CYSTIC LESIONS

OF PANCREAS
Morphologically Classified Into
 Unilocular cysts (cysts without septation or a solid component)
 Pancreatic Pseudocyst,

 Intraductal Papillary Mucinous Neoplasm (IPMN) And

 Mucinous Cystadenoma

 Microcystic lesions (collection of microcysts)

 Serous cystadenoma

 Macrocystic lesions (multilocular cysts with fewer compartments, each > 2 cm)
 Mucinous Cystadenoma,

 IPMN

 Lymphoepithelial Cyst

 Cysts with solid components, i.e., mucinous cystic neoplasm

 Pathological Classification

 Simple Retention Cysts

 Pseudocysts

 Cystic Neoplasms
 Retention cysts

 True or simple cysts,  Solitary cysts (congenital, duplication,dermoid) are rare

 Usually found incidentally

 Multiple pancreatic cysts more common
 They are usually small

 lined by cuboidal epithelium

Wall is covered by normal epithelium
 Von hippel – lindau disease (~ 50%)
with ductal and centroacinar cells
 ADPKD
 In 25% of patients with cystic fibrosis
 Rarely symptomatic

• No clinical significance
• No treatment indicated
 Pseudocysts
 Generally symptomatic (i.e. pain)
 If asymptomatic, think about another Dx

 History of acute or chronic pancreatitis

 Almost always pseudocyst with this history

 Look for associated findings

 Pancreatic inflammation, parenchymal calcifications, atrophy, typical intraductal
calcifications

 Can communicate with pancreatic duct

 Wide neck vs. narrow neck for IPMN

 Wall can calcify

 No mural nodules
 They do not have a true wall with normal pancreatic cells, their wall is formed by fibrous
and granulation tissue.

 Fluid of the cyst- usually dark in color and contains pancreatic enzymes and bicarbonates.

 INVESTIGATIONS
 Ultrasonogram

 CT

 EUS

 ERCP

 MRCP

 FNA
 Complications include
 Abscess /systemic sepsis

 SMV/PV thrombosis

 Intracystic hemorrhage/pseudoaneurysms

 Peritonitis/intraperitoneal bleeding

 Pressure effects

 Pancreatico-pleural fistula

 Symptomatic cysts require treatment

 Drainage (>5 cm)

 Percutaneous

 Endoscopic drainage under EUS guidance through the stomach or the duodenal wall

 Surgically (lap/open) by anastomosing the cystic wall to the stomach, duodenum or jejunum

 Resection
Serous cystadenoma
 Benign neoplasms

 Cuboidal, glycogen-rich, epithelial cells

 Rare neoplasm- 1 to 2%

 Slight predominance in head region

 Incidental finding at routine physical examination or at autopsy or VHL associated.

 Large mutiloculated mass with serous fluid in cystic cavities -

 Microcystic and locular

 Symptoms and signs of an expansile abdominal mass

 Women are more affected

 6th – 7th decade of life

 Malignant transformation is very rare (<1%)

 Polycystic (microcystic) or Oligocystic (macrocystic)

 Honeycomb appearance/spongelike
 well demarcated multicystic cluster of individual small cyst (< 2cms)

 Aspiration
 Non viscous

 Low CEA

 Low Amylase
 USG

 MRCP

 Endoscopic ultrasonography with FNA

 CT- Central sunburst, Radial or Stellate scar pattern on CT (20%)

 Treatment
 In select patients with large (>4 cm) or rapidly growing lesions, resection is
appropriate
Mucinous Cystic Neoplasms
 Most common type

 40 – 50% of all Pancreatic cystic neoplasms

 Women (M:F – 1:9)

 Mean age – 50 years

 Body and tail of pancreas (>95%)

 Solitary lesions

 Size range from 6 to 35 cms (8 – 10 cms)

 Fewer than six separate cysts (>2cm), rarely just one Macrocyst

 No communication with pancreatic duct

 Well encapsulated, spherical in shape

 Cysts have septa within them and may have solid, eccentric component

 Content of cyst – usually mucinous, may be haemorrhagic or watery or

necrotic.

 MCNs are lined by mucin secreting columnar epithelium

 Ovarian type stroma – pathognomonic of MCNs

 Eggshell Calcification – pathognomonic of MCNs

 Potentially premalignant lesion – malignant degeneration after a long

period
 Histological Classification of MCNs
 Mucinous cystadenoma (65%)
 Uniform single layer of benign, columnar mucinous epithelium
 Non-invasive proliferative MCNs (30%)
 Varying degree of atypia, dysplasia, papillary endothelial infolding and
carcinoma in situ
 Mucinous adenocarcinoma (5%)
 True invasive tumor

Spectrum of all these changes of epithelium may be found within the same
neoplasm.
 MCNs frequently contain mutations of
 K-ras2 oncogene

 p53 tumor suppressor gene

 Expression of DPC4 gene product is frequently lost in invasive MCNs

 Incidence of invasive cancer 6 to 20%

 Risk factors for malignancy

 Large tumor size (>4cm)

 Associated mass, mural nodule, asymmetrically thickened wall

 Eggshell calcification

 Advanced age

 Symptomatology – abd. pain, weight loss, jaundice, mechanical duodenal obstruction

 Splenic vein obstruction

 CT/MRI: *Aspiration
 Thick cyst wall  Viscous mucus
 Smooth sharp boundaries.  High levels of CEA
 Do NOT communicate with pancreatic ductal system  Low amylase
 Pancreatic duct dilation.  Drop sign
 Eggshell calcification  columnar or cuboidal mucinous epithelial
 Endoscopic ultrasonography with FNA cells
 Viscous fluid.  Ovarian type stroma
 CEA  Estrogen and Progesterone staining
 positive
Adenoma > 200 ng/mL
 Mucinous cystadenocarcinoma >6000 ng/mL
 PET-Scan.
 Surgical resection if any of the following:
 > 3 cm.
 Main duct dilation
 Mural nodule.
 Observation if no candidate with small tumors.
 Prognosis:
 Poor if Invasive disease.
 Follow up:
 Non invasive: Annually the first years.
 Invasive:
 Every 4 month the first 2 years.
 Biannually until year 5.
 Intraductal Papillary Mucinous Neoplasm
(IPMN)
Several names have been given:

 Mucin secreting carcinoma (Ohashi et al, 1982)

 Villous adenoma of the duct of Wirsung

 Diffuse intraductal papillary adenocarcinoma

 Intraductal cystadenoma

 Mucinous duct ectasia

 Intraductal papillary mucinous tumor

Types of IPMNs based on morphology:
 I. Main duct IPMN
 Dilation of main pancreatic duct
 Diffuse (generalized) or Segmental (usually involving body and tail)
 Larger with prominent intraductal papillary projections

 II. Branch duct IPMN

 Cystic dilation of side branch of main pancreatic duct system
 Usually in head or uncinate process
 Communicating with pancreatic ductal system
 Frequently smaller
 Indolent course as compared to main duct IPMN
 Multifocal (30%), involves multiple non-contiguous side branches

 III. Mixed type IPMN

Histologically (WHO) IPMN divided into:

 A. Benign
 Adenoma without dysplasia

 B. Borderline
 Adenoma with mild to moderate dysplasia

 C. Carcinoma
 Non-invasive or invasive

Hyperplastic or dysplastic epithelium may be flat, micro papillary or grossly papillary

 IPMN
 25% of the pancreatic cystic Neoplasm.

 Male = Female 50 – 70 years.

 Head > Body

 Presentation:

 Abdominal pain.

 Pancreatitis.

 Weight loss.

 Jaundice.

 New onset diabetes.

 Characteristics:

 Main duct dilation.

 Papillary projections

 Excessive mucin production

 Genetics:

 Mutations in K-Ras, CDKN-2a, RNF 43,

 Time from IPMN adenoma to invasive cancer – 3 to 6.4 years

 25 to 48% IPMN contains invasive carcinoma

 Types:
 According to the affected duct:
 Main duct type- Invasion 57 – 92 %.
 Branch duct type- Invasion 6 – 46%
 According to the dysplasia:
 Adenoma.
 Borderline.
 Carcinoma in situ.
 Frankly invasive
 CECT
 Main pancreatic or duct dilation.

 Involvement of any part of the pancreas or the whole pancreas.

 Continuity of cyst with ductal system.

 Irregular and poorly demarcated

 Mural nodules
 ERCP
 variable dilatation (segmental or diffuse or branch) depending on the type.

 Polypoid mural tumour or amorphous mucinous luminal filling defects may be identified.

 Mucinous material may be seen protruding from the ampulla of Vater- fish mouth
 Aspiration
 Mucinous
 Elevated CEA & amylase levels
 IPMN also exhibits different patterns of papillae
 Gastric (most commonly branch duct IPMN)

 Intestinal (Usually main duct IPMN)

 Pancreatobiliary

 Oncocytic

 Null

 Intestinal type IPMN are MUC2 positive

 progress to invasive colloid carcinoma. Better prognosis
 Pancreatobiliary IPMN are MUC1 positive
 progress to invasive ductal/tubular adenocarcinoma. Poor prognosis

 Malignant IPMN associated with lower incidence (22%) of lymph node metastases than
ductal adenocarcinoma and have favourable prognosis
 Risk factors of underlying malignancy
 Main Duct Disease
 Branch-duct dilation more than 3 cm
 Presence of a mural nodule(s).
 Advanced age (older than 70 years).
 Presence of symptoms –
 Pain (often as result of pancreatitis)
 weight loss
 Fatigue
 Jaundice
 30% of patients with malignant IPMNs are asymptomatic
 Increased telomerase activity in pancreatic cystic fluid
 Elevated CA 19-9 level

 Surgical Treatment:
 Imaging suggesting malignancy

 Partial Pancreatectomy with Frozen section analysis

 REVISE &
SUMMARISE
Management
 PEARLS
• Age & Gender
– “Daughter Lesion”: SPEN
– “Mother Lesion”: Mucinous cystic
– “Grandmother Lesion”: Serous cystadenoma
• Location
– Head/neck for serous & side branch IMPN
– Body/tail for mucinous cystic neoplasm
• Calcification
– Peripheral in mucinous cystic
– Central in serous cystadenoma
• Mural Nodularity (enhancement = neoplasm)
• Duct communication (narrow neck) favors IPMN
THANK
YOU
A