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Gastrointestinal Imaging |
1 From the Departments of Gastroenterology (T.Y., T.H., T.M., T.S., R.J.S.), Pathology (A.I.), Surgery (S.A.), and Radiology (H.O.), Fukuoka University Chikushi Hospital, Zokumyoin 377-1, Chikushino-shi, Fukuoka 818-8502, Japan. Received March 24, 1998; revision requested June 17; revision received April 15, 1999; accepted May 4. Address reprint requests to T.Y. (e-mail: ff036711@csat.fukuoka-u.ac.jp).
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Abstract |
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Index terms: Angiography, 75.124, 955.12, 955.72 • Arteries, calcification, 75.813, 955.72 • Arteries, mesenteric, 955.12, 955.72 • Colitis, ischemic, 75.266 • Colon, CT, 75.1211 • Veins, calcification, 75.813, 959.72 • Veins, mesenteric, 959.72
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Introduction |
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We encountered three patients in whom ischemic colitis caused by mesenteric phlebosclerosis was histopathologically diagnosed. We report the radiologic findings of these three patients and review previous case reports.
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Case Reports |
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Laboratory findings showed a C-reactive protein level of 19 mg/L and an erythrocyte sedimentation rate of 29 mm/h, but his white blood cell count was within normal limits (6.5 x 109/L). There were no other abnormal findings in the complete blood cell count or blood chemistry analysis, including electrolyte levels.
Abdominal conventional radiography showed multiple calcifications at the site of the ascending colon. The calcifications appeared threadlike and were arranged perpendicular to the bowel wall, which suggested vascular calcifications.
Abdominal computed tomography (CT) disclosed thickening of the wall of the ascending colon, of the hepatic flexure, and of part of the transverse colon. Mural thickening was most remarkable along the mesenteric attachment where the maximal width was 1.5 cm. There were many small calcifications in or near the colonic wall (Fig 1a).
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Radiography of the upper gastrointestinal tract did not show any abnormal findings, nor did endoscopy of the upper gastrointestinal tract reveal any abnormal findings such as varices.
Superior mesenteric angiography showed narrowing of the marginal arteries of the right colic artery and middle colic artery with tortuosity of the vasa recta (Fig 1c). In the venous phase of angiography, marked dilatation and tortuosity of the veins along the vasa recta in the right hemicolon were revealed (Fig 1d). However, there was neither obstruction of the portal vein nor collateral circulation according to the angiographic examinations, including a portogram via the superior mesenteric artery.
The patient underwent percutaneous transhepatic portography to rule out congenital abnormalities of the portal vein and its tributaries and to examine the portal pressure. Percutaneous transhepatic portography showed normal portal, splenic, and superior mesenteric veins, whereas no collateral veins were observed. The pressure study performed during percutaneous transhepatic portography showed that the pressures of the main portal vein, splenic vein, splenoportal junction, and superior mesenteric vein were all within normal limits. Since abdominal pain persisted despite treatment with total parenteral nutrition for 1 month, surgical intervention was performed in April 1995.
Gross findings at laparotomy showed thickening of the ileocecal valve and mild dilatation of the terminal ileum. The cecum and the ascending colon looked dark brown or blackish. The more distal along the colon, the more normal the color of the bowel appeared, with the gross appearance of the sigmoid colon almost normal. Since the surgeons were afraid of leakage if an anastomosis were constructed between the blackish colon and the small intestine, subtotal colectomy with ileosigmoidostomy was performed. The resected specimen showed marked mural thickening of the cecum and the ascending colon. The mucosa appeared edematous with congestion and looked dark brown.
Microscopic examination showed marked fibrosis in the submucosa. The mucosa was atrophic due to perivascular fibrosis. The veins in the submucosa, muscularis propria, and serosa were dilated and tortuous. Mural thickening of the veins by marked fibrosis, with hyalinization and calcification, and luminal narrowing were distinct. In addition, mucosal hemorrhage and vascular congestion of the arteries and veins in the mucosa and submucosa were noted, but no thrombus was found (Fig 1e, 1f).
Case 2
This case has been reported (3). A 57-year-old man had been informed that he had liver dysfunction 12 years prior to admission to the hospital. He began to have right flank pain 7 months prior to admission and underwent barium enema examination of the large bowel. Crohn disease was then diagnosed. He was hospitalized and treated with an elemental diet, but his symptoms did not ameliorate. He was referred to us and was admitted in January 1987 for further examination and treatment. The only abnormal finding at physical examination was tenderness of the right flank.
Complete blood cell count analysis showed pancytopenia: white blood cell count, 3.3 x 109/L; red blood cell count, 3.5 x 1012/L; hemoglobin level, 119 g/L; hematocrit level, 33.6% (0.336); platelet count, 96 x 109/L. Blood chemistry analysis showed mild liver dysfunction: glutamic-oxaloacetic transaminase level, 150 U/L; glutamic-pyruvic transaminase level, 251 U/L; lactate dehydrogenase level, 330 U/L. Although the erythrocyte sedimentation rate was elevated to 64 mm/h, the C-reactive protein level was normal: 1 mg/L. Electrolyte, total cholesterol, and serum amylase levels were also within normal limits.
Abdominal conventional radiography disclosed multiple threadlike calcifications suggestive of vascular calcifications at the site of the ascending colon (Fig 2a).
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The patient was treated with total parenteral nutrition for about 2 months. However, neither his symptoms nor the abnormalities visible at barium enema examination improved with this treatment. He underwent a subtotal colectomy with ileosigmoidostomy in April 1987.
Abnormalities were found macroscopically from the cecum to the descending colon. There was 1 cm of mural thickening of the cecum and the ascending colon, in addition to congestion and edema of the mucosal surface, with swelling or disappearance of the semilunar folds. The color of the surface was dark brown. These findings were mild in degree but similar to those observed in case 1.
Radiography of the resected right hemicolon revealed tortuous threadlike calcifications (Fig 2b). Microscopic examination showed almost the same findings as in case 1, such as marked fibrosis of the mucosa, irregular and tortuous arrangement of the veins, and venous wall thickening by marked fibrosis with hyalinization and calcification.
The patient was readmitted to the hospital because of a small amount of tarry stool in April 1990. A visceral angiogram obtained at that time did not show any abnormal findings in the superior mesenteric, celiac, and inferior mesenteric arteries, except for the loss of the ileocolic, right colic, and middle colic arteries owing to the previous colectomy and the lack of collateral circulation.
Case 3
A 54-year-old man with diarrhea visited a general practitioner in March 1991. Acute colitis was diagnosed. One week later, the diarrhea had ameliorated with use of medication. Two months later, he noticed tarry stool and underwent barium enema examination. Ischemic colitis was diagnosed, and the symptoms disappeared within 3 days.
In 1993, he visited a physician to undergo screening for colonic cancer. Because his feces were positive for occult blood, he underwent radiologic and endoscopic examination. Abnormal findings were observed in the right hemicolon, but a definite diagnosis could not be determined at that time.
In June 1994, the patient came to us, and phlebosclerotic colitis was diagnosed by means of reviewing abdominal conventional radiographic and barium enema examination results obtained at the previous institute. He was admitted to our hospital for further examination. His medical history included osteomyelitis of the right knee joint at the age of 24 years, and he had had hypertension for 20 years. Physical examination disclosed high blood pressure, 160/98 mm Hg, and a restricted range of flexion of his right knee joint.
Complete blood cell count, blood chemistry, electrolyte, urinalysis, and fecal examinations did not show any abnormal results. Signs of inflammation, such as erythrocyte sedimentation rate (2 mm/h) and C-reactive protein level (1 mg/L), were negative.
Abdominal conventional radiography showed multiple threadlike calcifications at the site of the ascending colon and a part of the transverse colon. CT of the abdomen showed calcifications of the right side of the colonic wall and, distant from it, of the veins that emptied into the superior mesenteric vein. However, the thickening of the colonic wall was less distinct compared with that seen in cases 1 and 2 (Fig 3).
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Superior mesenteric angiography showed narrowing of the marginal arteries of the right and middle colic arteries with tortuosity of the vasa recta, as well as dilatation of the veins along the vasa recta in the region of the right hemicolon. The pressure of the main portal vein, measured during percutaneous transhepatic portography, was within normal limits.
At the time of colonoscopic examination, endoscopic mucosal resection of an area of mucosal irregularities in the ascending colon was performed. Histologic examination of the endoscopically resected specimen, which included the mucosal and submucosal layers, revealed atrophy and fibrosis of the mucosa, fibrosis of the submucosa, thickening of the venous walls, and tortuosity of the veins, in addition to focal calcifications in the thickened venous walls. On the basis of these findings, phlebosclerotic colitis was diagnosed.
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Discussion |
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Phlebosclerosis is an adaptive change in the venous wall to prolonged and increased venous blood pressure, for example, owing to right-sided heart failure or portal hypertension (4). As for calcifications due to phlebosclerosis on abdominal conventional radiographs, calcifications of the portal vein, its tributaries, or both are known to occur (5–7). Such patients have portal hypertension. Esophageal varices and hepatosplenomegaly usually are seen concomitantly. Obstruction of the portal vein and extensive collateral circulation frequently are recognized at angiographic examination (5–7). There was no evidence of portal hypertension in the three cases in our study, and neither angiography nor percutaneous transhepatic portography revealed collateral circulation or abnormalities of the portal vein.
Calcifications of the portal vein and its tributaries have been described as having a tortuous tubular appearance expanding to either side of the midline, usually at the level of T12 to L1, at abdominal conventional radiography (5). However, in the cases in our study, calcifications were seen along the wall of the right hemicolon, and they had tortuous threadlike appearances. In one case, abdominal CT disclosed diffuse calcifications not only of the colonic wall but also at a site near the superior mesenteric venous trunk, which may imply that phlebosclerosis had developed diffusely in veins of the colonic wall and in those in the vicinity of the superior mesenteric venous trunk.
On the basis of the findings at abdominal conventional radiography, the radiographic changes at barium enema examination, the gross findings at laparotomy of the right hemicolon (such as a change in color to dark brown), and the histopathologic findings, we conclude that the cause of the disorder in the three cases in our study was ischemic colitis induced by phlebosclerosis in the tributaries of the superior mesenteric vein with subsequent disturbance in venous return from the colonic wall.
Using the National Library of Medicine's bibliographic database, or MEDLINE, we searched for case reports within the 12 years up to 1998 by using the key words "phlebosclerosis" or "ischemic colitis and calcification," but no such case reports were found. In Japan, we first reported case 2 in 1989 at a meeting of the Research Society for Early Gastric Cancer, held in Tokyo (3,8). Thereafter, six more Japanese cases were reported during 1991–1996 (9–13). Although some of these were not reported as cases of colitis with phlebosclerosis, all shared common findings at abdominal conventional radiography and barium enema examination. Two of these six cases were reported in English, but their histopathologic characteristics were not described, since surgical resection had not been performed (11). Among these six cases, some were reported as cases of portal phlebosclerosis. This confusion may have been caused by the lack of detailed examination. Angiography was performed in only three of these previously reported cases, and measurement of portal pressure was performed in none.
The three cases in our study had characteristic findings both radiologically and histopathologically; the disorder thus seems to represent a clinical entity. With regard to family history, past medical history, complications, and laboratory findings, the nine cases (the three cases in our study and the six previously reported cases) had nothing in common, and therefore the pathogenesis of this disorder cannot be speculated on.
If, in the future, other cases of this disorder are detected by means of the characteristic findings at conventional radiography, barium enema examination, and abdominal CT, then its clinicalpathologic features may become more fully clarified. Until then, we propose to call this disorder "phlebosclerotic colitis" and to distinguish it from ordinary ischemic colitis.
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Acknowledgments |
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Footnotes |
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This article has been cited by other articles:
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  M. Kusanagi, O. Matsui, H. Kawashima, T. Gabata, M. Ida, H. Abo, and K. Isse Phlebosclerotic Colitis: Imaging-Pathologic Correlation Am. J. Roentgenol., August 1, 2005; 185(2): 441 - 447. [Abstract] [Full Text] [PDF]
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V. Markos, S. Kelly, W. C. Yee, J. E. Davis, R. E. Cheifetz, and A. Alsheikh Phlebosclerotic Colitis: Imaging Findings of a Rare Entity Am. J. Roentgenol., May 1, 2005; 184(5): 1584 - 1586. [Full Text] [PDF]
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