ACUTE PANCREATITIS: NEW CLASSIFICATION OF AN OLD FOE T Barrow, A Nasrullah, S Liong, V Rudralingam, S A Sukumar
LEARNING OBJECTIVES q Through a series of cases illustrate the updated Atlanta symposium classification of acute pancreatitis complications. q Highlight the changes in the recent classification update. q Pictorial review of the imaging findings on computed tomography (CT), with MR correlation where appropriate, of local complications related to acute pancreatitis.
BACKGROUND q Originally published in 1992 the Atlanta symposium consensus classification of acute pancreatitis complications has undergone recent revision. 1 q An improved understanding of underlying pathophysiology, advanced diagnostic imaging and new therapy options drove the 2012 update. 2 q It is important that both radiologists and clinicians are aware of the new classification to ensure standard reporting and facilitate communication between the different subspecialities optimising patient care.
LEARNING OBJECTIVES q Through a series of cases illustrate the updated Atlanta symposium classification of acute pancreatitis complications. q Highlight the changes in the recent classification update. q Pictorial review of the imaging findings on computed tomography (CT), with sonographic correlation where appropriate, of local complications related to acute pancreatitis.
CHANGES TO CLASSIFICATION Changes were made in 2012 to the classification of NON-VASCULAR complications. 1992 Classification Acute fluid collection Pancreatic necrosis 2012 Classification Acute peripancreatic fluid collection Acute necrotic collection Infected acute necrotic collection Pancreatic necrosis Walled off necrosis Infected walled off necrosis Infected pancreatic necrosis Pancreatic pseudocyst Pancreatic abscess REMOVED from classification Infected pancreatic necrosis Pancreatic pseudocyst Infected pseudocyst ADDED to classification
COMPLICATIONS LOCAL COMPLICATIONS NON-VASCULAR Acute peripancreatic fluid collection Pancreatic necrosis Acute necrotic collection Infected necrosis Pancreatic pseudocyst Walled off necrosis (WON) VASCULAR Haemorrhage Pseudoaneurysm Thrombosis
NON-VASCULAR LOCAL COMPLICATIONS
COMPLICATIONS NON-VASCULAR <4 weeks >4 weeks Interstitial Oedematous Pancreatitis Acute Peripancreatic Fluid Collection (APFC) Pancreatic Pseudocyst (may become infected) Necrotising Pancreatitis Pancreatic Necrosis Acute Necrotic Collection (ANC) (may become infected) Walled Off Necrosis (WON) (may become infected) Infected necrosis refers to infected ANC/WON
ACUTE PERIPANCREATIC FLUID COLLECTION A Fig 1. Intravenous contrast enhanced axial CT images (A, B) in two different patients shows acute peripancreatic fluid collections, with no perceptible wall, within the anterior pararenal space representing an acute peripancreatitic fluid collection (APFC, arrow heads). Note the presence of a fat plane between the collection and the posterior gastric wall (arrow) allows differentiation from a lesser sac collection (B, star). APFCs represent homogeneous peripancreatic fluid, with no discernible wall, confined by peripancreatic fascial planes. The presence of a fat plane between the collection &posterior stomach wall allows differentiation from a lesser sac collection. The occurrence of lesser sac collections, contrary to common belief, is rare in our experience.
ACUTE PERIPANCREATIC FLUID COLLECTION Fig 2. Axial intravenous contrast enhanced CT image showing an acute fluid collection extending into the spleen (star) in a patient with acute pancreatitis. Acute peripancreatic fluid collections (APFCs) are associated with interstitial oedematous pancreatitis with no associated pancreatic necrosis. This entity occurs within the first 4 weeks post onset of interstitial oedematous pancreatitis.
PANCREATIC PSEUDOCYST Fig 3. Axial intravenous contrast enhanced CT images (A-C) of the same patient show the formation of a pseudocyst from an acute peripancreatic fluid collection over a 6 week period. Initial admission examination (A) demonstrates acute peripancreatic inflammatory fat stranding (arrows) and the interval CT performed 10 days later (B) shows the development of an acute peripancreatic fluid collection (arrow head). Subsequent CT performed at a 5 week interval (C) shows progression to a welldefined fluid collection with a thin wall (star), consistent with pseudocyst formation. Pancreatic pseudocysts are well-defined encapsulated homogeneous fluid collections that usually occur after 4 weeks post onset of interstitial oedematous pancreatitis. They usually occur outside the pancreas and have no/limited associated necrosis.
PANCREATIC PSEUDOCYST Fig 4. Axial intravenous contrast enhanced CT images (A, B) of the same patient shows the formation of a mediastinal pseudocyst (arrow) 6 weeks after the acute episode of pancreatitis. Note the presence of a moderate pericardial effusion (arrow head) and extensive upper abdominal ascites (star). Pancreatic pseudocysts are well-defined encapsulated homogeneous fluid collections that usually occur after 4 weeks post onset of interstitial oedematous pancreatitis. They usually occur outside the pancreas and have no/limited associated necrosis.
PANCREATIC NECROSIS Fig 5. Intravenous contrast enhanced axial CT images (A, B) show patchy parenchymal enhancement (arrow) and extensive peripancreatic fluid (star). Lack of pancreatic parenchymal enhancement following intravenous contrast administration is the hallmark of necrotising pancreatitis. In the acute setting enhancement may be patchy and identification of necrosis is aided by the addition of an unenhanced acquisition, which allows objective enhancement measurement.
ACUTE NECROTIC COLLECTION (ANC) Fig 6. Axial intravenous contrast enhanced CT images (A-C) of the same patient over a 6 week period shows the development of a walled of necrosis from an acute necrotic collection (ANC). Initial presentation CT image (A) shows extensive patchy pancreatic enhancement (arrow). 2 week interval CT (B) demonstrates the formation of heterogeneous non-liquid density collection, with no definable wall, involving the pancreatic and peripancreatic tissues ANC (star). Follow-up CT (C) performed at 6 weeks shows the formation of a wall around the collection (arrow head), representing early walled off necrosis (WON). ANCs are heterogeneous pancreatic/peripancreatic collections, containing varying amount of fluid and necrotic debris, that occur in the acute setting of necrotising pancreatitis. They have no definable wall unlike walled off necrosis (WON).
INFECTED NECROSIS Fig 7. Axial intravenous contrast enhanced CT image in a patient with severe acute pancreatitis and sepsis on admission showing extensive pancreatic necrosis with pockets of gas with ( soap bubble appearance, arrow) without a capsule, consistent with infected pancreatic necrosis. Note the presence of oedematous retroperitoneum (arrow heads). The presence of gas containing collection is characteristic of infected necrosis. Infected necrosis can occur in ANCs (without a wall) or WON (with a wall).
WALLED OFF NECROSIS (WON) B C Fig 8. Axial intravenous contrast enhanced CT images (A) shows a well defined homogeneous collection with a thin wall arising from the distal body and tail of the pancreas (star). Corresponding axial T2-weighted MR image (B) better depicts the necrotic component (star) of the encapsulated collection, consistent with a WON. Subsequent enhanced CT image (C) performed at a 2 week demonstrates the presence of fat within the increasingly heterogeneous collection (arrow), characteristic of WON. WON represents a mature, encapsulated collection of pancreatic/peripancreatic necrosis that has developed from an ANC. It usually occurs > 4 weeks after the onset of necrotising pancreatitis. T2 weighted MR better depicts the necrotic content of the WON.
WALLED OFF NECROSIS (WON) Fig 9. Axial intravenous contrast enhanced CT images (A-C) of a patient with necrotising pancreatitis 6 weeks post onset show a walled off subtly heterogeneous collection arising in the peripancreatic tissue (star). Note the pancreatic parenchyma can be seen separately from the collection (arrow) and the presence of calcification within the pancreatic head suggestive of chronic pancreatitis. Learning Point: WON may occur in the pancreatic, peripancreatic tissues or both.
VASCULAR LOCAL COMPLICATIONS
PSEUDOCYST HAEMORRHAGE A B Fig 10. Axial contrast enhanced CT images (A, B) of the same patient at a 5 month interval. Image A demonstrates the presence of an encapsulated homogeneous fluid collection within the anterior pararenal space (star), characteristic of a pseudocyst. Subsequent CT performed on acute admission with abdominal pain (B) shows interval enlargement of the pseudocyst with heterogeneous high density content (arrow), consistent with pseudocyst haemorrhage. Severe haemorrhage may complicate long standing pseudocysts, converting them into pseudoaneurysms. These may cause persistent compression & degeneration of vessel wall due to enzymatic content.
PSEUDOANEURYSM A B C Fig 11. Unenhanced axial CT image shows a focal vascular dilatation anterior to the aorta (arrow). Subsequent arterial (B) and portovenous phase (C) axial CT images at the same level demonstrate a pseudoaneurysm of the gastroduodenal artery (star). The gastroduodenal artery is the second most commonest artery to develop a pseudoaneurysm. Pseudoaneurysm may rupture into the peritoneal cavity, retroperitoneum or adjacent structures such as bowel.
PSEUDOANEURYSM HAEMORRHAGE Fig 12. Pseudoaneurysm secondary to complicated pancreatitis. Intravenous contrast enhanced porto-venous phase CT images (A, B) showing haemorrhagic pancreatitis with haematoma within the pancreatic bed extending into the right anterior pararenal space (arrow) and suspicious for an underlying pseudoaneurysm (star). Corresponding selective angiogram (C) confirms a pseudoaneurysm (arrow head) from a branch of the superior mesenteric artery, which was successfully embolised. Pseudoaneurysm formation occurs in up to 10% of cases of pancreatiitis. 3 Time interval from acute episode to pseudoaneurysm formation is variable (days to years).
SPLENIC VEIN THROMBOSIS Fig 13. Axial contrast-enhanced CT images (A-C) over a 2 year interval. Figure A shows a localised filling defect in the splenic vein (arrow) in keeping with an acute splenic vein thrombus. Interval CT performed 2 years later (B, C) demonstrate nonopacification of the splenic vein consitent with chronic thrombosis. Note the interval formation of multiple collateral vessels (arrow head). Note the incidental WON (star). Splenic vein thrombosis occurs in 10-40 % of the cases. It occurs due to local inflammation or compression from an adjacent pseudocyst. 4 It can result in isolated left sided portal hypertension, variceal formation and eventual GI bleeding.
PORTAL VEIN THROMBOSIS Fig 14. Portovenous contrast-enhanced axial CT slice shows a localised filling defect in the portal vein (yellow arrow) in keeping with portal vein thrombosis secondary to acute pancreatitis. Formation of portal vein thrombosis can lead to hepatic infarction. 5 Endovascular and systemic anti-coagulation can be used for treatment.
CONCLUSION q Complications of acute pancreatitis are frequently encountered. q It is important for the radiologist to be aware of the updated Atlanta symposium classification of acute pancreatitis. q Classification use facilitates communication with surgical colleagues and the initiation of timely potentially live-saving therapy where appropriate.
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