: 2014  |  Volume : 1  |  Issue : 1  |  Page : 50--55

Multihued complications in acute pancreatitis: A kaleidoscopic retrospective

Swarna Gupta Jain1, Brij Bhushan Thukral1, Avneet Singh Chawla2, Shalabh Jain1, Yatish Agarwal1,  
1 Department of Radiodiagnosis, Safdarjung Hospital and VM Medical College, New Delhi, India
2 Department of Surgery, Safdarjung Hospital and VM Medical College, New Delhi, India

Correspondence Address:
Dr. Swarna Gupta Jain
Department of Radiodiagnosis, Safdarjung Hospital and VM Medical College, New Delhi - 110 029


Acute pancreatitis is a diffuse inflammatory process in and around the pancreas triggered by the leakage of activated pancreatic secretions. It may remain localized within the pancreatic glandular tissue or spread to involve the adjacent or remote tissue planes and organs. Since the morbidity and mortality of acute pancreatitis is closely related to the extent of intra- and extra-pancreatic complications, cross-sectional contrast-enhanced computed tomography (CECT) imaging plays a major role in assessing the complications, stratifying the severity, and thus, prognosticating the outcome. Early diagnosis of complications allows for timely institution of specific measures that can help decrease the morbidity and mortality. This kaleidoscopic retrospective presents the complications of acute pancreatitis on CECT. The essay may benefit family physicians, surgeons, gastro-intestinal (GI) surgeons and GI physicians who manage such patients in their clinical practice, besides drawing the attention of residents and fellows practicing GI radiology.

How to cite this article:
Jain SG, Thukral BB, Chawla AS, Jain S, Agarwal Y. Multihued complications in acute pancreatitis: A kaleidoscopic retrospective.Astrocyte 2014;1:50-55

How to cite this URL:
Jain SG, Thukral BB, Chawla AS, Jain S, Agarwal Y. Multihued complications in acute pancreatitis: A kaleidoscopic retrospective. Astrocyte [serial online] 2014 [cited 2020 Jul 8 ];1:50-55
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 Pancreatic Complications

Pancreatic Necrosis

Nonenhancement of all or part of pancreas on contrast-enhanced computed tomography (CECT) scan is termed "necrosis" [1] [Figure 1]. CT is 100% specific for necrosis if greater than 30% of the gland is involved. [2] Necrosis develops between 24 and 48 h after the onset of acute pancreatitis, and therefore CT within the first 12 h may be falsely reassuring. [3] Pancreatic necrosis is a potential sequel of acute pancreatitis, which pathologically represents a collection of devitalized tissue. Appropriate therapeutic planning requires definition of this irreversibly damaged gland, the presence of which is not consistently diagnosed on the basis of clinical and laboratory data.{Figure 1}

Infected Pancreatic Necrosis

Distinction between a sterile and an infected necrosis is important because patients with infected necrosis usually need percutaneous, laparoscopic, endoscopic, or surgical intervention. [4] Infection can be suggested on CECT images if gas bubbles are present in the collection owing to the presence of gas-forming organisms [Figure 2]. [5] Gas can also be present in a collection after some drainage procedures. In the absence of gas in the collection, definitive proof can be obtained only by performing fine-needle aspiration of the collection with a positive Gram stain and culture for organisms. [6] {Figure 2}

Peripancreatic Fluid Collection

Peripancreatic fluid collections are caused by pancreatic and peripancreatic inflammation or by rupture of one or more small peripheral pancreatic side duct branches. They conform to the anatomic boundaries of the retroperitoneum and are usually seen immediately next to the pancreas without any discernible wall [Figure 3]. In the 1st week of acute pancreatitis, distinction between acute peripancreatic fluid collection and acute necrotizing collection may be difficult or impossible, because both collections may appear as areas of nonenhancement. If nonenhancing areas of variable attenuation are seen in these collections, the diagnosis of peripancreatic necrosis with nonliquefied components is suggested. [7] {Figure 3}

Peripancreatic Abscess

Peripancreatic abscess can be suggested on CECT images if gas bubbles are demonstrated within the collection [5] [Figure 4]. Spontaneous drainage into the gastrointestinal tract can lead to an erroneous diagnosis of infected collection. Careful analysis of the adjacent gastrointestinal walls can help prevent this diagnostic pitfall. Gas can also be present in a collection after some drainage procedures.{Figure 4}


Within 4 weeks from onset of acute pancreatitis, fluid collection may gradually transition into a pseudocyst. Pseudocyst occurs as a complication of acute pancreatitis in approximately 10%-20% of cases. [8] On CECT images, pseudocysts can be diagnosed as well-circumscribed, usually round or oval collections of homogeneously low attenuation that are surrounded by a well-defined enhancing wall consisting of fibrous or granulation tissue [Figure 5]. [7] {Figure 5}

 Extrapancreatic Complications

Pleural Effusion and Ascites

Ascites and effusion [Figure 6] and [Figure 7] are frequent during acute pancreatitis. They are accurate predictors of severity in these patients and are used as severity predictors in modified CT Severity Index for acute pancreatitis. [9] Because of the close relation of the pancreas, particularly in the tail, to the left hemidiaphragm, effusions are usually left sided or bilateral.{Figure 6}{Figure 7}

Vascular Complications

Vascular complications in pancreatitis are well recognized. The most common complications are hemorrhage into a pseudocyst, thromboses of the portal venous system, formation of pseudoaneurysms. Pancreatitis in combination with vascular complications is dangerous and potentially lethal. The survival of patients with pancreatitis and vascular complications depends on the early diagnosis of these complications.

Venous Thrombosis

Portal vein, splenic vein, and superior mesenteric vein thrombosis is a well-recognized complication of pancreatitis. The appearances on CECT are of an enlarged vein with a center of lower attenuation, which does not enhance following intravenous contrast injection [Figure 8] and [Figure 9]. Splenic vein thrombosis following pancreatitis should be considered in all patients as a cause of upper gastrointestinal hemorrhage from varices. [10] {Figure 8}{Figure 9}


A pseudoaneurysm has been reported to occur in 3.5%-10% of patients with pancreatitis. [11] The development of a pseudoaneurysm is due to severe inflammation necrotizing the vessel wall. The arteries involved include, in order of frequency, the splenic (40%), gastroduodenal (30%), pancreaticoduodenal (20%), gastric (5%), hepatic (2%), and others (superior mesenteric, jejunal, ileocecal, aorta) (1%-3%). [11] Nonenhanced CT scans demonstrate a low-attenuation rounded structure arising from the donor artery. Intermediate or high attenuation (hemorrhage) adjacent to the pseudoaneurysm indicates pseudoaneurysmal rupture, CECT demonstrates a contrast material-filled sac [Figure 10] and [Figure 11]. [12] However, the entire pseudoaneurysm may not fill with contrast material; a low-attenuation area may remain within the pseudoaneurysm, a finding that indicates partial thrombosis. The donor artery is adjacent to the pseudoaneurysm and can usually be seen communicating with it.{Figure 10}{Figure 11}

Gastrointestinal Complications

Gastrointestinal involvement in pancreatitis manifests as bowel wall thickening [Figure 12], stricture formation [Figure 13], or fistulous communication with collection [Figure 14]. Gastrointestinal fistula formation leads to the appearance of air foci within the collection, which has to be differentiated from infected collection.{Figure 12}{Figure 13}{Figure 14}

Fat Necrosis

Acute pancreatitis can result in fat necrosis. Mesenteric and retroperitoneal fat necrosis may be caused by fat saponification from pancreatitis, in which the damaged pancreas releases lipolytic enzymes, which autodigest the pancreatic parenchyma and peripancreatic fat tissues. [13] Scattered nodules of fat necrosis may be present throughout the retroperitoneum and abdominal cavity on CECT [Figure 15].{Figure 15}


1Ayub K, Slavin J, Imada R. Endoscopic retrograde pancreaticoduodenography in gallstone-related acute pancreatitis. Cochrane Database Sys Rev 2010;3:CD003630.
2Merkle EM, Gorich J. Imaging of Acute Pancreatitis. Eur Radiol 2002;12:1979-92.
3Osvaldt AB, Viero P, Borges da Costa MS, Wendt LR, Bersch VP, Rohde L. Evaluation of Ranson, Glasgow, APACHE-II, and APACHE-O criteria to predict severity in acute biliary pancreatitis. Int Surg 2001;86:158-61.
4Harris HW, Barcia A, Schell MT, Thoeni RF, Schecter WP. Necrotizing pancreatitis: A surgical approach independent of documented infection. HPB (Oxford) 2004;6:161-8.
5Vege SS, Fletcher JG, Talukdar R, Sarr MG. Peripancreatic collections in acute pancreatitis: Correlation between computerized tomography and operative findings. World J Gastroenterol 2010;16:4291-6.
6Ashley SW, Perez A, Pierce EA, Brooks DC, Moore FD Jr, Whang EE, et al. Necrotizing pancreatitis: Contemporary analysis of 99 consecutive cases. Ann Surg 2001;234:572-9.
7Thoeni RF. The revised Atlanta classification of acute pancreatitis: Its importance for the radiologist and its effect on treatment. Radiology 2012;262:751-64.
8Memiº A, Parildar M. Interventional radiological treatment in complications of pancreatitis. Eur J Radiol 2002;43:219-28.
9Mortele KJ, Wiesner W, Intriere L, Shankar S, Zou KH, Kalantari BN, et al. A modified CT severity index for evaluating acute pancreatitis: Improved correlation with patient outcome. AJR Am J Roentgenol 2004;183:1261-5.
10Belli AM, Jennings CM, Nakielny RA. Splenic and portal venous thrombosis: A vascular complication of pancreatic disease demonstrated on computed tomography. Clin Radiol 1990;41:13-6.
11Mallick IH, Winslet MC. Vascular complications of pancreatitis. JOP 2004;5:328-37.
12Knisely BL, Mastey LA, Collins J, Kuhlman JE. Imaging of cardiac transplantation complications. Radiographics 1999;19:321-41.
13Franco-Pons N, Gea-Sorlí S, Closa D. Release of inflammatory mediators by adipose tissue during acute pancreatitis. J Pathol 2010;221:175-82.