Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.

1. REFERENCES : RUMACK, RADIOPEDIA,
RADIOLOGY ASSISTANT.
BY : DR. JUHI PATEL
1st Year Resident Doctor

2.  ANATOMY.
 NORMAL APPEARANCE OF PANCREAS ON
ULTRASOUND.
 ACUTE PANCREATITS.
 CHRONIC PANCREATITIS.
 DIFFENETIAL DIAGNOSIS.

7. Patient position :
• Supine .
• Left lateral decubitus position.
Vascular landmarks are :
• Inferior vena cava (IVC) dorsally.
• SMA and SMV medially.
• GDA and pancreaticoduodenal arcade
anterolaterally.

9. Uncinate process :
Is a portion of the caudal pancreatic head
that wraps behind the SMA and SMV, ending
in a point oriented medially.
The uncinate process is medial and dorsal to
the SMA and SMV.

10.  Patient position :
• Supine.
• Left lateral decubitus.
• After water intake (sometimes combined with sitting
position).
 Body lies ventral to following vascular
landmarks :
• Splenic vein
• Its confuence with SMV
• SMA

11. A
SMA
SV
UNCINATE PROCESS
BODY

12. Patient position:
• After water intake ask the patient to lie in right
anterior oblique position.
• Right lateral decubitus position (coronal imaging
through spleen and left kidney).
Colour doppler reveals splenic artery and
vein which facilitates identification of tail.

14.  Echogenicity : is compared to liver.
• Iso or hyperechoic to liver.
• Echogenicity increases with age.
 Texture :
• Homogenous to lobular .
 Size :
• Head : 6 to 28 mm.
• Body : 4 to 23 mm.
• Tail : 5 to 28 mm.
 Pancreatic duct diameter:
• Head : 3 mm.
• Body : 2.1 mm.
• Tail : 1.6 mm.
22 mm (mean plus 3 standard
deviations)

15. ACUTE PANCREATITIS

16.  Gall stones : 40 %
 Alchoholism : 40 %
 Idiopathic : 10%
 Other : 10%
• injury (trauma).
• Hereditary.
• high fat levels in the blood.
• Surgery.

17.  Blockage of the pancreatic duct leads to increased
pressure in pancreatic duct and rupture.
 Pancreatic fluid (proteolytic and lipolytic enzymes)
ruptures into pancreas parenchyma and potential spaces.

18. Targets of Inflammatory spread
in Acute Pancreatitis
 1= spread into the
lesser sac
 2 = spread into the
transverse mesocolon
 3 = spread into the root
of the bowel mesentery
 4 = extension into the
duodenum
 5= inferior spread into
the remainder anterior
pararenal space
Gore and Levine, Textbook of Gastrointestinal Radiology

19. CLINICAL FEATURES:
History
 Acute-onset of severe
abdominal pain
 Typically epigastric pain,
radiating to back,
occasionally RUQ or LUQ
 Nausea, vomiting

21. Look for the changes in pancreas.
Look for secondary peripancreatic
changes.
Try to find out cause of acute pancreatitis
• Gall bladder and bile duct stones.
• Biliary sludge.

22.  In Pancreas look for :
1. Echogenicity :
May be normal.
Focal areas of hypo / hyperechogeicity and
inhomogenicity may occur.
2. Size of pancreas : 22 mm (mean plus 3 standard
deviations)
DECREASES INTERSTITIAL EDEDMA
INCREASES HEMORRHAGE, NECROSIS,
FAT SAPONIFICATION

25. Look for peripancreatic pathology :
pancreatitis associated inflammation.
• Extra pancreatic inflammatory changes may be
detected even when the pancreatic contour is
normal and the pancreas is not obviously
enlarged.
• Pancreatic inflammation is typically hypoechoic or
anechoic.

26. • Inflammation is most often seen ventral
and adjacent to pancreas in :
 prepancreatic retroperitoneum
 Right and left anterior pararenal spaces.
 The perirenal spaces.
 The transveres mesocolon

27. Pre pancreatic space inflammation.

28. Peri vascular space :
• Spread of inflammation especially around splenic
vein and spleno portal confluence, is characteristic
of Acute pancreatitis.
• This peri vascular inflammation may explain why
some patients develop thrombosis of portal and
splenic veins.

29. Splenic vein thrombosis

30. Anterior pararenal and perirenal space inflammation

31. Inflammatory masses may be present.

32.  GB sludge with pancreatitis :

33. LAB FINDINGS :
 Elevated pancreatic enzymes (Amylase and Lipase):
blockage of secretion leads to leakage through
basolateral membrane into circulation
Lipase: sensitivity 86-100%, specificity 50-99%
(Normal value : 0-160 U/L)
Amylase: sensitivity 75-92%, specificity 20-60%
(Normal value : 23-85 U/L. Some lab results upto 140
U/L)

34. LOCAL SYSTEMIC
Acute fluid collections ARDS
Pancreatic abscess Multiple organ dysfunction syndrome
Pseudocysts DIC
Necrosis Hypocalcemia
Infected necrosis Insulin dependent DM
Hemorrhage Pleural effusion
Venous thrombosis GI haemorrhage
Pseudoaneurysms

35. ACUTE FLUID COLLECTIONS :
• The Atlanta Classification suggests that
differentiation between acute fluid collection and
pseudocyst should be made after 4 weeks from
the onset of disease.
• Others studies suggest the fluid collection that
persist for 6 weeks can be considered a
pseudocyst.

36. Acute fluid collection

38. NECROSIS :
• Cannot be definitely diagnosed on ultrasound.
• CECT : non enhanced pancreatic parenchyma
greater then 3 cm or involving more than 30% of
area of pancreas.

39. ABSCESS :
• There are two different types of acute pancreatitis
associated abscess :
 The Atlanta Classification pancreatic abscess : an
infected fluid collection / pseudocyst (which has minimal
necrosis).
 Infected necrosis with fluid collection, which arises from
infetion of necrotic pancreatic tissue.

40. VASCULAR COMPLICATIONS :
• Pseudoaneurysm.
• Venous thrombosis.
PSEUDOCYST :

41. CHRONIC PANCREATITIS

42. Alcoholism.
Pancreatic duct obstruction caused by
strictures.
Hypertriglyceridemia.
Hypercalcemia.
Autoimmune pancreatitis.

43. Chronic pancreatitis is characterised by
intermittent pancreatic inflammation with
progressive, irreversible damage to gland.
CP ultimately leads to permanent structural
change and deficient endocrine and
exocrine function.

44. Some lasting morphologic changes include :
• Alteration in parenchymal texture.
• Glandular atrophy.
• Glandular enlargement.
• Focal masses.
• Dilatation and beading of pancreatic duct (often
with intra ductal calcification).
• Pseudocysts.

45.  Extensive pancreatic
calcification can be
seen in this image.

47. HALLMARK OF CP :
• Ductal dilatation.
• Calcifications (look for colour comet tail artifact -
CCTA).
CT is superior to sonography in detecting
calcifications and ductal dilatations.
• Areas of increased and decreased echogenicity are
related to effects of patchy fibrosis. These areas are
subjective and difficult to appreciate.

48. DUCTAL DILATATION

50. CALCIFICATIONS

52. Calcifications highlighted by CCTA

53. CP ASSOCIATED WITH :
• Pseudocysts.
• Portal and splenic vein thrombosis.
• Pseudoaneurysm.

54. PSEUDOCYSTS:
More common in chronic pancreatitis (20-
40%) than acute pancreatitis (5-16%).
Pseudocysts may present with :
• Various shapes.
• Contain necrotic debris.
• Haemorrhage.
• Completely solid pattern.

55. Pseudocyst with internal debris

57. Pseudocyst with debris within
(can be infection or hemorrhage)

58.  Causes of portal vein thrombosis in CP :
• Intimal injury from recurrent inflammation.
• Chronic fibrosis and inflammation.
• Compression by either a pseudocyst or enlarged pancreas.
 Pancreatitis associated thrombus in splenic or
portal vein often results in collaterals different from
those in portal hypertension from liver disease.
These collaterals, rather than conveying blood
away from the diseased liver, conduct blood
towards the liver, bypassing the clot.

59. Splenic vein thrombosis :
 Occur more frequently than portal vein thrombosis.
 Splenic vein thrombosis often results in left sided
(sinistral) portal hypertension.
 This can result in isolated gastric varices. (the
hepatopetal pathway to bypass splenic vein clot
includes short gastric collateral that lead to gastric
mural varices, then flow to liver in coronary vein).

61.  It may be difficult or impossible to detect splenic
vein clot or even the splenic vein itself.
 Therefore diagnosis of splenic vein clot may
depend on detection of collaterals, such as short
gastric varices or an enlarged coronary vein.

62. Short gastric collaterals from splenic vein clot

63. Portal vein thrombosis :
 When the main portal vein is clotted, blood
flows to the liver around the clot.
 If portal vein clot persist, these hepatopetal
collaterals may enlarge, resulting in
cavernous transformation of the portal vein.
 Gall bladder varices were present in 30% of
the cases.

64. Cavernous transformation

65. Gall bladder varices

66. It is the rare complication of pancreatitis,
much less common than thrombosis.
It can occur in gastroduodenal, spelnic,
superior mesenteric arteries.
It shows ying and yang (red blue) colour
doppler appearance representing the
blood swirling in the lesion.

69. Focal pancreatic masses occur in
approximately 30% CP patients.
Carcinoma and pancreatitis associated
masses are easy to differentiate clinically
and by imaging.

70. CHRONIC PANCREATITIS CARCINOMA
Calcifications are multiple and ductal. Few coarse calcifications, usually
unrelated to ducts.
Multiple dilated branch ducts in
pancreatic head.
Hyperechoic masses even without
discrete calcifications, are usually
related to CP.
Uncalcified iso or hypoehoic mass is
non specific and requires biopsy for
confirmation.
Pseudocysts are more common in CP.
Occur anywhere in the gland, usually
arising in the areas of necrosis.
Usually are peripheral to body and tail
lesions.

71. Mass associated with chronic pancreatitis

72. Calcification in mass revealed by CCTA

73. Autoimmune Pancreatitis (AIP) :
 Type of chronic pancreatitis more likely to be
confused for carcinoma.
 2 types :
 TYPE 1 – older age group, relapse common
 TYPE 2 – younger, relapse less likely
 Responds to steroids , prednisolone
 HYPERIgG4 disease

74. 1. Imaging appearance of pancreatic
parenchyma and pancreatic duct.
2. Serum IgG4 level
3. Other organ involvement with IgG4
related disease
4. Pancreatic histology
5. Response to steroid therapy

75. Mass in AIP.

76. DIFFERENTIAL DIAGNOSIS

77. Infiltrating Pancreatic Carcinoma
• Irregular, heterogeneous,
hypoechoic mass.
• Abrupt obstruction &
dilatation of pancreatic duct.
• Regional nodal metastases.
• Contiguous organ invasion
-Duodenum, stomach
& mesenteric root

78. • Nodular, bulky, enlarged
pancreas due to
infiltration.
• Retroperitoneal
adenopathy.
• Peripancreatic infiltration
(obliteration of fat planes).
• Primary may be seen in
case of metastatic
infiltration.
Lymphoma & Metastases

79. Perforated Duodenal Ulcer :
• Penetrating ulcers may infiltrate anterior
pararenal space, simulating pancreatitis.
• Less than 50% of cases have evidence of
extraluminal gas or contrast medium
collections.
• Pancreatic head may be involved.

80.  NBM : atleast for 6 hours is required.
 In acute pancreatitis changes may not be
apparent on ultrasound for 24 hours.
 Differentiation of certain masses from
pancreatitis associated masses may not be
possible.
 Necrosis cannot be definitely diagnosed on
ultrasound.

81. CT Scan:
• Modality of choice in acute and chronic
pancreatitis when ultrasound is not diagnostic.
• In acute pancreatitis to differentiate between
interstitial (80%) and necrotizing pancreatitis
(20%).
• Patients who do not manifest rapid clinical
response within 72hours with conservative
medical therapy.

82. MRI :
• It is particularly helpful in differentiating the fluid
and exudate component.
• When CT is not diagnostic, especially to
distinguish chronic pancreatitis from neoplasm.