1. SOLID LESIONS OF PANCREAS
Dr Siddaramu K S, 2nd yr M. Ch. Resident
Discussion: Dr Sanjay Nagral;
Consultant GI surgeon,
Mumbai

2. Case history
 67 yr/ M
 Progressive weight loss( 15 kg/ 6 months)
 Progressive jaundice
 No Health related problem in the past,
 No H/o tobacco in any form, nor alcohol.
 Exercised daily , Vegetarian .

3.  1st seen by Physician -- found to be healthy
and Fit
 Vitals Stable , Systemic exam Unremarkable.
 Hb - 13.5, TC - 6,500 , ESR - 13 mm at one
hour.
 Blood sugar was 481mg on fasting state.
 Diagnosed to have MOD, on Gliclazide 160
mg/d.
 Week later FBS 116mg and PPBS 174 mg .

4.  Continued to lose weight, slower rate.
 CBC -No change.
 Diabetes reasonably well controlled ,
 General examination again unremarkable.
 Thyroid Function- euthyroid status.

5.  US Abdomen
Mass 1.9 * 3.1 cms in head of pancreas,
Atrophic pancreas and mildly dilated PD.
CBD 9 mm dilated , smooth tapering lower end.
 LFT -
TB 4.3 mg- 70% conjugated,
SGPT- 75 i.u ALP -841 I.U.
 CA 19-9 was 14.5
 Chest X-ray was normal.

6.  CECT - similar finding to US.
Mass located within the pancreas.
Fat plane b/t pancreas and stomach
maintained.
 No involvement of major blood vessels.
 No metastatic disease detected .
 Clinical diagnosis -- Pancreatic head mass, most
probably neoplasm in back ground of chronic
pancreatitis.

7. Hmmmm………
 Q: What is your Analysis?
 What will you do next?

8.  Endoscopic Ultra sonography - carried out .
 Ill defined mass lesion in the head
 Pancreas atrophied and slightly hypo-
echoic,
 Mild MPD dilatation ,no stricture or stone .
 CBD appeared compressed inside the mass
but no stone

9.  Mass did not appear to involve major vessels
 Fat plane between the pancreas and stomach
intact.
FNA was obtained.
 Showed inflammatory cells only.

10. What should I do now?
 Refer to oncosurgeon?
 Repeat EUS?
 Review the FNA sample?

11. Evaluating Solid lesions of
Pancreas
 Epidemiology
 Most common presentations
 Imaging
 Serology
 Histology

12. Solid lesions -
Neoplastic
 Ductal adenocarcinoma( 85-90%)
 Neuroendocrine tumor (upto 5%)
 Solid psedopapillary neoplasm (1-2%)
 Pancreatoblastoma( 0.2%)
 Lymphoma(0.5%)
 Metastatic tumors (2-5%)
 Miscellaneous neoplasms

13. Non Neoplastic
 Focal Pancreatits, Autoimmune Pancreatitis, (
5-10%)
 Lipomatous pseudo hypertrophy(fatty
infiltration)
 Congenital anomalies (Bifid Pancreas,
Pancreatic Divisum, Prominent lobulation)
 Intra pancreatic accessory spleen
 Miscellaneous: Tuberculosis, Sarcoidosis,
Castleman

14. Epidemiology of Solid lesions
 1-10 yrs – Pancreatoblastoma,Congenital
anomalies.
 20-30 yrs -- Solid psedopapillary tumor(F:M
9:1)
 30-40 yrs -- Chronic Pancreatitis
 50-60 yrs -- NET,Metastasis, Lymphoma
 More than 60yrs - Ductal Adenocarcinoma,
Autoimmune pancreatitis (M:F 2:1)

15. Clinical Presentation of
solid lesions
 Nonspecific in Majority
 Abdominal pain , weight loss,progressive
obstructive Jaundice. – PDA
 Recurrent pain.--CP
 H/o RCC,Sarcoidosis,TB, Immuno deficiency
 Symptoms of lymphoma( fever,chills,night
sweats)

16. Imaging
 Trans Abd USG:
Accuracy is 50-70%
Contrast Enhanced Doppler US
Major limitations of US
Detection of small tumors (< 2 cm)
Lesions in the left side of the pancreatic gland,

17. After USG what?????
EUS or CECT ?

18. EUS
Advantages
 Detect masses as small as 0.2–0.3 cm.
 Clarify equivocal findings at CT or MR
 Allows biopsy of suspect lesions.
 More sensitive than CT (98% vs 86%)
 Accurate in local tumor staging (67% vs 47%).
Pitfalls
 It is highly operator dependent
 Presence of SA calcification, Billroth II,large Hiatus hernia,
varices
 Availability
 Narrow field of view

19. CECT VS EUS
Advantages of CECT:
1. Availability – widely used.
2. Resectability ,Distant Mets better tool
3. Vascular Anatomy -3D Reconstruction
4. Low cost
Limitations :
1.Difficulty in small lesions <1-2cm
2.Inflammtory mass- False appearance
3. Radiation.
4.Needle tract seeding (cutaneous & Peritoneal)

20. CECT Abdomen
 Investigation of choice in Majority(85-97%
sensitivity)
 Dual Phase Multi Detector CT
 Hypodense , irregular border,
Peripancreatic vessel involvement, PDA
Double duct sign
Upstream MPD Dilatation

21. Adenocarcinoma

22. NET
 Hypervascular tumor
 Calcification 20% vs 2% in PDA
 Vascular infiltration vs Encasement in PDA
 Less ductal involvement

23. Solid Pseudopapillary Tumor
 MC in Tail region
 Tendency to displace rather than invade
surrounding structures
 Rarely causes obstruction of the bile duct or
pancreatic duct.
 Pseudocapsule has low attenuation at CT
 Internal hemorragic & cystic degeneration

24. Solid Pseudopapillary Tumor

25. Lymphoma
 More CBD Dilatation than MPD
 Enlarged lymph nodes below Renal vein
 Invasive; No respect of Anatomic boundaries
 Vascular invasion less common

26. Metastasis
 Most common from Renal Cell Carcinoma, Ca
Lung, Ca Breast, CRC
 Hypervascular Mets--- Renal Cell Carcinoma
 Hypovascular Mets--- lung ,Breast, Colon
 Equivocal cases Require Biopsy.

27. RCC Mets

28. Focal Pancreatitis
Similar to Adenocarcinoma
 Hypo-attenuating
 Double Duct Sign
 Duct Stricture,
 Infiltration of fat, Vessels
 Duct Penetrating Sign
 PD irregularity Focal Pancreatitis
 Pancreatic Calcification.

29. MRI in solid lesions
 Fatty infiltration of pancreas & SPT- Inv of
Choice
 Mangafodipir Trisodium enhanced MRI –PDA
 Better for local extent,vascular involvement
than for Lymph node
 Not Superior to CECT in other lesions.

30. FDG-PET
 Preoperatively suspected distant metastasis.
 Differentiate benign vs malignant
 Investigate the response to neoadjuvant Rx
 Currently not a Preop Diagnostic Standard.

31. Role of ERCP ?
 Double duct sign in Adenocarcinoma, focal
Pancreatitis
 Biopsy & Brush Cytology- (less sensitive)
 Pre op Biliary Stenting

32. SEROLOGY: CA 19-9
 Most commonly valued marker (0-37 u/ml)
 Not specific, high levels seen in benign disease
 Normalization after resection improved
outcome
 Rising level after resection is a marker of relapse
 Levels > 1500 correlate with unresectable
tumors
 Not cost effective for screening

33. Serology
 Raised Ig G4, ANA
 Anti smooth muscle, Antihuman lactoferrin
 Functional Pan NET – Glucagon, Gastrin,VIP….
 Pancreatic Lipase – Acinar Cell Ca
 CEA,CA 242,CA 72-4.-PDA

34. Histology
 Difficult to differentiate b/t Ca and CP
More stroma and less of cells
 Small nests, scattered, round ,well delineated
units in exocrine back ground (NET)
 Lymphoplasmacytic infiltration in AIP

35. Coming back to our patient…
 IgG-4, grossly elevated
 Final diagnosis- Autoimmune pancreatitis,
with focal inflammatory Mass lesion.
 Patient was put on 30 mg of prednisolone
 At 4 wks of Rx, the Mass disappeared.

36. ERCP

37. AIP
 Classification:
 Two types
1. Type 1 Involves Adults or elderly
Idiopathic
Secondary to generalized autoimmune process.
2. Type 2 Seen in younger children.

38. AIP
Japanese Pancreas Society diagnostic
criteria(2002)
 I. Imaging studies show diffuse narrowing of
MPD with irregular wall (>1/3 of length ).
 II. Lab -abnormally elevated level ( IgG4), or the
presence of Auto Antibodies
 III. Histology shows fibrotic changes with
lymphocyte and plasma cell infiltrate.
 For diagnosis, criterion I must be present with
criterion II and/or III .

39. Take Home Message
 Accurate diagnosis can be challenging
 Multimodality imaging approach needed
 Not all Solid lesions are Malignant
 Knowledge of relevant clinical information
 Key radiologic features & Histology Helpful.

40. References
 Multimodality Imaging of and Non neoplastic Solid
lesionsof the pancreas, Radiographics journal,RSNA,2011.
993-1013
 Winter JM, Cameron JL, Lillemoe KD, et al. Periampullary
and pancreatic incidentaloma: a single institution’s
experience with an increasingly common diagnosis. Ann
Surg 2006;243(5):673–680; discussion 680–683.
 Ros PR, Mortelé KJ. Imaging features of pancreatic
neoplasms. JBR-BTR 2001;84(6):239–249.
 Blumgart’s Surgery of the liver,biliary tract,and Pancreas.