1. RMH Grand Rounds Pancreatitis
Dr. Stuart Cocquyt
February 9, 2018

2. No Disclosures

3. RMH Grand Rounds Pancreatitis
Dr. Stuart Cocquyt
February 9, 2018

4. RMH Grand Rounds Pancreatitis
Dr. Stuart Cocquyt
February 9, 2018

5. RMH Grand Rounds Pancreatitis Imaging of Acute pancreatitis
Dr. Stuart Cocquyt
February 9, 2018

6. RMH Grand Rounds Pancreatitis Imaging of Acute pancreatitis*
Dr. Stuart Cocquyt
February 9, 2018

7. RMH Grand Rounds Pancreatitis Imaging of Acute pancreatitis*
Dr. Stuart Cocquyt
February 9, 2018
*For The Clinician

8. Focus on describing the main imaging features of acute pancreatitis (AP) in the context of one of the more popular clinical and imaging classification systems:

9. Focus on describing the main imaging features of acute pancreatitis (AP) in the context of one of the more popular clinical and imaging classification systems:
Atlanta Classification of Acute Pancreatitis (2012)

10. The Atlanta Classification was partly developed for use by radiologists to describe the findings and severity of AP in a standardized way
Provides a common language for imaging findings which have important implications for guiding treatment of the patient with AP

11. The Atlanta Classification was partly developed for use by radiologists to describe the findings and severity of AP in a standardized way
Provides a common language for imaging findings which have important implications for guiding treatment of the patient with AP
Non-radiologist clinicians also need to have at least a basic understanding of the imaging criteria as well
Since treatment of AP is usually multi-disciplinary, most clinicians who order a CT scan for their patient with AP should be able to read and have the same level of understanding of the radiologist’s report

12. Objectives

13. Objectives
1. Review of basic anatomy of the pancreas and retroperitoneum

14. Objectives
1. Review of basic anatomy of the pancreas and retroperitoneum
2. Review epidemiology, pathogenesis and clinical features of AP

15. Objectives
1. Review of basic anatomy of the pancreas and retroperitoneum
2. Review epidemiology, pathogenesis and clinical features of AP
3. Present the Atlanta Classification System of AP focusing on the imaging criteria

16. Learning Objectives
1. Be able to describe the basic imaging findings in AP
2. Have a better understanding of the role of DI in diagnosis and management of AP
3. Be able to choose the best imaging test for the patient with AP
(Hint: Not every patient admitted with AP needs a CT!)

17. Anatomy of the Pancreas and Retroperitoneum

18. Pancreas is a 12-15 cm long RP digestive organ lying posterior to the stomach at about the L2 level
Both an exocrine gland secreting pancreatic juices which enter the duodenum via the pancreatic duct;
And endocrine gland secreting hormones like insulin and glucagon

19. Head: within the curve of the proximal duodenum; adjacent to or contains the CBD
Neck: lies anterior to the PV confluence
Body: forms part of the bed of the stomach and attachment for transverse mesocolon
Tail: usually contacts the hilum of the spleen

20. CT Imaging of the Pancreas
CT is the recommended first line modality because it is available and convenient/fast for all patients, including very ill
CT is performed with IV contrast (Omnipaque), if possible, to improve contrast resolution of all the tissues
Pancreatic CT protocol goes even one step by including an “early phase” of enhancement
Performed at 40 seconds
Improves contrast resolution specifically of the pancreatic parenchyma which is useful for small, subtle lesions like early adenocarcinoma

21. A full pancreatic CT protocol has 3 separate series of scans or phases:
Non-contrast phase
Highlights calcifications (gallstones, choledocholithiasis, pancreatic) & provides a “standard” with which to assess pancreatic parenchymal enhancement
Early enhancement phase
Optimized for pancreatic parenchyma
Portal venous phase
Performed 70 sec post IV contrast injection
“Standard” phase for most organ/viscera

22. The key to understanding CT imaging of the pancreas and AP is recognizing it is a RP organ
This is important because it determines the location and spread of inflammation in AP
Inflammation generally obeys the fascial planes, unless they are overwhelmed

26. Epidemiology, Pathogenesis and Clinical Presentation

27. Epidemiology, Pathogenesis and Clinical Presentation
Clinically and pathologically, pancreatitis occurs as a spectrum, mainly in duration and severity

28. Epidemiology, Pathogenesis and Clinical Presentation
Clinically and pathologically, pancreatitis occurs as a spectrum, mainly in duration and severity
Acute Pancreatitis: acute onset of abdominal pain resulting from enzymatic necrosis and inflammation of the pancreas
Chronic Pancreatitis: continuous or relapsing inflammation of the pancreas, typically causing pain, and leading to irreversible damage and impairment in function

29. Acute Pancreatitis
Relatively common disorder with incidence rate 5-35 per 100,000 (Western)
Leading GI cause of hospitalization in the US
Rising incidence in Europe and Scandinavia due to incr. alcohol consumption and more accurate diagnosis

30. AP Causes

31. AP Causes
1. Gallstones 40%

32. AP Causes
1. Gallstones 40%
2. Alcoholism 30%

33. AP Causes
1. Gallstones 40%
2. Alcoholism 30%
3. Multiple “other” 25%
Mechanical: pancreatic and periampullary tumours
Metabolic: hypertriglyceridemia, hyperCa2+
Infectious: mumps; CMV; HSV
Post-ERCP: 3-25% risk depending on type of ERCP

34. AP Causes
1. Gallstones 40%
2. Alcoholism 30%
3. Multiple “other” 25%
Mechanical: pancreatic and periampullary tumours
Metabolic: hypertriglyceridemia, hyperCa2+
Infectious: mumps; CMV; HSV
Post-ERCP: 3-25% risk depending on type of ERCP
4. Idiopathic 15%
No cause identified after exhaustive investigations

35. Pathogenesis

36. Pathogenesis
Not completely understood

38. The damage from autodigestion from activated enzymes ranges
Mild acute pancreatitis limited to interstitial edema
Severe acute necrotizing pancreatitis with actual parenchymal necrosis +/- hemorrhage in the pancreas from vascular damage

39. The damage from autodigestion from activated enzymes ranges
Mild acute pancreatitis limited to interstitial edema
Severe acute necrotizing pancreatitis with actual parenchymal necrosis +/- hemorrhage in the pancreas from vascular damage
Hospitalized mortality 10%
Up to 30% with severe necrotizing pancreatitis

40. AP Diagnosis

41. AP Diagnosis
1. History & Physical Exam

42. AP Diagnosis
1. History & Physical Exam
Abdominal pain: epigastric, constant and radiating to the back

43. AP Diagnosis
1. History & Physical Exam
Abdominal pain: epigastric, constant and radiating to the back
N/V; inflammatory fever; abdominal distension from ileus

44. AP Diagnosis
1. History & Physical Exam
Abdominal pain: epigastric, constant and radiating to the back
N/V; inflammatory fever; abdominal distension from ileus
Often non-specific!
Clinician may initially consider other DDx for acute abdomen: biliary colic, cholecystitis, cholangitis, perforated PUD, hepatitis, SBO, mesenteric ischemia

45. 2. Laboratory tests

46. 2. Laboratory tests
(Again, are generally non-specific..)
Leukocytosis
Anemia (if hemorrhage)
Hypocalcemia (ppt. of Ca2+ salts)
Hyperglycemia/Glycosuria

47. 2. Laboratory tests
(Again, are generally non-specific..)
Leukocytosis
Anemia (if hemorrhage)
Hypocalcemia (ppt. of Ca2+ salts)
Hyperglycemia/Glycosuria
LIPASE more specific

48. 3. Diagnostic Imaging:
May initially be performed before or after a diagnosis of AP is suspected

49. 3. Diagnostic Imaging:
May initially be performed before or after a diagnosis of AP is suspected
Before suspected:
If the presentation is non-specific, and/or the clinician suspects another problem for which imaging is requested

50. 3. Diagnostic Imaging:
May initially be performed before or after a diagnosis of AP is suspected
Before suspected:
If the presentation is non-specific, and/or the clinician suspects another problem for which imaging is requested
After suspected:
Current guidelines require at least 2 of the following 3 conditions be met for diagnosis of AP:
Characteristic pain
Lipase/Amylase elevated >3X upper normal
Characteristic imaging findings (usually CT > MRI or US)

51. 3. Diagnostic Imaging:
Therefore, it is completely appropriate to order a CT to confirm AP diagnosis, if a patient is suspected of having AP but does not fulfill the first 2 criteria (as can be the case with late presentation and elevated lipase but which does not reach threshold 3X value)

52. 3. Diagnostic Imaging:
After AP is diagnosed (whether requiring initial imaging or not), the role of DI becomes more selective and falls into 2 main categories:

53. 3. Diagnostic Imaging:
After AP is diagnosed (whether requiring initial imaging or not), the role of DI becomes more selective and falls into 2 main categories:
1. Determining the cause of AP

54. 3. Diagnostic Imaging:
After AP is diagnosed (whether requiring initial imaging or not), the role of DI becomes more selective and falls into 2 main categories:
1. Determining the cause of AP
2. Guiding management

55. Determining the cause of AP:

56. Determining the cause of AP:
Full discussion beyond the scope of this talk
In general, straightforward because there are only two main conditions which cause the majority of AP: gallstones and alcoholism

57. Therefore, ultrasound to assess for gallstones and/or choledocholithiasis is universally recommended for any patient’s first AP presentation
In an older patient (>40 years) or any atypical signs/symptoms (eg. weight loss with AP) CT may be considered to look for uncommon causes (eg.cancer)
Other modalities such as MRI, EUS and ERCP all have roles to play in investigating patients who may have uncommon causes of AP

58. Guiding management:

59. Guiding management:
Encompassed by the Atlanta Classification System for AP

60. Guiding management:
Encompassed by the Atlanta Classification System for AP
First published online Oct 2012 in journal Gut

61. A classification system of AP using clinical and cross-sectional imaging features (mainly CT)
Developed from several rounds of consensus consultation of pancreatologists world- wide which commenced in 2007
Update to the original 1992 Atlanta Classification of AP

62. Update was required to address:
short comings in the original system which included somewhat confusing descriptions of pancreatic and peri-pancreatic fluid collections
Incorporate new knowledge about the etiology and PP of the disease
Advances in imaging

63. It provides a consistent classification scheme including imaging terminology which is applicable world-wide:

64. It provides a consistent classification scheme including imaging terminology which is applicable world-wide:
Improves and standardizes clinicial assessment of severity of AP
Standardizes reporting of data (which)
Facilitates communication among treating physicians
Assists in the objective evaluation of treatments (current & new)

67. IEP

68. IEP
90-95% of AP
Represents non-necrotizing inflammation

69. IEP
90-95% of AP
Represents non-necrotizing inflammation
CT:
Focal or diffuse pancreatic enlargement
Wispy peripancreatic stranding or small fluid
No necrosis of either pancreas or peripancreatic tissues (which we know by comparing non-contrast and post IV enhanced images)

70. IEP in 28 yr man with alcohol-related AP
Wispy peripancreatic inflammation with normal pancreatic enhancement and no fluid collections

71. IEP

72. IEP
If fluid collection develops in first 4 weeks of IEP it is termed an Acute Peripancreatic Fluid Collection or APFC
Again, there is no necrosis CT
Homogeneous fluid collection, without a wall, that conforms to RP spaces

73. IEP with APFC in 49 yr man
One day after pain onset APFC seen as small, homogeneous fluid collection in L anterior pararenal space
Note normal enhancement of pancreas = no necrosis

74. IEP with APFC in 49 yr man
10 days later, multiple homogeneous APFCs (*) have increased in the lesser sac region

75. IEP with APFC in 49 yr man
10 days later, multiple homogeneous APFCs (*) have increased in the lesser sac region
Note again normal enhancing pancreas indicating IEP, not necrotizing pancreatitis

76. IEP

77. IEP
Most APFC resolve in 4 weeks; if it persists beyond 4 weeks it is termed a pseudocyst CT
By definition, still no necrosis, so pseudocysts still homogeneous fluid density collections
Because they are persistent, they are more organized and therefore show an enhancing, inflammatory wall

78. Pseudocyst in 36 yr man 6 weeks after onset gallstone IEP
Large homogeneous fluid collection (*) in the lesser sac
Timing since AP onset and thick wall characterize this finding as a pseudocyst, not APFC

80. Necrotizing Pancreatitis
5-10% of AP cases

81. Necrotizing Pancreatitis
Subdivided based on location of the necrosis:

82. Necrotizing Pancreatitis
Subdivided based on location of the necrosis:
Parenchymal necrosis only - 5%

83. Necrotizing Pancreatitis
Subdivided based on location of the necrosis:
Parenchymal necrosis only - 5%
Peripancreatic necrosis only – 20%

84. Necrotizing Pancreatitis
Subdivided based on location of the necrosis:
Parenchymal necrosis only - 5%
Peripancreatic necrosis only – 20%
Pancreatic and PP necrosis – 75%

85. Necrotizing Pancreatitis
Subdivided based on location of the necrosis:
Parenchymal necrosis only - 5%
Peripancreatic necrosis only – 20%
Pancreatic and PP necrosis – 75% CT
Pancreas: non-enhancing parenchyma
PP: heterogeneous density (not just fluid)
Soft tissue
Fat

86. Necrotizing Pancreatitis
There is an equivalent term for necrotizing pancreatitis in the first 4 weeks = Acute Necrotic Collection (ANC)

87. Necrotizing Pancreatitis
There is an equivalent term for necrotizing pancreatitis in the first 4 weeks = Acute Necrotic Collection (ANC)
Refers to any location of necrosis
If affects PP tissues can extend into the pelvis (hence why important to image the pelvis in AP patients)

88. Necrotizing pancreatitis in 58 yr woman
Notice the non-enhancing parenchyma (*) categorizing this as NP
Fluid extends into the PP tissues of the lesser sac , forming an ANC (not APFC)
As it involves pancreas AND PP tissues this is the combined type NP (most common)

89. NP in 18 yr man
Pancreatic paranchyma enhances normally (*), but there is large PP fluid collection
Not APFC because the collection is NOT homogeneous fluid density
Therefore this is NP or ANC affecting the PP tissues only

90. Necrotizing Pancreatitis

91. Necrotizing Pancreatitis
If a fluid collection in the setting of NP persists longer than 4 weeks, it is no longer an ANC but Walled Off Necrosis (WON)

92. Necrotizing Pancreatitis
If a fluid collection in the setting of NP persists longer than 4 weeks, it is no longer an ANC but Walled Off Necrosis (WON) CT
Similar to a pseudocyst, this is a mature collection, so see enhancing, thick wall
Unlike pseudocysts, WONs contain necrotic tissue, so appear heterogeneous

93. - NP in 48 yr woman at week 1 with necrotic pancreatic neck (*)

94. By week 5 the necrotic collection (
By week 5 the necrotic collection (*) has enlarged and now has an enhancing wall = WON
Notice the bit of heterogeneous tissue, indicating this is a WON and not pseudocyst

95. By week 7 a cystograstrostomy has been performed for drainage of the WON, by placement of stents endoscopically

97. Older, less specific terms such as “pancreatic abscess” and “acute pseudocyst” are discouraged

98. Older, less specific terms such as “pancreatic abscess” and “acute pseudocyst” are discouraged
Other findings which should specifically looked for and commented if present:

99. Older, less specific terms such as “pancreatic abscess” and “acute pseudocyst” are discouraged
Other findings which should specifically be looked for and commented if present:
1. INFECTION
Can complicate ANY fluid collection (APFC or ANC), but most common in NP
Rare in the first week and not correlated with extent of necrosis
Only reliable imaging finding is gas in a collection (alternatively FNA)
Infected necrosis associated higher mortality, especially if organ failure also present (up to 50%)

100. 37 yr woman previously diagnosed NP who experienced decompensation at week 6 and was readmitted to hospital
Multiple foci of gas in thick walled collection indicating an infected WON
Note absence of enhancing tail parenchyma confirming NP

101. 2. Vascular:
Up to 25% of AP and can cause significiant M&M
SV thrombosis or development of pseudoaneurysm (splenic > gastroduodenal and pancreaticoduodenal)

102. Implications of Atlanta Classification for Guiding Management:

103. Implications of Atlanta Classification for Guiding Management:
1. Most AP patients do not require CT imaging

104. Implications of Atlanta Classification for Guiding Management
1. Most AP patients do not require CT imaging
Most common form of AP is IEP without necrosis or fluid collections (90-95%)
Generally do well with supportive measures and make a complete recovery in 1-2 weeks
CT may be employed to make the initial diagnosis of AP, but no routine follow-up CT is usually required

105. 2. Conversely, CT imaging is completely appropriate when more severe form of AP is suspected clinically (anything other than IEP)

106. 2. Conversely, CT imaging is completely appropriate when more severe form of AP is suspected clinically (anything other than IEP)
Increased pain, fever, lipase, WBC, poor nutrition
Anything that suggests sepsis or organ failure

107. 2. Conversely, CT imaging is completely appropriate when more severe form of AP is suspected clinically (anything other than IEP)
Increased pain, fever, lipase, WBC, poor nutrition
Anything that suggests sepsis or organ failure
Caveat: CT may not be as accurate for early necrosis in the first week, therefore it is also appropriate to order a second CT in 5-7 days to reassess

108. 3. Nature of the local complication (NP or any fluid collection) on imaging can have a direct impact on the patient’s treatment plan (in combination with clinical status)
Full discussion beyond the scope of this talk
At most basic level can alter the management from the usual supportive measures to some form of intervention
FNA of a collection to determine infection
Percutaneous drainage of a symptomatic or infected collection
Open surgical necrosectomy

109. How can the clinician assist the rad interpretation of AP imaging studies?

110. How can the clinician assist the rad interpretation of AP imaging studies?
Timing of onset of symptoms (eg. < 1 week, > 4 weeks)
Affects accuracy of CT and description of fluid collections
Any concerns for sepsis or infection

111. Examples of useful histories for CT:

112. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”

113. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”
“Abdo pain onset 1 week ago - ?pancreatitis”

114. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”
“Abdo pain onset 1 week ago - ?pancreatitis”
“Pancreatitis”

115. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”
“Abdo pain onset 1 week ago - ?pancreatitis”
“Pancreatitis”
NOT appropriate history!

116. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”
“Abdo pain onset 1 week ago - ?pancreatitis”
“Pancreatitis”
NOT appropriate history!
Tells radiologist nothing about time course or clinical status, let alone whether the point of the CT is to diagnose AP or more worried about a complication

117. Examples of useful histories for CT:
“Pancreatitis onset 5 days ago, not improving”
“Pancreatitis onset 2 days ago, increasing pain/fever/WBC/not eating”
“Abdo pain onset 1 week ago - ?pancreatitis”
“Pancreatitis”
NOT appropriate history!
Tells radiologist nothing about time course or clinical status, let alone whether the point of the CT is to diagnose AP or more worried about a complication
Do not be surprised if the req. is returned for “more history pls.”!

118. Learning Objectives

119. Learning Objectives
1. Be able to describe the basic imaging findings in AP

120. Learning Objectives
1. Be able to describe the basic imaging findings in AP
Changes related to IEP or non-enhancement in NP
+/- fluid collections

121. Learning Objectives
1. Be able to describe the basic imaging findings in AP
Changes related to IEP or non-enhancement in NP
+/- fluid collections
2. Have a better understanding of the role of DI in diagnosis and management of AP

122. Learning Objectives
1. Be able to describe the basic imaging findings in AP
Changes related to IEP or non-enhancement in NP
+/- fluid collections
2. Have a better understanding of the role of DI in diagnosis and management of AP
Diagnosis: CT may be required to diagnose if clinical diagnostic criteria not met
Management: via the Atlanta Classification of AP combining imaging and clinical criteria to standardize the description of AP and its severity

123. 3. Be able to choose the best imaging test for the patient with AP

124. 3. Be able to choose the best imaging test for the patient with AP
Diagnosis: CT (if required)
Etiology of AP: US
+/- CT if unusual presentation features (eg. weight loss, jaundice, etc.)
Ongoing management: CT (if required) (because you’re worried about..)
Local complications (APFC or ANC +/- infection)
CT not as accurate in first week, so follow-up CT may be necessary

125. THANK-YOU!

126. BIBLIOGRAPHY
Banks, P. “Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus.” Gut 62 October 2012:
Cotran, R. Robbins Pathologic Basis of Disease - 6th Edition. Philadelphia: W. B. Saunders Company, 1999.
Foster, B. “Revised Atlanta Classification for Acute Pancreatitis: A Pictorial Essay.” Radiographics :
Santhi, S. “Etiology of acute pancreatitis.” UpToDate. Ed. David C Whitcomb. August February
Theoni, R. “The Revised Atlanta Classification of Acute Pancreatitis: Its Importance for the Radiologist and Its Effect on Treatment.” Radiology 262 March 2012:

128. (So, how is this Atlanta classification used to describe AP imaging findings and assess severity?
This table, in nutshell, summarizes the terms that should be used in describing the most important imaging findings
It recognizes two main subcategories of AP depending on whether or not necrosis is present. If no necrosis is present the AP is referred to as interstitial edematous pancreatitis or IEP. If any necrosis is present the term necrotizing pancreatitis or equivalently Acute Necrotic Collection, or ANC, should be used
Besides necrosis, the next most important criteria to consider is whether or not there are any fluid collections present. What a fluid collection is called is determined by whether there’s any necrosis AND by timing of onset of the AP. The timing of onset is usually defined as the time of onset of abdominal pain
We’ll now take a closer look at each subcategory and fluid collections including a brief overview of the imaging appearances)