CT AND MRCP FINDINGS OF ACUTE AND CHRONIC.pptx

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1. CT AND MRCP FINDINGS OF ACUTE AND CHRONIC PANCREATITIS DR. M H BHUYAN(MODERATOR) DR. P BORAH DR. DJ BORPATRAGOHAIN DR. L NATH DR. PN TAYE DR. SS BISWAS PRESENTED BY: DR. RISHAV SARMAH

2. ANATOMY The pancreas is a retroperitoneal organ with both endocrine and exocrine functions. It secretes hormones like (insulin, glucagon and somatostatin), and secretes pancreatic juice, involved in digestion. HEAD This is the thickest part of the pancreas and lies to the right of the superior mesenteric vessels. It is attached to the C loop of the duodenum. The uncinate process is a posterior extension of the head and lies behind the SMV Neck This is thinnest part of the pancreas and is located anterior to the superior mesenteric vessels. The portal vein formation occurs behind the pancreatic neck by the union of the SMV and Splenic vein. Body This is the main part of the pancreas and lies to left of the mesenteric vessels. The peritoneum and omental bursa cover the anterior and posterior surface of pancreas, respectively. Tail The layers of the splenorenal ligament enclose the pancreatic tail in the splenic hilum.

3. ACUTE PANCREATITIS Pancreatitis occurs due to a chain of events triggered by a temporary/permanent pancreatic duct obstruction. This leads to activation and release of pancreatic enzymes into pancreatic interstitium and peripancreatic tissues leading to severe auto digestion and necrosis of pancreas and adjacent tissues. Cli nically severe acute pancreatitis is characterized by two phases, an early phase and a late phase. The early phase is dominated by the systemic effects of release of inflammatory mediators such as cytokines – termed as systemic inflammatory response syndrome (SIRS). There is no correlation between the clinical severity of pancreatitis and morphological changes in this early stage. The later phase is dominated by effects of local complications due to pancreatic/peripancreatic necrosis

4. The Clinical diagnosis of acute pancreatitis requires two of the following three features: 1) Abdominal pain – which typically is epigastric and radiates to the back. 2) Serum amylase/lipase more than three times of the upper limit of normal. 3) Characteristic findings of acute pancreatitis on CT. If the first two findings are present without any significant SIRS then CT is not required.

5. Morphological classification There are two distinct forms of acute pancreatitis – interstitial oedematous pancreatitis and acute necrotising pancreatitis. Interstitial oedematous pancreatitis is a condition where there is only mild swelling of the pancreas with loss of normal lobulations and a diffuse decrease in attenuation of the pancreas. There may be heterogeneity of the pancreatic parenchyma due to varying degrees of interstitial oedema. The inflammatory changes may be restricted to the pancreas or extend into the peripancreatic regions. The inflammation in the peripancreatic regions manifests as acute pancreatic effusions.

6. Acute edematous pancreatitis: CECT image demonstrates homogenous enhancement of enlarged bulky pancreas. Acute edematous pancreatitis: STIR MR image demonstrates T2 hyperintense Interstitial edema in enlarged bulky pancreas.

7. Acute pancreatic fluid collections are enzyme-rich pancreatic juice collections seen in about 40% of patients with acute pancreatitis. The fluid collections occur due to exudation of pancreatic juices into the interstitium of the pancreas and subsequently leakage into the surrounding tissue spaces. As the exudative process continues, the parietal peritoneum overlying the pancreas may be disrupted with the inflammatory fluid entering the lesser sac. From the lesser sac the fluid can enter the peritoneal cavity via the foramen of Winslow or by dissecting the peritoneum along the anterior surface of the lesser sac. Posterior extension of the fluid collection in the anterior pararenal space may occur into a potential space between the laminae of the posterior pararenal fascia. Large fluid collections may dissect superiorly into the mediastinum or pericardial space

8. Series of CECT images in acute pancreatitis demonstrating acute pancreatic fluid collections of varying degrees.

9. Of these collections, 50% resolve spontaneously; the remainder may evolve after 4–6 weeks into pseudocysts Collection should be termed a pseudocyst only when a definite capsule develops, and the collection has been static for at least 4–6 weeks. Large collections of fluid are usually associated with a lesser degree of pancreatic necrosis as compared to extensive pancreatic necrosis associated with a lesser amount of fluid collection. The risk of complications such as rupture, infection and hemorrhage increases with the age of the collection.

10. ACUTE NECROTISING PANCREATITIS Acute necrotising pancreatitis is a fulminant form of pancreatitis in which there is necrosis of the pancreas, that is nonviable pancreatic tissue. These areas of nonviable pancreatic tissue do not enhance on CECT scan as compared to viable pancreatic tissue, which demonstrate significant enhancement. These areas may be diffuse or focal, small in size to complete glandular involvement. These necrotic areas have a very important bearing on the course of pancreatitis, as they are liable to undergo secondary infection and form pancreatic sepsis. Pancreatic necrosis may be seen in the pancreas only, peripancreatic tissues also or only in the peripancreatic region. Over time necrosis evolves and liquefies as well as the liquid component resorbs. If pancreatic necrosis is not resorbed it may get walled off or with time or may become infected. Encapsulation occurs between the third and fourth weeks. On CT, there is a spectrum of findings – solid, liquid containing debris (these may be nonwalled off/partially walled off).

11. CECT demonstrates focal areas of hypodensity in enlarged bulky pancreas representing areas of non viable parenchyma – pancreatic necrosis. Acute Necrotic collection: CECT demonstrates large ill-defined peripancreatic fluid collection with areas of varying densities representing an acute necrotic fluid collection.

12. COMPLICATIONS OF ACUTE PANCREATITIS

13. Pancreatic Pseudocysts Pseudocysts are round or oval encapsulated fluid collections containing only liquefied component. On CT, a pseudocyst appears as a well-defined fluid collection with a thin capsule. The most common location for pseudocysts is the lesser sac, though they may be found anywhere in the mediastinum, abdomen or pelvis as they may dissect along fascial planes, along vessels and through capsules of solid organs. When the contents of the pseudocyst are heterogeneous or uniformly increased in attenuation, the possibilities of infection or haemorrhage should be considered. Large pseudocysts greater than 6 cm in size can easily be drained percutaneously using intercostal drainage tube or pigtail catheter or endoscopically via the stomach.

14. CECT demonstrates multiple well defined thin walled homogenous fluid collections in a case of acute pancreatitis representing pseudocysts. T2 weighted MRI image demonstrates multiple well defined thin walled homogenous fluid collections in a case of acute pancreatitis representing pseudocyst.

15. Walled-off necrosis A s pancreatic/peripancreatic necrosis matures and evolves, an interface develops between necrosis and adjacent fatty tissue and an enhancing thickened wall is seen, resulting in a well-defined fluid collection with necrotic debris and fat necrosis. It is important to differentiate a pseudocyst from walled off necrosis, as a pseudocyst requires drainage and walled off necrosis requires surgical removal

16. CECT demonstrates large peripancreatic fluid collection with well defined margins, thick enhancing walls and internal densities representing walled of necrosis. T2 weighted MRI demonstrates large peripancreatic fluid collection with well defined margins and internal densities representing walled of necrosis.

17. Sepsis Pancreatic sepsis may occur following secondary infection of pancreatic and/or peripancreatic necrosis, acute pancreatic fluid collections and pseudocysts. The only specific sign to demonstrate sepsis is the presence of gas in a collection. This sign is unfortunately not common and seen in only one-third of cases. Gas is seen in the fluid collection as very dark well-defined air attenuation bubbles. Occasionally gas may be present due to a gastrointestinal fistula or previous surgery. Fat necrosis should not be confused with air bubbles, which are indicative of sepsis. A ir bubbles have well-defined margins and are homogeneously jet black, whereas fat is non-homogeneously grey with ill-defined margins. T he only other means to diagnose pancreatic sepsis is by CT-guided aspiration. Imaging-guided percutaneous drainage is the first step in treating pancreatic sepsis. Initially pig tail catheters were used but these are notorious to get blocked as the largest bore of a pigtail catheter is 12 F.Hence large bore ICD catheters with bore size of 16 to 30 F hav e been introduced.

18. Series of CECT demonstrating peripancreatic fluid collections with air within indicative of pancreatic sepsis. CT guided drainage of peripancreatic collection with a 24 FR ICD in situ – placed percutaneously.

19. Vascular and gastro-intestinal complications Vascular complications arise due to injury to the vessel wall by extravasated pancreatic enzymes. These injuries result in the formation of a pseudoaneurysm, which may rupture resulting in massive haemorrhage. On CT, these pseudo aneurysms are seen as densely enhancing rounded areas within or adjacent to fluid collections/necrotic areas. The commonly involved vessels are the splenic, gastroduodenal or pancreaticoduodenal arcade. Thrombosis of the portal vein, splenic and perisplenic veins may also occur. Gastrointestinal complications occur due to injury of bowel wall by pancreatic enzymes, similarly to vascular complications resulting in bowel fistulas The only indications of a bowel fistula on CT may be the presence of extraluminal/extravasation of oral contrast media or the presence of air in a fluid collection from a bowel fistula.

20. Vascular complication of acute pancreatitis due to autodigestion of vessel wall resulting in pseudoaneurysm. V enous thrombosis – coronal thick CECT MIP image demonstrates splenic vein thrombosis.

21. Prognostic role of CT CT may be used as a prognostic indicator of the severity of acute pancreatitis. There are two scoring systems: CT severity index and modified CT severity index. There are minor changes between the two, both perform equally well so either is fine to use providing similar prognostication.

22. Classification of Acute Pancreatitis According to Severity Index Score GRADE CTSI SCORE MODIFIED CTSI SCORE Mild acute pancreatitis 1-3 2 Moderate 4-6 4-6 Severe 7-10 8-10 Those with a score of 0 or 1 showed no mortality or morbidity. Patients with a score of 2 had no mortality and only 4% morbidity. Patients with scores between 7 and 10 had 17% mortality and a 92% complication rate. The clinical scoring systems such as the Ransons and APACHE are more sensitive to predicting systemic complications compared to the CT Severity Index, which is more sensitive than the clinical scoring systems in predicting pancreatic and peripancreatic complications.

23. The Role of MRI MRI has been found to be more sensitive than CT in detection of acute pancreatitis especially mild cases. Acute interstitial oedema is seen on T1WI fat sat images as a diffuse or focal enlargement of pancreas. The normal high signal intensity seen in the pancreas on T1WFS images is lost. On T2W fat sat images there may be hyperintensity in the pancreas due to pancreatic oedema, peripancreatic hyperintensity in the form of peripancreatic inflammation and fluid collections. Diffusion-weighted imaging shows hyperintense signal of the involved parenchyma with decreased ADC values. On MRCP the pancreatic duct may appear normal or compressed due to the pancreatic swelling.

24. In necrotizing pancreatitis there may be focal, segmental, diffuse high signal intensity on T1WI from hemorrhage or decreased signal intensity due to necrosis. These areas of haemorrhage or necrosis will not enhance on the contrast studies. Complications such as pancreatic duct rupture and non-liquefied contents of pancreatic/peripancreatic collections are better demonstrated on MRI than CT. MRCP also helps determine the underlying cause of pancreatitis, which may be choledocholithiasis, neoplasm or abnormalities of pancreatic duct such as pancreas divisum

25. Chronic Pancreatitis This is a chronic inflammatory disease that leads to progressive and irreversible structural damage to the pancreas, consequently leading to reduction in its exocrine and endocrine functions. Consumption of more than 100 g of alcohol in day results in a decrease in pancreatic secretion, reduction in bicarbonate concentration, diffusion of calcium into pancreatic ducts, as well as increase in protein secretion. In view of the high protein content in the ducts, protein plugs form, with the high calcium content in duct fluid they calcify. There is also progressive destruction of pancreatic secretory parenchyma by necrosis/apoptosis. Acinar cells disappear, duct cells are injured, fibrosis sets in and consequently there is functional impairment of exocrine and endocrine function leading to malnutrition and diabetes. The fibrotic tissue produces duct strictures with upstream dilatation and stasis. This usually results in atrophy and ductal calculi.

26. Etilogy : TIGAR-O Classification

27. Pathogenesis The hallmark of chronic pancreatitis is pancreatic ductal calcifications and ductal dilatation. Calcified proteinaceous plugs lie in the secondary ductules of the main pancreatic duct or main pancreatic duct. These may cause obstruction or inflammation of the ductal wall resulting in periductal inflammation which causes strictures due to fibrosis to the duct with resultant downstream dilatation of the duct. These may be visualized on a plain radiograph of the abdomen however plain radiographs have a poor sensitivity, as only in 30% of chronic pancreatitis calcification may be visible on a radiograph. The calcific plugs in the secondary ducts appear as calcific densities in the pancreatic parenchyma as the secondary ducts are not demonstrable on CT. Presence of ductal calculi in the main pancreatic duct is the most specific sign of chronic pancreatitis. The other findings are ductal dilatation and pancreatic glandular atrophy Chronic pancreatitis can have episodes of acute pancreatitis, complicating chronic pancreatitis due to ductal obstruction by calculi or pancreatic strictures.

28. IMAGING FINDINGS Parenchymal changes: In the initial stages of chronic pancreatitis as chronic inflammation and fibrosis sets in, there is loss of proteinaceous fluid in the pancreatic parenchyma. This results in reduction of normal T1-weighted hyperintense signal intensity of the pancreas. The normal pancreas enhances homogeneously in the late arterial phase and washes out in the venous phase. In chronic pancreatitis there is decreased heterogeneous enhancement in the arterial phase with delayed increased enhancement in the venous phase. The enhancement pattern in chronic pancreatitis is opposite of the enhancement pattern of normal pancreas. In late stage of chronic pancreatitis, there is pancreatic parenchymal atrophy.

29. Ductal changes: Pancreatic ductal abnormalities are the key findings, which help establish the diagnosis of chronic pancreatitis. In the early stages, there is dilatation and irregularity of the side branches. With progression, there is dilatation of the main pancreatic duct. The dilated main pancreatic duct may get complicated by strictures and intraductal calculi. Intraductal calculi may be seen as hypointense filling defects within the hyperintense fluid of the duct. There may be also multiple retention cysts of varying sizes.

30. CECT demonstrates dilated pancreatic duct with extensive calcific densities in pancreas. MRCP image demonstrates marked dilatation of pancreatic duct with prominent side branches, ductal calculi seen as filling defects in dilated main pancreatic duct.

31. Mass forming Pancreatitis vs Pancreatic adenocarcinoma

32. Imaging findings that favor diagnosis of a malignancy rather than an inflammatory condition : 1.Axial CT image shows diffuse calcifications in the background parenchyma and peripheral displacement of calcifications by a focal hypoattenuating lesion (dotted circle) in the pancreatic body. (2) MR cholangiopancreatogram shows dilatation of both the pancreatic duct (double arrows) and the common bile duct (single arrow). (d) Axial CT image shows the teardrop sign (arrows), a teardrop-shaped deformity of the SMV due to vascular encasement. (3) Axial CT image shows the SMA-to-SMV ratio.

33. Groove Pancreatitis This is an uncommon form of focal chronic pancreatitis affecting the pancreaticoduodenal groove, which is located between the head of the pancreas, duodenum and CBD. There are two forms, the pure form and the segmental form. In the pure form there is scar tissue between the duodenum and the head of the pancreas. In the segmental form there is scar tissue that involves the groove as well as pancreatic head. On imaging in the pure variety, a sheetlike tissue is seen between the duodenum and head of pancreas. S mall cysts representing pseudocysts may be seen along the duodenal wall. In the segmental form there is a sheet of tissue that is inseparable from the head of the pancreas that appears hypodense. There may be duodenal wall thickening and small pseudocysts. In addition, there may be pancreatic ductal dilation and consequently pancreatic atrophy.

34. Ill-defined inflammatory soft tissue between pancreas and duodenum representing groove pancreatitis. Hypodense soft tissue sheets in the pancreaticoduodenal groove, associated with inflammatory stranding within the surrounding fat

35. Tropical Pancreatitis This is a type of chronic pancreatitis seen in Asia, particularly India, predominantly in Kerala. Nearly two-thirds develop fibrocalcareous pancreatic diabetes in a decade after the onset of disease. The exact aetiology is unknown but considered to be due to protein malnutrition, cyanide toxicity, pancreatic duct anomalies and genetic mutations (SPINK1). On imaging the features are of a chronic pancreatitis. The pancreatic ductal calculi can measure unto 5 cm.

36. Autoimmune Pancreatitis This is a chronic fibroinflammatory process, part of IgG4 immunoglobulin systemic disease manifesting as sclerosing pancreatitis. AIP usually starts as a focal swelling progressing to a diffuse form. Consequently, there is diffuse pancreatic swelling with loss of normal parenchymal lobulations. The pancreas appears sausage shaped. With further progression in disease there is pancreatic tail retraction with the pancreatic tail not present. The margins of the pancreas are smooth. On MRI a capsule may be seen which is hypointense on T1/T2WIand shows delayed enhancement. In the focal variety, a mass lesion is seen usually in the body or tail, which is hypodense on CT, hypointense on T1 mildly hyperintense on T2WI and shows delayed enhancement. Sclerosing cholangitis is usually present in 88% of cases of AIP. This manifests as focal stenosis of the intrapancreatic CBD, with consequent upstream dilatation of CBD, less frequently multifocal intrahepatic biliary strictures.

37. Typical appearance of bulky pancreas with absence of tail of pancreas and abrupt rounding of pancreatic body. S ausage-shaped pancreas with decreased signal intensity on T1, and increased signal intensity on T2, mainly of the pancreatic head which shows areas of restricted diffusion.

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