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MDCT Imaging Features of Acute and Chronic Pancreatitis with its Complications: A Pictorial Review |
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Nagarajaiah Chandandur Pradeep Kumar, K Ramalakshmi, M Anvith, N Sanjana, Parmeshwar Ugran Prateek 1. Associate Professor, Department of Radiodiagnosis, Mysore Medical College, Karnataka, India. 2. Junior Resident, Department of Radiodiagnosis, Mysore Medical College, Karnataka, India. 3. Junior Resident, Department of Radiodiagnosis, Mysore Medical College, Karnataka, India. 4. Junior Resident, Department of Radiodiagnosis, Mysore Medical College, Karnataka, India. 5. Junior Resident, Department of Radiodiagnosis, Mysore Medical College, Karnataka, India. |
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Correspondence Address : M Anvith, S/o Manjunath T K, K C Street, Thirthahalli, Shivamogga-577202, Karnataka, India. E-mail: anvithmtth@gmail.com |
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ABSTRACT | ![]() | ||||||||||||||||||||||||||||||||||||||||||
The incidence of Acute Pancreatitis (AP) was 30.0 per 100,000 population overall. The two most common aetiological factors of AP are gallstones and alcohol abuse, while other causes such as metabolic, iatrogenic, vascular, infections, and toxic factors are less important and less common. Two laboratory tests, serum amylase and lipase levels, which have relatively good sensitivity and specificity, complement imaging in the diagnosis and treatment of some cases of AP. Imaging helps confirm the clinical diagnosis, determine the cause, grade the extent of AP, and assess its severity, in addition to clinical symptoms and laboratory studies. Chronic Pancreatitis (CP) is characterised by continuous inflammatory and fibrotic changes in the pancreas, eventually resulting in exocrine and endocrine dysfunction. Alcoholism is a factor in 70-90% of CP cases. Other causes include chronic ulcerative colitis, Sjogren’s syndrome, primary sclerosing cholangitis, etc. Early diagnosis of CP is challenging, as biochemical studies do not provide definitive diagnosis in the early stages. Imaging, mainly Contrast Enhanced Computed Tomography (CECT) and Magnetic Resonance Imaging (MRI), aids in the definitive diagnosis. The present pictorial article aimed to provide an image-rich overview of the morphological features associated with the early-stage and late-stage local consequences of acute and chronic pancreatitis. | |||||||||||||||||||||||||||||||||||||||||||
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Keywords : Aneurysm, Emphysematous, Fat stranding, Fluid collection, Multidetector computed tomography, Necrosis, Oedema, Pancreas, Thrombosis | |||||||||||||||||||||||||||||||||||||||||||
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INTRODUCTION | ![]() | ||||||||||||||||||||||||||||||||||||||||||
Pancreatitis is an inflammatory condition that refers to the autodigestion of the pancreas, where pancreatic enzymes damage pancreatic tissue, leading to dysfunction of the gland and potential damage to distant organs and systems. Pancreatitis can be either acute or chronic. Acute Pancreatitis (AP) Acute Pancreatitis is an acute inflammatory condition that develops when fluid containing activated proteolytic enzymes exudes from the pancreatic interstitium and leaks into the surrounding tissue (1). The AP is classified as mild or severe, based on the presence of local complications and organ failure. Morphologically, AP can be of two types, including acute oedematous or interstitial pancreatitis and acute Necrotising Pancreatitis (NP). Acute oedematous or interstitial pancreatitis comprises pancreatic oedema and inflammation, often having a modest clinical course and a self-limiting process. It has fewer local complications. Its pathological hallmarks are interstitial oedema and sporadic tiny regions of parenchymal necrosis (2). A much more severe form of pancreatitis known as NP is marked by significant fat necrosis, bleeding, and necrotic liquefaction of the pancreas (3). It is associated with local complications such as pseudocysts, Walled-off Necrosis (WON), and organ failure. Overall, the mortality associated with severe AP ranges from 10% to 30% (3). According to the updated Atlanta classification, to diagnose AP, two or more of the following criteria must be satisfied (4): a) Abdominal pain suggestive of pancreatitis; b) A serum amylase or lipase level that is three times higher than normal; or c) Distinctive imaging findings, for which the most common modality used is CECT. Imaging Technique-Computed Tomography The CECT is the most commonly used modality in the evaluation of AP. Guidelines for selecting the most appropriate criteria were created by the American College of Radiology (ACR) committee on appropriateness criteria and its expert panels in 2010 (5). CECT has received high score ratings in a variety of clinical settings when compared to imaging exams for the diagnosis and treatment of AP [5,6]. The CT identifies peripancreatic involvement and determines the presence and degree of necrosis. Additionally, using CT to guide percutaneous aspiration and drainage treatments related to pancreatic necrosis is a great concept. An ideal predictive approach should be accurate, simple to use, widely accessible, and have minimal interobserver variability to distinguish between patients with mild and severe pancreatitis. Hence, the CT severity index was introduced, focusing on the presence and degree of pancreatic inflammation and necrosis. However, this index had a few drawbacks, including the lack of a discernible relationship between the index score and the later occurrence of organ failure, extra pancreatic parenchymal problems, or peripancreatic vascular complications (7). As a result, the modified CT severity index was introduced to predict clinical outcomes more accurately. Interstitial Oedematous Pancreatitis versus Acute Necrotising Pancreatitis (NP) Interstitial oedematous pancreatitis is more common and represents the non necrotising form of AP. On contrast study, it shows diffuse or focal involvement, with focal involvement most commonly seen in the head or tail of the pancreas, occurring in 20% of cases (Table/Fig 1), (Table/Fig 2). The pancreas appears mildly heterogeneous with a loss of lobulated outline, and non enhancing areas are not seen in the parenchyma. Inflammatory changes are noted in the form of fat stranding or mesenteric haziness and hypodensity in the peripancreatic fat. There may be associated fluid, shown as ill-defined homogeneous low-attenuating areas (8). Most patients usually resolve on their own without complications. About 20% to 30% of instances of AP are caused by NP (9). It’s critical to realise that necrosis can occur in either the peripancreatic tissues or the pancreatic parenchyma. The scan should ideally be done five to seven days after the onset of symptoms. The NP is subdivided into three subtypes based on CECT according to the new Atlanta classification (4): • Combined pancreatic necrosis and peripancreatic necrosis, which is the most common, seen in around 75% of all NP (Table/Fig 3), (Table/Fig 4); • Peripancreatic tissue necrosis alone, which has a peripancreatic necrotic collection with normal homogeneous enhancement of the pancreas (less common, with an incidence of approximately 20%) (Table/Fig 5), (Table/Fig 6); • Pancreatic parenchymal necrosis alone (rare, with an incidence of only 5%). The extent of necrosis can be stratified as <30% (Table/Fig 3), (Table/Fig 4), 30-50% (Table/Fig 7), (Table/Fig 8), and >50% to grade the severity of pancreatitis. As the extent of necrosis increases, the chance of extra pancreatic complications increases. Acute Peripancreatic Fluid Collections (APFCs) and Pseudocyst The APFCs and acute necrotic collections are the current diagnostic names for local complications in the early stages of Acute Pancreatitis (ANCs). APFCs only appear in patients with Interstitial Oedematous Pancreatitis (IEP) during the first four weeks of treatment. APFCs solely contain fluid and are seen as homogeneous fluid-attenuation collections without a wall that tends to conform to the retroperitoneal spaces since the pathophysiology involves inflammation without necrosis. The most common sites are the lesser sac and anterior pararenal space. APFCs are always found in the peripancreatic region. Since most APFCs resolve on their own, drainage should not be done to avoid the danger of contaminating an otherwise sterile collection (9). If an APFC does not resolve within four weeks, it organises further and develops a capsule, which appears as an enhancing wall at CECT and contains only fluid without necrosis. At this time, the mass is referred to as a pseudocyst, which is a well-defined peripancreatic fluid accumulation surrounded by fibrous or granulation tissue (Table/Fig 9), (Table/Fig 10). About 50% of persistent pseudocysts develop clinical symptoms or consequences, which might include secondary infection, discomfort, haemorrhage due to erosion into nearby arteries, decompression or rupture, or localised mass effect. They typically resolve on their own. The diagnosis is not pseudocyst but WON, if there is even a modest area of fat or soft tissue attenuation in an otherwise fluid-attenuation collection (4). Acute Necrotic Collection and Walled-off Necrosis (WON) Acute necrotic collections, on the other hand, have the following characteristics: they occur only in NP (Table/Fig 3), (Table/Fig 4). They can be located in the peripancreatic and pancreatic regions, surrounding the pancreas or with intrapancreatic extension or both. They have a heterogeneous appearance due to containing variable amounts of necrotic material (3). Acute necrotic collections often extend beyond the boundaries of interfascial planes and can affect retroperitoneal spaces, interfascial planes, subperitoneal spaces, and other abdominal spaces (10). They are most commonly found in the lesser sac and the anterior pararenal spaces, followed by the transverse mesocolon, mesenteric root, and then the gastrohepatic (Table/Fig 11), (Table/Fig 12), gastrosplenic, and gastrocolic ligaments. These collections may also involve remote areas, such as the mediastinum and sidewalls of the pelvis. The WON occurs more than four weeks after acute NP. WON appears inhomogeneous and contains non liquefied components encapsulated with a well-defined wall. The WON can be intrapancreatic or extra-pancreatic (Table/Fig 13), (Table/Fig 14). Complications In addition to collections, complications such as vascular issues may also occur. Patients most frequently experience splenic vein thrombosis, which is a vascular issue in patients with AP. Vascular complications occur in a quarter of patients with AP and can cause substantial morbidity and mortality (11). Venous thrombosis: The most typical vascular consequence is splanchnic vein thrombosis, which may be caused by inflammatory responses, reduced venous flow, and mass effect by adjacent necrotic tissue on vascular structures (Table/Fig 15), (Table/Fig 16), (Table/Fig 17). In later stages, it may lead to splenomegaly and the formation of collaterals (12). Isolated superior mesenteric vein involvement is very uncommon and usually occurs together with splenic vein thrombosis. Haemorrhage: Secondly, the splenic artery, portal vein, and other peripancreatic veins are the most frequent sources of bleeding in AP because the release of pancreatic enzymes causes erosion of the surrounding vasculature, which may result in pseudoaneurysm formation and spontaneous haemorrhage (Table/Fig 18), (Table/Fig 19) (12). Pseudoaneurysm: The splenic artery is the most common artery involved in pseudoaneurysm formation (Table/Fig 20), (Table/Fig 21). It is a late and potentially fatal complication. Pseudoaneurysms can breach into the pancreatic parenchyma, the peritoneum, the gastrointestinal system, or the necrotic collection (13). Infection: About 20% of patients with NP experience infection as a complication, which is thought to be caused by bacterial translocation from the gut to nearby necrotic pancreatic tissue. Although gas is found in only a small percentage of cases of proven infection, the presence of gas during imaging indicates infection (Table/Fig 22) (12). Inflammation and mass effect on surrounding organs: The NP can displace and compress nearby organs due to the inflammatory changes and collections it causes. Complications are noted in the form of bowel obstruction, hydronephrosis, and inflammatory changes in the form of inflammatory thickening and adjacent fat stranding (12). Chronic Pancreatitis (CP) The CP is a progressive, irreversible inflammatory disease of the pancreas with clinical manifestations of chronic abdominal pain, weight loss, and permanent pancreatic exocrine and endocrine insufficiency (2). The histologic hallmarks of CP include fibrosis, chronic inflammation, and loss of acinar cells. Malnutrition and diabetes mellitus are the results of advanced-stage destruction of exocrine and endocrine pancreas tissue (14). In Western nations, 70-90% of cases of CP are caused by alcoholism. Additional significant risk factors include smoking, a high-protein diet, hypercalcaemia, hyperparathyroidism, pancreatic divisum, pancreatic or periampullary neoplasms, and ampullary stricture. Less common causes of CP include hereditary pancreatitis, autoimmune pancreatitis, malnutrition, and chronic renal insufficiency (15). Idiopathic CP is the term for the 30-40% of CP patients who have no known underlying aetiology (2). Computed Tomography The sensitivity of CT in detecting late stages of CP is 60-95% (16). However, it is limited in identifying early CP. The most common CT findings include ductal dilatation (68%), parenchymal atrophy (54%), and parenchymal and ductal calcification, which is the most specific feature (15). Depending on the degree of fibrosis or atrophy and the level of enzyme activity, the overall size of the pancreatic gland in CP may be normal, enlarged, or diminished. The presence and number of parenchymal calcifications are independent predictors of the degree of pancreatic fibrosis. Other less common complications include collections, bile duct dilatation, and heterogeneous glandular enhancement (16). Calcium buildup is a defining feature of chronic inflammation (Table/Fig 23), (Table/Fig 24). Pancreatic necrosis and inflammation cause local chemical changes that result in deposits of calcium carbonate and calcium phosphate. The location and volume of the calcium salt deposits can vary. Calcification most frequently starts in the head, but with persistent inflammation, it can spread to the body and tail as well (Table/Fig 23) (17),(18). Compared to calcifications, parenchymal atrophy and ductal dilatation are less distinctive signs because they can also be present in older people. The dilated duct may be smooth, crooked, or beaded (Table/Fig 24), (Table/Fig 25) (17). Pleomorphic ductal calculi may appear as sporadic regions of strictures and dilatation in the primary pancreatic duct. Complications Complications of chronic pancreatitis include pseudoaneurysm, biliary obstruction, venous thrombosis, and pancreatic pleural and peritoneal fistulae (19). CT is a great tool for locating problems associated with chronic pancreatitis. Fluid collection is one such problem that 30% of people experience. Although distant sites are seldom reported, fluid collections are typically seen inside (Table/Fig 25), (Table/Fig 26) or close to the pancreas. Pseudocyst/ Walled-off Necrosis (WON): The majority of fluid accumulations linked to chronic pancreatitis are tightly encapsulated, presenting as pseudocysts or WON. Free fluid near the pancreas is a sign of underlying acute pancreatitis (Table/Fig 25). Pseudocysts in chronic pancreatitis can communicate with the duct (Table/Fig 25), (Table/Fig 27), (Table/Fig 28) or be associated with ductal stricture. These pseudocysts are difficult to treat (14). Venous thrombosis: In vascular complications s/o chronic venous thrombosis, the most common is splenic vein thrombosis, which causes non visualisation of the same and is replaced by collaterals (Table/Fig 29), (Table/Fig 30), [Table/Fig-31]. Gastric and mesenteric varices may form in the presence of left-sided portal hypertension when the splenic vein is affected (2). Pancreatic pleural fistula: Pancreatic pleural fistula is an uncommon complication in chronic pancreatitis. Typically, when the posterior pancreatic duct is disrupted or a pancreatic pseudocyst extends into the pleural cavity, there is an aberrant communication to the pleural space [Table/Fig-32], [Table/Fig-33], [Table/Fig-34] (20). | |||||||||||||||||||||||||||||||||||||||||||
CONCLUSION | ![]() | ||||||||||||||||||||||||||||||||||||||||||
One of the most frequent pancreatic pathologies and medical/surgical emergencies seen in daily clinical practice is pancreatitis. The most challenging aspect of managing pancreatitis is identifying and managing its (systemic or local) consequences, rather than the pancreatitis itself. Local problems can be identified using imaging tests, and CT has long been considered one of the most effective imaging methods for this. | |||||||||||||||||||||||||||||||||||||||||||
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TABLES AND FIGURES |
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[Table / Fig - 1] [Table / Fig - 2] [Table / Fig - 3] [Table / Fig - 4] [Table / Fig - 5] [Table / Fig - 6] [Table / Fig - 7] [Table / Fig - 8] [Table / Fig - 9] [Table / Fig - 10] [Table / Fig - 11] [Table / Fig - 12] [Table / Fig - 13] [Table / Fig - 14] [Table / Fig - 15] [Table / Fig - 16] [Table / Fig - 17] [Table / Fig - 18] [Table / Fig - 19] [Table / Fig - 20] [Table / Fig - 21] [Table / Fig - 22] [Table / Fig - 23] [Table / Fig - 24] [Table / Fig - 25] [Table / Fig - 26] [Table / Fig - 27] [Table / Fig - 28] [Table / Fig - 29] [Table / Fig - 30] [Table / Fig - 31] [Table / Fig - 32] [Table / Fig - 33] [Table / Fig - 34]
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