Transverse Colon and Splenic Flexure

Since Price's report, however, the term "colon cut-off" sign has lost its original definition and has been applied to multiple sites of spasm and narrowing of the colon secondary to pancreatitis. Stuart12 employed it to designate collapse with absence of gas in the midportion of the transverse colon, which appeared to be cut off from the gas-containing hepatic and splenic flexures. This was a constant finding in both supine and erect plain films of the abdomen in six patients with acute pancreatitis. Brascho and co-authors13 found the gaseous dilatation to involve the ascending and entire transverse colon, with the cut-off point at the splenic flexure. In my ex-perience,2 as well as that of others,14-17 this is by far the most common single site involved.

Pancreatitis Edematosa

Fig. 11—6. Acute pancreatitis with extension to hepatic flexure.

Barium enema shows diffuse mild spasm and edematous mucosal changes of the hepatic flexure and distal ascending colon from extension of extravasated pancreatic enzymes via the right anterior pararenal compartment.

Fig. 11—6. Acute pancreatitis with extension to hepatic flexure.

Barium enema shows diffuse mild spasm and edematous mucosal changes of the hepatic flexure and distal ascending colon from extension of extravasated pancreatic enzymes via the right anterior pararenal compartment.

On plain films, the most common abnormality in the large intestine in cases of acute pancreatitis is gaseous distention of the transverse colon. This often represents a paralytic ileus secondary to the extravasated enzymes within the transverse mesocolon (Figs. 11-8 through 11-11). More directly irritative effects may be manifested by spasm and edema18 (Figs. 11-12 through 11-14).

Barium Enema Splenic Flexure

Fig. 11—7. Acute suppurative pancreatitis with extension to hepatic flexure.

(a and b) Barium enema and spot film demonstrate an annular constricting lesion of the distal ascending colon. The constant narrowing and overhanging shelflike margin mimic an "apple-core" carcinoma. Exploratory laparotomy disclosed a large peripancreatic abscess with retroperitoneal extension down to and involving the hepatic flexure and distal ascending colon, where an extramural inflammatory stricture was encountered. Areas of fat necrosis were present in the transverse mesocolon, pericolonic tissue, and greater omentum.

(Reproduced from Meyers and Evans. )

Fig. 11—7. Acute suppurative pancreatitis with extension to hepatic flexure.

(a and b) Barium enema and spot film demonstrate an annular constricting lesion of the distal ascending colon. The constant narrowing and overhanging shelflike margin mimic an "apple-core" carcinoma. Exploratory laparotomy disclosed a large peripancreatic abscess with retroperitoneal extension down to and involving the hepatic flexure and distal ascending colon, where an extramural inflammatory stricture was encountered. Areas of fat necrosis were present in the transverse mesocolon, pericolonic tissue, and greater omentum.

(Reproduced from Meyers and Evans. )

Fig. 11—8. Acute pancreatitis with extension in mesocolon approaching the transverse colon.

(a) During an episode of acute pancreatitis, CT shows enlargement of the pancreatic head (P) and phlegmonous extension into the transverse mesocolon (arrows).

(b) Three months later, the process has condensed and become encapsulated as a small pseudocyst within the transverse mesocolon (arrow). Note that the process stops just short of affecting the transverse colon (TC).

(Courtesy of Emil Balthazar, M.D., Bellevue Hospital, New York University School of Medicine, New York, NY.)

Splenic FlexureSplenic Flexure

Fig. 11—9. Mesocolic involvement by pancreatitis.

CT demonstrates multiple pseu-docysts of the pancreas (asterisks) have extended into the transverse mesocolon, whose fatty tissue is infiltrated by the inflammatory process.

Fig. 11—9. Mesocolic involvement by pancreatitis.

CT demonstrates multiple pseu-docysts of the pancreas (asterisks) have extended into the transverse mesocolon, whose fatty tissue is infiltrated by the inflammatory process.

Splenic FlexureSplenic Flexure

Fig. 11-10. Extension of acute pancreatitis to transverse colon.

(a) At the level of the uncinate process of the pancreas (P), inflammatory changes progress through the transverse mesoco-lon (arrows) toward the right, with associated conspicuous branches of the middle colic vessels.

(b) The infiltrate compresses and distorts the transverse colon

Fig. 11-10. Extension of acute pancreatitis to transverse colon.

(a) At the level of the uncinate process of the pancreas (P), inflammatory changes progress through the transverse mesoco-lon (arrows) toward the right, with associated conspicuous branches of the middle colic vessels.

(b) The infiltrate compresses and distorts the transverse colon

Dynamic Ileus

Fig. 11-11. Fulminant acute pancreatitis extending through the transverse mesocolon.

Phlegmonous changes involve the anterior pararenal spaces bilaterally and extend across the mesocolon (arrows) toward the transverse colon (TC), which exhibits ileus.

Fig. 11—12. Acute pancreatitis.

Plain film shows diffuse spasm and edema of the transverse colon due to extensive inflammatory exudate that also displaces the stomach superiorly and the transverse colon inferiorly.

Abdominal Splenic Flexure

Fig. 11—13. Acute pancreatitis.

Diffuse inflammation of transverse colon, shown by spastic narrowing and gross mucosal irregularities on delayed film of upper GI series.

Mucosa Images Transverse ColonAbdominal Splenic Flexure

Fig. 11-14. Acute pancreatitis.

Diffuse inflammation of transverse colon. Frontal (a) and oblique (b) views of barium enema study demonstrate mucosal edema. (Reproduced from Thompson et al. )

Fig. 11-14. Acute pancreatitis.

Diffuse inflammation of transverse colon. Frontal (a) and oblique (b) views of barium enema study demonstrate mucosal edema. (Reproduced from Thompson et al. )

The natural extension of the inflammatory process into the phrenicocolic ligament may result in severe spasm or an incomplete mechanical obstruction at the level of the anatomic splenic flexure immediately inferior to the tip of the spleen8 (Fig. 11-15). The obstruction need not be permanent and may resolve as pancreatitis subsides (Figs. 11-16 through 11-18). However, if the inflammation is more severe and particularly if it is accompanied by fat necrosis, barium enema study shows narrowing of the splenic flexure with irregular nodular or serrated margins and distorted mucosal folds secondary to the extramural inflammatory infiltrate. Occasionally, a significant degree of retrograde obstruction may be met, and the changes may simulate carcinoma.19 A granulomatous and fibrotic reaction may then result in a stricture of the splenic flexure. It is for these reasons that most colon strictures secondary to pancreatitis occur in the splenic flexure. 15-17,20

This is illustrated in Figure 11-19 in a case of traumatic pancreatitis. Barium enema examination discloses irregular flattening of the lower border of the transverse colon along its length, ending abruptly at the level of the anatomic splenic flexure (Fig. 11-19a) Distal to this site, the extraperitoneal descending colon resumes a normal haustral pattern. This pattern of asymmetric involvement of the lower contour of the mesenteric transverse colon is characteristic of extension of disease from the pancreas along the transverse mesocolon and phren-icocolic ligament.21 The narrowing with irregular nodular defects demonstrated in the splenic flexure (Fig. 11-19b, c) is obviously organic and not functional in nature and thus indicates direct passage of considerable pancre-

Splenic Flexure

Fig. 11—15. Acute pancreatitis extending into the phrenicocolic ligament.

Phlegmonous changes spread extensively through the mesocolon, and fluid extends into the phrenicocolic ligament (arrows) immediately lateral to the anatomic splenic flexure of the colon (C). Gallstones are present. (Courtesy of René Le Gall, M.D., Papeete, Tahiti.)

Pics Gallstones After Colonic

Fig. 11—16. Acute pancreatitis.

(a) Supine and (b) erect. Dilatation and air-fluid levels of the transverse colon extend to a narrowed segment of the splenic flexure (arrows).

Barium enema study 1 week after conservative therapy showed no abnormalities, indicating that these changes were due to spasm secondary to the irritating effects of enzymes within the phrenicocolic ligament. (Reproduced from Meyers and Evans.2)

Fig. 11—16. Acute pancreatitis.

(a) Supine and (b) erect. Dilatation and air-fluid levels of the transverse colon extend to a narrowed segment of the splenic flexure (arrows).

Barium enema study 1 week after conservative therapy showed no abnormalities, indicating that these changes were due to spasm secondary to the irritating effects of enzymes within the phrenicocolic ligament. (Reproduced from Meyers and Evans.2)

Splenic Flexure

Fig. 11—17. Pancreatic pseudocyst with pericolitis.

While the upper gastrointestinal series (a) demonstrates the pressure effect on the stomach produced by a large organizing pancreatic pseudocyst, the barium enema study (b) shows localized narrowing and spiculation of the mucosal pattern of the anatomic splenic flexure from extravasated pancreatic enzymes.

Transverse Colon Radiology

Fig. 11—18. Acute pancreatitis extending across the transverse mesocolon to the anatomic splenic flexure of the colon.

(a) CT shows gross extension of pancreatic inflammatory changes through the mesocolon (arrows) to the region of the phrenicocolic ligament (curved arrow).

(b) Barium enema reveals spasm of the splenic flexure with proximal colonic dilatation.

Fig. 11—18. Acute pancreatitis extending across the transverse mesocolon to the anatomic splenic flexure of the colon.

(a) CT shows gross extension of pancreatic inflammatory changes through the mesocolon (arrows) to the region of the phrenicocolic ligament (curved arrow).

(b) Barium enema reveals spasm of the splenic flexure with proximal colonic dilatation.

Transverse Colon

Fig. 11—19. Traumatic pancreatitis, with development of stricture of splenic flexure.

(a) Flattening of the inferior haustral contour of the transverse colon. Pseudosacculations result on the uninvolved superior border. The process ends at the level of the phrenicocolic ligament at the anatomic splenic flexure of the colon (arrow).

(b and c) Scalloped narrowing of the splenic flexure on filled and air studies. The intramural lesions end precisely at the level of the phrenicocolic ligament (arrows).

(d) Three months later, there is a marked fibrotic stenosis of the splenic flexure, reducing its lumen to a diameter of less than 3 mm. Surgical resection of the stricture, induced by fat necrosis, was required. (Reproduced from Meyers and Evans.2)

Fig. 11—19. Traumatic pancreatitis, with development of stricture of splenic flexure.

(a) Flattening of the inferior haustral contour of the transverse colon. Pseudosacculations result on the uninvolved superior border. The process ends at the level of the phrenicocolic ligament at the anatomic splenic flexure of the colon (arrow).

(b and c) Scalloped narrowing of the splenic flexure on filled and air studies. The intramural lesions end precisely at the level of the phrenicocolic ligament (arrows).

(d) Three months later, there is a marked fibrotic stenosis of the splenic flexure, reducing its lumen to a diameter of less than 3 mm. Surgical resection of the stricture, induced by fat necrosis, was required. (Reproduced from Meyers and Evans.2)

atic enzymes into the phrenicocolic ligament. From the severe changes in the splenic flexure, the probable development of a fibrotic stricture (Fig. 11-19d) should be anticipated and serial evaluations by barium enema studies obtained.

If the inflammatory process erodes through the wall of the colon at this site, extraperitoneal sinus tracts or fistulas to adherent small bowel loops may be demonstrated (Figs. 11-20 through 11-22).

Pancreatic pseudocysts may spontaneously rupture into an adjacent hollow viscus, the colon and particularly the splenic flexure being the most common site22-24

(Figs. 11-23 through 11-25). Fistulization does not occur in the initial acute phase of pancreatitis, but rather as a consequence of pancreatic suppuration or pseudocyst. Pancreatic gas may be the consequence of fistuli-zation, rather than secondary to pancreatic abscess

alone. The mechanism involves enzymatic digestion of the cyst wall or vascular insult that produces progressive necrosis and rupture. While temporary or even permanent remission may result from this spontaneous de-compression,24 major gastrointestinal bleeding is seen in about 30% because of erosion of large arteries,22,24 and sepsis with conversion of the pseudocyst into an abscess text continues on page 582

Splenic Flexure

Fig. 11-20. Gas-producing abscess of pancreas.

(a) Multiple gaseous lucencies of tail of pancreas at site of draining catheter. Barium enema demonstrates extension via the phrenicocolic ligament to anatomic splenic flexure with multiple sinus tracts of varying size.

(b) Four months later, multiple residual sinus tracts are present. (Reproduced from Meyers and Evans.2)

Fig. 11-20. Gas-producing abscess of pancreas.

(a) Multiple gaseous lucencies of tail of pancreas at site of draining catheter. Barium enema demonstrates extension via the phrenicocolic ligament to anatomic splenic flexure with multiple sinus tracts of varying size.

(b) Four months later, multiple residual sinus tracts are present. (Reproduced from Meyers and Evans.2)

Fig. 11—21. Acute pancreatitis with transmural erosion.

(a and b) Severe spread of enzymes into the phrenicocolic ligament produces a fixed and irregular narrowing of the anatomic splenic flexure of the colon. Transmural erosion is shown by faint barium extravasation laterally.

Fig. 11—22. Acute suppurative pancreatitis with transmural erosion.

Extravasated enzymes within the phrenicocolic ligament have resulted in incomplete obstruction of the splenic flexure (arrows) and transmural digestion with fistuli-zation to a small bowel loop and a long extraperitoneal sinus tract from the narrowed splenic flexure.

(Reproduced from Meyers and Evans.2)

Hepatic Flexure Polyp MriPhrenicocolic Ligament

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Responses

  • ruth
    What is Splenic flexure apple core lesion?
    4 years ago
  • robert
    What shape is an annular constricting lesion in the distal transverse colon?
    4 years ago
  • HAGOS
    Are the splenic flexure and transverse colon 2 different areas?
    2 years ago
  • aleksi
    Can pancreatitis cause narrowing of transverse colon at hepatic flexure?
    2 years ago

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