The document provides an overview of pancreatic anatomy, development, imaging, and pathology. It discusses the pancreas' gross anatomy, blood supply, embryological development, ductal anatomy, and relations to other structures. Common imaging modalities are described including their protocols and findings for evaluating inflammatory and neoplastic pancreatic conditions. Key pathological entities like acute pancreatitis, chronic pancreatitis, and pancreatic adenocarcinoma are summarized.

2. Welcome ladies and
gentlemen
&
It’s great honor for me to present
for you my lecture entitled

3. Pancreas;
Imaging Anatomy, Investigations and
Pathology
Ali M. Aboelsouad
Lecturer of Diagnostic Radiology
SECI-Assiut University

4. Intruduction
• The pancreas is a retroperitoneal
organ that has both: -
– Endocrine function through
production & secretion of
hormones into portal circulation
(Insulin, glucagon and
Somatostatin)
– Exocrine function through
production and secretion
of pancreatic juice into pancreatic
duct.

5. Gross Anatomy
The pancreas can be divided
into four main parts:
• Head: thickest part (AP
=3.5cm); lies to the right
SMA & SMV.
– uncinate process: posterior
extension of the head,
posterior to SMV.
• Neck: thinnest part (AP=
1.5cm); lies anterior to
confluence of SMV and
splenic vein to form portal
vein

6. Gross Anatomy
• Body:
– AP diameter= 2.5 cm.
– splenic vein lies in groove on the
posterior surface of body
– Splenic artery lies superior to
pancreas.
– Anterior surface is covered by
peritoneum, forming back
surface of lesser sac.
• Tail:
(AP diameter= 3cm) lies between
layers of the splenorenal
ligament in the splenic hilum

7. Gross Anatomy
• Pancreas lies in the abdomen obliquely horizontal with the tail
is the most superior part and head is the most inferior.
• This has an implication on visualization of pancreas on cross
sectional imaging.

9. Gross Anatomy
• (a) The gastroduodenal artery (arrow) is behind the pylorus (P). The posterior superior pancreaticoduodenal artery
(PSA) accompanies the bile duct (BD). The dorsal pancreatic artery (arrowhead) gives off a branch medial to the
pancreatic head. D = duodenum.
• (b) The gastroepiploic artery (large white arrow) is branching out from the gastroduodenal artery (small white
arrow),
• (c) The superior pancreaticoduodenal artery (large white arrow) and inferior pancreaticoduodenal artery (small
white arrow) form an arcade around the head of the pancreas.
• (d) Anterior to the uncinate process is the jejunal vein (small white arrow) draining into the SMW (large white

10. Blood Supply
• Arterial:
– Head by superior and inferior
PDA.
– Body & tail by branches from
splenic artery (dorsal and
great pancreatic artery)
• Venous:
– Splenic vein  portal
vein

11. Embryological Development of the Pancreas

12. Embryological Development of the
Pancreas
• It starts at the fourth week of gestation.
• The pancreas originates from the endodermal lining of
the duodenum as two outpouchings developed at the
junction of the foregut and midgut: -
• One ventral bud (caudal)
• One dorsal bud (cranial)
• The ventral pancreatic bud forms the head and the
uncinate process.
• The dorsal pancreatic bud forms the anterior part of
the neck, body, and tail of the pancreas.

13. Embryological Development of the
Pancreas
• The main pancreatic duct (Wirsung) is formed from the
proximal ventral duct and the dorsal duct.
• The accessory duct (Santorini) may be present due to
the persistence of the distal portion of the dorsal
pancreatic duct.
• At the sixth week of gestation, as the foregut
elongates, the ventral bud rotate clockwise posterior
to the duodenum and join the dorsal bud.
• At the seventh week of gestation, both buds fuse
together forming a single pancreas.

14. Ductal anatomy
• Main Pancreatic Duct (of
Wirsung):
– Begins at the tail and runs
to the head increasing in
size.
– Located in the anterior
half of pancreas.
– Joins the CBD at the
Ampulla of Vater to open
at the middle of medial
aspect of second part of
duodenum
– <3mm in diameter.

15. Ductal anatomy
• Accessory Pancreatic duct (of
Santorini):
– It’s the distal part of
dorsal bud duct and
drains via the minor
papilla into the
duodenum, 2cm proximal
to the ampulla of Vater.
– Occasionally
communicates with the
main duct.

18. Relations

19. Imaging investigations
1. Plain radiograph of the abdomen AP view.
2. Contrast meal.
3. Ultrasound transabdominal and endoscopic (EUS).
4. MSCT.
5. MRI.

20. Plain Radiograph
• Limited role.
• Detect:-
1. punctate calcifications
in chronic pancreatitis.
2. Colonic cutoff sign in
acute pancreatitis

21. Contrast Meal
• Limited role.
• Detect Frostberg
inverted 3 sign which
seen due to focal mass
and local edema in
cases of: -
– Pancreatic head
carcinoma
– Duodenal carcinoma.
– Pancreatitis

22. Ultrasonography
• Limited role due to the
overlying gas from the
transverse colon and stomach
that makes visualizing
pancreatic parenchyma
difficult or even impossible.
• On US, the pancreas is
slightly echogenic than liver
and has homogenous
appearance.

23. Ultrasonography
• Detect:-
1. GB Stones as etiology for
pancreatitis.
2. Biliary dilatation.
3. Complications of acute
pancreatitis as collection and
pseudo pancreatic cyst.
4. ?Pancreatic mass (Most focal
pancreatic lesions are
hypoechoic compared to
normal parenchyma)

24. MSCT Abdomen
• MDCT is the modality of choice for the evaluation of both
inflammatory and neoplastic conditions of the pancreas.
• Normally pancreas is slightly hyperdense than paraspinal
muscles with lobular outline and homogenous
enhancement in postcontrast study.

25. MSCT Abdomen
• In inflammatory conditions, MDCT not only
provides excellent visualization of the parenchymal
abnormalities, but also clearly depicts the extra
pancreatic spread of disease.
• In pancreatic neoplasms, MDCT accurately depicts
the tumor morphology, ductal anatomy, and its
relationship to the surrounding organs and vascular
structures.

26. MSCT Abdomen
• The typical MDCT protocol for pancreatic
evaluation involves administration of:
– Neutral oral contrast like water
– And positive intravenous contrast throughout 3
phases: -
1. pancreatic (late arterial after 40-45 s from injection)
phase to assess:
– Hyper vascular tumor as NET.
– Mesenteric vessels to assess tumor resectability
– Maximum differentiation between normal pancreatic parenchyma
and hypovascular tumor like adenocarcinoma
1. Porto venous phase.
2. Late phase on the liver to assess the mets.

27. MRI Abdomen
• Adv to MSCT:
– Superior soft-tissue contrast
even without IV contrast.
– Assessing the morphologic
features of pancreatic cysts.
– MRCP provides excellent
depiction of the pancreatic duct
anatomy and biliary channel.
• Disadv:
– Thicker slice thickness.
– More examination time.
– Sensitive to respiratory motion.

28. MRI Abdomen
• Precautions:
1. fasting for 4 hours.
2. Negative oral contrast.
• Protocol:
1. Axial T1 with and without fat sat.
2. Axial and coronal T2 with and without fat sat.
3. 3D T1 GE pre and post contrast.
4. 2d & 3D MRCP.

29. MRI Abdomen
• On T1 WI:
– Has the highest T1 signal of all
abdominal organs and used for:-
1. precontrast T1- weighted images are
the most sensitive sequence to
detect focal lesions, which are often
hypointense relative to normal
parenchyma
2. for detection of hemorrhage within
inflammatory collections.
• On T2 WI:
– Slightly hyperintense compared to the
adjacent muscle, and used for
depicting the ductal anatomy, cystic
lesions, and islet cell tumors, which
are hyperintense compared to normal
pancreas.

30. Imaging pathology
• Congenital:
• Agenesis.
• Pancreatic divisum.
• Annular pancreas
• Inflammatory:
• Acute pancreatitis.
• Chronic pancreatitis.
• Neoplastic:
– Exocrine: 99% of all primary
pancreatic neoplasms
• Pancreatic adenocarcinoma ~90-
95%
• cystic neoplasm
• Intraductal papillary
mucinous neoplasm (IPMN)
– Endocrine: 1% of all primary
pancreatic neoplasms
• non-functional
• functional
– Other
• Mets.
• Mesenchymal tumor
~5-10%

31. Pancreatic divisum
• The ventral bud failed to fuse
with dorsal bud during fetal
development.

32. Pancreatic divisum

33. Pancreatic divisum
• The pancreatic head and
uncinate process are drained
through the major papilla.
• The body and tail of the
pancreas are drained through
the minor papilla.
• As a result ,the dorsal
pancreatic duct drains most of
the pancreas via the minor
papilla that may lead to
recurrent attack of pancreatitis

34. Annular Pancreas
A ring of pancreatic tissue
that completely encircles
the duodenum

35. Acute pancreatitis
• The diagnosis of acute pancreatitis is made
by fulfilling two of the following three
criteria:
– acute onset of persistent, severe epigastric pain
– lipase/amylase elevation >3 times the upper limit of normal
– characteristic imaging features on contrast-enhanced CT, MRI
Imaging is only required to establish the diagnosis if the
first two criteria are not met. Imaging is crucial for:-
– to clarify the diagnosis when the clinical picture is confusing
– to assess severity (Balthazar & CTSI score) and thus to determine
prognosis
– to detect complications
– to determine possible causes

36. Acute pancreatitis
• Etiology: - [I GET SMS]
1. Idiopathic.
2. GB stones.
3. Ethanol abuse.
4. Trauma; accidental or iatrogenic in ERCP.
5. Steroids.
6. Mumps & Malignancy.
7. Scorpion sting.

37. Acute pancreatitis
• Imaging signs: -
– focal or diffuse parenchymal enlargement
– Hypo density corresponding to edema/necrosis.
– indistinct pancreatic margins owing to
inflammation
– Retroperitoneal fat stranding including:
– Peripancreatic fat.
– Left anterior pararenal space.
– Thickening of left Gerrota’s fascia.

38. Acute pancreatitis
There are two subtypes of
acute pancreatitis:
•Interstitial edematous
pancreatitis
– the vast majority (90-95%)
– most often referred to simply as
"acute pancreatitis" or
"uncomplicated pancreatitis"
•Necrotizing pancreatitis
– parenchymal necrosis i.e. non
enhancing hypodensity.
– peripancreatic necrosis
– combined type most common
All types of necrotizing pancreatitis may be
sterile or infected; air density is the best imaging
sign to suggest infection.

39. Acute pancreatitis
Complications:
1.Pancreatic fluid collections may be
developed either in presence or absence of
necrosis:
– If necrosis is absent i.e. interstitial
edematous pancreatitis, the fluid may
be:
1. acute peripancreatic fluid
collections (APFCs) (in the first 4 weeks)
2. pseudocysts: encapsulated fluid
collections after 4 weeks
– If necrosis is present i.e. necrotizing
pancreatitis
3. acute necrotic collections (ANCs):
develop in first 4 weeks
4. walled-off
necrosis (WON): encapsulated
collections after 4 weeks
5. emphysematous pancreatitis: if
secondarily infected

40. Acute pancreatitis
Complications:
2.vascular complications
– Hemorrhage: resulting from
erosion of blood vessels and
tissue necrosis
– pseudoaneurysm
– splenic vein thrombosis Gastric
varices without portal hypertension =
splenic vein occlusion
– portal vein thrombosis
3.Fistula formation : leakage of
pancreatic secretions into the
peritoneal cavity

41. Acute pancreatitis
Modified CTSI:
•Scores are generated by estimating pancreatic inflammation and necrosis :
– Pancreatic inflammation
• 0: normal pancreas
• 2: Inflammatory changes in pancreatic &/or peripancreatic tissue.
• 4: pancreatic or peripancreatic fluid collection.
– Pancreatic necrosis
• 0: none
• 2: 30% or less
• 4: more than 30%
– Extra pancreatic complications
• 2: pleural effusion, ascites, vascular complications, fistula formation
Total points are given out of 10 to determine the grade of pancreatitis
and aid treatment:
– 0-2: Mild pancreatitis carry best prognosis with 8% complications rate and 3% mortality.
– 4-6: moderate pancreatitis carry 35% complications rate and 6% mortality.
– 8-10: severe pancreatitis carry worst prognosis with 92% complications rate and 35%
mortality.

42. Chronic pancreatitis
• Dilatation of the MPD.
• Pancreatic calcifications.
• Changes in pancreatic size
(i.e. atrophy), shape, and
contour
• Pseudocyst

43. Pancreatic Adenocarcinoma
Imaging signs:
•Poorly defined masses
•Enhance poorly compared to adjacent
normal pancreatic tissue and thus
appear hypodense on arterial phase
and become isodense on delayed
scans i.e. hypovascular tumor.
•Double duct sign.
– DDx:-
1. Pancreatic head
carcinoma.
2. Ampullary carcinoma
3. Impacted ampullary stone.

44. Pancreatic adenocarcinoma
Curative treatment

45. Pancreatic Adenocarcinoma
Resectable or not?

46. Cystic Pancreatic Masses

47. Cystic Pancreatic Masses
Most of these cysts are
benign or low-grade
neoplasms.
•Pseudocyst - Think of it when
there is:-
1. History of pancreatitis or
abdominal trauma.
2. Unilocular cyst.
3. Contains non-enhancing
dependent debris.

48. Cystic Pancreatic Masses
• Cystic neoplasm- Think of it
when there is:
1. No history of pancreatitis or trauma,
2. The cyst has internal septa, a solid
component, central scar or wall
calcification.
• Mucinous cystic neoplasm
(MCN) - This is a uni macro
locular cyst, sometimes with wall
calcification, exclusively seen in
women.

49. Cystic Pancreatic Masses
• Serous cystic neoplasm
(SCN) - This is a multi micro
cystic lesion, sometimes with
characteristic scar which may
calcify without communication
of the PD or its side branches.
SCN is the only tumor that is not
premalignant.
• IPMN - This tumor is multi
micro cystic, but has no scar or
calcifications with connection to
the pancreatic duct or its side
branches.

52. Cystic Pancreatic Masses

53. Cystic Pancreatic Masses

54. Quiz case

55. Endocrinal tumors
• Arise from the pancreatic islet
cells.
• Associated with: -
• MEN I
• VHL
• TS
• C/O:
• syndromic tumors
– Insulinoma: most common
– Gastrinoma: 2nd
most common
– Glucaginoma, VIPoma and
Somatostatinoma.
• Non syndromic tumors: 3rd
most
common
• Prognosis:
– Insulinoma: 10% Malignant
– Gastrinoma: 60% Malignant
– Glucaginoma: 80% Malignant
– VIPoma and Somatostatinoma: each
75% Malignant
– non-functional: 85-100% malignant

56. Endocrinal tumors
• Ultrasound
– well-circumscribed with smooth margins, round or oval, hypoechoic
– Liver metastases may be hyperechoic or targetoid.
• CT
– Smaller tumors: hypervascular, tend to be homogenous and well circumscribed
– Larger tumors: heterogeneous and contain areas of cystic change
– May manifest as primarily cystic lesions and are distinguishable from other cystic neoplasms
by their hypervascular rim
• MRI (Sensitivity is similar to CT)
– T1: hypointense relative to pancreas
– T2: hyperintense relative to pancreas
– T1 C+ (Gad): hyperintense/hypervascular relative to pancreas
• Nuclear medicine
– Localize or confirm a functioning tumor and look for metastases.
– 111
In-octreotide SPECT: reported sensitivity is highest with gastrinomas >2 cm and lowest with insulinomas

57. Neuro/Endocrinal tumors
Important tips in pancreatic NET unlike
adenocarcinoma:
•Since they have a distinct capsule, so they displace rather than
invade surrounding structures as they grow in size  They less
frequently present with biliary obstruction.
•Endocrine tumors of the pancreas show peak contrast
enhancement in the early arterial phase (25-35 secs) and appear
isointense in late arterial phase.
•75% of patients with neuroendocrine tumors have metastatic
disease at presentation, most commonly in the liver and less
frequently in bone.

58. Pancreatic Mets
• RCC: commonest of
tumors that metastasize
to the pancreas
• Melanoma
• Breast Cancer
• Lung cancer
• Gastric Cancer
• Colorectal cancer

59. Mesenchymal tumors
• Benign
• Pancreatic neurofibroma
• pancreatic schwannoma
• pancreatic ganglioneuroma
• pancreatic desmoid tumor
• Pancreatic lipoma
• Pancreatic perivascular
epithelioid cell tumor
(Pancreatic PEComa)
• Pancreatic dermoid
• Pancreatic lymphangioma
• Malignant
• Pancreatoblastoma
• Pancreatic lymphoma.
• Pancreatic sarcoma

60. To conclude:
1. MSCT is the modality of choice to diagnose pancreatic lesions;
congenital (except divisum need MRCP), inflammatory and neoplastic.
2. MRI has equal accuracy to MSCT, however its affection by respiratory
motion, longer exam duration and its thicker slice thickness makes it
second choice.
3. MR will better demonstrate the cystic nature (CT can do that), the
internal structure of the cyst (septations, central scar, debris) (CT
cannot do that) and demonstrate the relationship of the cyst to the
pancreatic duct (CT cannot do that).

61. 4. CT can be helpful as it better depicts a
central calcification in SCN or peripheral
calcification in a mucinous cystic neoplasm
(MCN)
To conclude:

62. Thank you,
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