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Gastrointestinal Imaging |
1 From the Departments of Radiology ( J.Y.B., S.Y.Y., K.A.C., K.H.C., K.S.S.) and Internal Medicine (J.K.M., S.H.P., H.Y.K.), Kangnam St Mary's Hospital, College of Medicine, the Catholic University of Korea, 505 Banpo-Dong, Seocho-Ku, Seoul 137-040, Korea; the Department of Diagnostic Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea (H.K.H.); and the Department of Diagnostic Radiology, Hanyang University Hospital, Seoul, Korea (B.H.K.). Received December 31, 1997; revision requested February 24, 1998; revision received July 7; accepted October 20. Address reprint requests to J.Y.B.
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Abstract |
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MATERIALS AND METHODS: The authors retrospectively reviewed the images from 39 abdominal CT examinations performed in 33 patients with SLE and acute abdominal pain. Images were evaluated for bowel wall changes, mesenteric changes, fluid collection, retroperitoneal lymphadenopathy, peritoneal enhancement, and hepatomegaly as well as for changes in other abdominal organs. Ischemic bowel disease was diagnosed if at least three of the following signs were seen: bowel wall thickening, target sign, dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat.
RESULTS: Thirty-one (79%) of the 39 examinations had CT findings diagnostic of ischemic bowel disease, including symmetric bowel wall thickening (n = 29), target sign (n = 26), and mesenteric vascular engorgement and haziness (n = 31). In 24 cases, bowel wall thickening was multifocal, with variable length, and did not appear to be confined to a single vascular territory.
CONCLUSION: The most common CT finding in patients with SLE and acute abdominal pain is ischemic bowel disease. CT is useful for detecting the primary cause of gastrointestinal symptoms, planning treatment, and monitoring for infarction or perforation.
Index terms: Abdomen, CT, 70.12112, 70.12115 • Intestines, CT, 70.12112, 70.12115 • Intestines, infarction, 70.795 • Intestines, ischemia, 70.799, 70.612 • Lupus erythematosus, 70.612
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Introduction |
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Although nonspecific gastrointestinal symptoms are common in patients with SLE, abdominal pain is the most common manifestation of gastrointestinal involvement (3). Acute abdominal pain can occur as a consequence of various causes, but intraabdominal vasculitis resulting in ischemia and infarction of the intestine is the most common cause and the most dangerous manifestation in this illness (4,5).
The diagnosis of acute primary mesenteric ischemia poses a clinical challenge. The symptoms and signs at presentation are often varied and may overlap with those of bowel obstruction or peritonitis (6). Plain abdominal radiographs or contrast material–enhanced bowel radiographs are often normal or nonspecific. Although the role of computed tomography (CT) remains controversial and is still evolving, it is currently being used with increasing frequency in this clinical setting (7). Several articles have described the CT findings of bowel ischemia in patients with SLE (8–12). To our knowledge, however, the wide spectrum of CT findings in patients with SLE and acute abdominal pain has not been investigated.
The purpose of this study was to evaluate the CT features in patients with SLE and acute abdominal pain. Special emphasis was placed on the analysis of ischemic bowel disease.
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MATERIALS AND METHODS |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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CT was performed with a Somatom Plus or Somatom Plus 4 unit (Siemens, Erlangen, Germany). Scans were obtained with 8–10-mm-thick sections and 8–10-mm intervals. All scans were obtained after intravenous administration of contrast material. A total of 100 mL of iopromide 62.3% (Ultravist 300; Schering, Berlin, Germany) was administered by means of rapid bolus infusion in four cases and by using a mechanical power injector at a rate of 2–3 mL/sec in 35. Incremental sequential scanning (n = 20) and spiral CT (n = 19) was begun 45 seconds after the start of the injection, and the images covered the diaphragm to the symphysis. All patients received 500–700 mL of diluted diatrizoate meglumine (Gastrografin 2%; Schering), which was administered orally from 120 minutes to 30 minutes before scanning.
CT scans were retrospectively reviewed by two experienced radiologists (J.Y.B., H.K.H.), and the diagnosis was reached by consensus. Images were evaluated for bowel wall changes (bowel wall thickening patterns, involving sites, contrast enhancement patterns, dilatation of intestinal segments, and pneumatosis intestinalis) and mesenteric changes (engorged mesenteric vessels, comb sign, and increased attenuation of mesenteric fat). Other findings evaluated were the presence or absence of a fluid collection (ascites, pleural effusion, and pericardial effusion), retroperitoneal lymphadenopathy, peritoneal enhancement, and hepatomegaly. Any changes in other abdominal organs were also noted.
In the context of the clinical presentation and SLE history, the CT diagnosis of ischemic bowel disease was based on the presence of at least three of the following signs: bowel wall thickening, target sign, dilatation of intestinal segments, engorgement of mesenteric vessels, and increased attenuation of mesenteric fat.
Bowel wall thickening was diagnosed if the bowel wall was at least 3 mm thick in an area where the bowel was adequately distended (14).
Contrast enhancement patterns were classified as heterogeneous (target sign) or homogeneous. The target sign was defined as a thickened bowel wall with peripheral rim enhancement or an enhancing inner and outer rim with hypoattenuation in the center. Dilatation of intestinal segments was diagnosed if the dilated bowel segments had a diameter of more than 3 cm. The comb sign was defined as an increased number of visible vessels with a comblike pattern (12).
Because the amount of ascites could not be quantified exactly with CT, it was defined as small if fluid was confined to the pelvic cavity or localized within the peritoneal cavity and large if fluid overflowed into the peritoneal cavity from the pelvic cavity (15). Hepatomegaly was diagnosed when the craniocaudal dimension in the midclavicular line was greater than 15 cm (16). Splenomegaly was diagnosed when the craniocaudal span was greater than 14 cm. Lupus nephritis was diagnosed when kidneys were uniformly enlarged and had an abnormal contrast enhancement pattern in combination with proteinuria or cellular casts of any type at urinalysis (13).
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RESULTS |
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Ascites was present in 30 of the 39 cases; it was noted in 27 of the 31 cases with CT findings diagnostic of ischemic !bowel disease. Ascites was small in 17 of the 30 cases and large in 13.
All but one patient with CT findings of ischemic bowel disease were initially treated conservatively with intravenous high-dose steroid therapy and recovered from the acute gastrointestinal symptoms. Panperitonitis and impending bowel infarction were diagnosed clinically in one patient, and emergent exploratory laparotomy was performed. Surgery, however, showed edematous swelling and wall thickening of the jejunum representing mild reversible bowel ischemia; there was no evidence of bowel infarction.
Six patients with CT findings of ischemic bowel disease had another attack of acute abdominal pain after recovery from the acute gastrointestinal symptoms. Repeat CT scans were obtained 1–32 months after the initial CT scans. In five of these six patients, CT findings of ischemic bowel disease were again noted with partial regression (n = 2), little change (n = 1), and progression (n = 2) compared with findings on initial CT scans. One patient had no evidence of ischemic bowel disease on the repeat CT scan.
In one patient whose initial CT scan showed diffuse bowel wall thickening (Fig 5a), bowel infarction developed 6 months after initial remission. At the second admission, this patient had acute abdominal pain, and ultrasonography (US) showed concentric thickening of the jejunal wall (Fig 5b); CT was not performed at that time. Despite the use of intravenous steroid therapy, the patient's symptoms did not improve—even after 3 days—and mesenteric angiography was performed. The emergency superior mesenteric angiogram showed marked narrowing of the jejunal arteries and little vascular perfusion of the jejunal wall (Fig 5c), which indicates the presence of bowel infarction. Histopathologic examination performed after segmental resection of the jejunum showed typical necrotizing vasculitis affecting small vessels in submucosa, muscle, and subserosal layers (Fig 5d).
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DISCUSSION |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Although a wide range of abdominal symptoms has been noted in patients with SLE, abdominal pain is the most common, with reported frequencies of 33%–62% (24–26). These abdominal symptoms may result from a variety of disorders, such as central nervous system involvement, uremia, primary peritonitis, serositis, acute pancreatitis, ulcer, ileus, protein-losing enteropathy, and a variable degree of small- or large-bowel ischemia (19,21,22,25). Bowel ischemia due to vasculitis is the most serious gastrointestinal complication of SLE (10). Prompt and intensive radiographic evaluation is essential to differentiate the potential causes of abdominal distress.
The diagnosis of bowel ischemia is frequently difficult to make on the basis of plain radiography and barium studies. The advent of CT, however, with its ability to show both the bowel wall and the abdominal vasculature, raises the hopes for a more accurate method of diagnosing mesenteric ischemia (27). A thickened bowel wall and mesenteric change are displayed directly on CT scans. The common CT findings in mesenteric ischemia include dilated bowel, focal or diffuse bowel wall thickening, abnormal bowel wall enhancement (double halo or target sign), mesenteric edema, engorged mesenteric vessels, and ascites (27). The lack of specificity of these signs, however, is a limitation of the CT study because they can be seen in patients with pancreatitis, mechanical bowel obstruction, peritonitis, or inflammatory bowel disease, all of which may mimic intestinal ischemia clinically (27). Another problem with CT is the subjectivity in the interpretation of the various ischemic signs (28).
Vasculitis of the bowel due to SLE is known to be relatively uncommon (10). Our study, however, showed that 31 (79%) of the 39 CT examinations performed because of acute abdominal pain were diagnostic of ischemic bowel disease due to vasculitis. The high percentage of bowel ischemia in our study may be due to the fact that CT was performed in patients with acute abdominal pain and clinically suspected bowel ischemia. Unfortunately, pathologic proof of the presence of reversible vasculitis could not be obtained in these patients because improvement with steroid therapy negated the need for surgery. SLE history, clinical presentation, CT findings, and clinical improvement after intravenous steroid administration, however, strengthened the diagnosis of reversible ischemic bowel disease.
In our study, the jejunum and ileum were the most common sites of involvement. The segments of bowel wall thickening were multifocal and not confined to a single vascular territory in 24 of 29 cases with bowel wall thickening because mesenteric vasculitis may affect several vessels simultaneously (8). A recent study (12) has shown that lupus mesenteric vasculitis preferentially affected the territory supplied by the superior mesenteric artery, and no evidence of transverse or left side colon involvement was found at CT. In our study, however, the territory supplied by the inferior mesenteric artery was frequently involved: the transverse colon was involved in 10 (34%) of the 29 cases, the descending colon was involved in 11 (38%), and the rectosigmoid was involved in nine (31%). Although the rectum was involved in nine cases in our study (Fig 1c), isolated involvement of the rectum was not noted in any patient. Although the vasculitis and immune complex deposits are a systemic phenomenon and may involve any organ, rectal involvement is known to be rare. To our knowledge, only one case of isolated ischemic necrosis of the rectum has been previously reported (29). This may be due to the rich and multisource blood supply of the rectum.
CT is very sensitive in the detection of intramural gas collections, a well-known sign and characteristic finding of acute mesenteric ischemia. Pneumatosis intestinalis is very rare in lupus and, to our knowledge, has been documented in only six previously published case reports (10,17,30). In our series, there was only one case with a small amount of pneumatosis intestinalis in the jejunal wall (Fig 4). This patient was treated conservatively with intravenous steroid administration and improved clinically.
Mesenteric changes such as vascular congestion or mesenteric edema are common in patients with acute mesenteric ischemia (27). In our study, mesenteric changes were present in all 31 cases with CT findings of ischemic bowel disease.
A recent report stressed that a conspicuous prominence of mesenteric vessels with a palisade or comblike arrangement (comb sign) might be an early sign of lupus mesenteric vasculitis (12). Our data also showed that the comb sign was positive in 27 of the 31 cases with CT findings of ischemic bowel disease (Fig 3). The CT appearance of engorged mesenteric vessels, however, ranged from an enhancing nodular appearance (Fig 6a) to a comblike arrangement (Fig 6b), depending on the direction of the mesenteric vessels.
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The spectrum of renal disease in SLE is wide and ranges from minimal, nonprogressive disease to rapidly progressive glomerulonephritis (9). In our study, lupus nephritis and hydronephrosis were present in nine cases each, and lupus cystitis was noted in six cases. Lupus cystitis was seen in five of the nine cases with hydronephrosis. Although hydronephrosis occurs from many mechanisms in patients with SLE, vasculitis-related lupus cystitis is considered to be the most possible cause of hydronephrosis because obstruction at the ureterovesical junction may develop from detrusor muscle spasm associated with inflammation (32).
In our study, four cases of acute pancreatitis developed—three cases in association with ischemic bowel disease and one case without evidence of ischemic bowel disease. Although the etiology may be difficult to ascertain, vasculitis, thrombi in the pancreatic vessels, and a long-standing use of corticosteroids may cause acute pancreatitis (19,25). One case of pancreatic cancer was included in our study, but we consider this to be an incidental finding.
Although ischemic bowel disease was evident on CT scans in most of our patients with SLE and acute abdominal pain, bowel may be normal on CT scans in patients with acute abdominal pain or clinically suspected bowel ischemia. Because abdominal pain may have many causes, the source of pain cannot always be determined (25). In our series, variable CT findings were seen in eight cases without CT findings of ischemic bowel disease. These variable findings included pancreatitis, hydronephrosis, nephritis, cystitis, splenic infarction, thrombosis of inferior vena cava and renal vein, pancreatic cancer, and liver abscess, which might be the probable cause of abdominal pain. The cause of our one case of liver abscess was uncertain, although we consider this to be an incidental finding. CT is useful for differentiating variable causes of acute abdominal pain in patients with SLE.
The prompt diagnosis and treatment of patients with lupus and abdominal symptoms are often extremely difficult. In the absence of clinical signs of serious complications, intensive corticosteroid, antibiotic, and fluid therapy are indicated in most instances because these patients do not tolerate surgery well and have a propensity to form adhesions (33).
In conclusion, the results of our study show that the most common CT finding in patients with SLE and acute abdominal pain is ischemic bowel disease. CT is useful for detecting the primary cause of gastrointestinal symptoms, planning treatment, and monitoring for infarction or perforation.
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Footnotes |
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Author contributions: Guarantor of integrity of entire study, J.Y.B.; study concepts and design, J.Y.B., H.K.H., S.Y.Y., J.K.M.; definition of intellectual content, J.Y.B., H.K.H., S.Y.Y., J.K.M.; literature research, J.Y.B., H.K.H., S.Y.Y., J.K.M.; clinical studies, J.Y.B., J.K.M., S.H.P., H.Y.K.; data acquisition, J.Y.B., H.K.H., S.Y.Y., J.K.M., S.H.P., H.Y.K., K.A.C., B.H.K.; data analysis, J.Y.B., H.K.H., S.Y.Y., J.K.M.; statistical analysis, J.Y.B., S.Y.Y., J.K.M.; manuscript editing, J.Y.B., H.K.H., S.Y.Y., J.K.M., K.H.C.; manuscript review, J.Y.B., H.K.H, S.Y.Y., J.K.M., K.H.C., K.S.S.
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