Identifying Local Complications Associated with Acute Pancreatitis
Pancreatic Necrosis and Peripancreatic Fluid Collections
CECT can be used to diagnose pancreatic necrosis, which is associated with higher mortality and morbidity because it is patients with necrosis who most commonly develop persistent organ failure. Necrosis is best recognized by liquefaction, and is usually identified two to three days after onset of clinical symptoms [28]. Extrapancreatic necrosis (EXPN) may also be seen as a result of pancreatic enzymes extravasation into the tissues surrounding the pancreas. CECT shows extrapancreatic morphological changes exceeding fat stranding, with complete enhancement of the pancreatic parenchyma and no signs of pancreatic necrosis [29]. Figure 5.1 shows imaging differences between EXPN and pancreatic necrosis. Differentiating acute necrotizing pancreatitis (ANP) from EXPN alone is important as those with the latter have a better prognosis, including a lower risk of developing infected necrosis, need for intervention and mortality as well as a shorter hospital stay [29–31]. Those with EXPN are also less likely to develop diabetes and exocrine insufficiency as there is no loss of pancreatic parenchyma.
Figure 5.1 CT images of extrapancreatic necrosis and parenchymal pancreatic necrosis. (a) Morphological changes and necrosis (arrow) around the pancreas with a normal enhancing pancreas. (b) Hypoenhancement of the head and neck of the pancreas (arrow) consistent with parenchymal pancreatic necrosis with no extrapancreatic necrosis.
Source: courtesy of Elham Afghani.
CT imaging can differentiate an acute peripancreatic fluid collection (AFC) from an acute necrotizing collection (ANC). AFCs are fluid collections associated with interstitial edematous pancreatitis without necrosis, and typically develop within four weeks after onset. CECT of AFC shows a homogeneous collection with a fluid density that is confined to the peripancreatic fascial planes. There is no encapsulating wall which sets it apart from a pseudocyst, which is defined as an encapsulated fluid collection occurring more than four weeks after the onset of interstitial pancreatitis (Figure 5.2). CECT shows a well‐circumscribed homogeneous fluid density with only a liquid component and well‐defined wall [32]. ANC is associated with ANP and, on CECT, is demonstrated by a heterogeneous and non‐liquid density; it is without a definable wall and develops less than 4 weeks after symptom onset. It may be difficult to differentiate AFC from ANC in the first week after onset of symptoms. On the other hand, walled‐off necrosis (WON) is a mature and encapsulated collection of pancreatic or peripancreatic necrosis occurring more than four weeks after onset (Figure 5.3). On CECT, loculations of heterogeneous material is noted in the peripancreatic and/or extrapancreatic space [32]. CECT may also aid in distinguishing infected versus sterile ANC or WON by the presence of gas bubbles within the collection [1].
Figure 5.2 CT image of pancreatic pseudocyst shows a well‐encapsulated collection of fluid (arrow).
Source: courtesy of Elham Afghani.
Vascular Complications
MDCT is the most common imaging modality utilized to distinguish vascular complications associated with AP. It identifies peripancreatic vascular structures and involvement. Peripancreatic venous thrombosis of the splenic, portal, and/or superior mesenteric veins occurs as a result of stasis from spasm and mass effect from the surrounding pancreatic inflammation. Splanchnic vein thrombosis is the most common vascular complication of AP given that the splenic vein runs posteriorly and adjacent to the body and tail of the pancreas. It is seen in about 1.7% of all patients undergoing abdominal contrast‐enhanced cross‐sectional imaging [33] and 22.6% of patients with AP [34] and in 50% of patients with ANP [35]. It is often an incidental finding and may lead to severe complications such as mesenteric ischemia, non‐cirrhotic portal hypertension, and/or gastrointestinal bleeding. Splanchnic vein thrombosis can lead to engorgement of the short gastric vessels, leading to gastric varices with 12% risk of gastrointestinal bleeding [34]. On CT imaging, venous thrombosis is established by the presence of an enlarged vein with low attenuation in the center and does not enhance with the injection of intravenous contrast. There may also be extensive irregular enhancing vessels around the portal or splenic vein suggesting collateral formations. Focal segmental peripheral areas of lower attenuation may also be seen in the hepatic parenchyma that do not enhance with intravenous contrast, suggesting ischemic changes as a result of portal vein thrombosis [36,37].
Figure 5.3 Infected walled‐off necrosis: the arrow depicts the encapsulated collection of heterogeneous necrosis as well as air bubbles in the dependent portion of the collection.
Source: courtesy of Elham Afghani.
Arterial pseudoaneurysms are late complications of AP. The incidence is approximately 1.3–10% and can occur weeks to months after the onset of AP [36]. If not recognized early, it has up to a 90% mortality from hemorrhagic complications [37]. It occurs as a result of erosion of the wall of the vessel by the autodigestive action of proteolytic enzymes. On CT imaging, the pseudoaneurysm may appear as a saccular structure with an enhancing component and a possible thrombus. Pseudoaneurysms will enhance on arterial but not venous phase. Unenhanced images may suggest a pseudoaneurysm by a lesion with increased attenuation due to thrombosis. Pseudoaneurysms most commonly form in the splenic artery. Other locations include the gastroduodenal, superior mesenteric, pancreaticoduodenal, and hepatic arteries [36]. Pseudocysts can transform into pseudoaneurysms by mass effect and erosion into the surrounding arteries. On CT imaging, the pseudocyst/pseudoaneurysm does not appear cystic, but is dense on non‐contrast images and enhances on arterial and venous phases [36,38].
Other Complications
Obstruction of the bile and/or cystic duct, concomitant acute cholecystitis, extrahepatic bile duct necrosis, biliary stricture, and pancreatic choledochal fistula are possible biliary complications associated with AP [39–41]. CBD obstruction will commonly be seen as dilation of the CBD or cystic duct. CT imaging of cholecystitis demonstrates a distended gallbladder with an irregular wall. There may be biliary sludge and/or pericholecystic fluid [40]. Pancreatic choledochal fistulas occur as a result of direct inflammation and erosion between these two structures. CT scan of the abdomen with or without contrast shows a hypodense, thick fluid collection with gas in the pancreatic area [39].
Gastric, duodenal, jejunal, and colonic fistulization can also occur as a result of AP [42]. This occurs because of proteolytic enzyme autodigestion of the adjacent bowel from decompression of a pseudocyst or walled off necrosis as well as phlegmonous changes. The presence of gas on CT imaging may indicate fistulization [43].
Timing of CT in Acute Pancreatitis