Solid lesions of the Pancreas
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Transcript of Solid lesions of the Pancreas
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SOLID LESIONS OF PANCREAS
Dr Siddaramu K S, 2nd yr M. Ch. Resident
Discussion: Dr Sanjay Nagral; Consultant GI surgeon, Mumbai
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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 .
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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 .
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Continued to lose weight, slower rate.
CBC -No change. Diabetes reasonably well controlled , General examination again
unremarkable. Thyroid Function- euthyroid
status.
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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.
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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.
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Hmmmm………
Q: What is your Analysis?
What will you do next?
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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
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Mass did not appear to involve major
vessels Fat plane between the pancreas and
stomach intact.
FNA was obtained. Showed inflammatory cells only.
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What should I do now?
Refer to oncosurgeon?
Repeat EUS?
Review the FNA sample?
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Evaluating Solid lesions of Pancreas
Epidemiology Most common presentations Imaging Serology Histology
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Solid lesions -
NeoplasticDuctal adenocarcinoma( 85-90%)Neuroendocrine tumor (upto 5%)Solid psedopapillary neoplasm (1-
2%)Pancreatoblastoma( 0.2%)Lymphoma(0.5%)Metastatic tumors (2-5%)Miscellaneous neoplasms
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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
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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)
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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)
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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,
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After USG what?????
EUS or CECT ?
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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
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CECT VS EUS
Advantages of CECT: 1. Availability – widely used. 2. Resectability ,Distant Mets better tool 3. Vascular Anatomy -3D Reconstruction 4. Low costLimitations : 1.Difficulty in small lesions <1-2cm 2.Inflammtory mass- False appearance 3. Radiation. 4.Needle tract seeding (cutaneous &
Peritoneal)
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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
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Adenocarcinoma
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NET
Hypervascular tumor
Calcification 20% vs 2% in PDA
Vascular infiltration vs Encasement in PDA
Less ductal involvement
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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
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Solid Pseudopapillary Tumor
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Lymphoma
More CBD Dilatation than MPD
Enlarged lymph nodes below Renal vein
Invasive; No respect of Anatomic boundaries
Vascular invasion less common
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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.
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RCC Mets
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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.
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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.
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FDG-PET
Preoperatively suspected distant metastasis.
Differentiate benign vs malignant
Investigate the response to neoadjuvant Rx
Currently not a Preop Diagnostic Standard.
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Role of ERCP ?
Double duct sign in Adenocarcinoma, focal Pancreatitis
Biopsy & Brush Cytology- (less sensitive)
Pre op Biliary Stenting
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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
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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
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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
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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.
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ERCP
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AIP
Classification: Two types 1. Type 1 Involves Adults or
elderly Idiopathic Secondary to generalized autoimmune
process. 2. Type 2 Seen in younger
children.
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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 .
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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.
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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.
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