Imaging of Acute Pancreatitis

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1 Residents Section Structured Review rticle O Connor et al. Imaging of cute Pancreatitis Residents Section Structured Review rticle Residents inradiology Owen J. O Connor 1 Sebastian McWilliams 1 Michael M. Maher 1,2 O Connor OJ, McWilliams S, Maher MM Keywords: acute pancreatitis, CT abdomen, CT severity index, pancreatic pseudocyst DOI: /JR Received January 26, 2010; accepted after revision July 12, Department of Radiology, Cork University Hospital, University College Cork, Wilton, Cork, Ireland. ddress correspondence to M. M. Maher (m.maher@ucc.ie). 2 Department of Radiology, Mercy University Hospital, Cork, Ireland. WEB This is a Web exclusive article. JR 2011; 197:W221 W X/11/1972 W221 merican Roentgen Ray Society Imaging of cute Pancreatitis Educational Objectives 1. cute pancreatitis is an acute inflammatory process of the pancreas that may also involve adjacent or remote tissues and organs. 2. Imaging is frequently recommended to confirm the clinical diagnosis, ascertain the cause, and grade the extent and severity of acute pancreatitis. 3. Radiography, upper gastrointestinal series, and ultrasound are of limited value in the diagnosis of acute pancreatitis. 4. CT currently plays an important role in imaging of patients with acute pancreatitis, the identification of complications, and assessing the response to treatment. 5. lthough sensitive for the detection of acute pancreatitis, MRI is used less commonly than CT. MRI is especially useful for imaging patients with iodine allergies, characterizing collections, and evaluation of an abnormal or disconnected pancreatic duct that is easily overlooked. In addition, a heavily T2-weighted MRCP sequence may assist in diagnosis of choledocholithiasis. cute pancreatitis is an important cause of acute abdominal pain. Imaging plays a central role in the management of selected cases of acute pancreatitis, complementing laboratory investigations such as serum amylase and lipase levels that have relatively high sensitivity and specificity. In addition to clinical signs and laboratory investigations, imaging helps confirm the clinical diagnosis when there is uncertainty and elucidate the cause and grade the extent and severity of acute pancreatitis. Imaging also aids in the early detection of complications [1]. Pathophysiologic Basis cute pancreatitis is an acute inflammatory process of the pancreas that may involve adjacent or remote tissues and organs [2]. The causes of acute pancreatitis are protean (Table 1), with gallstones and alcohol responsible for approximately 90% of cases in the United States [1, 3] (Fig. 1). In practice, serum amylase or lipase levels greater than three times normal are used to confirm acute pancreatitis [4]. cute pancreatitis may be classified based on clinical, morphologic, or histologic criteria and many systems of classification exist, most based on the cause or severity [1, 2, 5]. Grading of Disease Severity The severity of acute pancreatitis may be broadly subdivided into mild and severe forms. Patients with mild acute pancreatitis tend to have acute interstitial pancreatitis whereas pancreatitis associated with hemorrhage, necrosis, or vasculitis is considered severe [6]. Most cases of acute pancreatitis are considered mild, with affected patients reporting modest abdominal pain and displaying mild abdominal tenderness. Patients with mild acute pancreatitis have either minimal or no organ and systemic dysfunction. Therefore, patients with mild acute pancreatitis should respond quickly to medical therapy, and their symptoms and laboratory values should normalize promptly [2]. Between 10% and 20% of cases of acute pancreatitis are considered severe [7]. Such patients will usually exhibit more severe abdominal pain, vomiting, and clinical signs of peritonism with tachycardia, fever, and leukocytosis. Patients with severe acute pancreatitis are more likely to have a protracted hospital stay and to develop systemic or organ failure with renal, respiratory, and cardiovascular failure; disseminated intravascular coagulation; or gastrointestinal hemorrhage [2]. The clinical evaluation of severe acute W221

2 O Connor et al. pancreatitis is unreliable. It is estimated that experienced clinicians predict which patients will develop severe acute pancreatitis in less than 40% of cases [8]. Examples of clinical systems that have been developed to more accurately and reproducibly grade the severity of acute pancreatitis include the cute Physiology and Chronic Health Evaluation II (PCHE II), Ranson s criteria, and the Glasgow original and modified systems [9, 10]. Ranson s score of 3 or more and an PCHE score of 8 or more suggest the presence of severe acute pancreatitis [10]. Scoring systems also help predict the likely course of acute pancreatitis at the time of presentation. This helps guide treatment-related decision making, such as the necessity for admission into an ICU or transfer to a tertiary referral center [3]. The sensitivity and specificity of the PCHE II system for assessing severe acute pancreatitis at the time of admission are 75% and 79%, respectively [11]. Clinical grading systems, such as the PCHE II system, indirectly estimate the degree of pancreatic damage. To directly evaluate and estimate the degree of parenchymal injury and to improve the early prognostic value of CT in acute pancreatitis, the CT severity index (CTSI) was developed [11]. The CTSI grades acute pancreatitis into five levels of increasing severity ( to E) using a 10-point scale. Points are awarded on the basis of the presence of pancreatic enlargement, fat stranding, and fluid collections and the amount of pancreatic necrosis. The CTSI is discussed in more detail in the systematic review of the complications of acute pancreatitis in an upcoming issue of the JR. new subgroup of acute pancreatitis has recently been described, termed moderately severe acute pancreatitis, consisting of patients with local complications similar to those with severe acute pancreatitis but lower morbidity, which is believed to be due to more transient organ dysfunction [12]. TBLE 1: Causes of cute Pancreatitis Type Mechanical Metabolic Drugs Infections Vascular Idiopathic Disease Epidemiology The incidence of acute pancreatitis is approximately 5 70 cases per 100,000 per year [13, 14]. Gallstones and alcohol are responsible for approximately 70% of cases [15]. mong patients with gallstones, acute pancreatitis has a higher incidence in men than women, but overall, gallstone acute pancreatitis is most frequent in women (generally between 40 and 50 years old) [16]. Gallstones and alcohol have been implicated in the development of recurrent attacks of acute pancreatitis. Interestingly, it has been observed in one cohort that only alcoholic patients progressed from acute to chronic pancreatitis [17]. In this group, a second attack of acute pancreatitis was associated with a 38% incidence of chronic pancreatitis [17]. The incidence of acute pancreatitis is increasing, and a 100% increase in the number of hospitalizations over the past two decades has been recorded TBLE 2: Indications for CT Imaging in cute Pancreatitis Type Diagnostic CT Delayed CT Causes Cholelithiasis; postoperative, ERCP, blunt, or penetrating trauma; anatomic variants (pancreas divisum, choledochocele, perivaterian duodenal diverticulum) lcohol, hyperlipidemia, hypercalcemia, hereditary, scorpion venom Corticosteroids, azathioprine, 6-mercaptopurine, thiazide diuretics, furosemide, aminosalicylic acid, sulfonamides, tetracycline, procainamide, and opiates Measles, mumps, IDS or HIV, cytomegalovirus, fungi (spergillus), and parasites (Toxoplasma) Polyarteritis nodosa, atheroembolism, and after abdominal and cardiac surgery Biliary sludge, microlithiasis, congenital in the United States [18]. This trend is possibly secondary to the increasing age of the population and increasing alcohol consumption, but mortality rates appear stable [14]. Indications for Imaging The clinical signs of acute pancreatitis are nonspecific, with serum amylase and lipase levels correlating poorly with disease severity B Fig. 1 CT in 54-year-old man with abdominal pain and raised serum amylase 3 days after blunt abdominal trauma. and B, CT images show disruption and discontinuity of pancreatic neck (arrow, ) and extensive stranding of retroperitoneal and intraperitoneal fat (arrowhead, B). Indications 1. When the diagnosis of acute pancreatitis is uncertain 2. Patients with hyperamylasemia, severe clinical pancreatitis, abdominal distention and tenderness, fever > 102, and leukocytosis for the detection of complications 3. Ranson score > 3 or PCHE score > 8 4. Patients who fail to improve after 72 hours of conservative medical therapy 5. cute change in clinical status, such as new fever, pain, and shock after successful initial medical therapy 1. Changing clinical status suggesting complication days after presentation if CT severity score is 3 10 at presentation or grade D E pancreatitis 3. fter surgery or interventional radiologic procedures to document response to treatment 4. Before discharge of patients with severe acute pancreatitis Note PCHE = cute Physiology and Chronic Health Evaluation. W222

3 Imaging of cute Pancreatitis B Fig. 2 CT of 35-year-old man with acute-on-chronic pancreatitis due to alcohol abuse., Control phase CT image shows several calcifications in head of pancreas (arrowhead) suggesting chronic pancreatitis. B, Contrast-enhanced CT image (pancreatic parenchymal phase) shows heterogeneous enhancement of pancreas, and pancreatic head appears edematous with associated stranding of peripancreatic fat. There are small peripancreatic fluid collections (acute pancreatic fluid collections) (arrowhead). Fig. 4 CT of 67-year-old woman with mild acute pancreatitis. Head of pancreas enhances homogeneously (long arrow) on portal venous phase imaging. There is extensive stranding of retroperitoneal fat, and acute fluid collections are seen in left anterior pararenal space (short arrow). [1]. Elevated plasma serum amylase and lipase levels are not specific to acute pancreatitis and may be elevated by bowel obstruction, infarction, cholecystitis, and perforated ulcer. Imaging is recommended to confirm the clinical diagnosis, diagnose its cause, exclude alternative causes of abdominal pain, and grade the extent and severity of acute pancreatitis [1, 13] (Table 2). Follow-up CT is not considered necessary if the CTSI score is between 0 and 2 on initial CT [2]. The British Society of Gastroenterology guidelines recommend imaging between 3 and 10 days after presentation [19]. Some groups recommend imaging within 24 hours to identify the cause of acute pancreatitis because ERCP and sphincterotomy within 72 hours in patients with gallstone-related acute pancreatitis have been proposed as a treatment strategy aimed at reducing the chance of developing severe or complicated acute pancreatitis [20]. t our institution, a three-phase (control, pancreatic parenchymal phase (40 seconds), and portal venous phase) protocol with positive oral contrast administration is used for the initial assessment of acute pancreatitis (Fig. 2). The pancreatic parenchymal phase is the optimal phase for assessment for necrosis because normal pancreatic tissue enhances greatest during this phase. Subsequent imaging with CT is generally performed using a single-phase technique in the portal venous phase. Many variations in CT technique exist. dual-phase technique (pancreatic and portal venous phases) is commonly used but risks missing hemorrhagic collections [21]. It is also recommended that thin-slice (3 mm) Fig. 5 CT image of abdomen of 67-year-old man with acute pancreatitis and acute hemorrhagic pancreatic collection. On unenhanced CT image, pancreas shows heterogeneous areas of increased density (arrows), consistent with blood in region of pancreatic head and tail on this unenhanced study. Note absence of wall around collection, as seen with pseudocyst. Fig. 3 Ultrasound of 74-year-old woman with mild acute pancreatitis. Pancreatic body and tail are hypoechoic due to edema anterior to pancreatic duct (arrow). CT should be used for imaging the pancreas; this may be of particular benefit for the planning of operative intervention [21]. The use of positive oral contrast material may mask hemorrhage or calculi, and for this reason many institutions use negative oral contrast material. The suggestion that IV administration of iodinated contrast material can increase the severity and duration of acute pancreatitis has led to conflicting opinions regarding IV contrast usage, and at present the benefits of IV contrast administration appear to outweigh the potential risks [22, 23]. MRI is comparable with CT for the assessment of acute pancreatitis [24]. In practice, MRI is particularly useful for the imaging of patients with iodine allergies; for the characterization of collections in cases in which there is diagnostic uncertainty; and for evaluating the biliary tract, including the bile ducts and pancreatic duct. Imaging ppearances Conventional radiography and upper gastrointestinal series no longer play an important role in the diagnosis of acute pancreatitis. Radiographic signs of acute pancreatitis include the sentinel loop sign (dilated air-filled duodenum or jejunum), the colon cutoff sign (dilated large bowel to the level of the splenic flexure), loss of the left psoas shadow, ascites, or a gasless abdomen [13]. Pleural effusions, atelectasis, or an elevated hemidiaphragm are suggestive of severe acute pancreatitis [25]. Thickened rugal and duodenal folds, indentation of the stomach, and enlargement of the C- loop of the duodenum are signs of acute pancreatitis on barium meal and follow-through studies [13]. Sonography of patients with acute pancreatitis is often negatively impacted by W223

4 O Connor et al. Fig. 6 CT of 45-year-old man with acute pancreatitis complicated by necrosis. On CT image, majority of pancreas fails to enhance apart from small portion of pancreatic body (arrow). This patient is at risk for disconnection of pancreatic duct because viable pancreatic tissue is separated from gastrointestinal tract by necrotic tissue. Fig. 7 Portal venous phase CT of abdomen of 75-year-old woman with acute pancreatitis who had profound sepsis. There is hypoattenuating collection replacing pancreatic neck (arrow) with stranding of peripancreatic fat. Note thick wall surrounding collection. spiration confirmed this to be abscess. difficulty visualizing the pancreas because of ileus and overlying bowel gas [10]. bnormal ultrasound findings are seen in 33 90% of patients with acute pancreatitis [10]. Interstitial edema in acute pancreatitis is depicted on ultrasound as an enlarged hypoechoic gland (Fig. 3). lthough ultrasound may be used to identify peripancreatic acute fluid collections, it is not useful for the detection of necrosis, and therefore its main role in the imaging of acute pancreatitis is limited to the detection of cholelithiasis and choledocholithiasis and identification of fluid collections in the peritoneum, retroperitoneum, and pleural spaces [10]. Contrast-enhanced CT is the imaging modality of choice for the diagnosis and staging of acute pancreatitis [3, 13]. The pancreas enhances uniformly in mild acute pancreatitis and may be normal or enlarged with a variable amount of increased attenuation in the adjacent fat, termed stranding [2, 26] (Fig. 4). Local edema is a common finding and may extend along the mesentry, mesocolon, and hepatoduodenal ligament and into peritoneal spaces. Extension of edematous fluid into the anterior perirenal space may create a mass effect and a halo sign with sparing of the perinephric fat [27]. Peripancreatic fluid collections consist of exudate, peripancreatic fat tissue necrosis, or hemorrhage [13] (Fig. 5). n organized peripancreatic fluid collection with a fibrous wall occurring greater than 4 weeks after the onset of symptoms is termed a pseudocyst [2]. Edema is differentiated from fluid collections by the identification of fat islands of normal tissue within edematous fluid [26]. It is usually possible to differentiate acute collections from necrosis. In cases in which CT is unable to accurately differentiate peripancreatic fluid collections from extrapancreatic fat tissue necrosis, it is thought to be safer to consider heterogeneous pancreatic collections as necrotic until proven otherwise [11]. Nonenhancement of all or part of the gland is termed necrosis [19] (Fig. 6). CT is 100% specific for necrosis if greater than 30% of the gland is nonenhancing [13]. Necrosis develops between 24 and 48 hours after the onset of acute pancreatitis, and therefore CT within the first 12 hours may be falsely reassuring [11]. Pancreatic abscess formation is usually observed 4 6 weeks after the onset of acute pancreatitis as an area of low attenuation containing pus and a thick wall that may enhance after IV contrast administration [2, 3]. Necrosis and abscess are considered among the most important imaging features of acute pancreatitis because they have prognostic relevance and may precipitate intervention by either interventional radiology or by the surgeons [26] (Fig. 7). Complications of acute pancreatitis, such as abscess and pseudoaneurysm formation, will be further discussed in an upcoming issue of the JR. The imaging of acute pancreatitis using MRI is comparable with that of CT, and the same descriptive terminology is used [10, 28]. MRI may be performed using unenhanced and contrast-enhanced T1-weighted and fat-suppressed T2-weighted gradient-echo sequences. Typically, an enlarged edematous gland that is low signal on T1-weighted and high signal on T2-weighed MRI is observed [10]. cute pancreatitis is sometimes associated with pancreatic ductal dilatation, which can be clearly identified and examined on T2-weighted images [13] (Fig. 8). T2-weighted images are also useful for the detection of acute pancreatic collections, pseudocysts, and hemorrhage [11]. The pancreatic duct should be carefully reviewed on T2-weighted images for the presence of disconnection, which can be easily overlooked Fig. 8 Fat-suppressed T2-weighted MR image of 41-year-old woman with mild acute pancreatitis. Pancreas is edematous and enlarged with diffusely increased signal and loss of normal lobular contour of body and tail (arrow). [29]. Disconnection occurs when necrosis affects the ductal epithelium and an isolated segment of viable pancreatic tissue is disconnected from the duodenum. This creates persistent fistulation and inflammation with an increased incidence of infection [29]. Diagnosis of disconnection of the main pancreatic duct requires visualization of a necrotic region of at least 2 cm in size, viable pancreatic tissue proximal to the necrosis, and extravasation at pancreatography [29]. The main pancreatic duct usually enters the necrotic material at a 90 angle. Evaluation for a disconnected pancreatic duct may be performed with CT or MRI. lthough early MRCP is generally of limited value for identifying the cause of acute pancreatitis because collections may compress the pancreatic and biliary ducts obscuring gallstones, MRCP may be of benefit when iodinated contrast administration is contraindicated or if disconnection of the main pancreatic duct is suspected [29]. Secretin-enhanced MRCP may be used for assessment of the pancreatic duct, although concerns regarding the risk of increasing pancreatic inflammation exist. Because ductal pressures approaching those at ERCP cannot be achieved, a normal MRCP is insufficient for exclusion of a disconnected duct in the presence of suspicious features [29]. Conclusion Imaging plays an important role in the management of the patient with acute pancreatitis. CT in particular has revolutionized pancreatic imaging, and what was once considered a hidden organ may now be accurately and noninvasively imaged. References 1. Millar FH, Keppke L, Balthazar EJ. Pancreatitis. In: Gore GM, Levine MS, eds. Textbook of W224

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