Pancreas: Pancreatitis: Multidetector CT Evaluation Of Acute Pancreatitis and Its Complications
Elliot K. Fishman, M.D., Professor of Radiology and Oncology, Johns Hopkins University School of Medicine
INTRODUCTION
Multidetector CT (MDCT) scanners using 4 and most recently 16 detector rows are the latest advancement in CT technology and have quickly become the gold standard for the evaluation of pancreatic pathology. The usefulness of CT in the detection and staging of pancreatic neoplasms has already been addressed in an earlier chapter. In this chapter, the role of MDCT in the evaluation of patients with known or suspected pancreatic inflammatory disease will be reviewed. Emphasis will be placed on the use of CT to guide patient therapy and to determine surgical versus medical management.
Acute Pancreatitis: An Overview
Acute pancreatitis is a complex inflammatory process involving the pancreactic gland. The pathological definition of acute pancreatitis is a nonbacterial inflammation of the pancreatic gland caused by the activation and the digestion of the gland by its own enzymes. The pathophysiology of pancreatitis is a chain of events that result from blockage of the pancreatic duct with subsequent release of pancreatic enzymes into the interstitium of the gland. Early on, pancreatitis is characterized by features of interstitial edema. Peripancreatic fat necrosis results from more severe involvement. Involvement of the parenchymal acini of the gland also occurs, resulting in foci of hemorrhage, vascular necrosis, disruption of the pancreatic ducts, and eventually pancreatic necrosis. Mild acute pancreatitis is characterized clinically by minimal symptoms, which respond rapidly to conservative management, with few patients progressing to severe pancreatitis. Severe pancreatitis presents with more pronounced signs and symptoms and can progress to hemorrhagic or necrotizing pancreatitis. These patients may demonstrate multisystem organ failure, hypotension, and shock, as well as hypocalcemia and disseminated intravascular coagulation.
The most common etiology of acute pancreatitis is gallbladder disease (i.e. cholelithiasis), which accounts for over 40% of cases. Alcoholic pancreatitis is the cause for nearly another 40% of patients. Other causes include hypercalcemic states of which the most commonly recognized conditions is hyperparathyroidism, as well as hyperlipidemia, familial pancreatitis, trauma including post procedure trauma (i.e. ERCP), drug induced pancreatitis (i.e. steroids, thiazide diuretics, and azathioprine), and rare causes like a scorpian bite. (1-5) (Figs. 1-3)
Role of MDCT in Pancreatitis
Most cases of acute pancreatitis are diagnosed clinically and do not rely on imaging (5). However, often the history and presentation of the patient may not be straight forward, and a reliable imaging modality is needed to establish the diagnosis (2-4, 6). For nearly two decades, CT has been the imaging procedure of choice in the initial evaluation and follow-up patients with suspected pancreatitis. The sensitivity of helical CT for the diagnosis of acute pancreatitis is not known, especially in very mild cases, but it is reasonable to assume that a good-quality contrast-enhanced helical CT scan will demonstrate definite changes in the vast majority of patients with moderate to severe involvement. Helical CT depicts all but the mildest forms of acute pancreatitis, demonstrates most major complications, and can help guide percutaneous aspirations and drainages. Helical CT is also indicated when there is failure of clinical response to treatment. In addition, helical CT can confidently detect other causes of abdominal pain in patients initially thought to have symptoms of acute pancreatitis. (Figs. 4-6)
Helical CT Technique
Diagnostic evaluation of the pancreas, with either single or multidetector row helical CT, has always required careful attention to study technique and protocols. Dual-phase helical scanning during both the arterial and portal venous phases has several advantages when imaging the pancreas. The arterial phase is superior to the portal venous phase visualization mesenteric and peripancreatic arteries. Opacification of the splenic vein, superior mesenteric vein, and portal venous confluence is better obtained during the more delayed portal venous phase. The pancreatic parenchyma is best seen in the parenchymal phase, which is around 50 seconds after the start of the injection. (7-8)
Although specific parameters will vary between scanners, several basic scanning concepts remain constant. Thin collimation scanning is essential. With single detection helical CT, slice collimation typically was between 3 and 5 mm with a reconstruction interval between 2 and 5 mm. With the newest MDCT scanners, typical study parameters are 3 mm slice thickness and data reconstructed at 3 mm for routine studies. When complications are suspected or when more detail is needed 1 mm detectors can be utilized on a 4 detector scanner to obtain 1.25 mm slice thickness, and reconstruct data at 1 mm intervals. On a 16-slice scanner we the .75 mm detectors can be used to create .75 mm slice thickness and reconstruct data at .5 mm intervals. Typically the entire abdomen and pelvis is scanned in order to fully evaluate the extent of pancreatic fluid collections and ascites.
Bolus intravenous contrast administration is also critical. The injection rate for evaluation of a suspected pancreatitis is typically 2-3 ml/s, with the higher injection rate helpful for vascular and 3D mapping. A total of 100-120 ml nonionic contrast agent (Omnipaque-350, Amersham Imaging, Princeton, NJ) is sufficient for most cases. Scans in the arterial phase begin around 25-30 s after the start of contrast injection, and at 50-60 seconds for portal phase imaging. Dual-phase studies combine both acquisitions and are recommended in most patients, especially when there are clinical concerns of hemorrhage, pseudoaneurysm, or necrosis. Additionally, initial noncontrast images of the pancreas can be helpful for the depiction of acute hemorrhage.
Classically, positive oral contrast (750 ml-1000 ml of 3% hypaque (Amersham Health, Princeton, NJ) was commonly used for delineating fluid collections from unopacified bowel in this clinical setting.. However, with the use of 4 and 16 slice MDCT we are now routinely using water as a neutral contrast agent. Water, when combined with bolus intravenous contrast administration, provides an alternative to positive contrast and is recommended when 3D imaging and vascular mapping are desired. 750 cc-1000 cc of water are routinely administered over a 15-20 minute period prior to the study.
With 16-slice MDCT, we are now routinely imaging the pancreas in a volume mode rather than as routine axial images. The combination of multiplanar imaging (coronal, sagittal) combined with 3D volume rendering is ideal for defining the true extent of disease. Volume displays are especially valuable in defining the inter-relationships between pseudocysts and adjacent organs, as well as in defining vascular complications ranging from pseudoaneurysms, venous thrombosis and/or collateralization
Grading of Pancreatitis with CT
The (2,5) International Symposium on Acute Pancreatitis classified pancreatitis into two subgroups -- mild acute pancreatitis and severe acute pancreatitis. Specifically, an attempt was made to try to create a classification system based on clinical and laboratory parameters and specific CT findings. Mild acute pancreatitis is a self-limiting disease and is the most common form of pancreatitis. The patients usually recover uneventfully without complications. On the other hand severe acute pancreatitis is associated with a protracted course with a high incidence of complications and a defined mortality rate. Injury to the pancreatic parenchyma is a key finding which explains why severe acute pancreatitis is also commonly referred to as necrotizing pancreatitis. The key to the successful management of a patient with pancreatitis is the early detection of necrotizing pancreatitis, which has an associated mortality of up to 23%. (9-12) (Figs. 7-8)
Although clinical signs of severe pancreatitis do exist and include tachycardia, hypotension, shock, respiratory distress, and peritonitis these often appear late in the course of the disease process. In fact, the clinical diagnosis of acute severe pancreatitis is missed in over 30% of cases in several large series. (12-14) In the past, a few attempts were made to correlate clinical signs with disease extent. The Ranson criteria for severity of acute pancreatitis was based on a series of 11 objective signs ranging from patient age to white blood count to calcium and serum glucose level. The more positive findings the worse the severity of disease and the higher the mortality rate. In patients with two or more signs there was no mortality but with 6 or more criteria the mortality rate was over 50%.
With the introduction of CT and the use of CT with IV the pancreatic gland itself can be well visualized and its appearance can be correlate with patient outcome. CT criteria for the diagnosis of pancreatic necrosis are dependent on the detection of areas which lack glandular enhancement, which may be focal, or more diffuse. Balthazar (15) showed that there was close correlation between the presence of necrosis and course of hospitalization including morbidity and mortality. In addition, the extent of necrosis was directly correlated with the rate of morbidity and mortality. Based on this work a CT severity index was developed which attempted to use CT as a numeric grading system for the radiological grading of pancreatitis. The system provides a score between 0 and 10 with higher morbidity and mortality found with higher scores. A severity score of 7-10 had a 92 % complication rate and a 17% mortality rate while a score of 0 or 1 had zero morbidity or mortality.
The extent of pancreatic enhancement will vary based on a number of technical parameters and study design features. Kim et al. (16) found the optimal time for imaging for necrosis is in the venous phase or 50-60 seconds after contrast injection. Injection rate should be in the 3-cc/sec range. The pancreatic enhancement is normally in the 100-150 HU range. Lack of enhancement of less than 30 HU is representative of decreased blood perfusion of the gland and correlated well with necrosis. Caution in defining pancreatic necrosis is important as areas of peripancreatic fluid can simulate areas of necrosis. Pancreatic necrosis is ideally detected on scans performed 48-72 hours after the onset of an attack of acute pancreatitis. Scans done within the first 24 hours may be falsely negative or equivocal. Although scans are commonly done at time of admission the need for a second study should be kept in mind for patients without rapid improvement initially. (Figs. 9-10)
TABLE 1 Balthazar Score
Grade A: normal
Grade B: focal or diffuse enlargement of the pancreas
Grade C: pancreatic gland abnormalities associated with peripancreatic inflammation
Grade D: fluid collection in a single location
Grade E: two or more fluid collections and/or the presence of gas in or adjacent to the pancreas
TABLE 2 CTSI (CT Severity Index)
CT Grade Based on Balthazar score plus pancreatic necrosis with a maximum score of 10 points
Grade A: 0 points
Grade B: 1 point
Grade C: 2 points
Grade D: 3 points
Grade E: 4 points
Points are given for necrosis with <30% being 2 points, 30-50% necrosis 4 points and >50% necrosis being 6 points.
Van den biezenbos et al. compared the success of the CTSI with the Simplified Acute Physiology (SAP) score in predicting patient outcomes in a series of 45 patients. The authors found that although CT scoring and the SAP score had no significant benefit in identifying patients with severe outcomes, the CTSI score was better in predicting a favorable outcome.
CT FINDINGS Uncomplicated Acute Pancreatitis
Mild cases of acute pancreatitis reveal a minimal increase in the size of the pancreas, often involving the entire gland. The pancreatic contour becomes irregular with inflammatory changes, and peripancreatic fat planes become blurred and appears thickened. Peripancreatic extension of the inflammatory processes is relatively common because the pancreas does not have a capsule. Thickening of the mesentery, renal fascia, and lateroconal fascia is common. More severe forms of pancreatitis can result in moderate to marked increase in the size of the gland. The enlarged gland commonly shows edematous changes of the parenchyma, with typical measurements in the range of 5-20 HU. There can be a total obliteration of the peripancreatic fat by relatively high-attenuation inflammatory exudates, necrotic tissue, and blood. (Figs. 11-12)
Fluid Collections and Exudates
As pancreatitis progresses, small fluid collections can accumulate in and around the gland. (18-20) Fluid collections lack a well-defined capsule and are confined by the anatomic space in which they arise. Many collections spontaneously resolve, but a certain percentage goes on to develop pseudocyst formation and secondary infection or hemorrhage. The most common site of extra pancreatic fluid collections is the lesser sac, located directly anterior to the pancreas and posterior to the stomach. The next most common location is the left anterior pararenal space. Larger fluid collections can extend over the psoas muscles to enter the pelvis and groin. Exudates can also invade the posterior pararenal space, perirenal space, mesocolon, and mesentery. These fluid collections can also tract upward and present as posterior mediastinal masses. (Figs. 13-14)
Pseudocysts
Pseudocysts are focal collections of pancreatic fluid that usually evolve from acute fluid collections and inflammatory exudates. They can become large, often measuring 5-10 cm in diameter. Pseudocysts have a dense peripheral fibrous capsule, which usually requires several weeks to mature. Pancreatic pseudocysts can persist for a relatively long time and may result in pain, secondary infection, hemorrhage, or biliary duct obstruction. Helical CT is excellent for demonstrating the capsule of the pseudocyst, which can show significant enhancement following bolus contrast administration. The degree of enhancement may relate to the "maturity" of the capsule and be a reliable indication for percutaneous drainage (21). Most often, though, the decision to drain pseudocysts is equally dependent on the patient’s clinical condition. Complications of pseudocysts also include compression and occlusion of the splenic vein, which can result in extensive collaterization around the spleen and stomach. This may in time become a source of GI bleeding. (Figs. 15-16)
CT with multiplanar reconstruction is valuable in helping determine the optimal pathway for pseudocyst drainage. Procedures such as cystgastrostomy can be planned off the sagittal and 3D volume mapping. Successful drainage of these collections can also be documented by CT scanning. (Fig. 17)
Pancreatic Necrosis
Pancreatic necrosis represents a severe complication of acute pancreatitis (22). Necrosis tends to occur early in the course of the disease. The diagnosis of necrosis is based on demonstrating a focal or diffuse, well-marinated area of parenchymal nonenhancement. The region should be at least 3 cm or larger in diameter or involve more than one-third of the gland. Excellent correlation between the lack of pancreatic enhancement on CT and necrosis has been documented. Edematous forms of acute pancreatitis with diminished glandular enhancement must not be confused with the nonenhancement of necrosis. Infected pancreatic necrosis is recognized at helical CT as bubbles of gas within areas of pancreas, or as a collection of gas and tissue within the retroperitoneum. Massive infected necrosis ("emphysematous pancreatitis") carries a grave prognosis. (Figs. 18-19)
Several authors (23-25) have discussed the importance of such parameters such as contrast injection rate and contrast volumes as well as timing of data acquisition relative to contrast bolus in determining the absolute values of pancreatic enhancement in the normal gland. Kim et al. found that higher dose (2 ml per kilogram vs. 1.5 ml per kilogram) and faster injection rates (5 ml/sec vs. 3 ml/sec) increased the maximum pancreatic enhancement value by between 13 and 24 HU. Other including Bonaldi et al. found that although peak enhancement increased overall image quality was similar. Tublin et al. noted that by varying injection rates between 2.5 ml/sec and 5.0 ml/sec that peak pancreatic enhancement as well time to peak enhancement varied. At 2.5 ml/sec the pancreas reached a peak enhancement at 69 seconds of 65HU while at 5.0 ml/sec the peak enhancement was at 43 sec and reached 84 HU.
Pancreatic Abscess
Pancreatic abscesses represent focal areas of infection in or around the pancreatic gland. Abscesses usually present 4 or more weeks after the onset of the acute pancreatitis, and probably result from secondary infection of pancreatic fluid collections or from areas of focal necrosis. The helical CT diagnosis is suggested with the demonstration of a focal fluid collection that contains gas bubbles. The nearby pancreas remains visible and enhances following contrast administration. Clinical correlation or percutaneous aspiration is often required to make the diagnosis. Even in the absence of air, the possible presence of abscess should always be considered in any febrile patient with a persistent fluid collection. One CT finding which may be helpful in suggesting infection is a mottled appearance within the area of inflammation. This finding has been very helpful in our experience. (Figs. 20-21)
Vascular Complications and Hemorrhage
Pseudocysts and chronic pancreatitis can result in vascular occlusion of the splenic vein, superior mesenteric vein, and/or portal vein. Splenic vein thrombosis is most common, and results in complications such as gastric varices. Helical CT can accurately depict sites of vascular thrombosis and demonstrate collateral vascular pathways. Hemorrhage in cases of pancreatitis usually occurs from vascular injuries produced by pancreatic enzymes with enzymatic autodigestion of arterial walls with a confined perivascular blood leak and subsequent pseudoaneurysm formation. Injuries commonly involve the splenic artery or the pancreatic-duodenal or the gastroduodenal arteries, which are intimately related to the pancreas. An arterial pseudoaneurysm may result, and is often the underlying etiology in cases of massive hemorrhage. CT with arterial phase MDCT can routinely detect the presence and location of pseudoaneurysms. 3D CT angiography may be helpful in defining the specific site of the pseudoaneurysm. In these cases the importance of rapid contrast bolus (3 cc/sec minimum) and arterial phase imaging cannot be over emphasized. (26-28) (Figs. 22-23)
Bleeding can also occur into a pre-existing pseudocyst. Helical CT is often very helpful in identifying the source of hemorrhage. Acute hemorrhage secondary to a bleeding pseudocyst or pseudoaneurysm has an associated mortality rate of 12-37%.
Involvement of Adjacent Organs
Classically, pancreatitis is a disease process where spread is not limited by adjacent organs, mesenteries or the omentum. While pancreatitis most commonly involves the pararenal spaces and lesser sac it can extend to and involve adjacent organs. For example, renal involvement is typically inflammatory extension into the anterior and sometimes posterior pararenal space. The left pararenal space is most commonly involved except when the cause of pancreatitis is post procedural like post-ERCP pancreatitis where right-sided involvement is more common. On occasion a pseudocyst can tract into the perirenal space and even beneath the renal capsule. This pseudocyst can at times, on select images, even simulate a renal cyst. When pancreatic fluid tracts beneath the capsule it can result in a Page kidney due to compressive forces on the renal parenchyma. Percutaneous drainage may be needed. Other unusual complications include renal vascular abnormalities such as narrowing of the renal vein, renal vein thrombosis, perirenal varices and asymmetric renal enhancement due to extrinsic pressure on one of the renal arteries. In one series of acute pancreatitis 7% of cases had renal and perirenal complications. (29) (Figs. 24-25)
Splenic involvement by pancreatitis is not uncommon especially when one considers the intimate relationship of the tail of the pancreas and the splenic hilum (30-31) (Fig. 26). In addition to vascular complications ranging from splenic artery pseudoaneurysm to splenic vein occlusion, pseudocysts may tract deep into the spleen. This can result in complications ranging form intrasplenic pseudocysts to splenic infarction to intrasplenic hemorrhage. Intrasplenic pseudocyst can weaken the pancreatic gland so that with even minor trauma splenic rupture may occur. Splenic abscess may develop as a rare complication of pancreatitis. Although rare (frequency of 1-5%) splenic involvement by pancreatitis can be life threatening and CT can be used as a guide to monitor these patients and to determine when aggressive intervention is necessary to avoid catastrophic clinical outcomes.
Interventional Guidance in Pancreatitis: Role of CT
Although the detailed role of CT in the guidance of interventional procedures in pancreatitis is beyond the scope of this chapter, a few brief comments are in order. Although there has often been some discussion as to the role of interventional percutaneous drainage of pancreatic abscess, pancreatic necrosis or pseudocyst in regard to timing or surgical intervention it is general accepted that percutaneous drainage is a safe and effective technique even in patients with infected acute necrotizing pancreatitis. In an article by Freeny, sepsis was controlled in 74% of patients permitting elective surgery for treatment of pancreatic fistulae, and 47% were cured without the need for surgery. CT is routinely used for guidance for catheter placement as well as to monitor response. In these cases, 3D display of the relationship of the catheter to the fluid collection may prove useful. (32) (Figs. 27-28)
Chronic Pancreatitis
Repeated episodes of insult to the pancreas lead to a series of changes, which can result in glandular atrophy and subsequent glandular scarring and fibrosis. Pancreatic calcifications involving part or the entire gland may occur as an isolated event or as part of the process of glandular atrophy. Calcifications are most commonly associated with chronic alcoholic pancreatitis. In this process the ducts become occluded with proteinaceous plugs that eventually accumulate calcium carbonate. Duct obstruction results in changes of duct ectasia and glandular fibrosis. In most cases the calcifications are in the 1-5 mm size while larger calcifications do occur. Occasionally these calcifications become strategically located and may obstruct the distal common bile duct. Lesniak et al noted that calcifications may also develop in pancreatitis secondary to hyperparathyroidism, tropical pancreatitis and idiopathic pancreatitis while other causes of pancreatitis including gallstones, drugs, trauma and viruses do not cause pancreatic calcifications. (33) (Figs. 29-32)
One of the classic diagnostic dilemmas with CT in the past has been the differential diagnosis of acute pancreatitis on a background of chronic pancreatitis simulating a pancreatic neoplasm. This is especially common in the pancreatic head where areas of the gland may appear mass-like especially relative to areas of glandular atrophy. With MDCT and rapid contrast bolus this is currently less of a problem but occasionally will remain a diagnostic challenge especially in the patient with changing clinical symptoms and weight loss. Two strategies can be employed depending on the clinical scenario. One of course is to do a fine needle biopsy which when positive is diagnostic. A second, possibly more reasonable, strategy is to get a repeat CT scan in 4-8 weeks. In our experience in most cases the mass like process will resolve without need for more invasive workup. (34)
CONCLUSION References
Helical CT scanning allows quick and accurate diagnosis and staging of pancreatitis. CT can assess the degree of involvement and enables detection of complications including development of pseudocysts, abscess, necrosis, hemorrhage, and vascular occlusion. The introduction of 4 and more recently 16-slice multidetector row CT scanners improved our ability to detect the earliest changes of pancreatitis as well as its complications.
1. Steer ML. Pathophysiology and pathogenesis of acute pancreatitis: In: Bradley EL III (ed) Acute pancreatitis: Diagnosis and therapy. Raven Press 1994, New York.
2. Balthazar EJ, Robinson DL, Megibow AJ, et al: Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174:331-336.
3. Balthazar EJ. CT diagnosis and staging of acute pancreatitis. Radiol Clin North Am 1989; 27:19-37.
4. Balthazar EJ, Ranson JHC, Naidich DP, et al.: Acute pancreatitis: prognostic value of CT. Radiology 1985; 156:767-772.
5. Ranson JHC, Rifkind KM, Roses DF, et al. Objective early identification of severe acute pancreatitis. Am J Gastroenterol 1974; 61: 443-451.
6. Thoeni RF, Blakenberg F. Pancreatic imaging: Computed tomography and magnetic resonance imaging. Radiol Clin North Am 1993; 31:1085-1113.
7. Bonaldi VM, Bret PM, Atri M, Garcia P, Reinhold C. A comparison of two injection protocols using helical and dynamic acquisitions in CT examinations of the pancreas. AJR 1996; 167:49-55.
8. Hollett MD, Jorgensen MJ, Jeffrey RB Jr. Quantitative evaluation of pancreatic enhancement during dual-phase helical CT. Radiology 1995; 195:359-361.
9. Bradley EL III. A clinically based classification system for acute pancreatitis. Arch Surg 1993; 128:586-590.
10. Banks PA . A new classification system for acute pancreatitis.Am J Gastroenterol 1994; 89:151-152.
11. Banks PA. Practice Guidelines in Acute Pancreatitis. Am J Gastroenterol 1994; 89:S78-S85.
12. McMahon MJ, Playforth MJ, Pickforth IR. A comparative study of methods for the prediction of severity of attacks of acute pancreatitis. Br J Surg 1980; 67:22-25.
13. Wilson C, Heath DI, Imrie CW. Prediction of outcome in acute pancreatitis: A comparative study of APACHE II, clinical assessment and multiple factor scoring systems. Br J Surg 1990; 77:1260-1264.
14. Corfield AP, Cooper MJ, Williamson RCN, et al. Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices. Lancet 1985:2: 403-407.
15. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JHC. Acute pancreatitis: Value of CT in establishing prognosis. Radiology 1990; 174:331-336.
16. Kim T, Murakami T, Takahashi S, et al. Pancreatic CT imaging: Effects of different injection rates and doses of contrast material. Radiology 1999; 212; 219-225.
17. Van den biezenbos AR, Kruyt PM, Bosscha K, et al. Added value of CT criteria compared to the clinical SAP score in patients with acute pancreatitis. Abdom Imag 1998; 23:622-626.
18. Kemppainen E, Sainio V, Haapianen R, Kivisaari AL, Kivilakso E, Puolakkainen P. Early localization of necrosis by contrast-enhanced computed tomography can predict outcome in severe pancreatitis. Br J Surg 1996; 83:924-929.
19. Yeo CJ, Bastidas JA, Lynch-Nyhan A, et al. The natural history of pancreatic pseudocysts documented by computed tomography. Surg Gynec Obstet 1990; 170; 411-417.
20. Donovan PJ, Sanders RC, Siegelman SS. Collections of fluid after pancreatitis: Evaluation by computed tomography and ultrasonography. Radiol Clin North Am 1982; 20:653-665.
21. Balthazar EJ, Freeny PC, vanSonnenberg E. Imaging and Intervention in acute pancreatitis. Radiology 1994; 193:297-306.
22. Balthazar E. Acute Pancreatitis: Assessment of severity with clinical and CT evaluation. Radiology 2002; 223:603-613.
23. Kim T, Murakami T, Takahashi S, et al. Pancreatic CT Imaging: Effects of Different Injection Rates and Doses of Contrast Material Radiology 1999; 212:219-225.
24. Bonaldi VM, Bret PM, Atri M, Garcia P, Reinhold C. A Comparison of Two Injection Protocols Using Helical and Dynamic Acquisitions in CT Examinations of the Pancreas. AJR 1996;167:49-55
25. Tublin ME, Tessler FN, Cheng SL, Peters TL, McGovern PC. Effect of Injection Rate of Contrast Medium on Pancreatic and Hepatic Helical CT. Radiology 1999; 210:97-101
26. Ishida H, Konno K, Komatsuda T, et al. Gastrointestinal bleeding due to ruptured pseudoaneurysm in patients with pancreatitis. Abdom Imaging 1999; 24:418-421.
27. Burke JW, Erickson SJ, Kellum CD, et al. Pseudoaneurysms complicating pancreatitis: detection by CT. Radiology 1986; 161:447-450.
28. Waslen T, Wallace K, Burbridge B, Kwauk S. Pseudoaneurysm secondary to pancreatitis presenting as GI bleeding. Abdom Imaging 1998; 23:318-321
29. Mortele KJ, Mergo PJ, Yaylor HM, Ernst MD, Ros PR. Renal and perirenal space involvement in acute pancreatitis: spiral CT findings. Abdom Imaging 2000; 25:272-278
30. Urban BA, Fishman EK. Helical CT of the Spleen. AJR 1998;170:997-1003
31. Fishman EK, Soyer P, Bliss DF, Bluemke DA, Devine N. Splenic Involvement in Pancreatitis: Spectrum of CT Findings. AJR 1995; 164:631-635
32. Freeny PC, Hauptmann E, Althaus SJ, Traverso LW, Sinanan S. Percutaneous CT guided catheter drainage of infected acute necrotizing pancreatitis: Techniques and results. AJR 1998; 170:969-975.
33. Lesniak RJ, Hohenwalter MD, Taylor AJ. Spectrum of causes of pancreatic calcifications. AJR 2002; 178:79-86.
34. Neff CC, Simeone JF, Wittenberg J. Inflammatory pancreatic masses: Problems in differentiating focal pancreatitis from carcinoma. Radiology 1984; 150:35-38.