1. Meyers MA, Whalen JP: Roentgen significance of the duodenocolic relationships: An anatomic approach. AJR 1973; 117:263-274.

2. Whalen JP, Riemenschneider PA: Analysis of normal anatomic relationships of colon as applied to roentgenographic observations. AJR Rad Ther Nucl Med 1967; 99:55-61.

3. Meyers MA: Treitz redux: The ligament of Treitz revisited. Abdom Imaging 1995; 29:421-424.

4. Chou CK, Chang JM, Tsai TC, et al: CT of the duodenojejunal junction. Abdom Imaging 1995; 20:425-430.

5. Fox RS, Fox CG, Graham W III: Vaclav Treitz (1819-1872): Czechoslovakian pathoanatomist and patriot. World J Surg 1985; 9:361-366.

6. Treitz W: Uber Einen Neven Muskel Am Duodenum. Vjschr prakt Heilk (Prague) 1853; 37:113144.

7. Akin JT Jr, Gray SW, Skandalakis JE: Vascular compression of the duodenum: Presentation of ten cases and review of the literature. Surgery 1976; 79:515522.

8. van der Zypen E, Revesz E: Investigation of development, structure and function of the phreni-cocolic and duodenal suspensory ligaments. Acta Anat 1984; 119:142-148.

9. Friedman SM: Position and mobility of duodenum in living subject. Am J Anat 1946; 79:147-165.

10. Treitel H, Meyers MA, Maza V: Changes in the duodenal loop secondary to carcinoma of the hepatic flexure of the colon. Br J Radiol 1970; 43: 209-213.

11. Vieta JO, Blanco R, Valentini GR: Malignant duo-denocolic fistula: Report of two cases, each with one or more other synchronous gastrointestinal cancers. Dis Colon Rectum 1976; 19:542-552.

12. Perri F, Annese V, Federici T, et al: Benign duo denocolic fistula: An unusual cause of gastrointestinal bleeding. Gastrointest Endosc 1993; 39:827830.

13. Korelitz BI: Colonic-duodenal fistula in Crohn's disease. Dig Dis 1977; 22:1040-1048.

14. Jacobson IM, Schapiro RH, Warshaw AL: Gastric and duodenal fistulas in Crohn's disease. Gastroenterology 1985; 89:1347-1352.

15. Herlinger H, O'Riordan D, Saul S, et al: Nonspecific involvement ofbowel adjoining Crohn disease. Radiology 1986; 159:47-51.

16. Tandon HD, Prakash A: Pathology of intestinal tuberculosis and its distinction from Crohn's disease. Gut 1972; 13:260-269.

17. Ha HK, Ko GY, Yu ES, et al: Intestinal tuberculosis with abdominal complications: Radiologic and pathologic features. Abdom Imaging 1999; 24:32-38.

18. Torrance B, Jones C: Three cases of spontaneous duodenocolic fistula. Gut 1972; 13:627-630.

19. Ghahremani GG, Meyers MA: The cholecystocolic relationships: A roentgen-anatomic study of the co-lonic manifestations of gallbladder disorders. AJR 1975; 125:21-34.

20. Ohtani T, Shirai Y, Hatakeyama K: Diagnosis and staging of gallbladder carcinoma by computed tomography. In Neoplasms of the Digestive Tract: Imaging, Staging and Management. Edited by MA Meyers. Lippincott-Raven, Philadelphia, 1998, pp 485-492.

21. Ohtani T, Shirai Y, Tsukada K et al: Spread of gallbladder carcinoma: CT evaluation with pathologic correlation. Abdom Imaging 1996; 21:195-201.

22. Wolloch Y, Glanz I, Dintsman M: Spontaneous biliary-enteric fistulas: Some considerations on the management of gallstones. Am J Surg 1976; 131: 680-683.

23. Shimono T, Nishimura K, Hayakawa K: CT imaging of biliary enteric fistula. Abdom Imaging 1998; 23:172-176.

24. Meyers MA: Leiomyosarcoma of the duodenum: Radiographic and arteriographic features. Clin Radiol 1971; 22:257-260.

Intestinal Effects of Pancreatitis: Spread Along Mesenteric Planes

Acute inflammation of the pancreas may be classified into four groups:

1. Acute edematous pancreatitis is the most common form; there is localized or diffuse swelling of the organ.

2. Acute hemorrhagic pancreatitis is caused by the digestive effects of liberated trypsin and elastase on pancreatic vessels. The first changes caused by this vascular necrosis are found in the outer layer, but the damage usually progresses rapidly to involve the entire thickness of the vessel wall, with disruption of the intima.1

3. Acute gangrenous pancreatitis is rare because of the rich vascularization of the pancreas.

4. Acute suppurative pancreatitis secondary to superimposed infection may range from a localized pancreatic abscess to diffuse involvement, perhaps as a gas-producing process.

Localized changes on characteristic portions of the small intestine and colon are produced by the extrava-sated enzymes of pancreatitis, which follow definite anatomic planes.2 The lesions range from transient spasm to ischemic atrophy and the development of obstructive strictures as well as remote exudative abscesses. Extension of the effects of pancreatitis may occur through the loose retroperitoneal tissue planes of the anterior pararenal spaces. Notably, however, the mesenteric pathways most often involved and that direct the spread of pancreatic enzymes to remote sites in the intestinal tract are the transverse mesocolon and the small bowel mesentery. These observations have been confirmed by computed tomography.3 5 Fat necrosis is most common in these two sites and in the omentum.6

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