Sometimes, the ischemic event persists long enough without reperfusion and becomes destined to its final outcome: necrosis of the whole bowel wall. The intramural arteriocapillaries first lose part of their volume as the earlier entered blood flows out from the veins, even though some blood may seep back from the veins. At this moment, the CT shows a thin, poorly or suboptimally enhanced bowel wall (Fig. 1,2,3,4A,4B). Occasionally, detailed ischemic mucosal folds can be seen (Fig. 5). Poor enhancement along the antimesenteric side is suggestive of nonocclusive ischemia (Fig. 6). The intestinal fluid is decreased because the enterocytes cannot produce a normal amount of secretions if the arterial supply is blocked. The bowel wall is first pale and then turns to black and becomes thinned as a result of intravascular volume loss and collapse of necrotic tissue [1, 5]. Not uncommonly, the infarcted bowel is described as grossly dark red or purple and filled with bloody fluid. In fact, this description represents a reperfused instead of a nonreperfused ischemic bowel because there should not be a lot of erythrocytes or plasma extravasating through the damaged and ruptured microvascular wall into the mucosa, submucosa, or bowel lumen if the arterial supply is severely reduced, either occlusively or nonocclusively, without a subsequent reperfusion taking place. Microscopically, inflammatory cell infiltration in response to bacterial invasion is much more prominent than RBC extravasation in the nonreperfused attenuated wall. The evolution of bloody diarrhea or bloody intraluminal fluid is most likely due to an outpouring of the reperfused blood from the infarcted mucosa or submucosa into the lumen. Even though the residual blood in the capillaries that flows back from the venules may cause extravasation of RBC in the mucosa (lamina propria of the villi) or scattered hemorrhagic foci in the submucosa or subserosa, it is unlikely for this small amount of hemorrhage to cause considerable wall thickening. As bacteria proliferate and more gas is produced, the intraluminal gas may dissect into the necrotic wall (pneumatosis intestinalis), spread through the mesenteric veins, and finally flow into the portal veins (Fig. 7A,7B).

If the pathologic processes were corrected (by lysis of the embolus, reestablishment of blood pressure, release of external compression, or prompt development of collateral circulation), the reentered blood might cause different CT appearances, depending on the degree of disruption of the vascular wall integrity. The intestinal microvessel derives its oxygen supply through direct diffusion from the blood. When the arterial supply is insufficient for a certain period and returns later, the microvascular endothelium and the mucosal epithelium become damaged, and the permeability increases proportionately to the duration of oxygen deprivation and the degree of the reperfusion injury. If the degree is mild, only water molecules leak into the extravascular space and cause a mucosal or submucosal edema appearance on CT (Fig. 8). When the damage becomes more severe, the molecules of contrast medium follow the previously escaped fluid and cause various degrees of mucosal or submucosal enhancement (Figs. 9A,9B and 10). As the ruptures between the damaged endothelial cells further enlarge, the RBC also leak, resulting in a thickened soft-tissue-density bowel wall with or without mucosal enhancement (Figs. 11A,11B and 12A,12B). The thickened mucosal folds or thumprinting appearance seen radiologically are caused by submucosal edema or hemorrhage. The mucosa may remain intact or become necrotic. In the case of reperfusion, the bowel is grossly dark red, the wall is thickened, and the lumen is largely filled with bloody fluid in contrast with appearances of the nonreperfused condition.

When the mesenteric venous drainage is impaired, the intravascular volume increases, and the hydrostatic pressure rises as the arterial blood continues flowing into the capillary bed and venules of the bowel and mesentery. The elevated hydrostatic pressure causes the molecules of water or contrast material, or even the erythrocytes, to escape through the enlarged fenestrations of the stretched arteriocapillary endothelium into the submucosa, appearing as submucosal and mesenteric edema or hemorrhage on CT (Figs. 13 and 14). These appearances are similar to those of reperfused ischemia previously described. However, the mechanism is different from that of a directly arterial origin, which is caused by oxygen-deprived and free radical-induced disruption of vascular wall integrity and resultant increased permeability. As the tissue tension in the extravascular compartment of the submucosa increases, the arterial supply may be compromised and the mucosal enhancement decreased. Tissue tension may reach an extent sufficient to cause a complete failure of the arterial supply because of stasis of blood flow or thrombosis of small arterioles and subsequent bowel necrosis (Fig. 13). The mesenteric veins are usually engorged during this condition.

Closed loop small-bowel obstruction is caused by adhesion, incarcerated hernia, or volvulus. Both the artery and vein are compressed. Because the arterial pressure is higher than the venous pressure, the arterial inflow is usually more than the venous outflow. Thus, the CT appearances are similar to those of impaired venous drainage (Fig. 15A). The relatively rich arterial supply may contribute to increased intestinal secretions and rapid fluid-filling of the lumen of the closed bowel loop, which is occluded at both ends. Theoretically, the arterial supply is still adequate if the mucosal enhancement is normal. If the artery were compressed more tightly, the wall enhancement might be suboptimal, and the thickness would not be increased. If the compression is tight enough from the beginning of the obstruction, the wall might be thin and totally unenhanced, similar to that of nonreperfused ischemia (Fig. 15B).

Mesenteric edema or hemorrhage (Fig. 15A) may result from increased vascular permeability as a result of oxygen deprivation or elevated intravascular hydrostatic pressure caused by impaired venous drainage, even though the latter is more common and prominent. Mesenteric vascular engorgement usually occurs with impaired venous drainage. The density of the intraluminal fluid may be increased if RBC are released into the lumen (Fig. 15C). This appearance may occur in all of the conditions previously mentioned.

Bowel ischemia may result from a broad spectrum of diseases and may have different appearances depending on various mechanisms and stages. Different appearances may coexist in adjacent segments. A correct diagnosis of bowel ischemia should be based on a correlation of the image findings, laboratory data, and clinical history.

Address correspondence to C. K. Chou.