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Hyperdense stone is present in the gallbladder in a patient with interstitial pancreatitis. Figure 8. CT of choledocholithiasis. Unenhanced CT depicts a calcified stone in the common bile duct arrow at the level of pancreatic head asterisk with little peripancreatic fat stranding arrowheads compatible with interstitial pancreatitis. Stones may be densely calcified, rim calcified or laminated or have a central nidus of calcification. Stones also may present as a soft-tissue density or a lucent filling defect within the bile. Some stones may contain gas.

MRI is an excellent, but costly alternative for US for depicting stones larger than mm in the gallbladder or common bile duct Figure 9. Figure 9. MRCP of choledocholithiasis. Heavily T2-weighted 3D sequence depicts 2 filling defects in the distal part of the common bile duct arrow representing stones.

Hence, current guidelines advocate performing cholecystectomy during hospitalization in those with mild acute pancreatitis Cross-sectional imaging may show secondary findings suggesting a biliary cause of pancreatitis. However, the sensitivity of this finding was not significant in the study by Yie et al and needs to be validated in large-scale studies. In this study, some other CT features were significantly associated with biliary pancreatitis, including pericholecystic fluid or fat stranding, pericholecystic increased attenuation of the liver, increased gallbladder wall enhancement, and gallbladder wall thickening 45, Further study is needed to validate these results.

The low rate of pancreatic injury after abdominal trauma is related to its retroperitoneal location. Isolated pancreatic injury is less commonly seen than concomitant duodenal and pancreatic injury. Coexisting injuries are often present owing to the central location of the pancreas and the close relationship with surrounding organs and vessels. Injury to the pancreas can cause acute pancreatitis posttraumatic pancreatitis that may present with equivocal clinical symptoms and laboratory findings, often masked by other organ injuries 19, 27, Posttraumatic pancreatitis should be considered when patients present with abdominal pain, nausea, and vomiting associated with increased serum amylase levels after blunt abdominal trauma.

Contrast-enhanced CT is the primary imaging modality in abdominal trauma as it may diagnose posttraumatic pancreatitis and readily depicts accompanying traumatic injuries to other parenchymal organs, vessels, and bony structures 57, Posttraumatic pancreatitis is likely in the right clinical setting combined with imaging features of pancreatitis. CT features of posttraumatic pancreatitis vary with the impact and severity of abdominal trauma and ranges from normal findings, mild pancreatic swelling, and exudate or soft tissue infiltration in the retroperitoneal spaces and mesenteries to hypo-enhancement of pancreatic parenchyma representing contusion or frank pancreatic transection with associated hemorrhage, fluid exudate, and duct disruption.

Most CT findings in posttraumatic pancreatitis lack specificity and are often indistinguishable from pancreatitis of other etiologies, except for transection or laceration depicted as a hypoattenuating linear density perpendicular oriented to the long axis of the pancreas and fracture of the pancreas clear separation of pancreatic fragments. These subtle findings may be overlooked initially especially when coexistent organ injuries are present.

How to scan upper retroperitoneum by ultrasound (horizontal view )

A diligent search for ductal injury should be undertaken in every patient with blunt abdominal trauma and posttraumatic pancreatitis as its integrity dictates clinical management: when intact, a conservative management is maintained, whereas a disrupted duct necessitates urgent surgical intervention. Delays in diagnosis and treatment of ductal injury results in subsequent increases in morbidity and mortality 19, 27, 47, 57, The main pancreatic duct is most prone to injury from blunt trauma at the pancreatic neck or body as it traverses the vertebral column.

Minor or major pancreatic duct rupture can cause pancreatic ascites from leakage of pancreatic fluid into the lesser and greater peritoneal compartments. On CT, ductal injury can be inferred when a pancreatic laceration of more than one-half the pancreatic diameter is observed or in case of a complete transection or pancreatic fracture along the expected course of the pancreatic duct.

A characteristic telltale sign of ductal injury is the presence of a posttraumatic pancreatic collection or pseudocyst. Occasionally, MRCP may be a helpful non-invasive adjunct to emergency abdominal CT to better assess pancreatic duct integrity. A long-term complication of posttraumatic pancreatitis is ductal scarring and stenosis, which may cause obstructive pancreatitis proximal to the stricture. Obstructive causes of acute pancreatitis due to pancreatic neoplasms involve periampullary tumors, cystic and solid pancreatic tumors, of which pancreatic adenocarcinoma is the most frequent and challenging diagnosis given the narrow therapeutic window for curative surgery.

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Pancreatic cancer may cause pancreatitis because of pancreatic duct obstruction. Yet, the triggering mechanism of acute inflammation is incompletely understood as a minority of patients with pancreatic adenocarcinoma develop pancreatitis. Fortunately, pancreatitis resulting from underlying malignancy is usually mild interstitial pancreatitis such that curative resection is still possible Figure Figure Interstitial pancreatitis due to pancreatic adenocarcinoma.

A slightly dilated pancreatic duct top is noted which ends abruptly due to a hypovascular mass in the body of the pancreas bottom. Mild exudate is present in the left retroperitoneal space. Patient underwent surgery and pancreatic adenocarcinoma was confirmed at pathology. Necrotizing pancreatitis caused by pancreatic adenocarcinoma is rarely reported and notoriously difficult to diagnose and treat, as the extensive peripancreatic changes associated with necrotizing pancreatitis would likely render curative resection impossible in the majority of cases Pancreatic adenocarcinoma as the cause of pancreatitis is surrounded by pitfalls in clinical presentation and diagnostic imaging features leading to delays in correct diagnosis and appropriate treatment 7, 30, 72, Often, the diagnosis of an occult pancreatic adenocarcinoma is masked by the clinical presentation of signs and symptoms of acute pancreatitis.

Also, on imaging, features of the inflammatory process may hamper the visualization of a pancreatic mass. On CT, primary diagnostic signs for pancreatic adenocarcinoma are an infiltrating irregular hypovascular mass, signs of invasion of surrounding organs and vascular structures, necrotic regional lymphnodes, and metastases in liver or peritoneum 7. Suspicious secondary imaging findings are an abrupt stop of the pancreatic duct with upstream duct dilation whether or not with associated atrophy of pancreatic parenchyma , as this is rarely, if at all, seen in acute pancreatitis of benign cause.

In most published reports, pancreatic adenocarcinoma has not been suspected clinically with a delay of diagnosis up to months 7, 30, 72, Also, in patients with suspicious findings on regular CT, a short interval weeks follow-up study is needed to ascertain the right diagnosis. The following two etiologies pancreas divisum and annular pancreas occasionally cause acute pancreatitis. The association between these congenital pancreatic anomalies and acute pancreatitis remains, however, controversial.

Pancreas divisum represents a fusion anomaly in which the dorsal containing the Santorini duct and ventral containing the Wirsung duct pancreatic anlagen fail to fuse. Accordingly, the ventral Wirsung duct drains only the pancreatic head via the major papilla, whereas the majority of the pancreas drains via the minor papilla through the dorsal Santorini duct. Pancreas divisum is usually asymptomatic and the clinical relevance has been the subject of considerable debate.

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However, it is undoubtedly more frequently diagnosed in patients with repeated episodes of acute pancreatitis and chronic pancreatitis than in the general population. MRCP with secretin stimulation may depict inadequate outflow of pancreatic secretions through the minor papilla.

CT of the Retroperitoneum

In the normal population, multidetector CT with its high spatial resolution and thin collimation also allows for accurate assessment of pancreas divisum when the dorsal Santorini duct courses directly from the tail and body of the pancreas through the anterior part of the pancreatic head draining into the minor papilla without evident connection with the ventral duct.

However, inflammatory changes of the pancreas such as pancreatic oedema, swelling, and necrosis often preclude accurate CT assessment of ductal anatomy in patients with acute pancreatitis 3. Recognition of cross-sectional findings suggestive for pancreatic divisum can guide patient management by recommending ERCP evaluation and assessment of minor papilla function. Possible treatments include stent placement in the minor papilla or minor papillotomy. Annular pancreas is usually diagnosed during infancy with severe duodenal obstruction requiring urgent surgery , but clinical manifestations may develop at any age.

Pancreatitis due to annular pancreas is often focal, confined to the pancreatic head and likely relates to the obstruction of pancreatic secretions through the annular duct Santorini duct. In adults presenting with pancreatitis, annular pancreas can be depicted on CT as a ring of inflammatory tissue isodense with pancreatic parenchyma surrounding the descending duodenum.

Sometimes CT may show an annular duct Santorini also encircling the duodenum. Ischemic and postoperative pancreatitis are rare etiologies of acute pancreatitis 11, Although their mechanisms in inducing acute pancreatitis are intimately intermingled, independently they may account for an acute episode of pancreatitis. The common denominator in the pathogenesis of both etiologies is the disturbance of pancreatic microcirculation; i. These factors both induce and propagate premature intracellular activation of autodigestive pancreatic proteases and the resultant inflammatory response.

Pancreatic ischemia may occur as a secondary event and, as such, may aggravate acute pancreatitis severity caused by other etiologies, but may also be the primary initiator of acute pancreatitis 38, 60, 81, Postoperative pancreatitis may occur after a variety of surgical procedures, among these are intra-abdominal procedures such as common bile duct exploration, sphincteroplasty, distal gastrectomy, splenectomy, and organ transplantation and operations distant from the gastrointestinal tract; both after major surgery like cardiovascular surgery, spinal, vascular, and esophageal surgery, but also after relatively minor procedures that do not involve manipulations near the pancreas, such as thyroidectomy, parathyroidectomy, and inguinal hernia repair 13, 22, Possible factors linking these surgical procedures with acute pancreatitis include drugs medication during cardiopulmonary bypass surgery, immunosuppressive drugs in organ transplantation , intraoperative or postoperative periods of low flow or hypotension resulting in reduced splanchnic flow and impaired pancreatic vascularization, thromboembolic events, mechanical factors direct pancreatic, duodenal or biliary manipulation , and metabolic factors.

The spectrum of symptoms associated with ischemia-induced acute pancreatitis may vary from asymptomatic hyperamylasemia e. The definition and diagnosis of ischemia-induced acute pancreatitis are difficult to determine and often delayed 13, 22, 38, 60, 79, 81, Imaging studies are necessary when the diagnosis of acute pancreatitis is uncertain. CT is a valuable objective imaging modality for the evaluation of patients with suspected ischemic or postoperative pancreatitis. In postoperative patients, CT may show findings of acute pancreatitis with or without parenchymal necrosis with peripancreatic collections that show varying degrees of encapsulation due to the often delayed diagnosis.

Also, it is important to bear in mind that in patients with ischemic acute pancreatitis, a possible coexistence of intestinal ischemia may occur, in particular of the right hemicolon, the transverse colon, or the gallbladder. Furthermore, special attention should be paid to the patency of the portomesenteric venous structures as well as the celiac trunk and superior mesenteric artery i. In conclusion, the diagnosis of ischemic or postoperative pancreatitis requires a high index of suspicion.

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Increased clinical awareness perioperatively appears to be the most effective strategy for early diagnosis and timely treatment of acute ischemic pancreatitis following cardiac or major vascular surgery. Liberal use of diagnostic imaging modalities, primarily CT, to establish an early diagnosis and institution of appropriate therapy is, therefore, warranted.

Steatosis of the liver may be seen in patients with an alcoholic etiology or metabolic disturbances such as hypertriglyceridemia, but may also be a pre-existent condition in case of obesity or usage of medication and, therefore, lacks specificity Figure The presence of liver abnormalities characteristic for cirrhosis caudate lobe hypertrophy, lobularity of liver contour, venous collaterals, splenomegaly may, however, suggest an alcoholic etiology.

Hepatic steatosis in drug-induced pancreatitis. Markedly hypodense liver parenchyma is seen representing severe hepatic steatosis in a patient with necrotizing pancreatitis and a thrombus in the portal vein arrowhead.


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The standard work-up of the cause of acute pancreatitis may vary significantly among different centers based on personal experience and acquired skills, available equipment, and institutional strengths and weaknesses. However, based on current available evidence and recommendations according to established guidelines, an abdominal US is advised in all patients presenting with acute pancreatitis, both at first presentation and in recurrent episodes of otherwise idiopathic pancreatitis 23, 55, , Depending on expertise, availability, and local practices, further testing by means of EUS or MRCP is indicated as a next step if US is negative but the clinical suspicion for a biliary etiology is high.

Additional imaging i. Acute pancreatitis is a serious disease with varying severity. The recently revised Atlanta Classification on acute pancreatitis RAC classified the severity of acute pancreatitis clinically on the basis of presence or absence of organ failure and morphologically on the basis of presence or absence of tissue necrosis Morphologically i. Interstitial pancreatitis is usually a self-limiting disease with a short hospitalization stay and represents the most common form of acute pancreatitis 46, These patients typically recover uneventfully without complications.

On imaging, interstitial pancreatitis may reveal a minimal increase in size of the pancreas, focally or diffusely Figure Interstitial pancreatitis CT top depicts a swollen and slightly heterogeneous enhancing pancreatic parenchyma with fluid in the peripancreatic and retroperitoneal spaces asterisks. Follow-up CT 9 days later bottom shows resolution of fluid and normalization of pancreatic parenchyma. The pancreatic contour becomes irregular with inflammatory changes; the peripancreatic fat planes become blurred with increased attenuation values.

Peripancreatic extension of the inflammatory process is relatively common because the pancreas lacks a well-defined capsule. Thickening of the small bowel mesentery, renal fascia, and lateroconal fascia is common. More severe forms of interstitial pancreatitis can result in moderate amounts of peripancreatic fluid 15, , The revised Atlanta Classification distinguishes three subtypes of necrosis depending on involvement of pancreatic parenchyma alone rare , peripancreatic tissues extrapancreatic necrosis or EXPN, more common , or the combination of both combined necrosis, most common Pancreatic parenchymal necrosis tends to occur early in the course of the disease, within the first h after symptom onset.

CT criteria for the diagnosis of pancreatic parenchymal necrosis are dependent on the detection of areas lacking enhancement, which may be focal or diffuse Figure Lack of pancreatic enhancement corresponds with decreased blood perfusion of the pancreatic gland and correlates well with necrosis. Accuracy for depicting areas of pancreatic parenchymal necrosis is excellent when the region measures at least 3 cm or larger in diameter or involves more than one-third of the gland.

Caution in defining pancreatic parenchymal necrosis is important as areas of intrapancreatic fluid or reversible ischemia can simulate areas of necrosis. Scans done within this timeframe may be falsely negative or equivocal. EXPN is a relatively new subtype of necrotizing pancreatitis which has received increasing attention in the literature over the past years 4, 84, Its diagnosis hinges on the detection of heterogeneous peripancreatic collections with preserved pancreatic parenchyma perfusion. On CT, EXPN is determined when a normally perfused pancreatic parenchyma is noted surrounded by collections composed of various densities fat, fluid, and non-liquid Hounsfield units Figure In general, EXPN heralds a better prognosis than combined necrosis when sterile, but similar prognosis when infection of necrotic tissue develops 4, Extrapancreatic necrosis.

CT depicts a normal enhancing pancreatic parenchyma surrounded by acute necrotic collections.

Note, calcified stone in the gallbladder. The clinical course of acute pancreatitis is highly variable ranging from mild self-limiting symptoms to rapidly progressive organ dysfunction potentially culminating in death if not treated appropriately. Proper initial management includes transfer of patients to specialized centers or admission to intensive care units for supportive treatment or for targeted therapy i.

Besides the need from a clinical management perspective, there are other potential benefits for early severity prediction of acute pancreatitis. Accurate stratification is essential for reliable comparison of clinical outcomes among institutions, for evaluation of novel therapeutic strategies, and for inclusion of patients in randomized controlled clinical trials Hence, considerable efforts have been targeted over the past decades to the early identification of those who will develop persistent organ failure in the early stages and infected necrosis and sepsis in the later phase.

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