(Radiographics. 2002;22:527-541.)
© RSNA, 2002
Mesenteric Venous Thrombosis: Diagnosis and Noninvasive Imaging1
Michelle S. Bradbury, MD, PhD,
Peter V. Kavanagh, MD,
Robert E. Bechtold, MD,
Michael Y. Chen, MD,
David J. Ott, MD,
John D. Regan, MD and
Therese M. Weber, MD
1 From the Department of Radiology, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1088. Presented as an education exhibit at the 2000 RSNA scientific assembly. Received March 23, 2001; revision requested May 30; final revision received August 24; accepted August 27. Address correspondence to M.S.B.
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Abstract
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Mesenteric venous thrombosis is an uncommon but potentially lethal cause of bowel ischemia. Several imaging methods are available for diagnosis, each of which has advantages and disadvantages. Doppler ultrasonography allows direct evaluation of the mesenteric and portal veins, provides semiquantitative flow information, and allows Doppler waveform analysis of the visceral vessels; however, it is operator dependent and is often limited by overlying bowel gas. Conventional contrast material–enhanced computed tomography (CT) allows sensitive detection of venous thrombosis within the central large vessels of the portomesenteric circulation and any associated secondary findings; however, it is limited by respiratory misregistration, motion artifact, and substantially decreased longitudinal spatial resolution. Helical CT and CT angiography, especially when performed with multi–detector row scanners, and magnetic resonance (MR) imaging, particularly gadolinium-enhanced MR angiography, enable volumetric acquisitions in a single breath hold, eliminating motion artifact and suppressing respiratory misregistration. Helical CT angiography and three-dimensional gadolinium-enhanced MR angiography should be considered the primary diagnostic modalities for patients with a high clinical suspicion of mesenteric ischemia. Conventional angiography is reserved for equivocal cases at noninvasive imaging and is also used in conjunction with transcatheter therapeutic techniques in management of symptomatic portal and mesenteric venous thrombosis.
© RSNA, 2002
Index Terms: Computed tomography (CT), angiography, 957.12916, 959.12916 • Magnetic resonance (MR), vascular studies, 957.12942, 959.12942 • Portal vein, thrombosis, 957.751 • Veins, mesenteric, 959.751 • Veins, thrombosis, 957.751, 959.751
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- List the specific types and causes of portomesenteric venous thrombosis.
- Describe the roles and limitations of various imaging modalities in noninvasive diagnosis of portomesenteric venous thrombosis.
- Discuss the role of transcatheter therapeutic techniques in management of symptomatic portal and mesenteric venous thrombosis.
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Introduction
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Mesenteric ischemia encompasses a broad spectrum of diseases but has traditionally been classified according to the various causes of acute arterial occlusive disease, nonobstructive mesenteric arterial insufficiency, mesenteric venous occlusion, and chronic mesenteric ischemia (1). In addition to distinguishing between the arterial and venous causes of this disease, this classification is useful from a therapeutic standpoint. Splanchnic venous occlusions account for a relatively small percentage of such cases, about 15%–20% (2,3), but remain an important cause of acute bowel infarction. Advances in rapid, noninvasive imaging techniques, as well as evolving endovascular treatment options, are the main focus of this article.
The nonspecific signs and symptoms of mesenteric vascular disease can delay diagnosis, contributing to the poor clinical outcome associated with this condition. High morbidity and mortality rates create an important role for radiology in aiding earlier recognition and detection. Many cases are slowly progressive, and extensive venous collateralization within the splanchnic circulation usually prevents progression to infarction. Clinically obvious cases with evidence of peritonitis usually mandate prompt surgical intervention. Suspected acute cases without associated peritonitis, as well as chronic disease, will benefit from earlier detection and diagnosis with a range of noninvasive techniques, which help triage patients to the most appropriate management option.
In this article, we review the causes, clinical features, radiologic findings, and management of portal or mesenteric venous thrombosis.
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Causes
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Mesenteric venous thrombosis can be classified on the basis of its cause as primary or secondary. Spontaneous, idiopathic thrombosis of the splanchnic veins not associated with any predisposing conditions has been termed primary mesenteric venous thrombosis. The number of patients in this group has significantly decreased over the past decade because of improvement in diagnosis and recognition of previously unknown naturally circulating thrombogenic agents (4). Patients with known medical conditions or factors associated with portal or mesenteric venous thrombosis, such as pancreatitis, hypercoagulability states, cirrhosis, or surgery, are said to have secondary mesenteric venous thrombosis (Table).
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Clinical Features
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Cases may also be classified into acute and chronic presentations for management purposes. Acute mesenteric venous thrombosis is defined as the process that exists in those patients with presenting symptoms of less than 4 weeks duration (4). In a study conducted by the Mayo Clinic (3), typical signs and symptoms of acute bowel ischemia were found to include pain out of proportion to the physical findings, nausea, vomiting, and constipation, with or without bloody diarrhea. Diffuse, intermittent abdominal pain may be present from several days to as long as weeks. Of these symptoms, disproportionate pain with slow progression, accompanied by low-grade symptoms for at least 48 hours, was most commonly found (3). Although abdominal distention is the most frequently present sign of acute mesenteric ischemia, it is not universally present and was found in only 51% of patients in the Mayo Clinic series (3). Results of laboratory tests are nonspecific but can be used in conjunction with other findings to support or refute the clinical impression. Almost all cases are associated with a metabolic acidosis, and mild to moderate leukocytosis is also common.
The differential diagnosis for acute mesenteric ischemia is extensive, comprising both intravascular and extravascular causes. Arterial causes include embolic or atheromatous disease, dissecting aortic aneurysm, arteritis, fibromuscular dysplasia, endotoxin shock, hypoperfusion (shock, hypovolemia), direct trauma, and disseminated intravascular coagulation. Arterial causes can be further subdivided into occlusive mesenteric infarction (embolus lodging distal to the middle colic artery or thrombosis of the superior mesen-teric artery) and nonocclusive mesenteric ischemia (preexisting atherosclerosis with a systemic low-flow state). Venous causes make up a much smaller percentage of cases and are generally seen in younger patients, typically in the setting of abdominal surgery. Extravascular causes include incarcerated hernia, volvulus, intussusception, and constricting adhesive bands.
Chronic mesenteric ischemia is difficult to detect on the basis of clinical criteria alone and is often considered only after exclusion of more common causes of abdominal pain, such as gastroesophageal reflux or gallbladder, pancreatic, or gastric disorders (5,6). Most patients with chronic disease are asymptomatic until late complications occur, such as variceal bleeding due to portal hypertension. Weight loss, food avoidance, vague postprandial abdominal pain, or distention may also be demonstrated. The pain usually occurs within the first hour after eating, diminishing over the next 1–2 hours. Mild leukocytosis was found in the Mayo Clinic series in less than 50% of chronic cases (2). Thrombosis in the portomesenteric vasculature is usually detected as an incidental finding during evaluation of other abdominal pathologic conditions, such as portal hypertension, malignancy, or chronic pancreatitis.
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Radiologic Findings
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Imaging findings of bowel ischemia are similar regardless of the cause. Radiographic findings of bowel ischemia or infarction demonstrated on plain radiograph or barium studies are usually nonspecific; most often, these studies demonstrate a nonspecific ileus pattern with dilated, fluid-filled loops of bowel. Thumbprinting (focal mural thickening secondary to submucosal hemorrhage), separation of bowel loops due to mesenteric thickening, intramural pneumatosis, and mesenteric or portal venous gas may occasionally be seen but usually indicate late-stage disease. More commonly, results of plain radiography are nonspecific and of little or no use in diagnostic evaluation.
Doppler Ultrasonography
Color Doppler ultrasonography (US) with duplex scanning is noninvasive and relatively inexpensive and can provide semiquantitative information about portomesenteric blood flow. Venous flow anomalies or thrombus (Figs 1, 2), a thickened bowel wall, free intraperitoneal fluid, and biliary disease can also be demonstrated. Limitations of this modality are its operator-dependent nature, sensitivity of the equipment to slow flow, inability to identify a suitable acoustic window, variable visualization of the entire portomesenteric vasculature due to overlying bowel gas, and potential failure to depict deep varices involving the retroperitoneal and mesenteric vessels. In addition, large periportal collateral vessels in portal venous thrombosis may be mistaken for a patent portal vein. Nonetheless, Doppler US techniques can be a valuable tool in experienced hands, particularly for evaluation of portal vein patency. Intravenous administration of US-compatible intravascular contrast agents, once approved, in conjunction with gray-scale harmonic imaging may increase vessel conspicuity and thereby provide substantial improvement in US evaluation of portal or mesenteric venous thrombosis.
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Figure 1a. Portomesenteric venous thrombosis in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain. (a) US image shows an enlarged portal vein with an extensive intraluminal thrombus (arrow). (b) Contrast material-enhanced computed tomographic (CT) image shows several smaller filling defects (arrows) in an enlarged splenic vein. Incidental note is made of an infarct (I) in the left kidney. (c) CT image shows a large filling defect in the superior mesenteric vein (SMV) (arrow). The filling defect contains a central focus of calcification, which is indicative of chronicity. Multiple infarcts (I) are seen in the left kidney. (d) CT image shows an additional large filling defect at the level of the portovenous confluence (black arrow) with evidence of small-vessel collateralization (white arrow). A subcapsular hematoma (H) is present in the liver.
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Figure 1b. Portomesenteric venous thrombosis in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain. (a) US image shows an enlarged portal vein with an extensive intraluminal thrombus (arrow). (b) Contrast material-enhanced computed tomographic (CT) image shows several smaller filling defects (arrows) in an enlarged splenic vein. Incidental note is made of an infarct (I) in the left kidney. (c) CT image shows a large filling defect in the superior mesenteric vein (SMV) (arrow). The filling defect contains a central focus of calcification, which is indicative of chronicity. Multiple infarcts (I) are seen in the left kidney. (d) CT image shows an additional large filling defect at the level of the portovenous confluence (black arrow) with evidence of small-vessel collateralization (white arrow). A subcapsular hematoma (H) is present in the liver.
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Figure 1c. Portomesenteric venous thrombosis in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain. (a) US image shows an enlarged portal vein with an extensive intraluminal thrombus (arrow). (b) Contrast material-enhanced computed tomographic (CT) image shows several smaller filling defects (arrows) in an enlarged splenic vein. Incidental note is made of an infarct (I) in the left kidney. (c) CT image shows a large filling defect in the superior mesenteric vein (SMV) (arrow). The filling defect contains a central focus of calcification, which is indicative of chronicity. Multiple infarcts (I) are seen in the left kidney. (d) CT image shows an additional large filling defect at the level of the portovenous confluence (black arrow) with evidence of small-vessel collateralization (white arrow). A subcapsular hematoma (H) is present in the liver.
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Figure 1d. Portomesenteric venous thrombosis in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain. (a) US image shows an enlarged portal vein with an extensive intraluminal thrombus (arrow). (b) Contrast material-enhanced computed tomographic (CT) image shows several smaller filling defects (arrows) in an enlarged splenic vein. Incidental note is made of an infarct (I) in the left kidney. (c) CT image shows a large filling defect in the superior mesenteric vein (SMV) (arrow). The filling defect contains a central focus of calcification, which is indicative of chronicity. Multiple infarcts (I) are seen in the left kidney. (d) CT image shows an additional large filling defect at the level of the portovenous confluence (black arrow) with evidence of small-vessel collateralization (white arrow). A subcapsular hematoma (H) is present in the liver.
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Figure 2a. Portomesenteric venous thrombosis in a 73-year-old woman with abdominal pain and cholecystitis. (a) Doppler US image shows absence of flow in the splenic vein (black arrow) and within the portovenous confluence (white arrow). There was also absence of flow in the right portal vein. (b) Contrast-enhanced CT image shows filling defects in the portal vein (arrow) with cavernous transformation at the porta hepatis. (c) CT image shows a thrombus in the SMV (white arrow). Prominence of the pancreatic head (black arrows) and several peripancreatic lymph nodes (arrowheads) are also seen. (d) CT image shows haziness of the adjacent fat (arrow). The patient proved to have acute pancreatitis. Follow-up imaging showed resolution of the inflammatory changes with no lymph nodes identified.
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Figure 2b. Portomesenteric venous thrombosis in a 73-year-old woman with abdominal pain and cholecystitis. (a) Doppler US image shows absence of flow in the splenic vein (black arrow) and within the portovenous confluence (white arrow). There was also absence of flow in the right portal vein. (b) Contrast-enhanced CT image shows filling defects in the portal vein (arrow) with cavernous transformation at the porta hepatis. (c) CT image shows a thrombus in the SMV (white arrow). Prominence of the pancreatic head (black arrows) and several peripancreatic lymph nodes (arrowheads) are also seen. (d) CT image shows haziness of the adjacent fat (arrow). The patient proved to have acute pancreatitis. Follow-up imaging showed resolution of the inflammatory changes with no lymph nodes identified.
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Figure 2c. Portomesenteric venous thrombosis in a 73-year-old woman with abdominal pain and cholecystitis. (a) Doppler US image shows absence of flow in the splenic vein (black arrow) and within the portovenous confluence (white arrow). There was also absence of flow in the right portal vein. (b) Contrast-enhanced CT image shows filling defects in the portal vein (arrow) with cavernous transformation at the porta hepatis. (c) CT image shows a thrombus in the SMV (white arrow). Prominence of the pancreatic head (black arrows) and several peripancreatic lymph nodes (arrowheads) are also seen. (d) CT image shows haziness of the adjacent fat (arrow). The patient proved to have acute pancreatitis. Follow-up imaging showed resolution of the inflammatory changes with no lymph nodes identified.
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Figure 2d. Portomesenteric venous thrombosis in a 73-year-old woman with abdominal pain and cholecystitis. (a) Doppler US image shows absence of flow in the splenic vein (black arrow) and within the portovenous confluence (white arrow). There was also absence of flow in the right portal vein. (b) Contrast-enhanced CT image shows filling defects in the portal vein (arrow) with cavernous transformation at the porta hepatis. (c) CT image shows a thrombus in the SMV (white arrow). Prominence of the pancreatic head (black arrows) and several peripancreatic lymph nodes (arrowheads) are also seen. (d) CT image shows haziness of the adjacent fat (arrow). The patient proved to have acute pancreatitis. Follow-up imaging showed resolution of the inflammatory changes with no lymph nodes identified.
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Conventional Angiography
Diagnostic angiographic procedures have conventionally included both direct and indirect portography. Direct portography includes percutaneous transhepatic portal venography, transjugular portography, and splenoportography (Fig 3). Indirect portography involves arterial injections into the superior mesenteric artery or splenic artery. The latter technique, previously used as the preferred nonsurgical approach for confirming splanchnic venous thrombosis, requires prolonged arterial infusion of contrast material followed by delayed imaging. Although these techniques are invasive, may be limited by flow dynamics, and require the use of potentially nephrotoxic iodinated contrast material and ionizing radiation, they can be combined with endovascular therapeutic maneuvers such as transcatheter delivery of vasodilators or thrombolytic agents in selected patients (Fig 4). Mesenteric arteriography with delayed venous phase imaging may demonstrate venous occlusion or an intraluminal thrombus. Superior mesenteric arterial spasm is frequently observed, although prolongation of the arterial angiographic phase and other subtle findings may also result from superior mesenteric venous occlusion. Diagnostic angiography is usually reserved for cases in which clinically suspected portomesenteric venous thrombosis is not established with noninvasive modalities.
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Figure 3a. Splenoportography. (a) Normal splenoportogram shows patency of the splenic vein (arrowhead) and portal venous system (arrow). (b) Splenoportogram shows no filling of the splenic vein. A spontaneous splenorenal shunt has formed, with extensive perisplenic venous collateral vessels communicating with the left renal vein (solid arrow) and draining into the inferior vena cava (open arrow).
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Figure 3b. Splenoportography. (a) Normal splenoportogram shows patency of the splenic vein (arrowhead) and portal venous system (arrow). (b) Splenoportogram shows no filling of the splenic vein. A spontaneous splenorenal shunt has formed, with extensive perisplenic venous collateral vessels communicating with the left renal vein (solid arrow) and draining into the inferior vena cava (open arrow).
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Figure 4a. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Figure 4b. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Figure 4c. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Figure 4d. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Figure 4e. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Figure 4f. Portal venography performed with a percutaneous transhepatic approach in a 31-year-old woman with protein S deficiency and recent onset of abdominal pain (same patient as in Figure 1). (a) Venogram obtained with the catheter advanced into the distal main portal vein (arrow) shows narrowing of the lumens of the main portal vein and SMV due to thrombosis. The right intrahepatic portal vein and splenic vein are chronically occluded with associated cavernous transformation (arrowheads). (b) Venogram obtained after transcatheter injection of a tributary of the SMV (arrowhead) shows an extensive network of peripheral mesenteric venous collateral vessels (arrows). (c) Venogram obtained 2 days after mechanical thrombectomy and chemical thrombolysis shows a large residual clot in the portal vein (arrowheads). (d) Venogram shows occlusion of the large portal venous branches seen earlier. This appearance is presumably due to embolization of the thrombus after thrombectomy attempts. (e) Venogram obtained after repeat thrombectomy shows improved patency of the main portal vein and splenic vein. (f) Venogram shows no significant remaining filling defects in the main and left portal veins, but the entire right portal vein and its tributaries remain occluded.
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Helical CT and CT Angiography
Contrast-enhanced CT has gained an increasingly important role in patients with acute mesenteric venous thrombosis and is considered the diagnostic test of choice at many centers. This technique permits evaluation of vascular structures, the bowel wall, and the adjacent mesentery. Sensitivity rates reach at least 90% (3,7). CT findings of portomesenteric venous thrombosis include persistent, well-defined intraluminal filling defects with central low attenuation (Figs 1, 2, 5, 6), which may be surrounded by well-defined, rim-enhancing venous walls. Accompanying collateral circulation, engorgement of mesenteric veins, and mesenteric edema may be present (2,7,8). Multivein occlusion is common in splanchnic venous thrombosis.
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Figure 5. SMV thrombosis in a 57-year-old man with a history of gallstones. CT image shows lack of enhancement of the SMV (solid arrow) with stranding in the fat around the vessel, findings consistent with acute thrombosis. Additional subtle infiltration of the peripancreatic and mesenteric fat (open arrows) suggests accompanying pancreatitis.
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Figure 6a. Portomesenteric venous thrombosis in a 66-year-old woman with pancreatic cancer. (a) Contrast-enhanced CT image shows a large pancreatic mass (M) around the celiac artery (arrowhead). The distal portion of the splenic vein is not identified, and there is extrinsic obstruction of the left renal vein (arrow). (b) CT image shows obliteration of the SMV (arrowhead) and proximal portal vein near the confluence. Diffuse tumor infiltration along the aorta is also present.
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Figure 6b. Portomesenteric venous thrombosis in a 66-year-old woman with pancreatic cancer. (a) Contrast-enhanced CT image shows a large pancreatic mass (M) around the celiac artery (arrowhead). The distal portion of the splenic vein is not identified, and there is extrinsic obstruction of the left renal vein (arrow). (b) CT image shows obliteration of the SMV (arrowhead) and proximal portal vein near the confluence. Diffuse tumor infiltration along the aorta is also present.
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The most common manifestation of accompanying bowel ischemia is bowel wall thickening (9). This nonspecific finding may manifest as a target sign, with alternating intramural areas of high and low attenuation resulting from submucosal edema or hemorrhage (10). The thickened bowel wall may appear hyperattenuating; this appearance is thought to be due to intramural venous engorgement. The triad of low attenuation in the SMV, thickening of the small bowel wall, and the presence of peritoneal fluid suggests that laparotomy should be performed, as bowel infarction is likely. The presence of peritoneal fluid indicates a greater severity of bowel ischemia secondary to splanchnic venous occlusion and will often warrant laparotomy. Conversely, nonsurgical treatment may be appropriate in the absence of peritoneal fluid.
Other important CT findings include bowel dilatation (Fig 7), which reflects aperistaltic activity; absent or poor enhancement of the bowel wall secondary to both venous and arterial perfusion abnormalities; and, less commonly, intestinal pneumatosis (Fig 8). The latter two findings are more specific signs of ischemic bowel disease. Infarction of other abdominal viscera may be present. Less commonly, but more ominously, the appearance of mesenteric or portal venous gas suggests dissection of intramural gas into the venous system. Free intraperitoneal air from perforation of an infarcted bowel segment may also be seen.
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Figure 7. Bowel dilatation in a 54-year-old woman with mesenteric venous thrombosis. CT image shows multiple loops of distended, fluid-filled small intestine (B) secondary to SMV thrombosis (arrowhead). There is no pneumatosis or free intraperitoneal air. Trace ascites is also present (arrow).
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Figure 8. Intestinal pneumatosis in a 59-year-old woman with progressive worsening of abdominal pain and distention after renal transplantation. CT image shows air along the course of the SMV (arrowhead), and pneumatosis is present (arrow) within the wall of the distal ileum, ascending colon, and transverse colon. Extensive portal venous gas was also noted. At laparotomy, no large vascular (arterial or venous) clot was identified; therefore, thromboembolic disease at a microvascular level was suspected to be the likely cause.
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Helical CT has improved image quality and permitted faster scanning times. Technical advances in volumetric CT scanning performed with helical CT have facilitated development of revolutionary applications, such as CT angiography. This technique combines high-resolution volumetric data acquisition with large-volume bolus administration of intravenous iodinated contrast material. Rapid volumetric acquisition of data in a single breath-holding period has minimized motion artifact, suppressed respiratory misregistration, facilitated bolus tracking methods, and increased longitudinal spatial resolution over a large anatomic volume, which is greater than that achievable with conventional CT (11).
Multi–detector row CT scanners, which are described elsewhere (12,13), offer the advantages of significantly shorter acquisition times, retrospective thin- or thick-section reconstruction from the same raw data, improved three-dimensional (3D) rendering with decreased helical artifact, and increased z-axis coverage without compromising image quality (12,14). Timing parameters can be optimized, allowing both arterial and venous phases to be imaged. Dynamic evaluation of the splanchnic veins may be performed prospectively with dedicated multi–detector row CT angiography during the venous phase of the bolus injection (Figs 9, 10). In this case, data acquisition should be performed at peak venous enhancement, with the delay between the start of injection and the commencement of image acquisition tailored for that purpose. Protocols typically use 55–70-second delays following administration of 125–150 mL of intravenous contrast medium at a rate of 3.5–5 mL/sec through a peripheral vein. Evaluation of the mesenteric veins can also be performed retrospectively by using postprocessing techniques applied to routine abdominal helical CT data sets (13). This method is more time-consuming and is not favored for routine clinical practice.
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Figure 9a. Thrombosis due to a tumor in a 76-year-old woman with weight loss, shortness of breath, and a history of smoking. (a) Coronal reformation image from portal venous phase CT angiography shows an ill-defined right hepatic mass (M), consistent with known hepatocellular carcinoma. The tumor invades the right portal vein (arrow) to the level of the portal venous confluence. (b) Coronal reformation image from portal venous phase CT angiography shows that the tumor also invades the right hepatic vein, extending into the inferior vena cava (arrow).
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Figure 9b. Thrombosis due to a tumor in a 76-year-old woman with weight loss, shortness of breath, and a history of smoking. (a) Coronal reformation image from portal venous phase CT angiography shows an ill-defined right hepatic mass (M), consistent with known hepatocellular carcinoma. The tumor invades the right portal vein (arrow) to the level of the portal venous confluence. (b) Coronal reformation image from portal venous phase CT angiography shows that the tumor also invades the right hepatic vein, extending into the inferior vena cava (arrow).
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Figure 10a. Thrombosis due to a carcinoid tumor. (a) High-resolution axial image from venous phase CT angiography shows an expansile thrombus in the intrahepatic portal vein (arrow). (b) High-resolution coronal reformation image from venous phase CT angiography shows extension of the thrombus into the extrahepatic portal vein (arrow) and SMV (arrowhead). There is cavernous transformation in the region of the porta hepatis.
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Figure 10b. Thrombosis due to a carcinoid tumor. (a) High-resolution axial image from venous phase CT angiography shows an expansile thrombus in the intrahepatic portal vein (arrow). (b) High-resolution coronal reformation image from venous phase CT angiography shows extension of the thrombus into the extrahepatic portal vein (arrow) and SMV (arrowhead). There is cavernous transformation in the region of the porta hepatis.
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Helical CT angiography provides exquisite anatomic detail; reveals intra- and extraluminal abnormalities, intimal calcifications, mural thrombosis, and mesenteric edema; and can image metallic and nonmetallic synthetic grafts. Hepatopetal extension of thrombosis into the intrahepatic portal venous system may also be detected, permitting the severity of disease to be assessed and appropriate management to be initiated. Furthermore, the remaining extravascular organ anatomy is exquisitely depicted.
Conventional MR Imaging
Conventional magnetic resonance (MR) imaging has permitted assessment of the portomesenteric venous vasculature with spin-echo, gradient-echo, and gadolinium-enhanced sequences. Flow dynamics, extrinsic compression, hepatic vascular anatomy, and atherosclerotic narrowing have been studied (1). Recent advances in MR imaging techniques have been exploited to evaluate physiologic derangements associated with small bowel ischemia. For example, oxygen desaturation in the SMV resulting from increased tissue extraction of blood oxygen has been measured in vivo in the setting of ischemia (15,16). Real-time interactive MR imaging has been used to observe segmental hypomotility of the small intestine under ischemic conditions (17,18).
MR Angiography
Traditional MR angiography techniques have relied on nonenhanced velocity-dependent inflow time-of-flight or phase-contrast methods to evaluate the portomesenteric circulation. These methods have been hampered by longer data acquisition times; motion, flow, or susceptibility artifacts from implanted metallic devices or surgical clips; signal loss secondary to areas of complex flow; and in-plane flow saturation effects (19–21). Nonetheless, phase-contrast methods are still useful in quantitative measurement of flow rates in the superior mesenteric artery and SMV.
The latest 3D gadolinium-enhanced MR angiography techniques with short acquisition times (single breath hold) avoid many of the problems associated with time-of-flight and phase-contrast MR angiography. The contrast between blood and tissue is much improved compared with that achieved with these older methods (22). Since contrast resolution among extravascular structures is reduced with this technique, it is usually combined with spin-echo or gradient-echo sequences to provide additional soft-tissue information.
This application has evolved from the use of fast imaging techniques on high-gradient-strength units in combination with intravascular gadolinium-based agents, such as gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ). Saturation effects and respiratory motion artifacts are minimized or eliminated altogether (22–27), permitting exquisite detail of the mesenteric vascular anatomy (Figs 11–13). By exploiting the T1-relaxivity mechanisms of these agents, the dependency on blood flow is precluded. The improvements in contrast resolution are achieved regardless of the plane of acquisition, therebyallowing reductions in both the number of image sections required to display a large vascular territory and the overall image acquisition time (24). Fat suppression decreases unwanted signal from background tissues, maximizing the conspicuity of vascular structures.
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Figure 11a. Portomesenteric venous thrombosis in a 51-year-old woman with lower back pain. (a) Axial spin-echo MR image shows a nonocclusive thrombus at the splenoportal venous confluence (arrow). (b) Axial gradient-echo MR image shows a nonocclusive thrombus in the SMV (arrow). (c) Sagittal maximum intensity projection image reconstructed from the gradient-echo source images clearly shows the SMV thrombus (arrow).
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Figure 11b. Portomesenteric venous thrombosis in a 51-year-old woman with lower back pain. (a) Axial spin-echo MR image shows a nonocclusive thrombus at the splenoportal venous confluence (arrow). (b) Axial gradient-echo MR image shows a nonocclusive thrombus in the SMV (arrow). (c) Sagittal maximum intensity projection image reconstructed from the gradient-echo source images clearly shows the SMV thrombus (arrow).
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Figure 11c. Portomesenteric venous thrombosis in a 51-year-old woman with lower back pain. (a) Axial spin-echo MR image shows a nonocclusive thrombus at the splenoportal venous confluence (arrow). (b) Axial gradient-echo MR image shows a nonocclusive thrombus in the SMV (arrow). (c) Sagittal maximum intensity projection image reconstructed from the gradient-echo source images clearly shows the SMV thrombus (arrow).
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Figure 12a. Extensive portomesenteric venous thrombosis in a 46-year-old man with renal cell carcinoma. (a) Axial gadolinium-enhanced spin-echo MR image shows a large heterogeneous mass (M) in the lower pole of the right kidney, consistent with renal cell carcinoma. A filling defect is seen in the SMV (arrow). (b) Coronal contrast-enhanced 3D MR angiogram shows a long thrombus in the SMV (arrows) that extends into the portal vein. (c) Coronal contrast-enhanced 3D MR angiogram obtained anterior to b shows the proximal extent of the clot in the portal vein (arrows). (d) Coronal contrast-enhanced 3D MR angiogram shows a thrombus that involves the inferior vena cava (arrow).
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Figure 12b. Extensive portomesenteric venous thrombosis in a 46-year-old man with renal cell carcinoma. (a) Axial gadolinium-enhanced spin-echo MR image shows a large heterogeneous mass (M) in the lower pole of the right kidney, consistent with renal cell carcinoma. A filling defect is seen in the SMV (arrow). (b) Coronal contrast-enhanced 3D MR angiogram shows a long thrombus in the SMV (arrows) that extends into the portal vein. (c) Coronal contrast-enhanced 3D MR angiogram obtained anterior to b shows the proximal extent of the clot in the portal vein (arrows). (d) Coronal contrast-enhanced 3D MR angiogram shows a thrombus that involves the inferior vena cava (arrow).
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Figure 12c. Extensive portomesenteric venous thrombosis in a 46-year-old man with renal cell carcinoma. (a) Axial gadolinium-enhanced spin-echo MR image shows a large heterogeneous mass (M) in the lower pole of the right kidney, consistent with renal cell carcinoma. A filling defect is seen in the SMV (arrow). (b) Coronal contrast-enhanced 3D MR angiogram shows a long thrombus in the SMV (arrows) that extends into the portal vein. (c) Coronal contrast-enhanced 3D MR angiogram obtained anterior to b shows the proximal extent of the clot in the portal vein (arrows). (d) Coronal contrast-enhanced 3D MR angiogram shows a thrombus that involves the inferior vena cava (arrow).
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Figure 12d. Extensive portomesenteric venous thrombosis in a 46-year-old man with renal cell carcinoma. (a) Axial gadolinium-enhanced spin-echo MR image shows a large heterogeneous mass (M) in the lower pole of the right kidney, consistent with renal cell carcinoma. A filling defect is seen in the SMV (arrow). (b) Coronal contrast-enhanced 3D MR angiogram shows a long thrombus in the SMV (arrows) that extends into the portal vein. (c) Coronal contrast-enhanced 3D MR angiogram obtained anterior to b shows the proximal extent of the clot in the portal vein (arrows). (d) Coronal contrast-enhanced 3D MR angiogram shows a thrombus that involves the inferior vena cava (arrow).
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Figure 13a. SMV thrombosis in a 50-year-old woman with Crohn disease and increasing abdominal pain. At abdominal CT, a filling defect in the SMV was suspected. (a) Oblique coronal maximum intensity projection MR image shows a long thrombus in the SMV (arrows) that extends into the portal vein (PV). (b) Oblique coronal maximum intensity projection MR image shows the superior extent of the filling defect (solid arrow) in the portal vein (PV). The filling defect in the SMV is not visualized due to absence of flow, but the inferior mesenteric vein is seen (open arrows). The hepatic vein (HV) and splenic vein (SV) are well visualized. (c) Venous phase superior mesenteric angiogram does not show the SMV trunk, although the peripheral branches are visible. The thrombus in the proximal portal vein (PV) is seen (arrow). (Reprinted, with permission, from reference 23.)
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Figure 13b. SMV thrombosis in a 50-year-old woman with Crohn disease and increasing abdominal pain. At abdominal CT, a filling defect in the SMV was suspected. (a) Oblique coronal maximum intensity projection MR image shows a long thrombus in the SMV (arrows) that extends into the portal vein (PV). (b) Oblique coronal maximum intensity projection MR image shows the superior extent of the filling defect (solid arrow) in the portal vein (PV). The filling defect in the SMV is not visualized due to absence of flow, but the inferior mesenteric vein is seen (open arrows). The hepatic vein (HV) and splenic vein (SV) are well visualized. (c) Venous phase superior mesenteric angiogram does not show the SMV trunk, although the peripheral branches are visible. The thrombus in the proximal portal vein (PV) is seen (arrow). (Reprinted, with permission, from reference 23.)
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Figure 13c. SMV thrombosis in a 50-year-old woman with Crohn disease and increasing abdominal pain. At abdominal CT, a filling defect in the SMV was suspected. (a) Oblique coronal maximum intensity projection MR image shows a long thrombus in the SMV (arrows) that extends into the portal vein (PV). (b) Oblique coronal maximum intensity projection MR image shows the superior extent of the filling defect (solid arrow) in the portal vein (PV). The filling defect in the SMV is not visualized due to absence of flow, but the inferior mesenteric vein is seen (open arrows). The hepatic vein (HV) and splenic vein (SV) are well visualized. (c) Venous phase superior mesenteric angiogram does not show the SMV trunk, although the peripheral branches are visible. The thrombus in the proximal portal vein (PV) is seen (arrow). (Reprinted, with permission, from reference 23.)
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Accurate timing of data acquisition is essential to depict the vascular structures of greatest interest. In practice, multiphase dynamic imaging is performed after intravenous administration of gadolinium contrast material, with the arteries best seen during the early phase and the veins during the later phases. Timing the bolus to exactly coincide with central k-space data acquisition demands a knowledge of the contrast material travel time, or the time for the bolus to travel from the site of injection to the vascular territory under consideration. A number of semiautomated methods are now available for this purpose, including SmartPrep (GE Medical Systems, Waukesha, Wis), MR fluoroscopy, and timing boluses, all of which are designed to reduce the margin for error in timing the administration of contrast medium.
A final approach, ultrafast 3D MR digital subtraction angiography, is independent of the contrast material travel time, as total 3D image acquisition times on the order of 10 seconds or less are achievable. Venous structures will be highlighted after subtraction of arterial phase images from equilibrium phase images.
Although 3D contrast-enhanced MR angiography is similar to contrast-enhanced helical CT angiography, several advantages of the former include (a) the more favorable safety profile of paramagnetic agents compared with that of iodinated contrast agents; (b) the ability to tailor the imaging plane of acquisition to correspond with the vascular territory under consideration; (c) simpler 3D reconstruction of projection images from the 3D MR angiography data set (24); (d) lack of ionizing radiation; and (e) application of 3D Fourier techniques, allowing manipulation of k space to enhance temporal resolution. However, as MR angiography indirectly relies on detection of vascular signal, degradation of the signal related to turbulence can be observed. Thus, the severity of stenosis can be overestimated. MR angiography techniques are less sensitive for detection of calcification, and spatial resolution is lower compared with that of CT angiography. Another limitation is the inability to visualize vessels with stents due to the signal void caused by metallic material. Typical protocols use 3D contrast-enhanced MR angiography supplemented with phase-contrast MR angiography for additional functional information in select cases; spin-echo and gradient-echo sequences will usually be performed as well for the assessment of extravascular anatomy. Such protocols take 30–60 minutes to complete, considerably longer than with CT angiography. However, it is often possible to achieve shorter examination times in response to a specific clinical question.
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Management
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Acute mesenteric ischemia with signs of bowel infarction or peritonitis is generally an indication for immediate surgery to resect involved segments of intestine. Uninvolved intestine within the same vascular territory is also resected. Surgical thrombectomy is feasible in cases of focal, acute thrombus within the proximal SMV (within 1–3 days) (4). In acute or subacute mesenteric ischemia with splanchnic venous occlusion and viable intestine at CT or MR imaging, or in cases of extensive portomesenteric venous thrombosis, transcatheter delivery of thrombolytic agents (urokinase, streptokinase, or tissue plasminogen activator) has been successfully performed in a small subset of patients (28–31). In the latter situation, surgical thrombectomy is ineffective because numerous clots typically extend into small portomesenteric venous radicles (28), inaccessible to standard balloon embolectomy approaches. Endovascular treatment techniques frequently begin with direct cannulation of the portal venous system via a percutaneous transhepatic or transjugular route. Such access routes permit transcatheter thrombolysis with both mechanical and chemical methods. Intraarterial infusion of thrombolytic agents into the superior mesenteric artery (28,32) is another well-established strategy. Percutaneous catheter placement directly into the SMV has also been performed (31). Chronic mesenteric ischemia usually relies on medical management (4), which is aimed at reducing the risk of gastrointestinal bleeding from varices and controlling associated cardiovascular abnormalities such as atrial fibrillation. As adequate collateral venous drainage is usually present, asymptomatic chronic mesenteric venous thrombosis requires no treatment.
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Conclusions
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Mesenteric venous thrombosis has often been a diagnosis of exclusion, usually suspected in the later stages of the disease after multiple diagnostic tests fail to identify the cause of the patient’s symptoms. The late diagnosis has been attributed to multiple factors, which include clinical features that overlap those of more common intestinal disorders, such as cholecystitis and gastroesophageal reflux; the relative rarity of the disease; the lack of sensitivity for clot detection; and the poor specificity of ancillary signs at noninvasive imaging. Traditionally, the standard of reference for diagnosis of mesenteric ischemia has been conventional angiography. Doppler US is limited in the evaluation of these patients due to its operator dependency and inability to accurately depict vascular anatomy in the presence of overlying bowel gas. CT and MR imaging optimally depict extravascular anatomy. This advantage allows detection of ancillary signs of mesenteric ischemia, which can be valuable in equivocal cases. These modalities also serve to identify alternative causes to explain the patient’s condition. Nonhelical contrast-enhanced CT is hampered by respiratory and motion artifacts and has largely been superseded by helical CT in most developed countries. Both CT angiography and MR angiography provide superior temporal and contrast resolution for evaluation of the portomesenteric circulation. Thrombosis involving the larger splanchnic veins is readily identified with either technique. However, owing to limits in spatial resolution, evaluation of the smaller, distal mesenteric branch vessels remains a challenge for all cross-sectional imaging methods. Noneth
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Abstract
LEARNING OBJECTIVES
