Published online before print January 15, 2003, 10.1148/radiol.2263011540
(Radiology 2003;226:635-650.)
© RSNA, 2003
CT of Acute Bowel Ischemia1
Walter Wiesner, MD2,
Bharti Khurana, MD,
Hoon Ji, MD, PhD and
Pablo R. Ros, MD, MPH
1 From the Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115. Received September 17, 2001; revision requested November 15; revision received December 21; accepted January 22, 2002. Address correspondence to P.R.R. (e-mail: pros@partners.org).
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ABSTRACT
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Bowel ischemia may be caused by many conditions and manifest with typical or atypical and specific or nonspecific clinical, laboratory, and radiologic findings. It may mimic various intestinal diseases and be confused with certain nonischemic conditions clinically and at computed tomography (CT). Bowel ischemia severity ranges from mild (generally transient superficial changes of intestinal mucosa) to more dangerous and potentially life-threatening transmural bowel wall necrosis. Causes of critically reduced blood flow to the bowel are diverse, ranging from occlusions of mesenteric arteries or veins to complicated bowel obstruction and overdistention. CT can demonstrate changes in ischemic bowel segments accurately, is often helpful in determining the primary cause of ischemia, and can demonstrate important coexistent findings or complications. Unfortunately, common CT findings in bowel ischemia are not specific, and specific findings are rather uncommon. Therefore, it often is a combination of nonspecific clinical, laboratory, and radiologic findings—especially detailed knowledge about the pathogenesis of acute bowel ischemia in different conditions—that helps most in correct interpretation of CT findings. To improve understanding of this complex heterogeneous entity, this article provides an overview of the anatomy and physiology of mesenteric perfusion and discussions of causes and pathogenesis of acute bowel ischemia, CT findings in various types of acute bowel ischemia, and potential pitfalls of CT.
© RSNA, 2003
Index terms: Colitis, ischemic, 75.266 • Intestines, CT, 74.12111, 74.12112, 75.12111, 75.12112 • Intestines, infarction, 74.266, 75.266 • Intestines, ischemia, 74.266, 75.266 • Review
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INTRODUCTION
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With the increase in average life expectancy, acute bowel ischemia represents one of the most threatening abdominal conditions in elderly patients (1–7). Acute bowel ischemia may involve the small or large bowel, be segmental or diffuse, and be only partial mural (meaning that it involves only the mucosa and submucosa, with or without parts of the muscularis) or transmural (meaning that it leads to continuous necrosis of all bowel wall layers [ie, infarction]). Ischemic colitis, as an example of only partial mural and superficial colonic ischemia, is the most common type of colitis in patients older than 50 years and is often self-limiting, whereas acute bowel infarction (accounting for approximately 1% of all cases of acute abdomen) has a higher annual mortality rate than colon cancer (1,3).
Despite its frequency and seriousness, acute bowel ischemia represents one of the most challenging abdominal conditions because of its wide range of clinical and pathologic manifestations, as well as its high mortality rate (50%–90%, depending on the cause of the event and the degree and extent of ischemic bowel wall damage) (1–7). The therapeutic approach to transmural bowel infarction still consists of surgical resection, an intervention that has not changed appreciably over the past century (8). However, the diagnostic approach to acute bowel ischemia changed dramatically with the introduction of angiography in 1960 (9,10). During the decade that followed, flexible fiberoptic endoscopy, ultrasonography (US), color Doppler US imaging, and computed tomography (CT) have markedly altered the diagnostic approach to acute bowel ischemia; not surprisingly, these diagnostic advances have also strongly influenced the therapeutic approach to nontransmural bowel ischemia in current practice (11–13). The purpose of this article is to document recent advances in understanding of acute bowel ischemia and to define the role of CT in the diagnosis of this complex and heterogeneous entity.
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ANATOMY AND PHYSIOLOGY
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The vascular supply of the small and large bowel is provided by three arteries: the celiac trunk, the superior mesenteric artery, and the inferior mesenteric artery. The celiac trunk provides the blood supply to the gastrointestinal tract from the distal esophagus to the descending duodenum (14). The gastroduodenal artery, usually the first branch of the common hepatic artery, provides an important connection between the celiac trunk and the superior mesenteric artery. The superior mesenteric artery supplies the transverse and ascending duodenum, the jejunum and ileum, and the large bowel to the splenic flexure, although the vascular supply of this particular region may be variable (14,15). The superior mesenteric artery has some important anastomotic connections to the inferior mesenteric artery, including the marginal artery of Drummond (marginal artery of the colon) and the arcade of Riolan (intestinal arterial arcade) (14– 16). The inferior mesenteric artery supplies the colon from the splenic flexure to the rectum, forming several anastomoses to the lumbar branches of the abdominal aorta, the sacral artery, and the internal iliac arteries (14–16). The branches of these arteries form up to four arcades, and the peripheral mesenteric vasculature is composed of several vascular circuits coupled both in series and in parallel. The three primary parallel circuits serve the muscularis propria, the submucosa, and the mucosa, while the five series-coupled components consist of the resistance arterioles, the precapillary sphincters, the capillaries, the postcapillary sphincters, and the venous capacitance vessels (17).
The superior and inferior mesenteric veins parallel their arteries and drain the respective parts of the gut. The inferior mesenteric vein empties into the splenic vein and joins with the superior mesenteric vein to form the portal vein (14). Numerous shared collateral vessels also characterize the mesenteric veins, which also maintain various connections to the systemic venous circulation. These connections range from anastomoses to gastric and esophageal veins to renal, lumbar, and pelvic veins (14–16).
Under normal circumstances, the human bowel receives around 20% of resting cardiac output, of which two-thirds supplies the intestinal mucosa (18,19). In the postprandial phase, splanchnic autoregulation may increase intestinal blood flow to as much as 35% of cardiac output. Interestingly, this response depends on the content of the ingested food, with the earliest rise seen after intake of carbohydrates and a slower, but overall larger, increase in intestinal perfusion after oral intake of fat and proteins (17–20). In contrast, intestinal perfusion may be reduced to 10% of cardiac output in critical situations, such as in conditions of "fight or flight" (21).
In addition to the local autoregulation of intestinal perfusion, which is mediated primarily by a direct myogenic response to a reduction in perfusion pressure, several neural and humoral agents, including vasopressin and angiotensin II, also play an important role in the physiology of mesenteric vasoconstriction (17,18). Under normal conditions, autoregulation of intestinal perfusion may maintain tissue viability below a systemic blood pressure of 70 mm Hg. However, in cases where systemic blood pressure is below 40 mm Hg and local myogenic autoregulation is overruled by systemic autoregulation, local protective mechanisms fail. This results in an increasingly ischemic bowel wall, similar to what would happen in the case of mesenteric underperfusion due to vascular occlusion (22,23).
The initial ischemic damage to the intestinal wall may then range from only mild and superficial necrosis limited to the mucosa (with or without involvement of the submucosa and focal areas of the muscularis) (ie, partial mural bowel ischemia, including ischemic colitis) to dangerous and life-threatening continuous necrosis of all bowel wall layers (ie, transmural bowel infarction) (24,25). Furthermore, the initial purely ischemic lesions of the intestine are typically followed by an inflammatory response due to the release of certain mediators such as cytokines, platelet-activating factor, and tumor necrosis factor, all of which are released from activated neutrophils, platelets, mast cells, and endothelial cells within the splanchnic circulation (26,27). These substances additionally damage the bowel wall and may contribute to the pathogenesis of bowel wall necrosis. As a consequence, the mucosal barrier breaks down and the bowel loses its resistance to bacterial invasion, leading to bacteremia and sepsis (28,29). Furthermore, toxic proteases, intraluminal bacteria and toxins, and free radicals (produced during reperfusion of the ischemic bowel segment) may subsequently also contribute to the pathogenesis of severe intestinal necrosis within ischemic bowel segments (30,31).
Partial mural bowel ischemia may be self-limiting, or it may progress to a serious and potentially life-threatening disease. The clinical consequences of acute bowel ischemia, therefore, may be extensive in type and degree. Besides local complications such as bleeding, intestinal perforation, abscess formation, and peritonitis, acute bowel ischemia may also have serious systemic effects, including bone marrow suppression, myocardial and renal failure, hemoconcentration, acidosis, disseminated intravascular coagulation, and multiple organ failure (32–36). While it has long been accepted that transmural bowel infarction causes this dramatic clinical picture, it appears more and more that even less pronounced partial mural bowel ischemia may also cause already dangerous systemic injury after disruption of the intestinal mucosal barrier (36).
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ETIOLOGY AND PATHOGENESIS
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Acute bowel ischemia may be caused by occlusions of the arteries or veins, as well as by nonocclusive reduction of intestinal perfusion (see Table 1). Acute occlusions of the superior mesenteric artery due to thrombosis or embolization are responsible for approximately 60%–70% of cases of acute bowel ischemia, whereas mesenteric venous thromboses account for 5%–10% of the total and nonocclusive conditions account for approximately 20%–30% of cases (1–7,13,37,38). Acute occlusions of the superior mesenteric artery may be proximal or distal and most commonly result from thromboembolism, where the embolus originates from the left atrium as a consequence of atrial fibrillation (39). Acute occlusions of the mesenteric arteries may be related to numerous other conditions, however, including atherosclerosis, thromboembolism from the aorta, mesenteric arterial thrombosis, aortic or mesenteric arterial dissection, spontaneous or postoperative cholesterol embolization, aortic surgery, stent placement, or therapeutic embolization of mesenteric vessels to treat gastrointestinal hemorrhage (40–43) (Figs 1–5). While isolated proximal occlusions of only one visceral artery may be rather well compensated by means of collateral circulation (as long as the other two visceral arteries are intact), very distal occlusions of mesenteric arteries, as occasionally identified histopathologically after disintegration and distal embolization of a thrombus or cholesterol embolus, usually lead to the worst ischemic damage to the bowel wall.
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Figure 1. Unenhanced transverse CT scan shows mild thickening of descending colon (arrowheads). Note pronounced circumferential calcification of infrarenal abdominal aorta and inferior mesenteric artery at its origin (arrow).
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Figure 2. Contrast material-enhanced transverse CT scan shows subtotal thrombosis of superior mesenteric artery (arrowheads). Note small well-perfused residual lumen dorsolaterally (arrow) and well-perfused branch, which prevented acute mesenteric infarction in this case.
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Figure 3a. (a) Contrast-enhanced transverse CT scan shows several infarcted small-bowel loops (arrows), which manifest with dilatation and air-fluid levels but no wall thickening, due to transmural small-bowel necrosis. (b) Contrast-enhanced transverse CT scan shows large cholesterol embolus (arrows) in the superior mesenteric artery, confirmed at surgery, which caused acute mesenteric infarction.
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Figure 3b. (a) Contrast-enhanced transverse CT scan shows several infarcted small-bowel loops (arrows), which manifest with dilatation and air-fluid levels but no wall thickening, due to transmural small-bowel necrosis. (b) Contrast-enhanced transverse CT scan shows large cholesterol embolus (arrows) in the superior mesenteric artery, confirmed at surgery, which caused acute mesenteric infarction.
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Figure 4a. Unenhanced transverse CT scans show sigmoid colon infarction after aortic stent placement. (a) Stent can be seen in an infrarenal aortic aneurysm (arrows). The stent caused occlusion of the inferior mesenteric artery and subsequent ischemia of the sigmoid colon. (b) Note moderate wall thickening of sigmoid colon (arrows), which has undergone transmural infarction.
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Figure 4b. Unenhanced transverse CT scans show sigmoid colon infarction after aortic stent placement. (a) Stent can be seen in an infrarenal aortic aneurysm (arrows). The stent caused occlusion of the inferior mesenteric artery and subsequent ischemia of the sigmoid colon. (b) Note moderate wall thickening of sigmoid colon (arrows), which has undergone transmural infarction.
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Figure 5. Unenhanced transverse CT scan shows pneumatosis (arrowheads) along the left-sided colon, due to transmural colonic infarction. The patient had low cardiac output, but the wrong position of the intraaortic balloon (arrow), which occluded the inferior mesenteric artery at its origin, might have been the main reason for the critical underperfusion of the left side of the colon.
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Occlusions of the mesenteric arteries may also be caused by antiphospholipid antibody syndrome and especially by various types of vasculitis and thrombotic microangiopathies. These conditions may cause occlusions of large (Takayasu arteritis, giant cell arteritis), medium (panarteritis nodosa, Kawasaki disease), or small (systemic lupus erythematosus, Schönlein-Henoch purpura, Wegener granulomatosis, Churg-Strauss syndrome, Buerger disease, rheumatoid vasculitis, Behçet syndrome, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome) mesenteric vessels (44–54) (Fig 6). The clinical and pathologic manifestations of resulting bowel ischemia may overlap considerably in all these types; however, these entities typically affect young patients at unusual sites such as the stomach, duodenum, or rectum. Furthermore, any small vessel disease, ranging from diabetic vasculopathy and amyloidosis to oxalosis, may also be a causal factor in intestinal underperfusion or may at least contribute to its pathogenesis in combination with some of the aforementioned causes (55,56). Last but not least, fibromuscular dysplasia involving the mesenteric arteries has also been reported as an extremely rare cause of acute mesenteric infarctions in children (57).
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Figure 6. Contrast-enhanced transverse CT scan shows segmental small-bowel with pronounced wall thickening (arrowheads) and mild periserosal haziness involving ileum and colon in a patient with generalized autoimmune vasculitis due to systemic lupus erythematosus.
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Occlusions of mesenteric veins may be primary or secondary and may be found proximally or distally. Mesenteric venous thrombosis may be caused by infiltrative, neoplastic, or inflammatory conditions (which, in rare instances, may encase mesenteric veins) or by various types of abdominal infection—with or without thrombophlebitis (58,59). Furthermore, thrombotic mesenteric venous occlusions may occur in patients with a hypercoagulability state caused by polycythemia vera; sickle cell disease and thrombocytosis; antithrombin III, protein C, and/or protein S deficiencies; or a hypercoagulability state caused by carcinomatosis, pregnancy, or use of oral contraceptives (1–7,13,58–64) (Fig 7). Isolated proximal mesenteric venous thromboses, however, usually do not lead to severe bowel ischemia because of the extended collateral network between mesenteric and systemic veins. In contrast, thrombosis of very distal mesenteric veins, which may occur in association with various hypercoagulability states, usually leads to severe hemorrhagic infarction of the bowel wall (Fig 7). Furthermore, certain types of vasculitis (eg, Wegener granulomatosis, systemic lupus erythematosus, Behçet syndrome) that primarily affect very small mesenteric arteries may cause additional occlusions of small and intramural mesenteric veins, which explains why, under these conditions, the ischemic bowel often shows pronounced wall thickening (20,44–54,65,66). Finally, enterocolic lymphocytic phlebitis has been reported as another rare entity in which inflammatory occlusions of small intramural colonic veins may lead to intestinal ischemia and necrosis (65,66).
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Figure 7. Contrast-enhanced transverse CT scan shows mesenteric venous infarction with massive small-bowel wall thickening (arrows), total absence of bowel wall enhancement, pronounced edema of mesenteric fat (arrowheads), and ascites ( ) in a patient with polycythemia vera who developed multiple thromboses of distal and intramural mesenteric veins.
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Bowel ischemia caused by primary mesenteric venous thrombosis is rare compared with that caused by acute occlusions of mesenteric arteries. However, complicated bowel obstruction may lead to acute bowel ischemia caused mainly by compromise of the venous circulation. This particular cause of bowel ischemia may be easily underestimated, since bowel ischemia represents only a coexistent finding in such cases. In fact, in cases of complicated bowel obstruction, bowel ischemia usually results from compression or strangulation of mesenteric veins, with or without subsequent thrombosis leading to severe ischemic damage or, in extreme scenarios, hemorrhagic infarction of the bowel wall. This is typically observed in cases of strangulated herniation, strangulated closed-loop obstruction, volvulus, and intussusception (20,38) (Figs 8, 9).
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Figure 8. Contrast-enhanced transverse CT scan shows ischemia of the ileum, with pronounced bowel wall thickening (arrows) and mesenteric fat stranding (arrowheads) in a patient with strangulated closed-loop obstruction. Note mural edema of strangulated bowel segment and mild perfusion of mucosal-submucosal and serosal-subserosal layers, causing a target sign.
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Figure 9. Contrast-enhanced transverse CT scan shows ischemia of several small-bowel loops, with mild thickening and diffuse hyperemia of bowel wall (arrows), as well as mesenteric fluid (arrowheads) adjacent to ischemic bowel segments, in a case of strangulated small-bowel herniation due to a congenital defect in the mesosigmoid.
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Bowel ischemia may also occur as a result of intestinal overdistention, which is usually observed in a prestenotically dilated colonic segment (Fig 10). In rare cases of ileocecal occlusion, however, ischemia may also occur in the small bowel (67,68). The pathogenesis of this type of distention-related bowel ischemia differs from that of other types of bowel ischemia resulting from strangulation. Distention-related ischemia results from compromise of the local mucosal microcirculation caused by the elevated intraluminal pressure, which leads to ischemia of the distended bowel; in certain cases, bacterial overgrowth within the prestenotic segment may also contribute to the pathogenesis of intestinal necrosis (67,68). Any increase in intraluminal pressure to more than 50 mm Hg will disturb the mucosal microcirculation, especially in patients with an already compromised colonic perfusion; therefore, in rare instances enemas or endoscopy may cause ischemic colitis or worsen the already preexistent mucosal ischemia (16–19,69,70).
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Figure 10. Unenhanced transverse CT scan shows parastomatal herniation of left-sided colon (large arrow) causing mechanical obstruction and prestenotic dilatation of right-sided colon. Massively distended right-sided colon shows mild (but on the basis of distention, abnormal) wall thickening (arrowheads), as well as pneumatosis (small arrows) due to ischemic colitis.
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Colonic ischemia may develop in patients with acute pancreatitis or other abdominal inflammatory conditions such as appendicitis, diverticulitis, and peritonitis (24,38). In acute pancreatitis, for example, bowel ischemia usually involves the transverse colon or the hepatic and splenic flexures and may range in severity to include transmural colonic necrosis (71). Colonic ischemia associated with pancreatitis seems to be related to encasement of branches of colonic vessels; vasospasm of mesocolic arteries due to local irritation; and/or systemic regulation following stress, pain, and fluid loss; or a combination of these factors (71). In certain cases, however, it may be difficult to assess how much colonic wall damage is caused by direct injury from pancreatic exudates. Mesenteric venous thrombosis in cases of acute pancreatitis usually does not cause marked intestinal ischemia, owing to the large collateral venous supply in the mesentery.
While all the aforementioned conditions are due to partial or total extrinsic or intrinsic occlusion of splanchnic vessels, acute bowel ischemia may also be caused by nonocclusive reduction of the mesenteric blood supply. Nonocclusive mesenteric ischemia was commonly reported in the past, and the decline in the frequency of this condition over the past decade is probably related to better monitoring of patients in intensive care and to proactive corrections of hemodynamic abnormalities that lead to systemic hypotension and attendant underperfusion of the intestine. If systemic blood pressure decreases precipitously in a patient with hemorrhagic, cardiogenic, or septic shock (the same condition has been observed in patients undergoing nonpulsatile cardiopulmonary bypass surgery), then systemic regulatory mechanisms, mediated chiefly by angiotensin II, overrule local regulatory mesenteric vasodilation by trying to reduce intestinal perfusion and preserve blood supply to brain, heart, and muscles. As a consequence, intestinal perfusion will decrease dramatically, and nonocclusive bowel ischemia may develop. The manifestation may range from a more localized and self-limiting superficial ischemia of the watershed areas (including splenic flexure, ileocecal junction, and rectosigmoid) to a diffuse and extended ischemic injury to the entire bowel ("shock bowel") (72–75) (Figs 11, 12).
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Figure 11. Contrast-enhanced transverse CT scan shows mild homogeneous wall thickening (arrows) of the splenic flexure. The homogeneously hypoattenuating appearance is caused by pronounced mural edema.
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Figure 12. Contrast-enhanced transverse CT scan shows diffuse mild wall thickening and prolonged bowel wall enhancement (arrowheads) in several dilated small-bowel loops. Also present are mesenteric and peritoneal fluid (arrow) and ascites () in this patient with cardiac shock who was treated with a high dose of intravenous blood pressure drugs. At autopsy, diffuse mucosal and submucosal necrosis was revealed throughout the intestine, but no transmural bowel infarction was found.
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Acute nonocclusive bowel ischemia has been reported (76–79) in patients with familial dysautonomy syndrome or pheochromocytoma and even in high-endurance athletes, in whom a combination of dehydration and stress likely contributes to the nonocclusive pathogenesis. Although most commonly found in the left-sided colon, nonocclusive ischemic colitis may occasionally involve the right side as well. It seems that right-sided colonic involvement is associated with more severe forms of ischemic colitis and that this occurs frequently in patients with chronic renal failure necessitating hemodialysis (80) (Fig 13).
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Figure 13. Unenhanced transverse CT scan shows mild wall thickening (small arrows) of left-sided colon, with mild paracolic fat stranding. Note much more pronounced bowel wall thickening (large arrows) and paracolic fat stranding along the right side of the colon, which, in addition to nontransmural ischemic bowel wall damage, also showed marked bacterial superinfection and subsequent inflammation.
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Trauma may cause bowel ischemia: directly, when mesenteric vessels and bowel wall are lacerated; or indirectly, when trauma leads to hemorrhagic shock and subsequent nonocclusive bowel ischemia as described above (1–7,13,14,38). Furthermore, acute bowel ischemia may be caused by radiation, corrosive injury, immunosuppression, chemotherapy, and a variety of pharmaceutical agents that lead to mesenteric vasoconstriction (eg, digitalis, vasopressin, adrenaline, noradrenaline, ergotamine), hypotension (antihypertensive drugs, diuretics, neuroleptics, antidepressants), or inhibition of prostaglandin synthesis (eg, indomethacin) (81–84) (Fig 14). Finally, use of cocaine, crack cocaine, and heroin has also been reported to cause nonocclusive bowel ischemia by leading to strong and selective mesenteric vasoconstriction (85,86).
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Figure 14. Contrast-enhanced transverse CT scan shows moderate thickening of ileum (arrows), as well as mild mesenteric fat stranding (arrowheads), representing acute radiation-induced enteritis. Patient had undergone radiation therapy to treat inoperable retroperitoneal metastasis (not shown) from colon cancer initially treated with right hemicolectomy.
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PATHOLOGY
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There are three stages of acute bowel ischemia. The first stage (stage I), known as reversible ischemic enteritis or colitis, is characterized by mucosal necrosis, mucosal erosions and ulcerations, and/or hemorrhage (24,25). In rare instances, mucosal plaques may slough off into the bowel lumen, but an ischemic bowel wall injury that is usually limited to the intestinal mucosa will eventually heal completely. However, if ischemic damage extends more deeply into the bowel wall and if it leads to necrosis of the deep submucosal and muscular layers (stage II), fibrotic strictures stemming from local reparative changes may ultimately develop (87,88). In contrast to stages I and II, which represent partial mural bowel ischemia, stage III acute bowel ischemia represents transmural bowel wall necrosis (ie, bowel infarction). Stage III is clearly differentiated from stages I and II because it is associated with a high mortality rate and, therefore, requires immediate surgical intervention.
Mucosal and intramural necrosis are always followed by edema and/or hemorrhage; clearly, the extent to which these findings are present may differ substantially on the basis of the pathogenesis of bowel ischemia. In bowel ischemia caused by mesenteric venous occlusion, both intramural edema and hemorrhage, as well as edema within mesenteric fat, will be more pronounced due to venous congestion than in cases with a purely arterio-occlusive pathogenesis (87). Furthermore, any ischemic bowel (especially the colon) may become superinfected after the mucosal barrier has broken down, and such superinfection may be an important contributor to the pathogenesis of bowel wall necrosis (89,90).
Therefore, the histopathologic manifestation of ischemic bowel segments may differ on the basis of pathogenesis (veno-occlusive or arterio-occlusive), severity of bowel ischemia with superficial mucosal or transmural bowel wall necrosis only, location (in small or large bowel), and presence and degree of hemorrhage and/or subsequent superinfection. These factors will also contribute to the CT appearance of acute bowel ischemia and help explain the possible overlap with various nonischemic diseases of the small and large bowel.
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CT OF BOWEL ISCHEMIA
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Value of CT
Since the mid-1980s, the authors of an impressive number of publications have addressed the role of CT in acute bowel ischemia and infarction (91–112). Advances in CT sensitivity in the past decade have been impressive: The sensitivity has increased markedly over the past several years from a low of 39% to a current high of 82% (comparable to the sensitivity of angiography [97–99]). However, nearly all studies that have focused on CT and acute bowel ischemia have included patients known to have bowel ischemia; in only one study (98) of which we are aware was the sensitivity and specificity of CT evaluated by analyzing the findings in a group of patients with mesenteric ischemia and in a control group of patients without ischemia. Furthermore, since the number of patients in the control group was smaller than the number of patients with acute bowel ischemia in that particular study and since prospective studies addressing this topic are lacking, it is impossible to determine the true specificity of CT in the prospective evaluation of this disease. Nevertheless, the authors of these studies have successfully described CT findings in acute bowel ischemia, and some have effectively demonstrated their relative frequency while further stressing the value of CT in patients who are suspected of having this disease (94,98–100,108).
Technique
Accurate CT imaging of acute bowel ischemia usually requires both oral and rectal administration of contrast material or water, as well as intravenous administration of iodinated contrast material. In cases where acute bowel ischemia and ischemic colitis are suspected, oral administration of 600–750 mL of contrast material or water 30–120 minutes before scanning or rectal administration of 400–800 mL of contrast material or water is important to achieve adequate bowel distention (Table 2). Rectal administration of water or contrast material is especially important in cases where acute colonic ischemia is suspected, such as in cases of ischemic colitis or ischemic proctosigmoiditis, since it may otherwise be impossible, when colonic segments are contracted, to decide whether bowel wall thickening is present or the CT findings only represent colonic contraction.
The question of whether to use positive or negative contrast material for bowel distention in possible acute bowel ischemia must be answered in future studies. It may be stated at this point, however, that positive contrast material is definitely indicated in cases of bowel obstruction and is also probably more advantageous for clear delineation of the inner bowel wall layers in case of pronounced hypoattenuation of the bowel wall. Water is probably more advantageous when assessing abnormal bowel wall enhancement in cases with absent or minor bowel wall thickening, especially if CT angiography is performed.
Intravenous administration of contrast material is necessary to demonstrate the presence of thrombi in the mesenteric arteries or veins, although additional acquisition of unenhanced CT scans may help delineate vascular calcifications, hyperattenuating intravascular clotting, and/or acute submucosal or intramural hemorrhage. Acquisition of both unenhanced and enhanced CT studies is essential for differentiation of hyperattenuating bowel wall caused by acute and diffuse intramural hemorrhage from that caused by hyperemia or hyperperfusion (discussed later in the CT Findings section on abnormal enhancement). Moreover, these bowel wall enhancement patterns are critical for the diagnosis of bowel ischemia associated with bowel obstruction.
From 100 to 150 mL of contrast material (300–370 mg of iodine per milliliter) is usually administered with a power injector at a rate of 2–4 mL/sec. In the past, image acquisition was performed during the portal venous phase (60 seconds after initiation of injection) with single-detector CT; if a biphasic acquisition was performed with single-detector CT, the arterial phase usually had to be limited to a part of the abdomen because of the longer acquisition time. By using multi–detector row dual-phase CT of the entire abdomen, demonstration of an arterial (25–30 seconds after initiation of injection) and a portal venous (60 seconds) phase of enhancement is easily achieved, and data sets from the arterial phase of enhancement may be used for various types of postprocessing (Table 2).
Three-dimensional imaging (ie, CT angiography and multiplanar reformatting) is a technology of increasing interest in the diagnosis of ischemic bowel disease (113). Sagittal, coronal, and curved multiplanar reformatted images and CT angiograms, all created at a workstation by using the acquired volume data sets, may be very helpful in identifying the site, level, and/or cause of bowel ischemia. The abdomen and pelvis are usually scanned with a collimation of 5–10 mm and a pitch of 1.0–1.5 with single-detector CT, whereas they are scanned at a collimation of 1.0–2.5 mm and a pitch of 6 with multi–detector row CT. Use of thinner sections or overlapping reformatted images may be advantageous in patients suspected of having bowel obstruction.
However, many patients with acute bowel ischemia, and especially those with acute bowel infarction, may not be able to drink adequately prior to the CT examination. Furthermore, many patients with acute bowel ischemia have substantially reduced renal function, and, since patients with acute bowel infarction may have severe electrolyte and fluid imbalances, administration of intravenous contrast material may be impossible. Although this restriction will decrease the diagnostic accuracy of CT, it also effectively demonstrates that the CT protocol depends to a great degree on the clinical presentation of patients suspected of having acute bowel ischemia.
Acquisition of arterial phase CT scans and CT angiograms is surely of great value in the assessment of mesenteric arteries. However, high-quality portal venous phase scans are usually sufficient to show occlusions of mesenteric arteries and definitely have the additional advantages of (a) depicting mesenteric veins; (b) allowing better assessment of abnormalities of the bowel wall itself; and (c) providing greater accuracy in the detection of perforation, abscess formation, and peritonitis, as well as in the diagnosis of other causes of acute abdomen. Therefore, future studies will have to be performed to show if CT in patients in whom acute bowel ischemia is clinically suspected ought to be limited to acquisition of unenhanced and portal venous phase CT scans in order to avoid a further increase in radiation dose to patients.
CT Findings
CT findings in acute bowel ischemia may consist of various morphologic changes, including homogeneous or heterogeneous hypoattenuating or hyperattenuating wall thickening, dilatation, abnormal or absent wall enhancement, mesenteric stranding, vascular engorgement, ascites, pneumatosis, and portal venous gas (101,102). Acute bowel ischemia may affect the small and/or large bowel and may be diffuse or localized, segmental or focal, and superficial or transmural; therefore, it can mimic various intestinal diseases (103,104).
Acute bowel ischemia may involve more typical regions such as the left-sided colon; under such circumstances or if there are more specific CT findings such as pneumatosis or portal venous gas, the correct diagnosis will usually be suspected by the radiologist in an appropriate clinical setting. In rare instances, however, acute bowel ischemia may affect rather short and atypical bowel segments such as the duodenum, cecum, or the rectosigmoid; in these situations, the correct radiologic diagnosis may become difficult if there are no other clinical or laboratory findings that support the diagnosis (105,106) (Figs 15, 16). Hence, the CT appearance of acute bowel ischemia will depend on its cause, severity, localization, extent, and distribution, as well as on the presence and degree of submucosal or intramural hemorrhage, superimposed bowel wall infection, and/or bowel wall perforation. Therefore, the CT findings in acute bowel ischemia may be as heterogeneous and nonspecific in these patients as their clinical and laboratory findings are.
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Figure 15. Unenhanced transverse CT scan shows pronounced homogeneous cecal wall thickening (arrows), representing transmural necrosis with superinfection in a patient with isolated cecal infarction.
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Figure 16. Unenhanced transverse CT scan shows pronounced circumferential thickening of rectal wall (arrows) and pararectal fat stranding (arrowheads) in a patient with nonocclusive ischemic proctitis, which is well depicted following rectal administration of contrast material and luminal distention.
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Bowel wall thickening.—The normal bowel wall thickness has been reported to range from 3 to 5 mm, though this strongly depends on the degree of bowel distention (114,115). In the colon, spastic contractions may cause a wall thickness of more than 5 mm, whereas a wall thickness of only 3 mm may be abnormal in colonic segments that show pronounced distention (Fig 10).
According to reports in the literature, the most common CT finding in acute bowel ischemia is bowel wall thickening, which is present in 26%–96% of reported cases (101). This wide range may be surprising at first, but it can be explained by the fact that often no distinction is drawn between small- and large-bowel ischemia or between bowel ischemia and bowel infarction. However, if we analyze only the results of studies that included larger groups of consecutive patients, exclude those of studies that just describe CT findings in small and preselected groups of patients, and separately address small-bowel and large-bowel ischemia and/or infarction, then we may observe that bowel wall thickening is common in cases of ischemic colitis and colonic infarction, as well as in cases of acute bowel ischemia caused by primary or secondary mesenteric venous occlusion, but is rare and even atypical in acute and exclusively arterio-occlusive transmural small-bowel infarction, where the necrotic small bowel may typically show dilated and fluid-filled or gas- and fluid-filled loops with a "paper thin wall" (94,98–100,108).
Bowel wall thickening detected on CT scans in patients with acute bowel ischemia is due to mural edema and/or hemorrhage and/or superinfection of the ischemic bowel wall, with the latter playing an especially important role in ischemic colitis and colonic infarction. The greatest incidence of bowel wall thickening is observed in cases of ischemic colitis (94%) and reversible mesenteric ischemia (80%), whereas it is much less common in patients with mesenteric infarction (26%–38%) (94,98–100,108). However, bowel wall thickening is also the least specific CT finding in cases of acute bowel ischemia, since it may be observed in a variety of nonischemic conditions affecting the small or large bowel (103,104).
In cases of transmural small-bowel infarction, intramural nerves and the intestinal musculature may be destroyed as well; therefore, infarcted bowel segments (usually small bowel) may manifest without bowel wall thickening, but this lack of thickening is due to total loss of tone, dilatation, and extreme thinning of the bowel wall. In this situation, detection with CT may be difficult, especially if there are no additional findings suggestive of the diagnosis (Fig 3). Therefore, when ischemic small bowel manifests with dilatation and bowel wall thinning rather than thickening, transmural small-bowel infarction has probably occurred. This would be consistent with the results of two studies (99,100) in which bowel wall thickening was shown to be less common in mesenteric infarction than in reversible mesenteric ischemia and that small-bowel wall thickening is, therefore, associated with a significantly good prognosis under these circumstances.
Bowel wall thickening in acute bowel ischemia or infarction does not differ according to its occlusive or nonocclusive pathogenesis. However, it is obvious that bowel wall thickening will be more pronounced in cases of bowel ischemia caused by occlusions of mesenteric veins (including primary or secondary mesenteric venous thrombosis, strangulated herniation, complicated bowel volvulus, and intussusception) than in cases of acute bowel ischemia caused exclusively by occlusions of mesenteric arteries, at least as long as intramural hemorrhage and/or superinfection are absent in the latter group (111,112) (Figs 7–9).
The presence and degree of bowel wall thickening do not correlate with the severity of ischemic bowel wall damage. As mentioned earlier, small-bowel infarction may manifest with a paper-thin bowel wall, whereas reversible shock bowel may manifest with mild but diffuse thickening of the small-bowel wall. Nontransmural ischemic colitis, on the other hand, may manifest with pronounced colonic wall thickening due to pronounced submucosal hemorrhage, inflammation, and/or superinfection and therefore be indistinguishable from transmural colonic infarction on CT scans, providing perforation has not yet taken place (89,101,108) (Figs 4, 13, 15, 17).
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Figure 17. Contrast-enhanced transverse CT scan shows pronounced heterogeneous colonic wall thickening (arrows), as well as mild pericolic fat stranding along the splenic flexure due to diffuse intramural hemorrhage in a patient with nontransmural ischemic colitis with diffuse intramural hemorrhage.
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Dilatation.—Luminal dilatation and/or air-fluid levels are quite common CT findings in acute bowel infarction (56%–91% of cases), though both findings are much less common in reversible bowel ischemia (40%) and in superficial ischemic colitis (94,98–100,108) (Fig 3). This phenomenon may be explained by the fact that ischemic bowel wall lesions in a still viable bowel segment usually lead to spastic contractions, a condition most commonly observed in the colon with only mild mucosal ischemia. In contrast, bowel dilatation may result either from interruption of intestinal peristalsis as a reflex to ischemic injury or, as discussed earlier, from irreversible and transmural ischemic damage to the bowel wall. While a finding of dilated and gas-filled bowel loops is not specific for adynamic ileus, the presence of dilated and mainly fluid-filled bowel loops, resulting from additional fluid exudation into the lumen of ischemic bowel segments (gasless abdomen), becomes more suggestive of acute bowel ischemia or infarction.
Stranding and ascites.—Mesenteric fat stranding, mesenteric fluid, and/or ascites are also nonspecific CT findings in acute bowel ischemia, and their presence depends heavily on the cause, pathogenesis, and severity of the ischemia, as well as on its location in the small or large bowel. Mesenteric fat stranding, mesenteric fluid, and ascites, respectively, have a sensitivity of 58%, 88%, and 75% and a specificity of 79%, 90%, and 76% for diagnosis of partial mural or transmural bowel ischemia in cases of complicated bowel obstruction (111). If two of the three findings are established, the specificity increases to 94% (111) (Figs 8, 9). However, none of these three findings allows for differentiation between transmural and partial mural infarction in cases of complicated bowel obstruction, since under these conditions mesenteric ischemia results from mesenteric venous occlusion, which alone causes transudation into the mesentery or the peritoneal cavity—even without underlying bowel ischemia. For the same reason, mesenteric fat stranding and ascites may appear at the onset of any intrinsic or extrinsic mesenteric venous occlusion, where they are of no value in the estimation of the severity of bowel ischemia (Fig 7).
In cases of acute mesenteric infarction, mesenteric fat stranding and ascites have been reported in 68%–69% and 49%–88% of cases, respectively (99,100). In our experience in cases of isolated small-bowel ischemia caused solely by mesenteric arterial occlusion, mesenteric fat stranding and ascites may be used to help estimate the severity of bowel wall damage, since both CT findings seem to be absent as long as transmural bowel wall necrosis has not developed. Unfortunately, the same is not true for cases of large-bowel ischemia. In large-bowel ischemia, paracolic streakiness and even paracolic fluid collections may result from superinfection of ischemic colonic segments. Paracolic streakiness and fluid collections may thus be present in 61% and 37% of cases of ischemic colitis, respectively, even if no transmural bowel wall necrosis has occurred (108) (Figs 13, 17–19).
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Figure 19. Contrast-enhanced transverse CT scan in a patient with ischemic colitis shows hypoattenuating colonic wall thickening with enhancement of mucosa and submucosa and serosa and subserosa, causing a target sign (arrows). Despite absence of transmural infarction, mild pericolic streakiness and fluid are present along the anterior pararenal and lateroconal fasciae (arrowheads).
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Therefore, CT findings of pericolic streakiness and paracolic fluid do not allow differentiation between transmural and partial mural colonic ischemia (ischemic colitis) when there are no additional CT findings suggestive of transmural colonic infarction such as signs of colonic perforation with or without pneumoperitoneum; large amounts of free intraperitoneal fluid, contrast material, or stool; local or diffuse peritonitis; and/or pronounced pneumatosis or portomesenteric venous gas.
Bowel wall attenuation.—An ischemic bowel segment may manifest with a hypoattenuating or hyperattenuating bowel wall. Hypoattenuation of bowel wall in acute bowel ischemia is usually homogeneous and caused by bowel wall edema; this appearance has been reported (108) in 61% of cases of ischemic colitis (Fig 11). It is therefore obvious that hypoattenuation of a thickened bowel wall, representing bowel wall edema, is more typical in cases of acute bowel ischemia caused by mesenteric venous occlusions (where bowel wall edema is typically pronounced [Fig 7]), although even under these circumstances intramural hemorrhage and hemorrhagic infarction may occasionally cause hyperattenuation of the thickened bowel wall, as well. Such an intramural hemorrhage may be diffuse or located predominantly in the submucosal layers and may also be encountered in cases of acute arterio-occlusive and nonocclusive bowel ischemia or infarction (101–103,108) (Figs 17, 18).
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Figure 18. Unenhanced transverse CT scan in a patient with ischemic colitis of descending and sigmoid colon shows marked heterogeneous wall thickening of sigmoid colon (small arrows) and mucosal and submucosal hyperattenuation (large arrows) due to hemorrhage.
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Abnormal enhancement.—Hyperemia and hyperperfusion of the bowel wall are two other factors that may cause hyperattenuation of ischemic bowel walls on contrast-enhanced CT scans, where it manifests as hyperenhancement. Also, if unenhanced CT is not performed prior to contrast-enhanced CT, differentiation between acute intramural hemorrhage and hyperemia and/or hyperperfusion may be difficult. Hyperemia of ischemic bowel segments without hyperperfusion typically occurs in cases of mesenteric venous occlusion and subsequent outflow obstruction, whereas hyperperfusion of ischemic bowel segments typically occurs during reperfusion following occlusive or nonocclusive bowel ischemia or as a result of superinfection and subsequent inflammation. Hyperemia and hyperperfusion of an ischemic bowel segment may be diffuse or primarily involve the mucosa and submucosa; in the latter conditions, hyperemia and hyperperfusion may cause a typical target sign in addition to the surrounding mural edema (72,101,102) (Fig 8). Contrarily, hyperenhancement of the bowel wall in shock bowel indicates neither hyperemia nor hyperperfusion but typically corresponds to prolonged enhancement of the bowel wall due to reduced arterial perfusion after vasospasm of the mesenteric arteries caused by the effects of angiotensin II or after reduced venous outflow due to contraction of mesenteric veins caused by the effects of adrenaline and noradrenaline.
Hyperperfusion and hyperemia of the bowel have been reported (99) to have a sensitivity of 33% and a specificity of 71% for acute mesenteric ischemia. The authors of that study (99) also showed that pronounced bowel wall enhancement is a good prognostic factor, probably since it represents viability of the bowel wall. In contrast, total absence of bowel wall enhancement is not as sensitive, and while Taourel et al (99) found it in only 18% of patients with acute bowel ischemia, Klein et al (98) reported a sensitivity of 62% for this CT finding. However, absence of bowel wall enhancement has been reported to be highly specific for acute mesenteric ischemia (specificity, 96%), a phenomenon that may also be effectively demonstrated with color Doppler US (99,115).
Pneumatosis and portomesenteric gas.—Pneumatosis and portomesenteric venous gas have been reported as less common but more specific findings of acute bowel ischemia, being present in 6%–28% and 3%–14% of cases, respectively (94,98–100,108). Pneumatosis may manifest with small isolated gas bubbles within an ischemic bowel wall or as broad rims of air dissecting the entire bowel wall into two layers (116) (Figs 5, 10, 20, 21). Portomesenteric venous gas may consist only of some small gaseous inclusions within the mesenteric veins or may extend into the intrahepatic branches of the portal vein, where it is typically found in the periphery of the liver (117) (Figs 22–24). The reported specificities of pneumatosis and portal venous gas for acute bowel ischemia usually approach 100%. However, this would surely not be the case if these numbers were assessed prospectively in a large sample of patients, since there are just too many other possible conditions to which these two CT findings may be attributed as well (see below).
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Figure 20. Contrast-enhanced transverse CT scan in a patient with occlusive transmural colonic infarction shows widely dilated colon with (based on the degree of distention) mildly thickened colonic wall, mesenteric gas, and mixed bubblelike (arrowheads) and bandlike (arrows) pneumatosis.
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Figure 21. Unenhanced transverse CT scan in a patient with embolic transmural small-bowel infarction shows massive circumferential and bandlike pneumatosis (arrows) of multiple necrotic loops and pronounced edema () of mesenteric fat.
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Figure 22. Unenhanced transverse CT scan in a patient with embolic transmural small-bowel infarction shows collection of mesenteric venous gas (arrows) in a branch of the superior mesenteric vein. The infarcted small bowel was dilated without wall thickening.
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Figure 23. Contrast-enhanced transverse CT scan in a patient with embolic transmural small-bowel infarction shows mesenteric venous gas with an air-contrast material level in the superior mesenteric vein (arrow). The infarcted small bowel shows minimal pneumatosis (arrowhead) but no wall thickening.
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Figure 24. Contrast-enhanced transverse CT scan in a patient with acute transmural mesenteric infarction shows pronounced intrahepatic portal venous gas (branching hypoattenuating areas) extending into the periphery of both liver lobes.
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Pitfalls
There are three major potential pitfalls regarding CT detection of bowel ischemia: (a) A colonic segment with superficial mucosal ischemic injury may react with spasticity, and CT findings may be misinterpreted as a simple contraction (providing there is no pericolic fat stranding, abnormal attenuation, or enhancement) (Figs 11, 19). Luminal distention by means of oral or rectal contrast material or water may be helpful in such cases. (b) Another common reason to miss acute colonic ischemia at CT is due to its presence in a widely distended colonic segment where, for example, a bowel wall thickness of 3–5 mm (which would be normal for a colonic segment with a lesser degree of distention) should nonetheless be interpreted by the radiologist as thickened (Figs 1, 10). (c) The third, but probably most important pitfall, is a tendency to misinterpret bowel wall dilatation and air-fluid levels as ileus or pseudo-obstruction in patients with acute arterio-occlusive small-bowel infarction (Fig 3). This may easily happen if there is no bowel wall thickening at all, since the radiologist usually expects bowel wall thickening in cases of acute bowel ischemia. However, it is exactly this patient with acute small-bowel infarction who has a very poor prognosis if the correct diagnosis is missed at CT and if he or she does not undergo surgery immediately, since there is usually no other modality that might enable the correct diagnosis. Therefore, one has to keep in mind that as long as there is no clinical history of vasculitis or other reason for primary or secondary mesenteric venous occlusions, one should not generally expect bowel wall thickening in cases of small-bowel infarction, since a necrotic small bowel in acute and purely arterio-occlusive small-bowel infarction may typically manifest only with dilatation and fluid-filled or gas- and fluid-filled bowel loops but without any bowel wall thickening at all (Fig 3).
CT findings of bowel ischemia may widely overlap with those of various nonischemic conditions affecting the small or large bowel; in particular, acute bowel ischemia affecting rather short and atypical segments may be easily misinterpreted (103,104). For example, CT findings of isolated cecal infarction may be mistaken for typhlitis; ischemia of the terminal ileum or segmental bowel ischemia, for Crohn disease; ischemic pancolitis, for infectious or ulcerative colitis; and isolated ischemic proctosigmoiditis, in particular, for infectious proctosigmoiditis or even for acute sigmoid diverticulitis in patients with diverticula.
Certain nonischemic conditions may also be misinterpreted as acute bowel ischemia, including various types of enteropathic and colopathic conditions (103,104). However, the most common cause of misinterpretation of nonischemic conditions for bowel ischemia is the presence at CT of pneumatosis or portal venous gas. According to the literature, pneumatosis and portal venous gas have a specificity of up to 100% for acute bowel ischemia; this might explain, to an extent, the risk of misinterpretation of these two findings in nonischemic conditions. However, these high specificities are surely too high, since they were drawn from retrospective studies in preselected groups of patients; moreover, it is not uncommon that pneumatosis and portal venous gas may both be related to nonischemic conditions.
The causes of pneumatosis intestinalis may range from infectious, inflammatory, neoplastic, or iatrogenic mucosal injury to increased intraluminal pressure and asthma. Furthermore, this condition must be differentiated from pneumatosis cystoides coli, a benign condition of unknown origin (24,25,116). Likewise, portomesenteric gas, although considered to be a highly specific and even ominous sign in patients with acute bowel ischemia, may also be related to various nonischemic conditions. These include the aforementioned causes of nonischemic pneumatosis, endoscopic or transcutaneous biopsy, gastrointestinal surgery, abdominal abscess drainage, and anaerobic abdominal infection (117). Furthermore, neither pneumatosis nor portomesenteric venous gas is absolutely specific for transmural bowel wall necrosis in cases of acute bowel ischemia, since both CT findings may also be observed in patients with only partial mural or even superficial mucosal and submucosal bowel ischemia, in which cases the findings are typically not associated with the same unfavorable clinical outcome (118).
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CONCLUSION
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One of the goals of modern medicine is to achieve an accurate and early diagnosis, as well as determine optimal treatment and achieve reduced mortality in patients with acute mesenteric infarction. This is often difficult, however, because of the variable clinical and radiologic-pathologic manifestations of the condition. Therefore, a strongly clinical-radiologic approach must be pursued in the detection, diagnosis, and treatment of this often fatal disease. Indeed, understanding of acute bowel ischemia and its
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ABSTRACT
INTRODUCTION
