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(Radiographics. 2000;20:29-42.)
© RSNA, 2000

SCIENTIFIC EXHIBIT

CT and MR Imaging Findings of Bowel Ischemia from Various Primary Causes1

Sung E. Rha, MD , Hyun K. Ha, MD, Soo-Hyun Lee, MD, Ji-Hoon Kim, MD , Jeong-Kon Kim, MD, Jung H. Kim, MD, Pyo N. Kim, MD , Moon-Gyu Lee, MD and Yong-Ho Auh, MD

1 From the Department of Diagnostic Radiology, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Poongnap-Dong, Songpa-Ku, Seoul 138-040, Korea. Recipient of a Certificate of Merit award for a scientific exhibit at the 1998 RSNA scientific assembly. Received February 19, 1999; revision requested March 16; revision received and accepted April 21. Address reprint requests to H.K.H.


   Abstract
Top
 Abstract
Introduction
 Causes of Bowel Ischemia
 Conclusions
 References
 
Ischemic bowel disease represents a broad spectrum of diseases with various clinical and radiologic manifestations, which range from localized transient ischemia to catastrophic necrosis of the gastrointestinal tract. The primary causes of insufficient blood flow to the intestine are diverse and include thromboembolism, nonocclusive causes, bowel obstruction, neoplasms, vasculitis, abdominal inflammatory conditions, trauma, chemotherapy, radiation, and corrosive injury. Computed tomography (CT) or magnetic resonance (MR) imaging can demonstrate the ischemic bowel segment and may be helpful in determining the primary cause. The CT and MR imaging findings include bowel wall thickening with or without the target sign, intramural pneumatosis, mesenteric or portal venous gas, and mesenteric arterial or venous thromboembolism. Other CT findings include engorgement of mesenteric veins and mesenteric edema, lack of bowel wall enhancement, increased enhancement of the thickened bowel wall, bowel obstruction, and infarction of other abdominal organs. However, regardless of the primary cause, the imaging findings of bowel ischemia are similar. Furthermore, the bowel changes simulate inflammatory or neoplastic conditions. Understanding the pathogenesis of various conditions leading to mesenteric ischemia helps the radiologist recognize ischemic bowel disease and avoid delayed diagnosis, unnecessary surgery, or less than optimal management.

Index Terms: Intestines, CT, 70.1211 • Intestines, infarction, 70.795 • Intestines, ischemia, 70.266 • Intestines, MR, 70.1214


   Introduction
Top
 Abstract
 Introduction
Causes of Bowel Ischemia
 Conclusions
 References
 
Bowel ischemia or infarction is a common but complex disorder with various primary causes and clinical presentations and high mortality. It is caused by insufficient blood flow to the intestine from various causes, including thromboembolism, nonocclusive causes, bowel obstruction, neoplasms, vasculitis, abdominal inflammatory conditions, trauma, drugs (chemotherapy), radiation, and corrosive injury.

Imaging findings of bowel ischemia are similar regardless of the primary cause. Radiographic findings of bowel ischemia at plain and barium studies have been well documented and include bowel wall thickening, submucosal focal mural thickening or thumbprinting, dilated bowel loops, intramural pneumatosis, and mesenteric or portal venous gas (1). Angiography may show arterial or venous occlusion or demonstrate vasospasm and diminished flow in nonocclusive ischemia (1). The computed tomographic (CT) or magnetic resonance (MR) imaging findings represent a combination of those seen at plain radiography, barium studies, and angiography. Moreover, CT or MR imaging may be helpful in determining the primary cause of bowel ischemia as well as allowing direct evaluation of the bowel wall, adjacent mesentery, and vascular structures.

The most common CT finding in bowel ischemia is bowel wall thickening, although it is nonspecific (2). The thickened bowel wall is sometimes associated with the target sign, alternating layers of high and low attenuation within the thickened bowel wall, which results from submucosal edema or hemorrhage. However, the bowel wall is thinned or occasionally invisible when the involved bowel segment becomes gangrenous.

Other CT findings of bowel ischemia reported in the literature include arterial occlusion, mesenteric or portal vein thrombosis, bowel dilatation, engorgement of mesenteric veins and mesenteric edema, intramural gas (intestinal pneumatosis), mesenteric or portal venous gas, lack of bowel wall enhancement, increased enhancement of the thickened bowel wall, and infarction of other abdominal organs (eg, liver, spleen, or kidneys) (3). Bowel dilatation reflects the interruption of peristaltic activity in ischemic segments. It is a common but nonspecific finding in bowel ischemia. Engorgement of mesenteric veins reflects venous congestion secondary to stasis. Owing to the edema that accompanies bowel ischemia, the mesenteric fat may be abnormally increased in attenuation (4). Intramural gas is a less common but more specific CT sign of ischemic bowel disease. The intramural gas is caused by dissection of luminal gas into the bowel wall across the compromised mucosa. Mesenteric or portal venous gas is an even less common CT manifestation of ischemic bowel disease and represents the propagation of intramural gas into the mesenteric venous system. Free intraperitoneal gas is an ominous CT sign in ischemic bowel disease because it indicates perforation of an infarcted bowel segment (2). Absent or poor enhancement of the bowel wall appears to be the most specific finding for bowel ischemia. In some cases, the ischemic segment shows prolonged enhancement. An abnormal enhancement pattern in ischemic segments is attributable mainly to perfusion problems (ie, delayed return of the venous blood with subsequent slowing of the arterial supply or arteriospasm).

In this article, we present the broad spectrum of radiologic findings of bowel ischemia from various primary causes. The pathophysiology and pathologic findings of each category of disease are also reviewed.


   Causes of Bowel Ischemia
Top
 Abstract
 Introduction
 Causes of Bowel Ischemia
Conclusions
 References
 
Thromboembolism
Superior mesenteric artery (SMA) embolus associated with cardiovascular problems (Fig 1) is the most common cause of acute mesenteric ischemia, accounting for approximately 50% of cases (1). Thrombosis in the SMA or superior mesenteric vein (SMV) is a less common cause. SMV thrombosis can be confidently detected with CT, even in the peripheral branches, if good enhancement of the mesenteric vessels is achieved (5) (Fig 2). Conversely, the accuracy of CT in diagnosis of mesenteric arterial occlusion is debatable, with the sensitivity ranging from 37% to 80% (3,6). This wide range may be due to a different rate of distal occlusion and different techniques of contrast material administration in each study (3).



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  		Figure 1.   Bowel infarct due to mesenteric arterial occlusion of the ileocolic branch with iodized oil (Lipiodol; Guerbet, Roissy, France) in a 57-year-old man. The iodized oil was infused during hepatic arterial embolization for hepatocellular carcinoma. Contrast material-enhanced CT scan shows bowel wall thickening in the ileum with intestinal pneumatosis (arrowheads), as well as thickening of the ascending colon with the target sign (small arrows). Large arrow = iodized oil.

 


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  		Figure 2a.   Bowel infarct due to mesenteric venous thrombosis in a 52-year-old man. (a) Contrast-enhanced CT scan shows diffuse bowel wall thickening in the jejunum (arrows) and a hypoattenuating thrombus in the SMV (arrowhead). (b) Follow-up CT scan obtained 5 weeks later shows that the thickened bowel wall has become much thinner (arrows). However, at surgery, the involved bowel segment was gangrenous with microperforation.

 


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  		Figure 2b.   Bowel infarct due to mesenteric venous thrombosis in a 52-year-old man. (a) Contrast-enhanced CT scan shows diffuse bowel wall thickening in the jejunum (arrows) and a hypoattenuating thrombus in the SMV (arrowhead). (b) Follow-up CT scan obtained 5 weeks later shows that the thickened bowel wall has become much thinner (arrows). However, at surgery, the involved bowel segment was gangrenous with microperforation.

 
Various causes of hypercoagulable states also cause spontaneous mesenteric vascular occlusion. Among them, antiphospholipid antibody syndrome recently has been regarded as one of the important causes. The diagnosis of this syndrome can be made if the combination of recurrent venous thrombosis, arterial embolism, and recurrent fetal loss is present (7).

Nonocclusive Causes
Nonocclusive ischemia is a condition in which the mesenteric arteries and veins are patent, but flow through them is too slow to deliver enough oxygenated blood to the intestine. The cause is usually decreased cardiac output from any cause, including primary cardiac disease, infarction, arrhythmia, and hypovolemia. Nonocclusive ischemia may be caused by a combination of low mesenteric flow and secondary reflex mesenteric arterial vasoconstriction. Mesenteric arterial vasoconstriction is a condition in which arterial vasospasm reduces flow through patent but acutely contracted arteries. The vasoconstriction may occur reflexly because of hypotension or may occur after administration or abuse of medications, such as digitalis, ergot preparations, vasopressin or other pressor agents, amphetamine, and cocaine (8).

Shock bowel is a subtype of nonocclusive ischemia and involves diffuse small bowel ischemia in patients with hypovolemia (9). Hypoperfusion results in increased bowel permeability to macromolecules and albumin, which leads to diffuse bowel wall thickening (Fig 3), increased enhancement on CT scans due to slowed perfusion and interstitial leakage of molecules of contrast material, and accumulation of intraluminal fluid secondary to the failed resorption capacity (10). However, shock bowel resolves with resolution of hypovolemia; this fact suggests that this finding represents a reversible ischemic change without clinical significance.



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  		Figure 3.   Shock bowel in a 26-year-old woman after cesarean section. Contrast-enhanced CT scan shows diffuse bowel wall thickening in the ileum (arrows) with a large intraperitoneal fluid collection due to hemoperitoneum.

 
Bowel Obstruction
Intestinal strangulation is usually caused by bands and adhesions, hernia, volvulus, or intussusception and develops when circulation to the obstructed segment is impaired. It is characterized by three coexisting phenomena: proximal mechanical obstruction of an involved bowel segment, closed-loop obstruction of the involved segment, and venous congestion of the involved loop (11). The bowel segment proximal to an obstruction can become ischemic due to severe bowel distention. This distention is a reason for bowel wall and mucosal edema, pneumatosis, and perforation proximal to a small bowel or colonic obstruction.

The important CT findings for a diagnosis of strangulated obstruction include poor or absent enhancement, the serrated beak sign, a large amount of ascites, diffuse mesenteric haziness or vascular engorgement, and an unusual vascular course (12–15) (Figs 4, 5). The serrated beak sign indicates the presence of a closed loop associated with regional mesenteric vascular engorgement as well as bowel wall thickening at the obstructed segment (15). Unusual mesenteric vascular courses seen at CT include the whirl sign (16), converging of the mesenteric vessels toward one point (17), and reversed apposition of the mesenteric artery and vein.



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  		Figure 4a.   Strangulated bowel obstruction due to an internal hernia in the lesser sac in a 50-year-old woman. (a) Contrast-enhanced CT scan shows bowel wall thickening with poor enhancement of the strangulated bowel segment (arrows) in the lesser sac. Regional mesenteric vascular engorgement and haziness are also seen. (b) Photograph of the resected specimen shows diffuse dark discoloration of the ischemic segment of the intestine.

 


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  		Figure 4b.   Strangulated bowel obstruction due to an internal hernia in the lesser sac in a 50-year-old woman. (a) Contrast-enhanced CT scan shows bowel wall thickening with poor enhancement of the strangulated bowel segment (arrows) in the lesser sac. Regional mesenteric vascular engorgement and haziness are also seen. (b) Photograph of the resected specimen shows diffuse dark discoloration of the ischemic segment of the intestine.

 


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  		Figure 5a.   Strangulated bowel obstruction due to bands and adhesions in a 25-year-old pregnant woman. (a) Coronal contrast-enhanced MR image shows diffuse small bowel dilatation and poor enhancement (arrows) in the strangulated segment. (b) Coronal half-Fourier single-shot fast spin-echo MR image shows bowel wall thickening with a target appearance (black arrows) and regional mesenteric vascular engorgement (white arrows).

 


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  		Figure 5b.   Strangulated bowel obstruction due to bands and adhesions in a 25-year-old pregnant woman. (a) Coronal contrast-enhanced MR image shows diffuse small bowel dilatation and poor enhancement (arrows) in the strangulated segment. (b) Coronal half-Fourier single-shot fast spin-echo MR image shows bowel wall thickening with a target appearance (black arrows) and regional mesenteric vascular engorgement (white arrows).

 
Information regarding the viability of strangulated bowel loops is important for determining the prognosis and surgical strategy. However, CT has some limitations in clearly determining the viability of bowel loops because early, reversible signs of strangulated obstruction may overlap with the findings of simple bowel obstruction (15). Therefore, the combined use of clinical criteria suggesting intestinal strangulation, such as tenderness, tachycardia, leukocytosis, and fever, would help improve the diagnostic accuracy of CT in equivocal cases. If early decompression of a strangulated bowel obstruction is not performed, bowel gangrene is subsequently produced. In most patients with gangrene, a large amount of intraperitoneal fluid is present; gas can be demonstrated in the mesenteric or portal vein or bowel wall in some instances, and the bowel wall is thinned with poor or absent enhancement.

Neoplasms
Bowel ischemia can also develop in tumorous conditions. The most representative example is colonic carcinoma. The prevalence of ischemic colitis coexisting with colonic carcinoma ranges from 1% to 7%. In such cases, the ischemic change proximal to the colonic carcinoma is usually a consequence of bowel distention due to mechanical obstruction (18). However, proximal ischemia can develop without bowel obstruction. In these cases, proliferation of bacteria due to stagnation of bowel contents above the stricture or mechanical vascular occlusion may contribute to this pathologic change (19).

CT allows distinction of an ischemic segment from a tumoral segment in 75% of such cases (20). Most often, an ischemic segment is concentrically and smoothly thickened with a mean thickness of 1 cm, whereas a tumoral segment is irregularly thickened with a mean thickness of 2 cm (Fig 6). The CT finding of the target sign indicates the presence of an ischemic segment, but this finding appears to not be common (20% of cases). Ischemia can develop at sites remote from the obstructing region with intervening normal-appearing colonic mucosa. This finding may be attributable to the fact that tension in the bowel wall increases both with increasing intraluminal pressure and with increasing diameter of the obstructed segment (19). When colonic carcinoma partially or completely obstructs the ileocecal valve, ischemia can also develop in the small intestine. Although CT is useful for detecting an ischemic segment, barium study appears to be more useful for this purpose. The presence of thumbprinting, loss of abrupt transition, or prominent transverse ridging at the proximal end of the tumoral segment raises the possibility of proximal ischemic changes.



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  		Figure 6a.   Colonic carcinoma with proximal ischemic colitis in a 72-year-old man. (a) Contrast-enhanced CT scan shows concentric bowel wall thickening in the ischemic sigmoid colon (open arrows) with an intervening normal-appearing segment separating the ischemic segment from the tumoral segment in the rectum (solid arrows). (b) Photograph of the resected specimen shows normal colonic mucosa between the tumoral segment (arrows) and ischemic segment (arrowheads).

 


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  		Figure 6b.   Colonic carcinoma with proximal ischemic colitis in a 72-year-old man. (a) Contrast-enhanced CT scan shows concentric bowel wall thickening in the ischemic sigmoid colon (open arrows) with an intervening normal-appearing segment separating the ischemic segment from the tumoral segment in the rectum (solid arrows). (b) Photograph of the resected specimen shows normal colonic mucosa between the tumoral segment (arrows) and ischemic segment (arrowheads).

 
Although relatively uncommon, another tumorous condition that can produce bowel ischemia is pancreatic carcinoma invading the root of the mesentery. Under such circumstances, bowel ischemia results from direct invasion of the SMA or SMV or from squeezing of these vessels.

Vasculitis
Systemic vasculitis affecting the gastrointestinal tract is not common but is one of the causes of bowel ischemia. The frequency of gastrointestinal involvement in systemic vasculitis depends on the type of vasculitis, with the highest prevalence (50%–70%) in cases of polyarteritis nodosa (21). Usually, vasculitis narrows or occludes the smallest peripheral visceral vessels. The bowel changes, like those due to vasculitis elsewhere, are the result of local ischemia and may result in mucosal ulceration, local areas of gangrene with perforation and peritonitis, large areas of gangrene with stricture formation and obstruction, or hemorrhage (22). In general, without knowledge of the clinical information, it may be difficult to determine whether mesenteric ischemia is caused by vasculitis on the basis of CT findings alone. However, mesenteric vasculitis usually demonstrates a relatively long length of bowel involvement and a nonsegmental distribution. Involvement of the duodenum by ischemic change is nearly always indicative of vasculitis. One of the most important features of mesenteric vasculitis is multiplicity; it has a tendency to concomitantly involve both the jejunum and the ileum, as well as both the small and large intestine (Fig 7). In many instances, skip areas between the involved segments can be observed (23). When the territorial extent of mesenteric vascular changes is considered, the prevalence of vasa recta involvement is higher in patients with mesenteric vasculitis (Fig 8). In addition, the prevalence of genitourinary involvement and splenomegaly is high (24).



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  		Figure 7a.   Systemic lupus erythematosus with mesenteric ischemia in a 20-year-old man. (a) Contrast-enhanced CT scan shows diffuse circumferential bowel wall thickening in the small intestine with the target sign and mesenteric vascular engorgement and haziness. (b) Contrast-enhanced CT scan obtained at a lower level shows concentric rectal wall thickening (white arrows) and bladder wall thickening (black arrows) due to lupus cystitis.

 


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  		Figure 7b.   Systemic lupus erythematosus with mesenteric ischemia in a 20-year-old man. (a) Contrast-enhanced CT scan shows diffuse circumferential bowel wall thickening in the small intestine with the target sign and mesenteric vascular engorgement and haziness. (b) Contrast-enhanced CT scan obtained at a lower level shows concentric rectal wall thickening (white arrows) and bladder wall thickening (black arrows) due to lupus cystitis.

 


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  		Figure 8a.   Polyarteritis nodosa with bowel ischemia in a 58-year-old man. (a) Contrast-enhanced CT scan shows bowel wall thickening in the jejunum (arrows) with minimal engorgement of the vasa recta and the arcade of the jejunal vascular branches. (b) Coronal half-Fourier single-shot fast spin-echo MR image shows bowel wall thickening in the jejunum (arrows) with mesenteric haziness (arrowheads). (c) Digital subtraction angiogram shows multiple berry aneurysms in the proximal SMA (arrows) and multifocal areas of luminal narrowing.

 


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  		Figure 8b.   Polyarteritis nodosa with bowel ischemia in a 58-year-old man. (a) Contrast-enhanced CT scan shows bowel wall thickening in the jejunum (arrows) with minimal engorgement of the vasa recta and the arcade of the jejunal vascular branches. (b) Coronal half-Fourier single-shot fast spin-echo MR image shows bowel wall thickening in the jejunum (arrows) with mesenteric haziness (arrowheads). (c) Digital subtraction angiogram shows multiple berry aneurysms in the proximal SMA (arrows) and multifocal areas of luminal narrowing.

 


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  		Figure 8c.   Polyarteritis nodosa with bowel ischemia in a 58-year-old man. (a) Contrast-enhanced CT scan shows bowel wall thickening in the jejunum (arrows) with minimal engorgement of the vasa recta and the arcade of the jejunal vascular branches. (b) Coronal half-Fourier single-shot fast spin-echo MR image shows bowel wall thickening in the jejunum (arrows) with mesenteric haziness (arrowheads). (c) Digital subtraction angiogram shows multiple berry aneurysms in the proximal SMA (arrows) and multifocal areas of luminal narrowing.

 
Abdominal Inflammatory Conditions
Intraabdominal vasculatures can be injured in cases of abdominal inflammatory conditions, which include pancreatitis, appendicitis, diverticulitis, diffuse peritonitis, and parasitic infestation (8). Acute pancreatitis can result in many vascular complications, both arterial and venous. Among these, venous thrombosis involving the splenic or portal vein is relatively more common than arterial involvement and is possibly associated with stasis, spasm, or mass effect from surrounding inflamed pancreatic tissue. SMV thrombosis also occurs infrequently (25). The pathophysiology of SMV thrombosis is not clear, but possible factors include hypovolemia and local release of thrombogenic factors either by invading bacteria or as part of an inflammatory response. Most patients with SMV thrombosis do not develop significant ischemia in the small intestine due to the large collateral venous supply in the mesentery (25). However, colonic ischemia sometimes develops from direct encasement of the branches of left colic vessels (Fig 9). In cases of regional colonic wall thickening in patients with acute pancreatitis, differentiation of colonic ischemia from an inflammatory infiltrate of the colon due to pancreatitis may be difficult with CT.



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  		Figure 9a.   Chronic pancreatitis with diffuse colonic necrosis in a 44-year-old man. (a) Contrast-enhanced CT scan shows evidence of extensive pancreatitis with diffuse phlegmonous changes and a fluid collection in the peripancreatic space as well as involvement of the duodenum (arrows). (b) CT scan obtained at a lower level shows bowel wall thickening along the descending and sigmoid colon (arrows). (c) Photograph of the gross pathologic specimen after total colectomy shows diffuse ischemic changes in nearly the entire colon, which are especially severe at the sigmoid colon (S) and rectum (R). The ischemia resulted from direct encasement of the branches of mesenteric vessels by the pancreatitic process.

 


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  		Figure 9b.   Chronic pancreatitis with diffuse colonic necrosis in a 44-year-old man. (a) Contrast-enhanced CT scan shows evidence of extensive pancreatitis with diffuse phlegmonous changes and a fluid collection in the peripancreatic space as well as involvement of the duodenum (arrows). (b) CT scan obtained at a lower level shows bowel wall thickening along the descending and sigmoid colon (arrows). (c) Photograph of the gross pathologic specimen after total colectomy shows diffuse ischemic changes in nearly the entire colon, which are especially severe at the sigmoid colon (S) and rectum (R). The ischemia resulted from direct encasement of the branches of mesenteric vessels by the pancreatitic process.

 


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  		Figure 9c.   Chronic pancreatitis with diffuse colonic necrosis in a 44-year-old man. (a) Contrast-enhanced CT scan shows evidence of extensive pancreatitis with diffuse phlegmonous changes and a fluid collection in the peripancreatic space as well as involvement of the duodenum (arrows). (b) CT scan obtained at a lower level shows bowel wall thickening along the descending and sigmoid colon (arrows). (c) Photograph of the gross pathologic specimen after total colectomy shows diffuse ischemic changes in nearly the entire colon, which are especially severe at the sigmoid colon (S) and rectum (R). The ischemia resulted from direct encasement of the branches of mesenteric vessels by the pancreatitic process.

 
Trauma
Abdominal trauma is a well-recognized cause of bowel ischemia (26). Penetrating trauma can cause direct damage to the major vessels, including the aorta, SMA, and inferior mesenteric artery, resulting in extensive hemoperitoneum or acute mesenteric ischemia. If localized tissue necrosis is produced by trauma, complete healing or a segmental intestinal stricture develops. However, perforation or localized peritonitis can also occur if transmural necrosis develops.

As demonstrated by several researchers, blunt abdominal trauma is one of the causes of segmental intestinal stenosis in association with acute ischemic insult to the intestine (27). There may be an interval of months or years between the injury and the appearance of the ischemia-related stricture. Such strictures are likely to occur near the proximal or distal extremes of the small intestine, where mesenteric mobility commences. In many instances, focal deprivation of the blood supply secondary to the tear in the mesenteric attachment contributes to the development of posttraumatic ischemia (Fig 10). Alternatively, the intestine may be crushed against the spine, usually as part of a seat belt injury. Barium studies of the colon or small intestine show tubular or circumferential luminal narrowing with an irregular contour, usually in a short segment (28).



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  		Figure 10.   Ischemia of the ileum after blunt trauma in a 35-year-old man. Contrast-enhanced CT scan shows bowel wall thickening in the ileum (open arrows) with diffuse mesenteric haziness (solid arrows).

 
Drugs (Chemotherapy)
Chemotherapeutic agents can induce spontaneous gastrointestinal necrosis and even perforation (29–32). As demonstrated by some researchers, such complications can occur in patients receiving long-term immunosuppressive drugs to prevent homograft rejection or in those receiving long-term chemotherapy for leukemia or lymphoma. The precise cause of the perforations remains unclear, but it may be complex. The fact that bowel ischemia and perforation occur so frequently in immunosuppressed patients lends support to the hypothesis that steroids are partly related (30). Similar pathologic findings in patients who receive cytotoxic agents further suggest that there is a breakdown of intestinal mucosal resistance and that bacterial toxins might also be involved (29).

At CT, chemotherapy-induced enteropathy appears as nonspecific focal or diffuse bowel wall thickening with or without the target sign (Fig 11) or as regional mesenteric vascular engorgement and haziness (Fig 12); occasionally, bowel perforation occurs. Such findings can be seen in either diseased or disease-free intestinal segments.



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  		Figure 11a.   Chemotherapy-induced enteropathy with diffuse intestinal necrosis in the ileum in a 65-year-old woman who received chemotherapy for leukemia. (a) Contrast-enhanced CT scan shows bowel wall thickening in the distal ileum with a target appearance (arrows) and a regional fluid collection due to hemoperitoneum. (b) CT scan obtained at a lower level shows homogeneous bowel wall thickening in the ileum (open arrows) and a localized collection of intraperitoneal free gas (solid arrows).

 


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  		Figure 11b.   Chemotherapy-induced enteropathy with diffuse intestinal necrosis in the ileum in a 65-year-old woman who received chemotherapy for leukemia. (a) Contrast-enhanced CT scan shows bowel wall thickening in the distal ileum with a target appearance (arrows) and a regional fluid collection due to hemoperitoneum. (b) CT scan obtained at a lower level shows homogeneous bowel wall thickening in the ileum (open arrows) and a localized collection of intraperitoneal free gas (solid arrows).

 


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  		Figure 12a.   Chemotherapy-induced enteropathy with diffuse intestinal necrosis in a 72-year-old man who received chemotherapy for central nervous system lymphoma. (a) Contrast-enhanced CT scan shows extensive portal venous gas. (b) CT scan obtained at a lower level shows intestinal pneumatosis (black arrows) and gas in the mesenteric vascular branches (white arrows).

 


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  		Figure 12b.   Chemotherapy-induced enteropathy with diffuse intestinal necrosis in a 72-year-old man who received chemotherapy for central nervous system lymphoma. (a) Contrast-enhanced CT scan shows extensive portal venous gas. (b) CT scan obtained at a lower level shows intestinal pneumatosis (black arrows) and gas in the mesenteric vascular branches (white arrows).

 
Radiation
Radiation-induced small-vessel occlusions may produce chronic ischemia anywhere in the alimentary tract. Radiation enteritis develops in patients who receive 4,500 cGy or more of radiation. The underlying pathologic process is endarteritis obliterans, and compromise of the microvascular circulation is an important factor in the natural history of radiation changes in the intestine (33). Factors that predispose to the development of chronic radiation enteritis include prior abdominal surgery with adhesive changes, peritonitis before radiation therapy, hypertension, atherosclerosis, and diabetes (34). Radiographic findings include thickened valvulae conniventes, wall thickening, later effacement of the mucosal fold pattern, ulceration, single or multiple stenoses, adhesions, and occasional sinuses and fistulas (35,36). CT and MR imaging show bowel wall thickening with occasional visualization of the target sign (37) (Figs 13–15). The important clue for diagnosis is that the bowel changes are confined to the radiation port.



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  		Figures 13.   (13) Acute radiation enteritis in a 61-year-old woman with a history of radiation therapy after hysterectomy for cervical cancer. (a) Image from a small bowel follow-through study shows luminal narrowing and a thickened bowel wall (open arrows) and mucosal irregularity due to ulceration (solid arrows). (b) Coronal half-Fourier single-shot fast spin-echo MR image also shows luminal narrowing and a thickened bowel wall (arrows).

 


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  		Figures 13.   (13) Acute radiation enteritis in a 61-year-old woman with a history of radiation therapy after hysterectomy for cervical cancer. (a) Image from a small bowel follow-through study shows luminal narrowing and a thickened bowel wall (open arrows) and mucosal irregularity due to ulceration (solid arrows). (b) Coronal half-Fourier single-shot fast spin-echo MR image also shows luminal narrowing and a thickened bowel wall (arrows).

 


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  		Figure 14.   Acute radiation enteritis in a 71-year-old man with a history of radiation therapy for periureteral metastases from rectal cancer. Contrast-enhanced CT scan shows diffuse bowel wall thickening with the target sign (arrows) confined to the radiation port.

 


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  		Figure 15.   Chronic radiation enteritis in a 48-year-old man with a history of radiation therapy after surgery for paraganglioma in the paraaortic space. Contrast-enhanced CT scan shows a stricture of the jejunum with considerable bowel wall thickening (arrows) due to desmoplastic reaction.

 
Corrosive Injury
Alkalis are potent lipid solvents and cause injury by liquefaction necrosis with saponification of tissues. Penetration of the mucosa by strong alkali occurs extremely rapidly. Concentrated acids produce coagulative necrosis. A potentially protective eschar develops rapidly and may limit penetration to the deeper muscle layer (38,39).

The esophagus and stomach are the most common sites of involvement, but in severe cases the small intestine can be injured with the development of ischemia (Figs 16, 17).



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  		Figure 16.   Corrosive enteritis in a 70-year-old man with a history of ingestion of acetic acid. Contrast-enhanced CT scan shows heterogeneous bowel wall thickening in the jejunum (arrows) and a large amount of ascites.

 


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  		Figure 17a.   Massive corrosive gastritis and enteritis in a 48-year-old woman with a history of ingestion of acetic acid. (a) Contrast-enhanced CT scan shows pneumatosis involving the gastric wall (arrowheads) and portal venous gas (arrows) with multifocal hepatic infarction. Free air is also noted in the perihepatic space. (b) CT scan obtained at a lower level shows intestinal pneumatosis in the jejunum as well as poor bowel wall enhancement.

 


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  		Figure 17b.   Massive corrosive gastritis and enteritis in a 48-year-old woman with a history of ingestion of acetic acid. (a) Contrast-enhanced CT scan shows pneumatosis involving the gastric wall (arrowheads) and portal venous gas (arrows) with multifocal hepatic infarction. Free air is also noted in the perihepatic space. (b) CT scan obtained at a lower level shows intestinal pneumatosis in the jejunum as well as poor bowel wall enhancement.

 

   Conclusions
Top
 Abstract
 Introduction
 Causes of Bowel Ischemia
 Conclusions
References
 
Regardless of the primary cause, mesenteric ischemia usually produces similar radiologic features and simulates many other inflammatory or neoplastic conditions. Therefore, understanding the pathogenesis of various conditions leading to mesenteric ischemia helps the radiologist recognize ischemic bowel disease and avoid delayed diagnosis, unnecessary surgery, or less than optimal management.


   Footnotes
 
Abbreviations: SMA = superior mesenteric artery SMV = superior mesenteric vein

CME FEATURE This article meets the criteria for 1.0 credit hour in category 1 of the AMA Physician's Recognition Award. To obtain credit, see the questionnaire on pp 244-252.

LEARNING OBJECTIVES After reading this article and taking the test, the reader will be able to: • Describe the broad spectrum of clinical, radiologic, and pathologic manifestations of bowel ischemia. • List the various signs of bowel ischemia and infarction in a variety of radiologic studies and understand their pathophysiology. • Summarize the pathogenesis of bowel ischemia according to the various primary causes.


   References
Top
 Abstract
 Introduction
 Causes of Bowel Ischemia
 Conclusions
 References
 

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