Vascular complications of pancreatitis: what to look for

Transcription

1 Vascular complications of pancreatitis: what to look for Award: Cum Laude Poster No.: C-1905 Congress: ECR 2012 Type: Educational Exhibit Authors: C. N. Tentugal, J. Brito, A. R. R. G. costa, L. Silva, C. Soares, F. Aleixo; Portimão/PT Keywords: Abdomen, Pancreas, Vascular, CT-Angiography, Ultrasound, Diagnostic procedure, Ischemia / Infarction, Hemorrhage DOI: /ecr2012/C-1905 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 36

2 Learning objectives To illustrate the imaging findings of vascular complications of pancreatitis. To present a systematic approach on items to look for when dealing with patients with pancreatitis, in order to detect such complications. Background Although most cases of acute pancreatitis are mild and self-limited, approximately one quarter of these patients may develop vascular complications, which may represent a life-threatening event. In patients with chronic pancreatitis, vascular complications are also a frequently serious medical problem. The technological development of the multidetector computed tomography (MDCT) scanner allows not only a more rapid acquisition of axial images but also volumetric scanning in a desired anatomic area during selected phases of contrast enhancement. MDCT angiography (MDCTA) has become an established noninvasive imaging method to define vascular anatomy and pathology affecting vascular structures, as well as for presurgical treatment planning. Imaging findings OR Procedure details VASCULAR ANATOMY OF THE PANCREAS The pancreas has complex diagnostic and management needs. Therefore, imaging postprocessing is now integral to all CT angiography (CTA) applications in this organ. Although a variety of postprocessing protocols have been advocated, the most frequently used approaches include multiplanar reconstruction (MPR), maximum intensity projections (MIP), minimum intensity projections (MinIP), volume rendering (VR), 3D, and curved planar reformation (CPR). Each has a specific role for assessing regional anatomy and relationship of lesions in the vicinity. Page 2 of 36

3 Vascular complications of pancreatitis is also well characterized by MRI but is not usually readily available. Therefore it is only used in selected cases such as equivocal CT findings, contraindications to iodonate contraste administration or pregnancy. MR imaging assessment of both pancreatic ductal and parenchymal diseases can be performed in a single setting, using a combination of T1, T2-weighted images, magnetic resonance cholangiopancreatography (MRCP), and dynamic post-gadolinium fat-suppressed T1-weighted sequences. The celiac trunk is the first major aortic branch below the diaphragm, giving rise to 3 vessels: common hepatic artery (CHA) splenic artery (SA) left gastric artery (LGA) The superior mesenteric and inferior mesenteric arteries are the next anterior visceral branches. The arterial blood supply of the pancreas is derived from the celiac trunk (CT) and the superior mesenteric artery (SMA). Page 3 of 36

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5 Fig. 1: Volume rendered CT image demonstrating the major arterial blood supply of the pancreas. CT - celiac trunck; LGA - left gastric artery; SA - splenic artery; CHA common hepatic artery; SMA - superior mesenteric artery References: C. N. Tentugal; Portimão, PORTUGAL The splenic artery (SA) courses along the superior margin of the pancreas, giving rise to the dorsal pancreatic artery, pancreatica magna artery, and distal arterial branches to the tail. The SMA arises from the aorta just below the celiac trunk and posterior to the pancreatic neck; it courses inferiorly to become anterior to the uncinate process of the pancreas, alongside the SMV. The gastroduodenal artery, which arises from the common hepatic artery, branches into the anterior and superior pancreatoduodenal arteries, which in turn anastomose with the inferior pancreaticoduodenal branch of the SMA, forming an arcade around the head and uncinate process. The transverse pancreatic artery connects the pancreaticoduodenal arcade, dorsal pancreatic, and pancreatica magna arteries. The portal vein (PV) is formed by the confluence of the superior mesenteric vein (SMV) and splenic vein posterior to the neck of the pancreas. Most commonly, it divides into the right and left portal veins at the porta hepatis. The splenic vein is posterior to the body and tail of the pancreas and joins the SMV behind the neck. VASCULAR COMPLICATIONS OF PANCREATITIS The most common complications are: Hemorrhage into a pseudocyst Erosions of the upper gastrointestinal arteries Thromboses of the portal venous system Pseudoaneurysm Arterial complications Page 5 of 36

6 1.Hemorrhage Hemorrhage is one of the most lifethreatening complications of pancreatitis. Hemorrhage is usually due to erosion of a major pancreatic or peripancreatic artery or due to the formation and subsequent rupture of an arterial pseudoaneurysm. The pathogenesis of hemorrhagic complications is multifactorial. One of the factor is mediated by severe pancreatic inflammation and pancreatic necrosis which takes place during the early phase of acute pancreatitis. Local spread of the inflammatory process and extravasation of proteolytic and lipolytic enzymes further exacerbate the necrotizing process and initiate the damage of any vascular structure proximal to the necrotizing process, rendering them susceptible to rupture or subsequent pseudoaneurysm formation. Hemorrhage tends to occur rather frequently in patients requiring operation for necrosectomy and debridement of infected pancreatic sequestra (sequestrectomy). Another mechanism that may lead to severe hemorrhage is associated with the development of pancreatic and peripancreatic abscesses. This is more often observed weeks to months after the onset of a necrotizing form of severe pancreatitis or after necrosectomy and insufficient debridement. The combination of ischaemic necrosis, enzymatic destruction of tissues and bacterial contamination may lead to severe vessel damage as well as perforation of adjacent organs. In such events, bleeding can take place within the abscess cavity and from that to any other intra-abdominal or retroperitoneal space. A third pathogenic mechanism is mediated by long-standing pseudocysts. Vessels may be eroded as a consequence of persistent compression, ischemia, and elastolytic action of the enzymatic content of pseudocysts. Frequently, these mechanisms can lead to the formation of pseudoaneurysms. Their rupture or a direct vessel rupture within a pseudocyst converts it into a pseudoaneurysmatic pseudocyst (pulsatile pseudocyst), which may eventually rupture in the retroperitoneum or peritoneal cavity or communicate with adjacent hollow structures such as the stomach, jejunum, colon, and Wirsung duct (haemosuccus pancreaticus). Page 6 of 36

7 Fig. 2: 79-year-old woman with acute pancreatitis. Axial CT image shows a spontaneously high attenuation image (white arrow) that corresponds to a hematoma in the pancreatic head. Note the multiple hyperdense calculi inside the gallbladder (black arrow) References: C. N. Tentugal; Portimão, PORTUGAL 2.Pseudoaneurysm The formation of pseudoaneurysms occurring as a result of pancreatitis is well established. A pseudoaneurysm has been reported to occur in 3,5-10% of patients with pancreatitis. The arteries involved include, in order of frequency: splenic artery (40%) Fig. 3 on page 20 and Fig. 4 on page 21 gastroduodenal artery (30%) Fig. 5 on page 22 pancreaticoduodenal artery (20%) Fig. 6 on page 23 gastric artery (5%) hepatic artery (2%) others: superior mesenteric, jejunal, ileocaecal, intrapancreatic, aorta (1-3%) Fig. 7 on page 24, Fig. 8 on page 25 and Fig. 9 on page 26 Page 7 of 36

8 Fig. 3: 54-year-old male patient with history of pancreatectomy 10 years prior due to chronic alcoholic pancreatitis. Now presents with epigastric pain and melena. Contrast enhanced axial CT shows a well defined low attenation area that corresponds to the pseudoaneurysm sac (thin arrow) and its patent lumen (thick arrow) which shows the same attenuation as the aorta. References: C. N. Tentugal; Portimão, PORTUGAL Page 8 of 36

9 Fig. 5: Gastroduodenal artery pseudoaneurysm in a 27-year-old female with history of acute pancreatitis 1 month prior; now presents with continuous epigastric pain. Contrast enhanced axial CT demonstrates a pseudoaneurysm consisting of the aneurysm sac with a hypodense thrombus inside (black arrow) and the patent lumen filled with contrast material (white arrow). References: C. N. Tentugal; Portimão, PORTUGAL Page 9 of 36

10 Fig. 7: 40-year-old male with chronic pancreatitis. A and B: coronal and oblique MIP images demonstrating a small intrapancreatic pseudoaneurysm (black arrow). Note the atrophic pancreas with multiple hyperdense calcifications along its parenchyma. References: C. N. Tentugal; Portimão, PORTUGAL Rupture of a pseudoaneurysm is a disastrous complication of pancreatitis. A pseudoaneurysm may rupture into a pseudocyst, the gastrointestinal tract, peritoneal cavity or pancreatic parenchyma. The size of the pseudoaneurysm is not a determinant of rupture. The MDCTA has a sensitivity of %for detecting pseudoaneurysms. Angiography is indicated for diagnosing small pseudoaneurysms as well as for endovascular treatment with embolization, with a success rate of %. Venous complications Thrombosis and hemorrhage Thrombosis of the venous system affects mainly the splenic vein due to its proximity to the body and tail of the pancreas, but it can extend into the portal and superior mesenteric vein. Page 10 of 36

11 Different mechanisms are involved in venous thrombosis after pancreatitis, all of them leading to blood stasis which in the end will lead to thrombosis. 1. Splenic vein thrombosis Isolated splenic vein thrombosis (SVT) is relatively common in patients with chronic pancreatitis, occurring in as many as 10-40% of cases. Fig. 10: 77-year-old male with severe acute pancreatitis. Contrast enhanced axial CT shows necrosis of the pancreatic body and tail, with rearranging, low attenuation fluid collections(*) with small air bubbles inside (emphysematous pancreatitis). Splenic vein thrombosis is also evident (arrow). References: C. N. Tentugal; Portimão, PORTUGAL Page 11 of 36

12 When there is SVT the splenic artery remains intact and thus enables continued high pressure in the spleen, which forces an abnormal outlet through collaterals. Therefore, regardless of the mechanism of SVT, venous blood is forced to return to low pressure systems via collaterals. Increased blood flow through the short gastric veins to the left gastric vein or through the gastroepiploic vein to the pancreaticoduodenal vein creates a localized form of "left-sided" portal hypertension with dilatation of the submucosal veins within the stomach wall, producing the formation of gastric varices Fig. 11 on page 27 along the greater curvature and the fundus of the stomach. A second pathway involves the portosystemic collaterals, which develop along the lower end of the esophagus, with direct connection to the azygous system. Because portal venous pressure is normal and esophageal veins can usually drain through the patent left gastric vein, the development of associated oesophageal varices is usually prevented. SVT may be silent or present with symptoms. Gastrointestinal bleeding of various severities (anemia, hematemesis, melena, or hematochezia) is the commonest manifestation of the syndrome (15-50%). Splenomegaly is also a frequent accompaniment of SVT. 2. Portal vein thrombosis Portal vein thrombosis is a possible complication of pancreatitis although not as common as SVT. On MDCTA, an acute portal vein thrombus can be hyperdense and obscured on contrast-enhanced MDCTA. Chronic portal vein thrombus is relatively hypodense to adjacent soft tissues, presenting as a clearly defined filling defect within the enhanced portal vein lumen. The hepatic segment supplied by the occluded venous branch appears hyperdense on arterial phase imaging owing to compensatory arterial flow, and hypodense in comparison with the remaining hepatic parenchyma on the portal venous phase imaging. Page 12 of 36

13 Fig. 12: 50-year-old male with history of chronic pancreatitis. Contrast enhanced axial CT image demonstrates a linear,low attenuation, intraluminal filling defect in the portal vein (circle) in a long-standing PV thrombosis. References: C. N. Tentugal; Portimão, PORTUGAL Page 13 of 36

14 Fig. 13: Portal vein thrombosis. Doppler-US shows a hypoecoic portal vein with no blood flow. References: C. N. Tentugal; Portimão, PORTUGAL Page 14 of 36

15 When segmental occlusion of the portal venous system occurs, local collateral venous pathways form relatively quickly in response to occlusion of the main portal vein or one of its intrahepatic branches. Cavernous transformation of the portal vein is defined as a masslike network of intertwined veins in the hepatoduodenal ligament and porta hepatis that provide an alternative pathway around an occluded main portal vein or lobar branch. Compensatory arterial flow to the peripheral segments of the liver deprived of portal venous flow occurs and results in hyperattenuation in the arterial phase Fig. 14 on page 30. Fig. 15: Cavernous transformation of the portal vein and portal biliopathy. Contrast enhanced axial CT shows a network of collateral channels occupying the area of the former thrombosed portal vein (thick arrow). Extensive collateral circulation is also evident - gastric varices (arrowhead). Note the dilatation of the biliary duct (thin arrow) as a consequence of portal hypertension - portal biliopathy. References: C. N. Tentugal; Portimão, PORTUGAL Page 15 of 36

16 3. Superior mesenteric vein thrombosis SMV thrombosis is a rare complication of pancreatitis and may lead to mesenteric ischemia. Intestinal ischemia following mesenteric vein thrombosis is due to resistance in the mesenteric venous blood flow causing profound wall edema, fluid efflux into the bowel lumen with resulting systemic hypotension and increase in blood viscosity. As a result, arterial flow is diminished leading to submucosal hemorrhage and bowel infarction. Fig. 16: 86-year-old male with acute pancreatitis and SMV thrombosis. Contrast enhanced axial CT imaging demonstrates a filling defect in the SMV corresponding to the thrombus and a hyperattenuating wall (arrow). References: C. N. Tentugal; Portimão, PORTUGAL Page 16 of 36

17 Fig. 17: Superior mesenteric vein thrombosis. Doppler US image shows absence of flow in the superior mesenteric vein (SMV). SMA - superior mesenteric artery. References: C. N. Tentugal; Portimão, PORTUGAL VASCULAR CHECKLIST OF THE PANCREAS In a patient with pancreatitis the vascular structures around the pancreas must be checked in a systematic way in order to avoid misdiagnosis. These are the structures that must be carefully depicted: Arteries Splenic Gastroduodenal Pancreaticoduodenal Gastric Hepatic Superior mesenteric Veins Page 17 of 36

18 Splenic Superior mesenteric Portal Indirect signs Collateral circulation Transient hepatic attenuation differences (THAD) Splenomegaly Splenic infarction Images for this section: Page 18 of 36

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20 Fig. 1: Volume rendered CT image demonstrating the major arterial blood supply of the pancreas. CT - celiac trunck; LGA - left gastric artery; SA - splenic artery; CHA - common hepatic artery; SMA - superior mesenteric artery Fig. 2: 79-year-old woman with acute pancreatitis. Axial CT image shows a spontaneously high attenuation image (white arrow) that corresponds to a hematoma in the pancreatic head. Note the multiple hyperdense calculi inside the gallbladder (black arrow) Page 20 of 36

21 Fig. 3: 54-year-old male patient with history of pancreatectomy 10 years prior due to chronic alcoholic pancreatitis. Now presents with epigastric pain and melena. Contrast enhanced axial CT shows a well defined low attenation area that corresponds to the pseudoaneurysm sac (thin arrow) and its patent lumen (thick arrow) which shows the same attenuation as the aorta. Page 21 of 36

22 Fig. 4: Volume-rendered CT image demonstrating peri-pancreatic arteries and a splenic pseudoaneurysm. Page 22 of 36

23 Fig. 5: Gastroduodenal artery pseudoaneurysm in a 27-year-old female with history of acute pancreatitis 1 month prior; now presents with continuous epigastric pain. Contrast enhanced axial CT demonstrates a pseudoaneurysm consisting of the aneurysm sac with a hypodense thrombus inside (black arrow) and the patent lumen filled with contrast material (white arrow). Page 23 of 36

24 Fig. 6: 79-year-old female that presents with acute pancreatitis. Contrast enhanced coronal CT image demonstrates a pseudoaneurysm of the pancreaticoduodenal artery with its low attenuation sac (white arrow) and patent lumen (black arrow). Page 24 of 36

25 Fig. 7: 40-year-old male with chronic pancreatitis. A and B: coronal and oblique MIP images demonstrating a small intrapancreatic pseudoaneurysm (black arrow). Note the atrophic pancreas with multiple hyperdense calcifications along its parenchyma. Page 25 of 36

26 Fig. 8: Volume rendered CT demonstrating the small intrapancreatic pseudoaneurysm. Fig. 9: Coronal T1-weighted MR image obtained after the administration of gadoliniumbased contrast material showing a intrapancreatic pseudoaneurysm (arrow). Page 26 of 36

27 Fig. 10: 77-year-old male with severe acute pancreatitis. Contrast enhanced axial CT shows necrosis of the pancreatic body and tail, with rearranging, low attenuation fluid collections(*) with small air bubbles inside (emphysematous pancreatitis). Splenic vein thrombosis is also evident (arrow). Page 27 of 36

28 Fig. 11: 72-year-old male with prior history of acute pancreatitis shows gastric varices along the fundus and greater curvature. This patient had a splenic vein thrombosis, a late complication of pancreatitis. Contrast enhanced axial CT reveals prominent gastric veins along the fundus and greater curvature (circle). Page 28 of 36

29 Fig. 12: 50-year-old male with history of chronic pancreatitis. Contrast enhanced axial CT image demonstrates a linear,low attenuation, intraluminal filling defect in the portal vein (circle) in a long-standing PV thrombosis. Page 29 of 36

30 Fig. 13: Portal vein thrombosis. Doppler-US shows a hypoecoic portal vein with no blood flow. Page 30 of 36

31 Fig. 14: Transient hepatic attenuation differences (THAD). Contrast enhanced CT axial image in the arterial phase shows segmental arterial hyperperfusion due to portal vein obstruction. Page 31 of 36

32 Fig. 15: Cavernous transformation of the portal vein and portal biliopathy. Contrast enhanced axial CT shows a network of collateral channels occupying the area of the former thrombosed portal vein (thick arrow). Extensive collateral circulation is also evident - gastric varices (arrowhead). Note the dilatation of the biliary duct (thin arrow) as a consequence of portal hypertension - portal biliopathy. Page 32 of 36

33 Fig. 16: 86-year-old male with acute pancreatitis and SMV thrombosis. Contrast enhanced axial CT imaging demonstrates a filling defect in the SMV corresponding to the thrombus and a hyperattenuating wall (arrow). Page 33 of 36

34 Fig. 17: Superior mesenteric vein thrombosis. Doppler US image shows absence of flow in the superior mesenteric vein (SMV). SMA - superior mesenteric artery. Page 34 of 36

35 Conclusion MDCT is the most frequently used imaging modality to evaluate pancreatitis and it has the ability to detect most vascular complications. In order to avoid misdiagnosis, it is useful to be familiar with a checklist of the mostly involved vascular structures. The prompt recognition of these complications will allow timely intervention. Personal Information Cláudia Tentúgal Radiology Resident. Radiology Department. Centro Hospitalar do Barlavento Algarvio, Portimão/Portugal. claudiatentugal@gmail.com References 1. Rocio Perez-Johnston, MD, Dipti K. Lenhart, MD, Dushyant V. Sahani, MD. CT Angiography of the Hepatic and Pancreatic Circulation. Radiol Clin N Am 48 (2010) Ismail H. Mallick, Marc C. Winslet. Vascular complications of pancreatitis. JOP. J Pancreas (Online) 2004; 5(5): Savastano S, Feltrin GP, Antonio T, et al. Arterial complications of pancreatitis: diagnostic and therapeutic role of radiology. Pancreas 1993;8: Emil J. Balthazar, MD. Complications of acute pancreatitis: Clinical and CT evaluation. Radiol Clin N Am 40 (2002) De Perrot M, Berney T, Buhler L, et al. Management of bleeding pseudoaneurysms in patients with pancreatitis. Br J Surg 1999;86: Page 35 of 36

36 6. Anuradha Saokar, MD, Chad B. Rabinowitz, MD, Dushyant V. Sahani, MD. CrossSectional Imaging in Acute Pancreatitis. Radiol Clin N Am 45 (2007) Preet S. Kang, MD, James W. Spain, MD, PhD. Multidetector CT Angiography of the Abdomen. Radiol Clin N Am 43 (2005) Karen M. Horton, MD, Elliot K. Fishman, MD. CT Angiography of the Mesenteric Circulation. Radiol Clin N Am 48 (2010) David H. Kim, MD, Perry J. Pickhardt, MD. Radiologic Assessment of Acute and Chronic Pancreatitis. Surg Clin N Am 87 (2007) John N. Ly, Frank H. Miller. MR imaging of the pancreas: A practical approach. Radiol Clin N Am 40 (2002) Page 36 of 36