SOLID LESIONS OF PANCREAS

Dr Siddaramu K S, 2nd yr M. Ch. Resident

Discussion: Dr Sanjay Nagral; Consultant GI surgeon, Mumbai

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 .

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 .

Continued to lose weight, slower rate.

CBC -No change. Diabetes reasonably well controlled , General examination again

unremarkable. Thyroid Function- euthyroid

status.

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.

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.

Hmmmm………

Q: What is your Analysis?

What will you do next?

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

Mass did not appear to involve major

vessels Fat plane between the pancreas and

stomach intact.

FNA was obtained. Showed inflammatory cells only.

What should I do now?

Refer to oncosurgeon?

Repeat EUS?

Review the FNA sample?

Evaluating Solid lesions of Pancreas

Epidemiology Most common presentations Imaging Serology Histology

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

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

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)

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)

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,

After USG what?????

EUS or CECT ?

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

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)

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

Adenocarcinoma

NET

Hypervascular tumor

Calcification 20% vs 2% in PDA

Vascular infiltration vs Encasement in PDA

Less ductal involvement

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

Solid Pseudopapillary Tumor

Lymphoma

More CBD Dilatation than MPD

Enlarged lymph nodes below Renal vein

Invasive; No respect of Anatomic boundaries

Vascular invasion less common

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.

RCC Mets

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.

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.

FDG-PET

Preoperatively suspected distant metastasis.

Differentiate benign vs malignant

Investigate the response to neoadjuvant Rx

Currently not a Preop Diagnostic Standard.

Role of ERCP ?

Double duct sign in Adenocarcinoma, focal Pancreatitis

Biopsy & Brush Cytology- (less sensitive)

Pre op Biliary Stenting

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

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

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

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.

ERCP

AIP

Classification: Two types 1. Type 1 Involves Adults or

elderly Idiopathic Secondary to generalized autoimmune

process. 2. Type 2 Seen in younger

children.

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 .

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.

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.