(Radiographics. 2001;21:1475-1490.)
© RSNA, 2001
Root of the Small-Bowel Mesentery: Correlative Anatomy and CT Features of Pathologic Conditions1
Yuriko Okino, MD,
Hiro Kiyosue, MD,
Hiromu Mori, MD,
Eiji Komatsu, MD,
Shunro Matsumoto, MD,
Yasunari Yamada, MD,
Koji Suzuki, MD and
Kenichiro Tomonari, MD
1 From the Department of Radiology, Oita Medical University, Hasama-machi, Oita 879-5593, Japan. Presented as an education exhibit at the 2000 RSNA scientific assembly. Received February 7, 2001; revision requested April 6 and received July 9; accepted July 23. Address correspondence to Y.O. (e-mail: hosya@oita-med.ac.jp).
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Abstract
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The root of the small-bowel mesentery (SBM) is an important peritoneal fold that is contiguous to other peritoneal ligaments and mesocolons. Several pathologic conditions can occur in the SBM itself, and diseases that spread through the connections from adjacent organs frequently involve it. The root of the SBM is contiguous to the hepatoduodenal ligament around the superior mesenteric vein (SMV) and contiguous to the right side of the transverse mesocolon around the gastrocolic trunk. The inferior mesenteric vein, which is a landmark of the descending mesocolon, runs along the left side of the root of the SBM. Malignant neoplasms can spread to the SBM by means of direct extension, extension along the neural plexus, extension along neighboring ligaments, or extension along lymphatic vessels. Inflammatory conditions such as pancreatitis and perforation of a jejunal diverticulum can also spread to the SBM. Anomalies that can occur in the SBM include rotation anomalies and internal hernia. Vascular lesions of the SBM include thrombosis of the superior mesenteric artery (SMA), acute SMV thrombosis, SMA dissection, arterioportal fistula, and portal venous gas. Other pathologic conditions that can occur in the SBM are edema or congestion, mesenteric tear, mesenteric panniculitis, and tumors or tumorlike lesions.
Index Terms: Mesenteritis, 792.295 • Mesentery, 792.92 • Mesentery, gas, 792.71, 792.783 • Mesentery, injuries, 792.41 • Mesentery, ischemia, 95.70 • Mesentery, neoplasms, 792.30 • Peritoneum, abnormalities, 792.146, 792.158 • Peritoneum, fluid, 792.77 • Retroperitoneal space, fibrosis, 87.893, 98.827
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LEARNING OBJECTIVES FOR TEST 4
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After reading this article and taking the test, the reader will be able to:
- Describe the normal anatomy of the SBM and its relationships to the other peritoneal folds.
- List the various pathologic conditions that involve the root of the SBM and their characteristic CT features.
- Recognize vessels that are landmarks of the SBM, such as the gastrocolic trunk and inferior mesenteric vein.
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Introduction
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The root of the small-bowel mesentery (SBM) is located in the central portion of the abdomen, connecting intraperitoneal structures, and is contiguous to other peritoneal ligaments and mesocolons. Several pathologic conditions can occur in the SBM itself, and diseases from other organs that spread via connections with the SBM also frequently involve the root of the SBM. This article describes the normal anatomy of the root of the SBM and presents specific computed tomographic (CT) features of secondary SBM lesions that spread via the SBM root and primary SBM lesions.
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Normal Anatomy
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The SBM is a voluminous, fat-laden peritoneal reflection that fixes the jejunum and ileum to the posterior abdominal wall. The attached parietal border, which is approximately 15 cm long, runs obliquely down from the duodenojejunal flexure to the ileocecal region (1). Its root is a bare area continuous with the anterior pararenal space of the retroperitoneum (2). The root of the SBM contains two major vessels, the superior mesenteric artery (SMA) and superior mesenteric vein (SMV).
There are many important structures and organs in the vicinity of the root of the SBM. The root of the SBM is contiguous superiorly to the hepatoduodenal ligament around the SMV and portal vein, contiguous anteriorly to the transverse mesocolon, and contiguous posterolaterally to the ascending and descending mesocolons (anterior pararenal space) (Figs 1–3). The gastrocolic trunk, which is formed by union of the gastroepiploic vein, right colic vein, and anterior superior pancreaticoduodenal vein, runs anterior to the surface of the pancreatic head and joins the right aspect of the SMV. The gastrocolic trunk is a landmark of the junction between the transverse mesocolon and the root of the SBM. The inferior mesenteric vein, which is a landmark of the descending mesocolon, joins the SMV or splenic vein on the left side of the root of the SBM.
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Figure 1. Drawing of the anatomy near the root of the SBM (RSBM). The root of the SBM (area within dashed circle) is contiguous superiorly to the hepatoduodenal ligament (HDL) along the SMV, anteriorly to the transverse mesocolon (TM), and posterolaterally to the ascending mesocolon and descending mesocolon (DM). The gastrocolic trunk (GT) is a landmark of the junction between the transverse mesocolon and the root of the SBM. The inferior mesenteric vein (IMV) is a landmark of the descending mesocolon and joins the SMV or splenic vein on the left side of the root of the SBM. IPDA = inferior pancreaticoduodenal artery, IPDV = inferior pancreaticoduodenal vein, PV = portal vein, SRL = splenorenal ligament.
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Figure 2. Massive ascites in a patient with ovarian cancer. Coronal magnetic resonance (MR) image of the peritoneal folds clearly shows the relationships of the ligaments and mesenteries. Note that the root of the SBM (*) is contiguous to the hepatoduodenal ligament (HDL) and the right side of the transverse mesocolon (TM). SRL = splenorenal ligament.
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Figure 3a. Contrast material-enhanced CT scans of the peritoneal folds and ligaments. (a) The root of the SBM is contiguous to the hepatoduodenal ligament (arrows) around the portal vein (PV) and SMV. CHA = common hepatic artery. (b, c) The root of the SBM is contiguous to the right side of the transverse mesocolon (TM) in the vicinity of the gastrocolic trunk (GT). The right side of the root is contiguous to the ascending mesocolon (arrowheads), which contains the right colic vein (RCV). The left side is contiguous to the descending mesocolon (arrows), which contains the inferior mesenteric vein (IMV). A = SMA, D = horizontal portion of the duodenum, J = jejunum, V = SMV. (d) The posterior attachment of the SBM (arrows) fixes the SBM to the posterior abdominal wall. IMV = inferior mesenteric vein.
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Figure 3b. Contrast material-enhanced CT scans of the peritoneal folds and ligaments. (a) The root of the SBM is contiguous to the hepatoduodenal ligament (arrows) around the portal vein (PV) and SMV. CHA = common hepatic artery. (b, c) The root of the SBM is contiguous to the right side of the transverse mesocolon (TM) in the vicinity of the gastrocolic trunk (GT). The right side of the root is contiguous to the ascending mesocolon (arrowheads), which contains the right colic vein (RCV). The left side is contiguous to the descending mesocolon (arrows), which contains the inferior mesenteric vein (IMV). A = SMA, D = horizontal portion of the duodenum, J = jejunum, V = SMV. (d) The posterior attachment of the SBM (arrows) fixes the SBM to the posterior abdominal wall. IMV = inferior mesenteric vein.
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Figure 3c. Contrast material-enhanced CT scans of the peritoneal folds and ligaments. (a) The root of the SBM is contiguous to the hepatoduodenal ligament (arrows) around the portal vein (PV) and SMV. CHA = common hepatic artery. (b, c) The root of the SBM is contiguous to the right side of the transverse mesocolon (TM) in the vicinity of the gastrocolic trunk (GT). The right side of the root is contiguous to the ascending mesocolon (arrowheads), which contains the right colic vein (RCV). The left side is contiguous to the descending mesocolon (arrows), which contains the inferior mesenteric vein (IMV). A = SMA, D = horizontal portion of the duodenum, J = jejunum, V = SMV. (d) The posterior attachment of the SBM (arrows) fixes the SBM to the posterior abdominal wall. IMV = inferior mesenteric vein.
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Figure 3d. Contrast material-enhanced CT scans of the peritoneal folds and ligaments. (a) The root of the SBM is contiguous to the hepatoduodenal ligament (arrows) around the portal vein (PV) and SMV. CHA = common hepatic artery. (b, c) The root of the SBM is contiguous to the right side of the transverse mesocolon (TM) in the vicinity of the gastrocolic trunk (GT). The right side of the root is contiguous to the ascending mesocolon (arrowheads), which contains the right colic vein (RCV). The left side is contiguous to the descending mesocolon (arrows), which contains the inferior mesenteric vein (IMV). A = SMA, D = horizontal portion of the duodenum, J = jejunum, V = SMV. (d) The posterior attachment of the SBM (arrows) fixes the SBM to the posterior abdominal wall. IMV = inferior mesenteric vein.
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In terms of the neural plexus, the pancreatic capital plexus, which includes a first branch and a second branch, is attached to the medial margin of the pancreatic head near the SMA and celiac trunk (Fig 4). The second branch of this plexus is located around the inferior pancreaticoduodenal artery and inferior pancreaticoduodenal vein (3). In terms of lymphatic vessels, there is the peripancreatic nodal group, which includes the anterior and posterior peripancreatic nodes, and the pancreaticoduodenal nodes, which continue to the nodes of the SMA trunk along the inferior pancreaticoduodenal artery (4).
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Figure 4. Drawing of the neural plexus near the pancreatic head. The pancreatic capital plexus is attached to the medial margin of the pancreatic head near the SMA and celiac trunk. The second branch of the plexus (II) surrounds the inferior pancreaticoduodenal artery and vein.
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Secondary SBM Lesions That Spread via the SBM Root
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Malignant Neoplasms
Direct Extension.—
The pancreas is located in the retroperitoneum adjacent to many structures and organs and has no fibrous capsule. Thus, pancreatic cancer commonly manifests as direct invasion of surrounding structures, generally resulting in a poor prognosis due to its limited resectability. Cancer of the pancreatic body may spread directly to the root of the SBM (Fig 5). Although malignant tumors of the jejunum and duodenum are rare, they can directly involve the root of the SBM (Fig 6).
Extension along the Neural Plexus.—
Neural plexus invasion is a common manifestation of pancreaticobiliary cancers and is found during surgery in 91% of patients with cancer of the pancreatic head and 88% of patients with distal bile duct cancer (3). Cancer of the pancreatic head or distal common bile duct frequently spreads to the SBM root via the second branch of the neural plexus. Tumors may infiltrate toward the posterior aspect of the SMA or the jejunal mesentery via the second branch of the plexus along the inferior pancreaticoduodenal artery or inferior pancreaticoduodenal vein. Neural plexus invasion is recognized on CT scans as an irregular mass or areas of increased attenuation or stranding of retroperitoneal fat around the inferior pancreaticoduodenal artery, inferior pancreaticoduodenal vein, or SMA (Fig 7).
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Figure 7a. Neural plexus invasion by cancer of the lower bile duct. Postcontrast CT scans show a tumor (* in a) of the lower bile duct. Neural plexus invasion is seen as extension of the mass through the root of the SBM and along the inferior pancreaticoduodenal artery and first jejunal artery (arrows in b) to the right aspect of the SMA (arrowheads in a). D = duodenum, P = pancreatic head, V = SMV.
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Figure 7b. Neural plexus invasion by cancer of the lower bile duct. Postcontrast CT scans show a tumor (* in a) of the lower bile duct. Neural plexus invasion is seen as extension of the mass through the root of the SBM and along the inferior pancreaticoduodenal artery and first jejunal artery (arrows in b) to the right aspect of the SMA (arrowheads in a). D = duodenum, P = pancreatic head, V = SMV.
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Extension along Neighboring Ligaments.—
The root of the transverse mesocolon extends across the descending duodenum and the pancreatic head, continuing along the lower edge of the pancreatic body and tail. It merges with the root of the SBM around the uncinate process of the pancreas. Cancer of the pancreatic head located near the gastrocolic trunk extends into the SMV and may infiltrate the root of the transverse mesocolon. Pancreatic cancer may also extend to the SBM and ligaments, including the hepatoduodenal ligament, splenorenal ligament, gastrohepatic ligament, and gastrosplenic ligament, either directly or via the transverse mesocolon (Fig 8). In addition, hepatobiliary cancer or gastroduodenal cancer may extend to the root of the SBM through the hepatoduodenal ligament, and descending colon cancer or retroperitoneal sarcomas may extend to the root of the SBM through the transverse mesocolon or descending mesocolon (2).
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Figure 8. Cancer of the pancreatic body extending through the ligaments. Postcontrast CT scan shows a tumor (T) of the pancreatic body, located in the SBM, extending to the splenorenal ligament (arrows) through the transverse mesocolon.
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Extension along Lymphatic Vessels.—
Because of the rich lymphatic networks around the pancreas, lymph node metastases are common in pancreatic tumors. Most lymph node metastases are found in the peripancreatic nodal group (which includes the anterior and posterior peripancreatic nodes), in the pancreaticoduodenal nodes along the inferior pancreaticoduodenal artery, and in the nodes of the SMA trunk. In distal bile duct cancer, the lymph node involvement extends from the hepatoduodenal ligament or posterior pancreaticoduodenal region to the area around the SMA.
Ampullary cancer most frequently spreads to the posterior peripancreatic nodal group, to the nodes of the inferior pancreaticoduodenal artery, and then to the nodes of the SMA trunk.
Inflammation
Pancreatitis.—
In severe forms of pancreatitis, extensive pancreatic necrosis and inflammation of the peripancreatic fat are present and may result in fluid accumulations. This fluid, including digestive enzymes, may directly extend to the anterior pararenal space by autolysis. The SBM is continuous with the transverse mesocolon at the inferior portion of the pancreas. Thus, the pancreatic fluid can spread to remote sites such as the ileal loops, transverse colon, or cecum along the SBM or transverse mesocolon (Figs 9, 10). For the pathway of pancreatic fluid via the transverse mesocolon, there are lateral limits of the hepatic flexure on the right side and the splenic flexure on the left side. In contrast, for the pathway of pancreatic fluid via the SBM, there is an inferior limit of the ileocecal region (5) (Fig 9). Vascular injury due to pancreatic fluid is often observed, including portal vein thrombosis and pseudoaneurysm of the peripancreatic artery. In rare cases, pancreatic fluid extends into the portal venous system (Fig 11).
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Figure 9. Drawing of the pathways for pancreatic fluid to the SBM. Pancreatic fluid can spread to remote sites along the ligaments and mesentery. For the pathway via the transverse mesocolon (TM), the lateral limits are the hepatic flexure on the right side and the splenic flexure on the left side. For passage of pancreatic fluid via the SBM, the inferior limit is the ileocecal region. PCL = phrenocolic ligament, SRL = splenorenal ligament.
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Figure 10a. Acute pancreatitis. (a) Drawing of the pathway for pancreatic fluid shows the fluid extending through the root of the SBM anteriorly into the transverse mesocolon (TM) and in a left lateral direction into the anterior pararenal space behind the descending mesocolon (DM). Note the relationship between the inferior mesenteric vein (IMV) and the pathway for pancreatic fluid from the root of the SBM to the left anterior pararenal space behind the descending mesocolon. DC = descending colon, P = pancreatic head. (b, c) Postcontrast CT scans (b obtained superior to c) show pancreatic fluid extending to the SBM and transverse mesocolon (arrowheads). The fluid also extends laterally to the left anterior pararenal space behind the descending mesocolon (*) and to the right anterior pararenal space behind the ascending mesocolon (**). The inferior mesenteric vein, which is the landmark for the descending mesocolon, is clearly visualized (arrow).
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Figure 10b. Acute pancreatitis. (a) Drawing of the pathway for pancreatic fluid shows the fluid extending through the root of the SBM anteriorly into the transverse mesocolon (TM) and in a left lateral direction into the anterior pararenal space behind the descending mesocolon (DM). Note the relationship between the inferior mesenteric vein (IMV) and the pathway for pancreatic fluid from the root of the SBM to the left anterior pararenal space behind the descending mesocolon. DC = descending colon, P = pancreatic head. (b, c) Postcontrast CT scans (b obtained superior to c) show pancreatic fluid extending to the SBM and transverse mesocolon (arrowheads). The fluid also extends laterally to the left anterior pararenal space behind the descending mesocolon (*) and to the right anterior pararenal space behind the ascending mesocolon (**). The inferior mesenteric vein, which is the landmark for the descending mesocolon, is clearly visualized (arrow).
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Figure 10c. Acute pancreatitis. (a) Drawing of the pathway for pancreatic fluid shows the fluid extending through the root of the SBM anteriorly into the transverse mesocolon (TM) and in a left lateral direction into the anterior pararenal space behind the descending mesocolon (DM). Note the relationship between the inferior mesenteric vein (IMV) and the pathway for pancreatic fluid from the root of the SBM to the left anterior pararenal space behind the descending mesocolon. DC = descending colon, P = pancreatic head. (b, c) Postcontrast CT scans (b obtained superior to c) show pancreatic fluid extending to the SBM and transverse mesocolon (arrowheads). The fluid also extends laterally to the left anterior pararenal space behind the descending mesocolon (*) and to the right anterior pararenal space behind the ascending mesocolon (**). The inferior mesenteric vein, which is the landmark for the descending mesocolon, is clearly visualized (arrow).
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Figure 11a. Acute pancreatitis with pancreatic fluid extending through the portal venous system. (a, b) Postcontrast CT scans show a pseudocyst (* in b) in the uncinate process of the pancreas. A low-attenuation area within the portal venous system is also identified (arrows in a). (c) Endoscopic retrograde cholangiopancreatogram shows contrast medium filling the biliary tract and entering the portal venous system through the pseudocyst (*). C = common bile duct, PV = portal vein, SPV = splenic vein. (d) MR cholangiopancreatogram shows high signal intensity of the portal venous system in contiguity with the pseudocyst (*). C = common bile duct, MPD = main pancreatic duct, PV = portal vein, SPV = splenic vein.
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Figure 11b. Acute pancreatitis with pancreatic fluid extending through the portal venous system. (a, b) Postcontrast CT scans show a pseudocyst (* in b) in the uncinate process of the pancreas. A low-attenuation area within the portal venous system is also identified (arrows in a). (c) Endoscopic retrograde cholangiopancreatogram shows contrast medium filling the biliary tract and entering the portal venous system through the pseudocyst (*). C = common bile duct, PV = portal vein, SPV = splenic vein. (d) MR cholangiopancreatogram shows high signal intensity of the portal venous system in contiguity with the pseudocyst (*). C = common bile duct, MPD = main pancreatic duct, PV = portal vein, SPV = splenic vein.
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Figure 11c. Acute pancreatitis with pancreatic fluid extending through the portal venous system. (a, b) Postcontrast CT scans show a pseudocyst (* in b) in the uncinate process of the pancreas. A low-attenuation area within the portal venous system is also identified (arrows in a). (c) Endoscopic retrograde cholangiopancreatogram shows contrast medium filling the biliary tract and entering the portal venous system through the pseudocyst (*). C = common bile duct, PV = portal vein, SPV = splenic vein. (d) MR cholangiopancreatogram shows high signal intensity of the portal venous system in contiguity with the pseudocyst (*). C = common bile duct, MPD = main pancreatic duct, PV = portal vein, SPV = splenic vein.
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Figure 11d. Acute pancreatitis with pancreatic fluid extending through the portal venous system. (a, b) Postcontrast CT scans show a pseudocyst (* in b) in the uncinate process of the pancreas. A low-attenuation area within the portal venous system is also identified (arrows in a). (c) Endoscopic retrograde cholangiopancreatogram shows contrast medium filling the biliary tract and entering the portal venous system through the pseudocyst (*). C = common bile duct, PV = portal vein, SPV = splenic vein. (d) MR cholangiopancreatogram shows high signal intensity of the portal venous system in contiguity with the pseudocyst (*). C = common bile duct, MPD = main pancreatic duct, PV = portal vein, SPV = splenic vein.
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Perforation of a Jejunal Diverticulum.—
Small-bowel diverticula predominantly involve the proximal jejunum. Apart from the Meckel diverticulum, these diverticula are acquired and are most frequently seen in the sixth and seventh decades of life (6). They are false diverticula and have thin walls with no muscular layer. Herniation can occur on the mesenteric side of the bowel wall, where the blood vessels pass through. Perforation is the most severe complication of jejunal diverticula, with a mortality rate of up to 40% (7). Since the diverticula usually exist on the mesenteric side of the bowel wall, the air perforations can extend to the root of the SBM through the SBM itself. CT can demonstrate these air perforations in the vicinity of the root of the SBM, the intestine, and mesenteric vessels (Fig 12).
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Figure 12a. Perforation of a jejunal diverticulum. Nonenhanced CT scans show air perforations within the root of the SBM and the retroperitoneal fat (straight arrows in a). Intraluminal gas is seen in the small intestine (curved arrow in b).
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Figure 12b. Perforation of a jejunal diverticulum. Nonenhanced CT scans show air perforations within the root of the SBM and the retroperitoneal fat (straight arrows in a). Intraluminal gas is seen in the small intestine (curved arrow in b).
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Primary SBM Lesions
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Anomalies
Rotation Anomalies.—
Rotation anomalies of the midgut loop include nonrotation, incomplete rotation, and reversed rotation.
Nonrotation of the midgut, a relatively common condition, is generally asymptomatic; however, since the peritoneal fixation is weak, twisting of the intestines (volvulus) can occur. Nonrotation occurs when the midgut loop does not rotate, resulting in the small intestine being on the right side and the large intestine on the left side (8). CT clearly shows this abnormality in the mesenteric vessels, with the SMA on the right side of the SMV (9) (Fig 13). If volvulus occurs, a "whirl sign" around the SMA may be identified at CT (Fig 14).
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Figure 13. Rotation anomaly (nonrotation). Postcontrast CT scan shows dilated bowel loops due to sigmoid colon cancer. The whole colon is located on the left side of the abdominal cavity. Note that the SMA (straight arrow) is to the right of the SMV. The inferior mesenteric vein (curved arrow) is in the normal position within the right margin of the descending mesocolon.
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Figure 14. Midgut volvulus. Precontrast CT scan shows a typical whirl sign (arrowheads) around the SMA (the root of the SBM). Note the high-attenuation structure (arrow) in the whirled loops, which represents a thrombus within the SMA.
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Incomplete rotation results from failure of the midgut loop to complete the final 90° of rotation. In this case, the cecum lies just inferior to the pylorus of the stomach and is fixed to the posterior abdominal wall by peritoneal bands passing over the duodenum. These bands or the volvulus of the intestine causes duodenal obstruction (8).
In the case of reversed rotation, which is rarely seen, the midgut loop rotates in a clockwise rather than a counterclockwise direction. As a result, the duodenum lies anterior to the SMA and the transverse colon lies posterior to the SMA. In this situation, the transverse colon may be obstructed by the pressure of the SMA (8).
Internal Hernia.—
Paraduodenal hernias are the most common type of internal abdominal hernias and result from congenital abnormalities in mesenteric peritoneal fixation (10). They are three times more frequent on the left side than on the right. Patients are frequently asymptomatic, and the hernia is thus discovered incidentally. The clinical manifestations result from partial or complete obstruction of the small intestine, which occurs in 50% of cases (11).
Left paraduodenal hernia develops through a peritoneal defect (the paraduodenal fossa) situated at the duodenojejunal junction, which is the confluent zone of the descending mesocolon, transverse mesocolon, and SBM. It extends into the descending mesocolon and the left portion of the transverse mesocolon. This portion of the transverse mesocolon or the descending mesocolon at the neck of the hernia sac contains the inferior mesenteric vein and left colic artery (11,12) (Fig 15). Recognition of the inferior mesenteric vein is useful because it is the most important landmark of the duodenojejunal junction. It runs superiorly along the right margin within the descending mesocolon and joins the splenic vein or SMV at the transverse mesocolon–SBM junction. CT can clearly demonstrate an encapsulated bowel loop that displaces the inferior mesenteric vein anteriorly (Fig 16), suggesting that the trapped loop is located behind the descending mesocolon. The trapped small-bowel loops are dilated; when the loops are strangulated, congestion of the SBM of the loops is sometimes also observed.
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Figure 15. Drawing of a left paraduodenal hernia. The jejunum enters the hernia sac behind the descending mesocolon through a peritoneal defect situated near the inferior mesenteric vein. (Adapted and reprinted, with permission, from reference 12.)
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Figure 16a. Left paraduodenal hernia. Axial (a) and coronal (b) postcontrast CT scans show an encapsulated bowel loop (black arrows) in the left paraduodenal fossa. The inferior mesenteric vein (arrowheads) is displaced anterolaterally by the bowel loop and joins the SMV through the root of the SBM. Note the mesenteric fat and the jejunal vein (white arrows) within the bowel loop.
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Figure 16b. Left paraduodenal hernia. Axial (a) and coronal (b) postcontrast CT scans show an encapsulated bowel loop (black arrows) in the left paraduodenal fossa. The inferior mesenteric vein (arrowheads) is displaced anterolaterally by the bowel loop and joins the SMV through the root of the SBM. Note the mesenteric fat and the jejunal vein (white arrows) within the bowel loop.
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Right paraduodenal hernia involves the mesentericoparietal fossa of Waldeyer, which is located just behind the root of the SBM, with the SMA and SMV running along the free edge of the right paraduodenal hernia sac (Fig 17). The right colic vein is a landmark of the ascending mesocolon. The right colic vein runs within the ascending mesocolon and joins the gastrocolic trunk through the transverse mesocolon. Right paraduodenal hernia occurs most frequently in the setting of a nonrotated small intestine. CT clearly demonstrates that the encapsulated small-bowel loops in the right midabdomen displace the right colic vein anteriorly (Fig 18), suggesting that the trapped loop is located behind the ascending mesocolon. In addition, looping of the small intestine around the SMA and SMV at the root of the SBM can be observed. Besides malrotation, right paraduodenal hernia is associated with two additional findings: location of the SMV to the left of and ventral to the SMA and absence of the normal horizontal duodenum (13).
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Figure 17. Drawing of a right paraduodenal hernia. The jejunum enters the mesentericoparietal fossa of Waldeyer (yellow arrow). The right colic vein (RCV), a landmark of the ascending mesocolon, runs within the ascending mesocolon and joins the gastrocolic trunk (GT) through the transverse mesocolon. (Adapted and reprinted, with permission, from reference 12.)
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Figure 18a. Right paraduodenal hernia. (a) Postcontrast CT scan shows an encapsulated bowel loop (arrows) in the Waldeyer fossa. The right colic vein (arrowheads) is displaced anteriorly by the bowel loop. (b) Surgical photograph obtained after withdrawal of the herniated bowel loops shows the hernial hiatus (Waldeyer fossa) (*). Note the congestion of the SBM. PJ = proximal jejunum withdrawn from the sac, T = Treitz ligament.
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Figure 18b. Right paraduodenal hernia. (a) Postcontrast CT scan shows an encapsulated bowel loop (arrows) in the Waldeyer fossa. The right colic vein (arrowheads) is displaced anteriorly by the bowel loop. (b) Surgical photograph obtained after withdrawal of the herniated bowel loops shows the hernial hiatus (Waldeyer fossa) (*). Note the congestion of the SBM. PJ = proximal jejunum withdrawn from the sac, T = Treitz ligament.
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Vascular Lesions
There are major mesenteric vessels and their tributaries in the root of the SBM, which feed to or drain from the small intestine and the right side of the colon.
SMA Thrombosis.—
SMA thrombosis can cause severe mesenteric ischemia. The etiology of acute occlusion consists of embolism and thrombosis. Acute emboli generally lodge at the bifurcation of the middle colic artery and the SMA (14). Thrombosis more often involves the proximal SMA. At precontrast CT, a hyperattenuating SMA may suggest SMA thrombosis. In addition, the key finding of SMA thrombosis is a filling defect of the contrast medium or ringed enhancement of the SMA at postcontrast CT (Fig 19). Decreased enhancement of the bowel wall, bowel wall thickening, and bowel dilatation have also been observed, all of which represent ischemic changes in the intestine. In addition, acute embolic infarction of the kidney or spleen is an important finding, as 20% or more of patients will also have embolization in other arteries during the current embolic event (15). The treatment for SMA thrombosis depends on the reversibility of the mesenteric ischemia. Bowel dilatation and intraluminal or intraportal venous gas are important clues in predicting the irreversibility of the ischemia.
Acute SMV Thrombosis.—
Acute mesenteric vein thrombosis occurs in up to 10% of cases of small-bowel ischemia. The etiology includes blood dyscrasia associated with hypercoagulability. Other causes include trauma, portal hypertension, infection, carcinoma, and use of oral contraceptive pills (16). Occlusion of the proximal SMV rarely causes bowel necrosis. In contrast, occlusion of the distal SMV or its branches involving the vasa recta causes bowel necrosis by preventing collateral flow. Precontrast CT can show enlarged diameter and increased attenuation of the SMV (reflecting the thrombi). After administration of contrast material, filling defects of the SMV, gross edema of the small-bowel wall, and uniform homogeneous waterlogging of the mesentery can also be seen (Fig 20). Treatments include intravenous or intraarterial (from the SMA) injection of heparin or thrombolytic agents and resection of the necrotic lesion.
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Figure 20a. Acute SMV thrombosis. (a) Postcontrast CT scan shows a filling defect in the SMV (arrow). (b) Postcontrast CT scan shows a dilated small-bowel loop (SB) with a thickened wall, an appearance suggestive of congestive change. The increased attenuation of the SBM represents mesenteric congestion or edema (arrows).
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Figure 20b. Acute SMV thrombosis. (a) Postcontrast CT scan shows a filling defect in the SMV (arrow). (b) Postcontrast CT scan shows a dilated small-bowel loop (SB) with a thickened wall, an appearance suggestive of congestive change. The increased attenuation of the SBM represents mesenteric congestion or edema (arrows).
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SMA Dissection.—
Spontaneous dissection of a visceral artery is a very rare condition, and the SMA is the visceral artery most frequently affected. Cystic medial necrosis and fibromuscular dysplasia have been shown to be etiologic factors. Microscopic findings include fragmentation of the elastic fiber, loss of smooth-muscle tissue, areas of cystic degeneration, and atheromatous changes in the arterial wall. The clinical symptoms include sudden bowel ischemia or intraperitoneal hemorrhage. The dissection usually begins a few centimeters from the origin of the SMA (17). At precontrast CT, enlarged diameter of the SMA and increased attenuation of the fat plane in the root of the SBM are seen. After administration of contrast material, enlarged diameter of the SMA with narrowing of the lumen can be seen (Fig 21).
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Figure 21. SMA dissection. Postcontrast CT scan shows enlarged diameter of the SMA (arrows) with narrowing of the lumen. Increased attenuation in the root of the SBM is also seen (arrowheads).
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Arterioportal Fistula.—
Extrahepatic and mesenteric arterioportal fistulas, which can be congenital or acquired, are rare. Congenital arterioportal fistula in the region of the pancreas is often associated with Osler-Weber-Rendu disease. Acquired mesenteric arterioportal fistula is a rare entity caused by trauma or pancreatitis (18). Arterioportal fistula is frequently associated with portal vein thrombosis. The relation between portal vein hypertension or obstruction and arterioportal fistula has been extensively discussed but remains controversial. The symptoms of arterioportal fistula include abdominal pain, upper digestive tract bleeding, and ascites (19). Imaging features at postcontrast CT are increased attenuation of the SBM, dilated vessels, and enhancing lesions of the pancreas, peripancreatic mesentery, or retroperitoneum. Cavernous transformation secondary to portal vein thrombosis is often observed.
Portal Venous Gas.—
Portal venous gas occurs due to entrance of intraluminal gas into the mesenteric venous system when the gastrointestinal mucosa is disrupted. According to some researchers, the most common cause of portal venous gas is bowel ischemia or obstruction (20). The pathogenesis is as follows: (a) luminal bacterial overgrowth with gas-forming organisms invading the submucosa and veins of the bowel wall, (b) bowel necrosis with gas infiltrating directly through the damaged bowel wall into the intestinal venules, and (c) elevated intraluminal pressure in conjunction with mucosal ulceration. The gas, originating from the intestine, extends through the mesenteric veins, reaching the SMV and portal vein. At CT, portal venous gas manifests as air attenuation in the portal venous system, which is recognized as a branching pattern in the periphery of the liver (Fig 22). In addition, pneumatosis of the bowel wall is seen in one-half of cases (20).
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Figure 22. Gas gangrene involving the small intestine. CT scan shows air attenuation in the SMV (arrows). The presence of Clostridium perfringens in the bowel wall was proved after resection of the jejunum.
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Edema or Congestion
Mesenteric edema is caused by many conditions, including hypoalbuminemia, liver cirrhosis, nephrosis, heart failure, portal vein thrombosis, mesenteric artery or vein thrombosis, and vasculitis. When fluid or inflammatory cells infiltrate the SBM, the attenuation of the mesenteric fat increases to the -40 to -60 HU range relative to the mean attenuation (21). The increased attenuation in the root of the SBM caused by mesenteric edema should be differentiated from that caused by other pathologic conditions, such as infiltration by a malignant neoplasm, inflammation, or SMA dissection. Mesenteric edema secondary to systemic disease often coexists with generalized subcutaneous edema and ascites. The mesenteric haziness extends from the serosal surface of the intestine to the root of the SBM at the origin of the SMA and SMV. In contrast, mesenteric edema secondary to mesenteric artery or vein thrombosis tends to be focal, although it may also be diffuse. The CT findings of mesenteric edema or congestion are diffuse changes or focal elevation of the attenuation of the mesentery and loss of the sharp interfaces between mesenteric vessels and mesenteric fat.
Trauma
Bowel and mesenteric injuries are found in approximately 5% of patients undergoing laparotomy after blunt abdominal trauma. The presence of a mesenteric hematoma should prompt a careful search for evidence of gastrointestinal perforation or laceration of mesenteric vasculature. The mesenteric side of the intestine is more prone to vascular tears, whereas the antimesenteric side is more prone to perforations (22). Occasionally, the mesenteric injury extends to the root of the SBM. Mesenteric injury should be suspected in a patient with increased attenuation or a hematoma in the root of the SBM at CT. Small areas of hemorrhage may result in streaky soft-tissue infiltration of normal mesenteric fat. Larger, more confluent hematomas may exert significant mass effect on adjacent bowel loops, and a convex, high-attenuation mass adjacent to the tear can be identified at CT (Fig 23).
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Figure 23a. Mesenteric tear. (a) Precontrast CT scan shows a convex, high-attenuation mass (arrows) within the SBM, which represents a mesenteric hematoma. The irregular areas of increased attenuation (arrowheads) in the root of the SBM represent a mesenteric tear with small areas of hemorrhage. (b) Surgical photograph shows the mesenteric tear (arrows), which runs from the root of the SBM to the mesenteric border.
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Figure 23b. Mesenteric tear. (a) Precontrast CT scan shows a convex, high-attenuation mass (arrows) within the SBM, which represents a mesenteric hematoma. The irregular areas of increased attenuation (arrowheads) in the root of the SBM represent a mesenteric tear with small areas of hemorrhage. (b) Surgical photograph shows the mesenteric tear (arrows), which runs from the root of the SBM to the mesenteric border.
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Inflammation
Mesenteric panniculitis is a rare disorder characterized by chronic nonspecific inflammation involving the adipose tissue of the bowel mesentery. The etiology is unclear; it may occur independently or in association with other disorders. This disease has been related to a variety of conditions such as vasculitis, granulomatous disease, rheumatic disease, malignancies (especially malignant lymphoma), and pancreatitis (23). Mesenteric panniculitis can involve the root of the SBM. CT shows a well-defined mass composed of heterogeneous fatty tissue. Preservation of the fat nearest the mesenteric vessels, the so-called fat ring sign or fatty halo, is commonly observed. A hyperattenuating stripe (tumoral pseudocapsule) surrounding the mass is also a characteristic CT finding, seen in one-half of patients (24).
Tumors or Tumorlike Lesions
Retroperitoneal Fibrosis.—
The cause of retroperitoneal fibrosis is idiopathic in two-thirds of cases. It usually manifests as an isolated fibrotic plaque anterior to the lumbar spine. The great vessels are often surrounded and encased. Retroperitoneal fibrosis is associated with fibrotic processes elsewhere in the body in up to 15% of cases, but the root of the SBM is rarely involved. In its early stages, histologic analysis shows inflammatory cells and edema in a loose collagen network. The mature plaque consists of dense fibrosis with minimal cellular infiltration (25). The attenuation of a well-developed plaque is usually equivalent to that of adjacent muscles. After intravenous administration of contrast material, the plaque shows various forms of enhancement depending on the stage of development of the fibrous process (Fig 24).
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Figure 24. Retroperitoneal fibrosis. Postcontrast CT scan shows a mass of soft-tissue attenuation (arrows) encircling the SMA in the root of the SBM. Biopsy at laparotomy revealed diffuse fibrosis of the pancreas and peripancreatic mesentery. Note the left hydronephrosis (H) caused by ureteral involvement. Ao = aorta.
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Lymphoma.—
Malignant lymphoma predominantly occurs in the lymph nodes, but it can involve any of the organs. At CT, malignant lymphoma occurring within the root of the SBM appears as multiple or conglomerated areas of increased attenuation or stellate infiltration of the mesentery. The mass extends along the SBM and to the other ligaments and mesocolons. The mesenteric vessels may be involved and encased by the mass, but the patency of the vessels is usually preserved (Fig 25). Rarely, malignant lymphoma occurs or grows within the portal vein and SMV.
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Figure 25. Mesenteric lymphoma. Postcontrast CT scan shows a mass of soft-tissue attenuation (arrows) in the root of the SBM. The patency of the vessels within the mass is preserved.
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Other Tumors.—
Other tumors can originate from the SBM and rarely extend through the root of the SBM to other ligaments. Once the tumor extends to the confluent zone, it can spread directly to other organs or along the ligaments. Sarcomas such as liposarcoma, leiomyosarcoma, malignant fibrous histiocytoma, and fibrosarcoma most frequently occur in this region. CT can clearly demonstrate the tumor origin and encasement or patency of mesenteric vessels (Fig 26).
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Figure 26. Retroperitoneal teratoma located at the root of the SBM. Postcontrast CT scan shows a multiloculated mass (arrows) in the root of the SBM. The medial part of the mass (arrowhead) extends between the SMV and SMA.
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Conclusions
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Many pathologic conditions can occur in the SBM itself, and diseases from other organs that spread via the root of the SBM also frequently involve the root of the SBM. CT scans can clearly demonstrate these pathologic conditions and their anatomic relationships with adjacent structures. Therefore, radiologists should pay special attention to abnormalities of the root of the SBM seen at CT.
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Acknowledgments
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We thank Hisayuki Aikawa for providing us with some interesting cases. In addition, the authors appreciate the help of Naoko Akada in preparing the manuscript.
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Footnotes
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Abbreviations: SBM = small-bowel mesentery,
SMA = superior mesenteric artery,
SMV = superior mesenteric vein
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References
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Abstract
LEARNING OBJECTIVES FOR TEST...
