteric veins. Most cases have been reported from East Asia, and the long-term use of geniposide (major constituent of Gardenia fruits) in herbal medicines has been associated with its development. Some patients are asymptomatic, and others present with abdominal pain, distension, and diarrhea [25].

Colonoscopy is the diagnostic procedure of choice. The endoscopic examination has to be performed with caution and minimizing air insufflation to avoid perforation. The mucosa of the affected segment usually appears edematous, hemorrhagic, and ulcerated (Fig. 12.5a). When bowel necrosis is present, colonoscopy reveals cyanotic, grey or black mucosa (Fig. 12.5b). Biopsy often demonstrates nonspecific findings of vascular congestion, submucosal hemorrhage, intestinal edema, inflammatory infiltration, loss of superficial cells, and intravascular platelet thrombi.

In mesenteric phlebosclerosis, endoscopic reveals an edematous dark-purple mucosa with ulcerations of various sizes in the right hemicolon. Cross-sectional imaging demonstrates marked thickening of the colonic wall and linear calcification of many branches of mesenteric vein.

Eosinophilic gastroenteritis is a heterogeneous collection of disorders of varied causes with similar clinicopathological features. Allergic phenomena have been proposed to account for eosinophilic gastroenteritis. About 70% of patients have a history of allergic disorder, especially asthma, hay fever, drug sensitivity, and food hypersensitivities. The clinical manifestations of eosinophilic gastroenteritis depends on the gastrointestinal (GI) site primarily affected and the layer of bowel wall predominantly involved. The stomach and intestine are most commonly involved, but the disease may affect any part of the gastrointestinal tract as well as the pancreatic and biliary tree [26]. Klein’s classification divides cases into three types: mucosal/submucosal type, muscular type, and subserosal type (Table 12.1) [27]. When the predominant involvement is mucosal, the condition behaves like other forms of inflammatory bowel diseases (IBD). If the eosinophilic infiltration is extensive, there may be malabsorption, weight loss, protein-losing enteropathy, hemorrhage, and perforation [26]. A low level of peripheral eosinophilia occurs in most cases (up to 90%) [28].