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Acute pancreatitis
•Mild - No organ failure and
no local or systemic
complications.
•Moderate - Presence of
transient organ failure less
than 48h and/or presence of
local complications.
•Severe - Persistent organ
failure > 48 hour.
15-20% of cases
Morphologically, there are two types of acute pancreatitis:
1.Acute oedematous or interstitial pancreatitis.
2.Acute necrotizing pancreatitis.
•Usually the necrosis involves both the pancreas and the peripancreatic tissues.
•Less commonly only the peripancreatic tissues.
•Rarely only the pancreatic parenchyma.
• The role of imaging is manifold:
• to clarify the diagnosis when the clinical picture is confusing
• to assess severity (e.g. Balthazar score) and thus to determine
prognosis
• to detect complications
• to determine possible causes
• Plain radiograph
• Radiographs are insensitive for evidence of acute pancreatitis: many
patients have normal exams. Moreover, none of the signs is specific enough
to establish the diagnosis of pancreatitis.
• Abdominal radiographs may demonstrate:
• localized ileus of the small intestine (sentinel loop)
• spasm of the descending colon (colon cut-off sign)
• Chest radiographs may demonstrate:
• pleural effusion, usually left-sided
• hemidiaphragm elevation
• basal atelectasis
• pulmonary edema suggestive of acute respiratory distress syndrome
• Ultrasound
• The main role of ultrasound is:
• to identify gallstones as a possible cause
• diagnosis of vascular complications, e.g. thrombosis
• identify areas of necrosis that appear as hypoechoic regions
• assessment of clinically similar etiologies of an acute abdomen
• ultrasonographic features congruent with acute pancreatitis include:
• increased pancreatic volume with a marked decrease in echogenicity
• volume increase quantified as a pancreatic body exceeding 2.4 cm in
diameter, with marked anterior bowing and surface irregularity
• decreased echogenicity secondary to fluid exudation, which may result in a
marked heterogeneity of the parenchyma
• displacement of the adjacent transverse colon and/or stomach
secondary to pancreatic volume expansion
• Contrast-enhanced computed tomography shows
• diffuse or focal (20%— head or tail) enlargement of the pancreas with
mild heterogeneous contrast enhancement.
• " Non-enhancing areas are not seen in the parenchyma.
• The lobulated outline of pancreatic parenchyma may be lost.
• There is soft tissue stranding and hypodensity in the peripancreatic
fat with thickening of anterior pararenal and lateroconal fascia.
• There may be associated fluid collections (APFC), seen as ill-defined
homogeneous low density areas,
• ascites
• and pleural effusion, often left sided.
• The pancreatic duct is usually normal,
• unless acute inflammation occurs in the background of chronic calcific
pancreatitis
Acute necrotising pancreas
• Areas of non enhancement can be seen in pancreas and or surrounding peripancreatic
tissue
• There are 3 subtypes of necrotizing pancreatitis:
1.Necrosis of both pancreatic parenchyma and peripancreatic tissues (most common).
2.Necrosis of only extrapancreatic tissue without necrosis of pancreatic parenchyma (less
common).
3.Necrosis of pancreatic parenchyma without surrounding necrosis of peripancreatic tissue
(very rare).
• Necrosis of the pancreatic parenchyma can be diagnozed on a contrast-enhanced CT ⩾
72 hours.
•
Necrosis of peripancreatic tissue can be vary difficult to diagnose, but is suspected when
the collection is inhomogeneous, i.e. various densities on CT..
complications
Non vascular complications
• Collections
• Atlanta Classification of Fluid Collections
• The 2012 Revised Atlanta Classification discerns 4 types of peripancreatic fluid collections in acute
pancreatitis depending on the content, degree of encapsulation and time.
1. Content
1. Fluid only in acute peripancreatic fluid collection (APFC) and Pseudocyst.
2. Mixture of fluid and necrotic material in acute necrotic collection (ANC) and walled-off-necrosis (WON).
2. Degree of encapsulation
1. None or partial wall in APFC and ANC.
2. Complete encapsulation in pseudocyst and WON.
3. Time
1. Within 4 weeks: APFC and ANC
2. After 4 weeks: pseudocysts and WON. It takes about 4 weeks for a capsule to form.
Acute Peripancreatic Fluid Collection - APFC
• Intraabdominal fluid collections and collections of necrotic tissue are common in acute pancreatitis.
• These collections develop early in the course of acute pancreatitis.
In the early stage, such a collection does not have a wall or capsule.
Preferred locations of fluid collections are:
• Lesser sac
• Anterior and posterior pararenal space of the retroperitoneum.
• Transverse mesocolon
• Small bowel mesentery.
• These collections are the result of the release of activated pancreatic enzymes which also cause necrosis of
the surrounding tissues.
This explains why many of these collections harbor solid necrotic debris.
• About 50% of these collections show spontaneous regression (figure).
The remaining 50% either remain stable or increase and undergo organization and demarcation with
liquefaction.
They may remain sterile or develop infection.
Pseudocyst
• A Pseudocyst is a collection of pancreatic juice or fluid enclosed by a
complete wall of fibrous tissue
It occurs in interstitial pancreatitis and the absence of necrotic tissue
is imperative for its diagnosis.
• Communication with the pancreatic duct may be present.
A pseudocyst requires 4 or more weeks to develop.
• The differential diagnosis includes walled-off necrosis and sometimes
a pseudoaneurysm or even a cystic tumor.
Most often, they occur in the lesser sac.
• Walled-off Necrosis - WON
• Based on CT alone it is sometimes impossible to determine whether a
collection contains fluid only or a mixture of fluid and necrotic tissue.
•
Consequently it is sometimes better to describe these as
'indeterminate peripancreatic collections'.
Infected necrosis
• Infected necrosis is:
• Infection of necrotic pancreatic parenchyma or extrapancreatic fatty
tissue - i.e. infected ANC or infected WON, depending on degree of
encapsulation.
• Usually occurs in the 2nd-4th week and rarely in the first week.
• Most severe local complication of acute necrotizing pancreatitis.
• Most common cause of death in patients with acute pancreatitis.
• Diagnose infected necrosis when there are gas bubbles on CT (seen in
40%) or when FNA is positive for bacteria.
• .Bowel ischemia and necrosis are a rare but serious complications of acute
pancreatitis.
• They are seen typically in patients of ANP due to extension of
inflammation along the mesentery to involve the vessels in the mesentery
and walls of the bowel.
• Transverse colon and splenic flexure are the most common sites.
• The involved bowel segment shows circumferential wall thickening with
maintained stratification on CECT scan.
• As the inflammation progresses, bowel necrosis and perforation may occur
which is seen as pneumoperitoneum and extraluminal leak of oral contrast
on CECT scan.
• Other complications include bowel obstruction and ileus.
• Pancreatic fistula is a complication which develops as a result of
necrosis of pancreatic ductal walls.
• This results in leak of pancreatic secretions causing persistence of
collections.
• Such collections have high amylase levels on sampling
• .Management involves endoscopic stenting or surgery.
• Other abdominal complications include cholecystitis, pancreatic duct
strictures and splenic infarcts.
• Extra-abdominal complications are also seen, most common being
pleural effusion.
Vascular complications
• Vascular complications may involve arterial or venous structures.
• Involvement of arteries may result in arteritis and erosion of the
arterial wall by pancreatic enzymes
• which may lead to formation of pseudoaneurysms, rupture and
thrombosis.
• Arterial hemorrhage and pseudoaneurysms are seen in up to 5% of
patients with acute pancreatitis and are usually solitary.
• It most commonly involves the splenic artery (60-65%; Fig. 21.15A),
followed by the gastroduodenal artery (20-25%; Figs 21.15B and C)
• Other arteries involved include
• left gastric,
• hepatic,
• inferior pancreaticoduodenal
• and gastroepiploic arteries.
From distal splenic artery
Pseudoaneurysm in the region of
head of pancreas, arising from
gastro duodenal artery
• CT angiography (from dome of diaphragm to iliac crest) should be
done in all cases where there is gastrointestinal bleed, hypotension or
drop in hemoglobin.
• On imaging, plain CT scan may be done to show hemorrhage (high
density area) in the collection or in the adjoining bowel loops.
• The angiography images show a variable-sized smooth or irregular
contrast filled out pouching from an artery or its branch.
• Pseudoaneurysms with a very narrow neck may not opacify in the
arterial phase, and may fill in the venous phase.
• Hence, both arterial and venous phases are needed in the evaluation
of hemorrhage in patients of acute pancreatitis.
• Venous complications most commonly include
• thrombosis of splenic vein, portal vein and superior mesenteric vein
which may result in formation of perigastric and splenic hilar
collateral venous channels and portal hypertenson.
Radiology of pancreatitis. Acute and chronic
Radiology of pancreatitis. Acute and chronic

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Radiology of pancreatitis. Acute and chronic

  • 2. •Mild - No organ failure and no local or systemic complications. •Moderate - Presence of transient organ failure less than 48h and/or presence of local complications. •Severe - Persistent organ failure > 48 hour. 15-20% of cases
  • 3. Morphologically, there are two types of acute pancreatitis: 1.Acute oedematous or interstitial pancreatitis. 2.Acute necrotizing pancreatitis. •Usually the necrosis involves both the pancreas and the peripancreatic tissues. •Less commonly only the peripancreatic tissues. •Rarely only the pancreatic parenchyma.
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  • 6. • The role of imaging is manifold: • to clarify the diagnosis when the clinical picture is confusing • to assess severity (e.g. Balthazar score) and thus to determine prognosis • to detect complications • to determine possible causes
  • 7. • Plain radiograph • Radiographs are insensitive for evidence of acute pancreatitis: many patients have normal exams. Moreover, none of the signs is specific enough to establish the diagnosis of pancreatitis. • Abdominal radiographs may demonstrate: • localized ileus of the small intestine (sentinel loop) • spasm of the descending colon (colon cut-off sign) • Chest radiographs may demonstrate: • pleural effusion, usually left-sided • hemidiaphragm elevation • basal atelectasis • pulmonary edema suggestive of acute respiratory distress syndrome
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  • 9. • Ultrasound • The main role of ultrasound is: • to identify gallstones as a possible cause • diagnosis of vascular complications, e.g. thrombosis • identify areas of necrosis that appear as hypoechoic regions • assessment of clinically similar etiologies of an acute abdomen
  • 10. • ultrasonographic features congruent with acute pancreatitis include: • increased pancreatic volume with a marked decrease in echogenicity • volume increase quantified as a pancreatic body exceeding 2.4 cm in diameter, with marked anterior bowing and surface irregularity • decreased echogenicity secondary to fluid exudation, which may result in a marked heterogeneity of the parenchyma • displacement of the adjacent transverse colon and/or stomach secondary to pancreatic volume expansion
  • 11. • Contrast-enhanced computed tomography shows • diffuse or focal (20%— head or tail) enlargement of the pancreas with mild heterogeneous contrast enhancement. • " Non-enhancing areas are not seen in the parenchyma. • The lobulated outline of pancreatic parenchyma may be lost. • There is soft tissue stranding and hypodensity in the peripancreatic fat with thickening of anterior pararenal and lateroconal fascia.
  • 12. • There may be associated fluid collections (APFC), seen as ill-defined homogeneous low density areas, • ascites • and pleural effusion, often left sided. • The pancreatic duct is usually normal, • unless acute inflammation occurs in the background of chronic calcific pancreatitis
  • 13. Acute necrotising pancreas • Areas of non enhancement can be seen in pancreas and or surrounding peripancreatic tissue • There are 3 subtypes of necrotizing pancreatitis: 1.Necrosis of both pancreatic parenchyma and peripancreatic tissues (most common). 2.Necrosis of only extrapancreatic tissue without necrosis of pancreatic parenchyma (less common). 3.Necrosis of pancreatic parenchyma without surrounding necrosis of peripancreatic tissue (very rare). • Necrosis of the pancreatic parenchyma can be diagnozed on a contrast-enhanced CT ⩾ 72 hours. • Necrosis of peripancreatic tissue can be vary difficult to diagnose, but is suspected when the collection is inhomogeneous, i.e. various densities on CT..
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  • 20. Non vascular complications • Collections • Atlanta Classification of Fluid Collections • The 2012 Revised Atlanta Classification discerns 4 types of peripancreatic fluid collections in acute pancreatitis depending on the content, degree of encapsulation and time. 1. Content 1. Fluid only in acute peripancreatic fluid collection (APFC) and Pseudocyst. 2. Mixture of fluid and necrotic material in acute necrotic collection (ANC) and walled-off-necrosis (WON). 2. Degree of encapsulation 1. None or partial wall in APFC and ANC. 2. Complete encapsulation in pseudocyst and WON. 3. Time 1. Within 4 weeks: APFC and ANC 2. After 4 weeks: pseudocysts and WON. It takes about 4 weeks for a capsule to form.
  • 21. Acute Peripancreatic Fluid Collection - APFC • Intraabdominal fluid collections and collections of necrotic tissue are common in acute pancreatitis. • These collections develop early in the course of acute pancreatitis. In the early stage, such a collection does not have a wall or capsule. Preferred locations of fluid collections are: • Lesser sac • Anterior and posterior pararenal space of the retroperitoneum. • Transverse mesocolon • Small bowel mesentery. • These collections are the result of the release of activated pancreatic enzymes which also cause necrosis of the surrounding tissues. This explains why many of these collections harbor solid necrotic debris. • About 50% of these collections show spontaneous regression (figure). The remaining 50% either remain stable or increase and undergo organization and demarcation with liquefaction. They may remain sterile or develop infection.
  • 22. Pseudocyst • A Pseudocyst is a collection of pancreatic juice or fluid enclosed by a complete wall of fibrous tissue It occurs in interstitial pancreatitis and the absence of necrotic tissue is imperative for its diagnosis. • Communication with the pancreatic duct may be present. A pseudocyst requires 4 or more weeks to develop. • The differential diagnosis includes walled-off necrosis and sometimes a pseudoaneurysm or even a cystic tumor. Most often, they occur in the lesser sac.
  • 23. • Walled-off Necrosis - WON • Based on CT alone it is sometimes impossible to determine whether a collection contains fluid only or a mixture of fluid and necrotic tissue. • Consequently it is sometimes better to describe these as 'indeterminate peripancreatic collections'.
  • 24. Infected necrosis • Infected necrosis is: • Infection of necrotic pancreatic parenchyma or extrapancreatic fatty tissue - i.e. infected ANC or infected WON, depending on degree of encapsulation. • Usually occurs in the 2nd-4th week and rarely in the first week. • Most severe local complication of acute necrotizing pancreatitis. • Most common cause of death in patients with acute pancreatitis. • Diagnose infected necrosis when there are gas bubbles on CT (seen in 40%) or when FNA is positive for bacteria.
  • 25. • .Bowel ischemia and necrosis are a rare but serious complications of acute pancreatitis. • They are seen typically in patients of ANP due to extension of inflammation along the mesentery to involve the vessels in the mesentery and walls of the bowel. • Transverse colon and splenic flexure are the most common sites. • The involved bowel segment shows circumferential wall thickening with maintained stratification on CECT scan. • As the inflammation progresses, bowel necrosis and perforation may occur which is seen as pneumoperitoneum and extraluminal leak of oral contrast on CECT scan.
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  • 27. • Other complications include bowel obstruction and ileus. • Pancreatic fistula is a complication which develops as a result of necrosis of pancreatic ductal walls. • This results in leak of pancreatic secretions causing persistence of collections. • Such collections have high amylase levels on sampling • .Management involves endoscopic stenting or surgery.
  • 28. • Other abdominal complications include cholecystitis, pancreatic duct strictures and splenic infarcts. • Extra-abdominal complications are also seen, most common being pleural effusion.
  • 29. Vascular complications • Vascular complications may involve arterial or venous structures. • Involvement of arteries may result in arteritis and erosion of the arterial wall by pancreatic enzymes • which may lead to formation of pseudoaneurysms, rupture and thrombosis.
  • 30. • Arterial hemorrhage and pseudoaneurysms are seen in up to 5% of patients with acute pancreatitis and are usually solitary. • It most commonly involves the splenic artery (60-65%; Fig. 21.15A), followed by the gastroduodenal artery (20-25%; Figs 21.15B and C) • Other arteries involved include • left gastric, • hepatic, • inferior pancreaticoduodenal • and gastroepiploic arteries.
  • 31. From distal splenic artery Pseudoaneurysm in the region of head of pancreas, arising from gastro duodenal artery
  • 32. • CT angiography (from dome of diaphragm to iliac crest) should be done in all cases where there is gastrointestinal bleed, hypotension or drop in hemoglobin. • On imaging, plain CT scan may be done to show hemorrhage (high density area) in the collection or in the adjoining bowel loops. • The angiography images show a variable-sized smooth or irregular contrast filled out pouching from an artery or its branch.
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  • 34. • Pseudoaneurysms with a very narrow neck may not opacify in the arterial phase, and may fill in the venous phase. • Hence, both arterial and venous phases are needed in the evaluation of hemorrhage in patients of acute pancreatitis.
  • 35. • Venous complications most commonly include • thrombosis of splenic vein, portal vein and superior mesenteric vein which may result in formation of perigastric and splenic hilar collateral venous channels and portal hypertenson.