Applied Radiology

Dr. Helmberger is an Associate Professor of Radiology in the Department of Clinical Radiology at Ludwig-Maximilians University, Munich, Germany.

Dr. Helmberger states that there is no actual, potential, or apparent conflict of interest regarding this article.

Portions of this article were presented at the 34th International Diagnostic Course held in Davos, Switzerland, April 6-12, 2002 and at the Society of Gastrointestinal Radiologists and the European Society of Gastrointestinal and Abdominal Radiology (SGR/ESGAR) joint meeting held in Orlando, FL, April 14-18, 2002. Parts of this article were published in the syllabi of the above mentioned meetings.

Pancreatitis is a common disease with an incidence of up to 80 per 100,000 admissions. The manifestations of pancreatitis range widely from mild and self-limiting to severe, lethal forms in acute pancreatitis, and to permanent loss of exocrine and/or endocrine function in chronic pancreatitis. ^1,2

Acute pancreatitis--Clinical overview

Acute pancreatitis (AP) is more often seen in the elderly population (in the 5th to 6th decade). The most common causes for AP are cholelithiasis (75%) and alcohol abuse (15%). Other causes include metabolic disorders (eg, hypercalcemia, hyperlipidemia type I and type V), infections (eg, parasites, hepatitis, HIV), trauma (eg, penetrating ulcer, abdominal surgery, endoscopic retrograde cholangiopancreatography [ERCP]), drugs (eg, azathioprine, furosemide, sulfonamides, steroids), and structural abnormalities (eg, pancreas divisum, choledochocele). In 10% to 15% of patients, no obvious etiology can be found; however, biliary microlithiasis might be the most likely cause in such cases. The most likely factors leading to AP are: 1) pancreatic hypersecretion; 2) intravasation and extravasation of pancreatic secretions; and 3) premature activation of pancreatic enzymes followed by autodigestion and necrosis of the pancreatic gland and peripancreatic tissues.

From the clinical point of view, AP can be divided into a mild and severe form almost paralleled by the pathophysiological finding of an interstitial (edematous) and necrotizing form. ^3-5 The mild form of AP (approximately 50% of the cases) is characterized by mild symptoms and transitory elevation of amylase levels that recover rapidly without complications. In general, the gland may be enlarged due to moderate edema, and peripancreatic fluid collections can be present. However, in 30% of cases, no morphological changes can be appreciated. In cholelithiasis, a segmental pancreatitis--mainly of the pancreatic head--can be found in up to 20% of cases (Figure 1).

Diagnostic imaging

Ultrasound (US) may reveal a normal to mildly enlarged gland with homogenous (hypoechoic) echogenicity. Sufficient visualization by US is possible only in 60% to 70% of cases. In contrast-enhanced computed tomography (CT) as well as in magnetic resonance imaging (MRI) (usually not necessary), the gland is diffuse and enlarged, with a small amount of fluid outlining the gland can be seen (Figures 1 and 2). Moreover, imaging is needed to rule out other underlying conditions that can be accompanied by hyperamylasemia, such as bowel obstruction, bowel infarction, gangrenous cholecystitis, or perforated ulcers. In advanced mild to moderate degrees of AP, the contour of the gland becomes shaggy. On CT and MRI, the appearance of the parenchyma may become heterogeneous, and small intraglandular and/or retroperitoneal fluid collections adjacent to the organ may develop (Figure 2).

In the most severe form of AP, there may be a delayed response or no response to conservative therapy, or there may even be deterioration during therapy. The mortality rate in the late stage of AP is almost 100%. Typical findings in severe (necrotizing) AP are varying degrees of parenchymal necrosis accompanied by progressive exudation, superinfection of necrotic tissue, hemorrhage, abscess formation, phlegmon (inflammatory pannus), and vascular erosion. In cases of severe AP, the pancreas and its surroundings present a wide spectrum of imaging findings. In severe cases, US imaging is often compromised by overlying gas, peripancreatic exudation, and phlegmonous changes. In necrosis, the pancreatic appearance becomes increasingly hypoechoic without differentiation of vital from necrotic tissue. Therefore, US is generally used as a second-line, complementary study in follow-up to detect fluid formations as pseudocysts. Parenchymal necrosis is best displayed on contrast-enhanced CT during the portal-venous phase. Characteristic findings are patchy areas of lack of enhancement, (pseudo)fragmentation, and liquifaction necrosis. Additionally, increasing peripancreatic exudates dissecting along retroperitoneal fascial planes into the mesocolon and the small-bowel mesentery, peripancreatic inflammatory tissue (phlegmon), and infected areas are frequently seen. In <10% of cases, small amounts of intraperitoneal fluid (ascites) are seen; large volumes of intraperitoneal fluids are very rare (Figure 3).

The literature indicates that MRI is not significantly superior to CT in the diagnosis of AP and related complications. However, the superior tissue contrast resolution of MRI and its higher sensitivity to slight edematous or necrotic changes, hemorrhage, or fluid dissecting through fat planes somewhat favors MRI. However, these advantages are often hampered by the impaired study conditions in severely ill patients that may degrade the image quality. ^5-8 In severe AP, pancreatic flow can be reduced by administration of iodinated contrast agents, resulting in an increased rate of necrosis and mortality that may make MRI the preferred staging tool in AP. ^9,10

Local inflammatory conditions are often complicated by regional and systemic involvement induced by autodigestion and activation of systemic inflammatory mediators.

The rapid pathologic changes occurring within the pancreas and the entire abdomen demand an adequate diagnostic and therapeutical regime to avoid a disastrous outcome (Figure 3). Several clinical and laboratory scoring systems were established to stage and predict the clinical course of severe AP (Ranson's score, APACHE II, Glasgow criteria, Serum-Methemalbumin, Trypsin-activated peptid, C-reactive protein). However, these scoring systems are primarily dependent upon systemic alterations and are therefore quite nonspecific without addressing the extent of pancreatic pathology. ^4,6 Balthazar et al ^11,12 found that contrast-enhanced CT was most helpful diagnostically in detecting complications that may necessitate medical, surgical, or interventional management, and in predicting patient outcome based on the CT findings specific to the pancreas. The proposed 5-grade scoring system (Table 1) functions by estimating the presence and degree of pancreatic and peripancreatic inflammation and fluid accumulation and by detecting the presence and extent of pancreatic necrosis together with an estimation of lack of gland enhancement (<30%, 30% to 50%, >50%). These factors can be translated into a CT-severity index that allows the estimation of complications (morbidity) and mortality (Figure 4). If >50% of the volume of the pancreas is necrotic, the morbidity rate rises to almost 100%. ^7,8 Nevertheless, approximately one-fifth of patients without necrotic changes of the pancreas will also develop local complications. Fluid collections will be seen in up to 50% of patients with AP. In approximately half of these patients, such collections will resolve spontaneously within several weeks. In the rest, however, the fluid collections will persist, eventually followed by encapsulation, superinfection (abscess), or formation of a pseudocyst.

Complications in acute pancreatitis

Pseudocysts are fluid collections with a noticeable capsule. They typically develop 4 to 5 weeks after the onset of AP. On US, CT, or MRI, they present a typical cyst-like appearance, in general without septations. Since large cysts are prone to complications (eg, rupture, infection, hemorrhage, biliary obstruction, or fistulization to the GI tract), cysts >5 to 7 cm should be treated by percutaneous drainage or operative marsupialization. In a septic patient, non­water-like fluid collections with rim enhancement on contrast-enhanced CT or MRI studies should be considered abscesses until proven otherwise. Gas, as a characteristic sign of an infected fluid collection, is detected in only 20% of cases of pancreatic abscesses. Percutaneous aspiration or drain-placement is the appropriate treatment.

In contrast to abscess formation, superinfected necrotic areas of the pancreas are much more difficult to treat. Due to the more solid consistency of the infected tissue, percutaneous drainage therapy is usually frustrating; therefore, a biopsy is often needed to establish the diagnosis. In most cases, surgical intervention must be considered.

Pseudoaneurysm formation and hemorrhage may result from the extravasated pancreatic enzymes that cause vascular injury and are typically late complications that occur after several episodes of severe AP. While pseudoaneurysms are generally detected easily by any kind of imaging modality, retroperitoneal hemorrhage is best depicted by contrast-enhanced CT or unenhanced MRI (Figure 5). Angiography with arterial embolization is the treatment of choice and, in general, is superior to the surgical therapy. Groove pancreatitis is a rare, late complication that develops after several attacks of AP and is defined as an inflammatory reaction and fluid collection located in the groove between the head of the pancreas and the duodenum. The anterior anlage of the pancreas seems to be mainly affected, with duodenal stenosis and/or strictures of the common duct occurring in approximately 50% of cases. ^13,14

Chronic pancreatitis

Chronic pancreatitis (CP) is defined as continuing inflammatory disease of the gland characterized by irreversible morphological and functional damage. The most common causes are chronic alcohol abuse (70%) and cholelithiasis (20%). In general, patients in their 3rd to 4th decade of life present with a history of epigastric pain (95%), weight loss (95%), and signs of endocrine or exocrine deficiency (diabetes mellitus, 58%; malabsorption syndrome and steatorrhea, 80%). Acute exacerbations of CP are accompanied by episodes of abdominal pain that can mimic an acute abdomen. However, CP becomes painless after several years with progressive destruction of the gland. In approximately 1.5% to 12% of cases, CP can be complicated by pancreatic cancer. ^1,2

Imaging findings are determined by the macrostructural changes occurring in the organ. The most characteristic findings are scattered glandular and ductal calcifications (40% to 50%), and ductal protein plugs that cause dilatation of the pancreatic main duct and side branches (70% to 90%), together with small cystic changes. The grade and shape of ductal dilatation may help to differentiate chronic (benign) obstructions from malignant occlusions. In CP, the contour of the pancreatic duct and its side branches is commonly irregular (73%), while this is true only in 15% of cases of pancreatic malignancy. Additionally, the duct is commonly <50% of the pancreatic anteroposterior diameter in CP, while the opposite is true in pancreatic cancers (due to obstructive atrophy). ^2,10,15-17

The pancreas can present a normal appearance in 15% to 20% of cases of CP. However, the most common finding is a diffuse (50%; Figure 6) or focal (25%; Figure 7) enlargement that may raise the suspicion of neoplasm. With time, atrophy of the organ will occur in 10% to 50% of patients (Figure 8). The varying appearance of CP explains the shortcomings in establishing the diagnosis. Without gross morphologic changes, it is very difficult to diagnose incipient forms of CP. Moreover, morphologic changes correlate very poorly with any functional exocrine and endocrine deficit.

Pancreatic calcifications are depicted easily by plain radiographs and US. Additionally, US can display ductal dilatation, micro- and macrocystic changes, and the gland itself (Figure 9). Contrast-enhanced CT is well established in assessing ductal changes, calcifications, the form and shape of the pancreatic gland, and potential concomitant conditions, such as pseudocysts. MRI, using unenhanced and gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced T1-weighted sequences (with or without fat suppression), is very capable of displaying the pancreatic duct and its side arms, including small calculi. Heavily T2-weighted sequences are best suited for that purpose (Figure 10). Nevertheless, ERCP will show initial ductal changes superior to all other imaging modalities, but the clinical significance of these minor changes remains controversial. ^8,10,15,16 Pancreatic cancer is the most crucial complication in CP and is the biggest diagnostic challenge because focal enlargement of the gland induced by a fibrotic inflammatory pseudotumor may be indistinguishable from pancreatic carcinoma (Table 2). Biopsy or even surgical exploration may be necessary in such cases.

Conclusion

Due to the relatively high incidence of biliary stone disease and alcohol abuse, inflammatory diseases of the pancreas are quite common in the Western world. In general, clinical and laboratory findings and the patient's history are adequate to establish a diagnosis of acute or chronic pancreatitis. Conventional plain radiographs and oral contrast studies are of very limited use in displaying ongoing processes within and around the pancreas. Therefore, US, contrast-enhanced CT, and, increasingly, MRI are the methods of choice to identify and characterize the extent and severity of inflammatory changes of the pancreas and to assess for potential complications. CT may be particularly helpful as a prognostic tool. AR