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Pancreatic Tumor Classification
Preoperative evaluation in
Whipple’s Procedure
Dr.Bhavin Vadodariya
DNB Resident Doctor
Department of Surgical Oncology
Apollo CBCC Cancer Care
Apollo Hospital,Ahmedabad
Date- 06/01/2018
 The most unforgiving organ in the human body.
Outline
•Classification
PDAC
Cystic neoplams
SPN
Endocrine Tumor
•Preoperative Management
•Assement of resectability
•Management of Obstructive jaundice
Neoplasms of the pancreas
 Solid tumors (AdenoCarcinomas)
 Cystic Neoplasms
 Endocrine tumors
Pancreatic adeno carcinoma
 5-year survival rate of only 6%.
 9th most common cancer in the US , but 4th in terms
of cancer deaths.
 74% of patients die within the first yearafter
diagnosis.
 Common age >60 years, median age is 72years.
 Incidence is about 8 to 9 cases per 1,00,000
 Incidence is lowest in India and parts of middle
east 8.1 and 7.0 per 1,00,000 in men and
women respectively
Pathology
 Pancreatic cancer probably arises through a stepwise
progression of cellular changes.
 From Pancreatic intra epithelial neoplasia to invasive adeno
carcinoma.
 75% are ductal adenocarcinoma
 Uncommon varieties include Adeno squamous and Acinar cell
carcinoma.
Adenosquamous carcinoma -
It has both glandular and squamous differentiation.
The biologic behaviour similar to typical ductal
adenocarcinoma.
Acinar cell carcinoma - presents as a large tumour,
often 10 cm in diameter or more, the prognosis of patients
with these tumours may be better than with ductal cancer.
Pancreatic Intraepithelial
Neoplasia(PanIN)

•Pre cursor lesions for invasive carcinoma
•Three stages of pancreatic intraepithelial neoplasia have
been defined. From PanIN 1 – PanIN 3
•With progressive cellular atypia and architectural
disarray.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Location of the tumour
 About two-thirds of pancreatic adenocarcinomas
arise within the head or uncinate process of the
pancreas
 15% are in thebody
 10% in thetail,
 remaining tumours demonstrating diffuse
involvement of the gland.
 Tumours in the pancreatic body and tail are generally
larger at the time of diagnosis, and therefore, less
commonly resectable.
 Tumours in the head of the pancreas are typically
diagnosed earlier because they cause obstructive
jaundice.
Cystic Neoplasms of Pancreas
Pathological classification of cystic
neoplasms of the pancreas: The who
international classification.
 Serous cystic neoplasm (SCN)
 Mucinous cystic neoplasm (MCN)
 Intra-ductal papillary mucinous neoplasm
(IPMN)
Serous cystic neoplasm (SCN)
 Microcystic adenoma
 Oligocystic adenoma
Mucinous cystic neoplasm (MCN)
Mucinous cystadenoma
Mucinous cystic tumour–borderline
Mucinous cystadenocarcinoma
Non-invasive (carcinoma in situ)
Invasive
Intra-ductal papillary mucinous
neoplasm (IPMN)
 Adenoma/low-grade dysplasia
 Borderline/moderate-grade dysplasia
 Carcinoma in situ
 Invasive carcinoma
SEROUS CYSTIC NEOPLASM
 First described by Comagno and Oertel in 1978 as
microcystic and glycogen rich and they distinguished
these lesions from mucinous cysts.
PATHOLOGY
 Cell of origin is centroacinar cell.
 Soft mass which includes numerous small cysts filled
with clear serous fluid arranged in a characteristic
honeycomb-like pattern.
 unique central calcification give rise to charecterstic
central sunburst,radial or stellate scar pattern on CT.
 <10 % are serous oligocystic ( macrocystic )SCNhave
fewer cysts, usually >2cm but histopathologic
appearance is similar to that of microcystic.
 Histologically they are have bland cuboidal epithelial
lining without nuclear pleomorphism or mitoses.
 Syndromic association betweenVHL
 EUS-FNA and analysis of fluid – SCN low amylaseand
viscosity.
 CEA < 5ng/ml, CA 19-9 < 37U/L, excludes MCN and
IPMN.
MUCINOUS CYSTIC NEOPLASMS
 They are mucin secreating cystic tumours that lack
communication with the pancreatic duct and contain
mucin secreting columnar epithelium.
 Grossly, individual cysts are typically greater than
2cm and the tumour mass can be as large as
25cm.these tumours are round with smooth surface
and fibrous pseudocapsule.
 MCNs are generally contain less than 6 cysts and are
spherical in shape.
 MCNs are typically located in body and tail ( 95 %
).peripheral eggshell like eccentric calcification occur in 15%
of cases and are considered pathognomonic.
 Ovarian like stroma surrounding the columnar epitheliumis
also pathognomonic and it is the presumed reason that are
almost exclusively seen in females( >95% ).
 MCNs exhibit characteristics of an adenoma-
carcinoma - sequence
INTRADUCTAL PAPILLARY MUCINOUS
NEOPLASM
 IPMNs constitute 15-30% of allcysticlesions.
 They are intraductal proliferation of neoplastic
mucinous cells leading to dilatation of main panreatic
duct or branch ducts.
 WHO classification
1. Adenoma
2. Borderline
3. Ca in situ
Morphology - IPMN
 main duct type
 branch duct type
 combined type
Histology
 Gastric foveolar type – Tall columnar cells, mucin,
scattered Goblet cells – Common in branch type.
 Villous intestinal type- Resemble colonic villous
adenoma- Common in Main duct type.
 Pancreato biliary – lined by cuboidalcells
Extra pancreatic malignancies in
patients with IPMN
 Colorectal adenomas andcarcinopmas
 Barrets mucosa and gastriccarcinoma
Analysis of the Cystic Fluid
 Differential Diagnosis of Pancreatic Cystic Neoplasms Based on
Analysis of Intracystic Fluid
Cystic Lesion Amylase CEA Viscosity Mucin Stain Cytology
 SCN ↓ ↓ ↓ Negative Glycogen rich
 MCN ↓ ↑↑↑ ↑ Positive Mucinous
 IPMN
 Pseudocyst
↑
↑↑↑
↑↑↑
↑ ↓
↑ Positive
Negative
Mucinous
Inflammatory
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Solid Pseudopapillary Tumor
(Papillary Cystic Cancer Or Frantz Tumor)
• Approximately 90% of solid pseudopapillary tumor
harbor APC/beta-catenin mutation
• Typically occur in women in the second or third
decade of life
Regarded as low grade malignant potential tumor.
Pathology
• Lesions may be large, encapsulated, evenly
distributedthroughout the pancreas.
• Strongly positive for beta-catenin, progesterone
receptors, vimentin, CD-10 and CD-56Q.
It can mimic the histologic appearance of NET but lacks
the nuclear features of NET and lacks the
neuroendocerine markers such
as chromagranin and synaptophysin.
Pancreatic neuro endocrine tumours
PNET
 Rare ,annual incidence of approximately 5 cases per
1,000,000 population.
 Functioning and Non functioning
 Sporadically or as a part ofsyndromes.
Syndromic pNETS
 10% are associated with an underlying genetic syndrome
(MEN1) and type IV (MEN4) –pNETS in 80-100% of patients
 Small, multifocal and microscopic
 Gastrinomas (>80% duodenal) develop in 54% of MEN-1 patients,
insulinomas in 18% and glucagonomas, VIPomas, somatostatinomas in <5%
 Von Hippel-Lindau disease (VHL),-10% patients develop pNETS
 Neurofibromatosis type I (NF1), tuberous sclerosis complex (TSC)
 2% of total pancreatic mass areislets
 APUD cells – 4 cell types, α, β, γ,δ
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Insulinoma
 Most common 60%
 Origin- β cells almost universally
within the pancreas (1/3head –
1/3 body – 1/3 tail)
 F>M
 90% benign, 10% malignant
 Most solitary, 10% multiple(MEN 1)
 21% MEN 1 – insulinomas
 The median age at diagnosis- 47yrs
Gastrinoma /Zollinger-Ellison
Syndrome
 Second most frequent
 1 / 2.5 million
 60% malignant (mets to liver)
 75 % sporadic
 M>F
 Average age -50 years,5 to 10 years earlier in MEN-1
 25 % MEN-1
VIPOMA(Verner-Morrison Syndrome)
 0.05-0.2 new cases per million adults
 Third most common neuroendocrine tumor of the pancreas
 Solitary, found in body or tail, usually detected at >3cm size
 2/3 malignant
 Male-to-female ratio in children - 1:1,
in adults. - 1:3
Glucagonoma
 Tumor of islet alpha cells
 Mainly body and tail
 1 per 20 million
 Mean age of 55 years (19-84 years).
 W>M
 50% malignant
 5-10 cm at diagnosis
 Migratory necrolytic erythema 2/3 cases – aminoacid
and trace element deficiency
 4D syndrome (dermatitis, diabetes, diarrhea, DVT)
 Fasting plasma glucagon >50pmol/ml:Diagnostic
Somatostatinoma
 Rare fewer than 100 cases in literature
 70% to 90% of tumours – malignant
 Location – usually head
 Clinical findings – unpredictable
 Diarrhea
 Gallstones – 59 %
 Steatorrhea
 Mild diabetes – 75%
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Preoperative Evaluation in
Whipple’s Surgery
Assessment of Resectability
CT Scan for pancreas
 Multi-detector spiral CT and is the single most useful
diagnostic and staging modality.
 It gives information about adjacent vascular
structures such as the portal, superior mesenteric,
and splenic veins, as well as the superior mesenteric
artery (SMA) and celiac axis.
Phases of an pancreatic protocol
 Early arterial phase (15-20 s after injection of
contrast)
 Late arterial phase (35-40 s)
 Hepatic or portal venous phase(50-60s)
 Nephrogenic Phase (100s)
 Delayed phase (6-10minutes)
 The non contrast phase - pancreatic calcifications, for
localization of the precise levels the post contrast
study.
 The early arterial phase permits evaluation of
pancreatic vasculature without interference from
venous opacification.
 The late arterial phase - distinguish pancreatic
neoplasms from adjacent normal pancreatic tissue, to
evaluate hyper-vascular liver metastases
(neuroendocrine tumors of the pancreas).
 The 4th phase portal venous phase - for hypo-
vascular liver metastases
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Unresectability in CT
 Unresectability is defined on multiphase CT by
involvement of
1. ≥ 180 degrees of the celiac axis
2. hepatic or superior mesenteric artery, enlarged lymph
nodes outside the boundaries of resection
3. ascites, and distant metastases.
 Invasion of the superior mesenteric vein or portal vein is
not in itself a contraindication to resection as long as the
veins are patent. Resection of vein with reconstruction is
possible.
CT images
Dilated intrahepatic ducts. Double-duct sign” with dilated common bile duct and
pancreatic ducts. There is a stent in the common bile duct
(S)
Pancreas cancer mass with stent through it (arrow).
Superior mesenteric artery (SMA) (A) is adjacent to
tumor.
Tree-dimensional CT vascular reconstruction
Portal and superior mesenteric veins
do not appear involved.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
ERCP
 ERCP may be of benefit in patients with biliary
obstruction and cholangitis - endoscopic stent can be
placed for decompression.
 With current capabilities of CT and MRI, ERCP is rarely
necessary.
Endoscopic retrograde cholangiopancreatogram
(ERCP) of patient with pancreas cancer with abrupt
cut-off of main
pancreatic duct secondary to tumor.
ERCP of patient with pancreas cancer with obstruction
of both main pancreatic duct and common bile duct
Completion cholangiogram after endoscopic placement of
stent
Indications for pre operative
decompression of biliary system.
 Cachexic patient for nutritionalimprovement.
 In patients withcholangitis
 If plan is non operativemanagement.
If bilirubin is > 12 mg%,
Sepsis, Hepatorenal syndrome,
•Surgery is done after 2-3 weeks once bilirubin level
drops down adequately.
•If ERCP is not possible then percutaneous transbiliary
drainage (PTBD) or cholecystostomy using Foley’s or
Malecot’s catheter is done.
•Surgical resection (Whipple’s) is done after 3 weeks.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
In a large multicenter randomized trial comparing early
surgery vs preoperative biliary drainage followed by
surgery in patients with cancer of the pancreas head,
the rates of serious complications were 39% (37 of 96
patients) in the early surgery group and 74% (75 of 106
patients) in the patients submitted to preoperative
biliary drainage (P ≤ 0.001).
A follow-up report from the same trial showed that
there was a significant delay in time to surgery (1 wk vs
5 wk), but no influence on survival rate.
While there was an increase in overall infectious
complications following surgery in the stented group,
the detrimental effects of pre-operative biliary stenting
were likely limited to those with subsequent bacterial
colonization of the biliary tree due to stent placement
Tissue diagnosis
 A tissue diagnosis of adenocarcinoma is not
required prior to an attempt at a curative
resection.
 Fibrosis in pancreatic cancer- may miss the
malignant glands, so sensitivity is less.
 Does not change treatment decision in a
planned curative surgery.
FNA is required if
1.Patients undergoing neoadjuvant therapy.
2. If the diagnosis of carcinoma is uncertain.
3.In suspected neuroendocrine cancers, lymphomas,
cystic lesions, FNA result may alter the treatment.
Medical Management of Obstructive
Jaundice
Hydration
•Adequate hydration is important in prevention of
dehydration postoperatively.
•Dehydration is common in obstructive
jaundice.
•Repeated monitoring by doing electrolytes
•Correction of hypoglycaemia and dilutional
hyponatraemia due to water retention; avoiding isotonic
saline infusion
Coagulopathy
•Correction of coagulopathy, prevention of renal failure,
infection, hepatic encephalopathy and electrolyte
imbalance
•Injection vitamin K IM 10 mg for 5 days.
•Fresh Frozen plasma—often requires 6 bottles or more
Blood transfusion in case of anaemia.
•Repeated monitoring by doing prothrombin time.
•
•Antibiotics like third generation cephalosporins.’
•Often TPN may be required preoperatively which is also
continued postoperatively.’
♦ Pulmonary function study and respiratory physiotherapy to
have adequate postoperative pulmonary function.
Role of Mannitol
Patient is prone to develop hepatorenal syndrome
postoperatively, leading into renal failure due to
sludging of the bile salts, due to toxins and sepsis; and
so mannitol should be given intravenously for 3 days
prior to surgery to flush the kidney (200 ml IV twice a
day).
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Preoperative smoking and alcohol consumption
•For alcohol abusers, 1 month of abstinence before
surgery is beneficial and should be attempted.
•For daily smokers, 1 month of abstinence before surgery
is beneficial.
•For appropriate groups, both should be attempted.
Preoperative nutrition
Routine use of preoperative artificial nutrition is not
warranted, but significantly malnourished patients
should be optimized with oral supplements or enteral
nutrition preoperatively
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Perioperative oral immunonutrition (IN)
The balance of evidence suggests that IN for 5-7 days
perioperatively should be considered because it may
reduce the rate of infectious complications
in patients undergoing major open abdominal surgery.
Oral bowel preparation
Extrapolation of data from studies on colonic surgery
and retrospective studies in PD show that MBP has no
proven benefit. MBP should not be used.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Preoperative fasting and preoperative treatment
with carbohydrates
•Intake of clear fluids up to 2 h before anaesthesia does not
increase gastric residual volume and is recommended
before elective surgery.
•Intake of solids should be withheld 6 h before anaesthesia.
•Data extrapolation from studies in major surgery
suggests that preoperative oral carbohydrate treatment
should be given in patients without diabetes.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Anti-thrombotic prophylaxis
•LMWH reduces the risk of thromboembolic
complications, and administration
should be continued for 4 weeks after hospital discharge.
•Concomitant use of epidural analgesia necessitates close
adherence to safety guidelines.
•Mechanical measures should probably be added for
patients at high risk
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Antimicrobial prophylaxis and skin preparation
•Antimicrobial prophylaxis prevents surgical-site
infections, and should be used in a single-dose manner
initiated 30-60 min before skin incision.
•Repeated intraoperative doses may be necessary
depending on the half-life of the drug and duration of
procedure.
Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure
Epidural analgesia
Mid-thoracic epidurals are recommended based on
data from studies on major open abdominal surgery
showing superior pain relief and fewer respiratory
complications compared with intravenous opioids.
Thank you

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Pancreatic Carcinoma Classification and Preoperative evaluation in Whipple's Procedure

  • 1. Pancreatic Tumor Classification Preoperative evaluation in Whipple’s Procedure Dr.Bhavin Vadodariya DNB Resident Doctor Department of Surgical Oncology Apollo CBCC Cancer Care Apollo Hospital,Ahmedabad Date- 06/01/2018
  • 2.  The most unforgiving organ in the human body.
  • 3. Outline •Classification PDAC Cystic neoplams SPN Endocrine Tumor •Preoperative Management •Assement of resectability •Management of Obstructive jaundice
  • 4. Neoplasms of the pancreas  Solid tumors (AdenoCarcinomas)  Cystic Neoplasms  Endocrine tumors
  • 5. Pancreatic adeno carcinoma  5-year survival rate of only 6%.  9th most common cancer in the US , but 4th in terms of cancer deaths.  74% of patients die within the first yearafter diagnosis.  Common age >60 years, median age is 72years.
  • 6.  Incidence is about 8 to 9 cases per 1,00,000  Incidence is lowest in India and parts of middle east 8.1 and 7.0 per 1,00,000 in men and women respectively
  • 7. Pathology  Pancreatic cancer probably arises through a stepwise progression of cellular changes.  From Pancreatic intra epithelial neoplasia to invasive adeno carcinoma.  75% are ductal adenocarcinoma  Uncommon varieties include Adeno squamous and Acinar cell carcinoma.
  • 8. Adenosquamous carcinoma - It has both glandular and squamous differentiation. The biologic behaviour similar to typical ductal adenocarcinoma. Acinar cell carcinoma - presents as a large tumour, often 10 cm in diameter or more, the prognosis of patients with these tumours may be better than with ductal cancer.
  • 9. Pancreatic Intraepithelial Neoplasia(PanIN)  •Pre cursor lesions for invasive carcinoma •Three stages of pancreatic intraepithelial neoplasia have been defined. From PanIN 1 – PanIN 3 •With progressive cellular atypia and architectural disarray.
  • 11. Location of the tumour  About two-thirds of pancreatic adenocarcinomas arise within the head or uncinate process of the pancreas  15% are in thebody  10% in thetail,  remaining tumours demonstrating diffuse involvement of the gland.
  • 12.  Tumours in the pancreatic body and tail are generally larger at the time of diagnosis, and therefore, less commonly resectable.  Tumours in the head of the pancreas are typically diagnosed earlier because they cause obstructive jaundice.
  • 14. Pathological classification of cystic neoplasms of the pancreas: The who international classification.  Serous cystic neoplasm (SCN)  Mucinous cystic neoplasm (MCN)  Intra-ductal papillary mucinous neoplasm (IPMN)
  • 15. Serous cystic neoplasm (SCN)  Microcystic adenoma  Oligocystic adenoma
  • 16. Mucinous cystic neoplasm (MCN) Mucinous cystadenoma Mucinous cystic tumour–borderline Mucinous cystadenocarcinoma Non-invasive (carcinoma in situ) Invasive
  • 17. Intra-ductal papillary mucinous neoplasm (IPMN)  Adenoma/low-grade dysplasia  Borderline/moderate-grade dysplasia  Carcinoma in situ  Invasive carcinoma
  • 18. SEROUS CYSTIC NEOPLASM  First described by Comagno and Oertel in 1978 as microcystic and glycogen rich and they distinguished these lesions from mucinous cysts.
  • 19. PATHOLOGY  Cell of origin is centroacinar cell.  Soft mass which includes numerous small cysts filled with clear serous fluid arranged in a characteristic honeycomb-like pattern.  unique central calcification give rise to charecterstic central sunburst,radial or stellate scar pattern on CT.
  • 20.  <10 % are serous oligocystic ( macrocystic )SCNhave fewer cysts, usually >2cm but histopathologic appearance is similar to that of microcystic.  Histologically they are have bland cuboidal epithelial lining without nuclear pleomorphism or mitoses.  Syndromic association betweenVHL
  • 21.  EUS-FNA and analysis of fluid – SCN low amylaseand viscosity.  CEA < 5ng/ml, CA 19-9 < 37U/L, excludes MCN and IPMN.
  • 22. MUCINOUS CYSTIC NEOPLASMS  They are mucin secreating cystic tumours that lack communication with the pancreatic duct and contain mucin secreting columnar epithelium.  Grossly, individual cysts are typically greater than 2cm and the tumour mass can be as large as 25cm.these tumours are round with smooth surface and fibrous pseudocapsule.
  • 23.  MCNs are generally contain less than 6 cysts and are spherical in shape.  MCNs are typically located in body and tail ( 95 % ).peripheral eggshell like eccentric calcification occur in 15% of cases and are considered pathognomonic.  Ovarian like stroma surrounding the columnar epitheliumis also pathognomonic and it is the presumed reason that are almost exclusively seen in females( >95% ).
  • 24.  MCNs exhibit characteristics of an adenoma- carcinoma - sequence
  • 25. INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM  IPMNs constitute 15-30% of allcysticlesions.  They are intraductal proliferation of neoplastic mucinous cells leading to dilatation of main panreatic duct or branch ducts.
  • 26.  WHO classification 1. Adenoma 2. Borderline 3. Ca in situ
  • 27. Morphology - IPMN  main duct type  branch duct type  combined type
  • 28. Histology  Gastric foveolar type – Tall columnar cells, mucin, scattered Goblet cells – Common in branch type.  Villous intestinal type- Resemble colonic villous adenoma- Common in Main duct type.  Pancreato biliary – lined by cuboidalcells
  • 29. Extra pancreatic malignancies in patients with IPMN  Colorectal adenomas andcarcinopmas  Barrets mucosa and gastriccarcinoma
  • 30. Analysis of the Cystic Fluid  Differential Diagnosis of Pancreatic Cystic Neoplasms Based on Analysis of Intracystic Fluid Cystic Lesion Amylase CEA Viscosity Mucin Stain Cytology  SCN ↓ ↓ ↓ Negative Glycogen rich  MCN ↓ ↑↑↑ ↑ Positive Mucinous  IPMN  Pseudocyst ↑ ↑↑↑ ↑↑↑ ↑ ↓ ↑ Positive Negative Mucinous Inflammatory
  • 33. Solid Pseudopapillary Tumor (Papillary Cystic Cancer Or Frantz Tumor)
  • 34. • Approximately 90% of solid pseudopapillary tumor harbor APC/beta-catenin mutation • Typically occur in women in the second or third decade of life
  • 35. Regarded as low grade malignant potential tumor. Pathology • Lesions may be large, encapsulated, evenly distributedthroughout the pancreas. • Strongly positive for beta-catenin, progesterone receptors, vimentin, CD-10 and CD-56Q.
  • 36. It can mimic the histologic appearance of NET but lacks the nuclear features of NET and lacks the neuroendocerine markers such as chromagranin and synaptophysin.
  • 38. PNET  Rare ,annual incidence of approximately 5 cases per 1,000,000 population.  Functioning and Non functioning  Sporadically or as a part ofsyndromes.
  • 39. Syndromic pNETS  10% are associated with an underlying genetic syndrome (MEN1) and type IV (MEN4) –pNETS in 80-100% of patients  Small, multifocal and microscopic  Gastrinomas (>80% duodenal) develop in 54% of MEN-1 patients, insulinomas in 18% and glucagonomas, VIPomas, somatostatinomas in <5%  Von Hippel-Lindau disease (VHL),-10% patients develop pNETS  Neurofibromatosis type I (NF1), tuberous sclerosis complex (TSC)
  • 40.  2% of total pancreatic mass areislets  APUD cells – 4 cell types, α, β, γ,δ
  • 42. Insulinoma  Most common 60%  Origin- β cells almost universally within the pancreas (1/3head – 1/3 body – 1/3 tail)  F>M  90% benign, 10% malignant  Most solitary, 10% multiple(MEN 1)  21% MEN 1 – insulinomas  The median age at diagnosis- 47yrs
  • 43. Gastrinoma /Zollinger-Ellison Syndrome  Second most frequent  1 / 2.5 million  60% malignant (mets to liver)  75 % sporadic  M>F  Average age -50 years,5 to 10 years earlier in MEN-1  25 % MEN-1
  • 44. VIPOMA(Verner-Morrison Syndrome)  0.05-0.2 new cases per million adults  Third most common neuroendocrine tumor of the pancreas  Solitary, found in body or tail, usually detected at >3cm size  2/3 malignant  Male-to-female ratio in children - 1:1, in adults. - 1:3
  • 45. Glucagonoma  Tumor of islet alpha cells  Mainly body and tail  1 per 20 million  Mean age of 55 years (19-84 years).  W>M  50% malignant  5-10 cm at diagnosis
  • 46.  Migratory necrolytic erythema 2/3 cases – aminoacid and trace element deficiency  4D syndrome (dermatitis, diabetes, diarrhea, DVT)  Fasting plasma glucagon >50pmol/ml:Diagnostic
  • 47. Somatostatinoma  Rare fewer than 100 cases in literature  70% to 90% of tumours – malignant  Location – usually head  Clinical findings – unpredictable  Diarrhea  Gallstones – 59 %  Steatorrhea  Mild diabetes – 75%
  • 51. CT Scan for pancreas  Multi-detector spiral CT and is the single most useful diagnostic and staging modality.  It gives information about adjacent vascular structures such as the portal, superior mesenteric, and splenic veins, as well as the superior mesenteric artery (SMA) and celiac axis.
  • 52. Phases of an pancreatic protocol  Early arterial phase (15-20 s after injection of contrast)  Late arterial phase (35-40 s)  Hepatic or portal venous phase(50-60s)  Nephrogenic Phase (100s)  Delayed phase (6-10minutes)
  • 53.  The non contrast phase - pancreatic calcifications, for localization of the precise levels the post contrast study.  The early arterial phase permits evaluation of pancreatic vasculature without interference from venous opacification.
  • 54.  The late arterial phase - distinguish pancreatic neoplasms from adjacent normal pancreatic tissue, to evaluate hyper-vascular liver metastases (neuroendocrine tumors of the pancreas).  The 4th phase portal venous phase - for hypo- vascular liver metastases
  • 60. Unresectability in CT  Unresectability is defined on multiphase CT by involvement of 1. ≥ 180 degrees of the celiac axis 2. hepatic or superior mesenteric artery, enlarged lymph nodes outside the boundaries of resection 3. ascites, and distant metastases.  Invasion of the superior mesenteric vein or portal vein is not in itself a contraindication to resection as long as the veins are patent. Resection of vein with reconstruction is possible.
  • 61. CT images Dilated intrahepatic ducts. Double-duct sign” with dilated common bile duct and pancreatic ducts. There is a stent in the common bile duct (S)
  • 62. Pancreas cancer mass with stent through it (arrow). Superior mesenteric artery (SMA) (A) is adjacent to tumor. Tree-dimensional CT vascular reconstruction Portal and superior mesenteric veins do not appear involved.
  • 64. ERCP  ERCP may be of benefit in patients with biliary obstruction and cholangitis - endoscopic stent can be placed for decompression.  With current capabilities of CT and MRI, ERCP is rarely necessary.
  • 65. Endoscopic retrograde cholangiopancreatogram (ERCP) of patient with pancreas cancer with abrupt cut-off of main pancreatic duct secondary to tumor. ERCP of patient with pancreas cancer with obstruction of both main pancreatic duct and common bile duct
  • 66. Completion cholangiogram after endoscopic placement of stent
  • 67. Indications for pre operative decompression of biliary system.  Cachexic patient for nutritionalimprovement.  In patients withcholangitis  If plan is non operativemanagement. If bilirubin is > 12 mg%, Sepsis, Hepatorenal syndrome,
  • 68. •Surgery is done after 2-3 weeks once bilirubin level drops down adequately. •If ERCP is not possible then percutaneous transbiliary drainage (PTBD) or cholecystostomy using Foley’s or Malecot’s catheter is done. •Surgical resection (Whipple’s) is done after 3 weeks.
  • 70. In a large multicenter randomized trial comparing early surgery vs preoperative biliary drainage followed by surgery in patients with cancer of the pancreas head, the rates of serious complications were 39% (37 of 96 patients) in the early surgery group and 74% (75 of 106 patients) in the patients submitted to preoperative biliary drainage (P ≤ 0.001).
  • 71. A follow-up report from the same trial showed that there was a significant delay in time to surgery (1 wk vs 5 wk), but no influence on survival rate. While there was an increase in overall infectious complications following surgery in the stented group, the detrimental effects of pre-operative biliary stenting were likely limited to those with subsequent bacterial colonization of the biliary tree due to stent placement
  • 72. Tissue diagnosis  A tissue diagnosis of adenocarcinoma is not required prior to an attempt at a curative resection.  Fibrosis in pancreatic cancer- may miss the malignant glands, so sensitivity is less.  Does not change treatment decision in a planned curative surgery.
  • 73. FNA is required if 1.Patients undergoing neoadjuvant therapy. 2. If the diagnosis of carcinoma is uncertain. 3.In suspected neuroendocrine cancers, lymphomas, cystic lesions, FNA result may alter the treatment.
  • 74. Medical Management of Obstructive Jaundice
  • 75. Hydration •Adequate hydration is important in prevention of dehydration postoperatively. •Dehydration is common in obstructive jaundice. •Repeated monitoring by doing electrolytes •Correction of hypoglycaemia and dilutional hyponatraemia due to water retention; avoiding isotonic saline infusion
  • 76. Coagulopathy •Correction of coagulopathy, prevention of renal failure, infection, hepatic encephalopathy and electrolyte imbalance •Injection vitamin K IM 10 mg for 5 days. •Fresh Frozen plasma—often requires 6 bottles or more Blood transfusion in case of anaemia. •Repeated monitoring by doing prothrombin time. •
  • 77. •Antibiotics like third generation cephalosporins.’ •Often TPN may be required preoperatively which is also continued postoperatively.’ ♦ Pulmonary function study and respiratory physiotherapy to have adequate postoperative pulmonary function.
  • 78. Role of Mannitol Patient is prone to develop hepatorenal syndrome postoperatively, leading into renal failure due to sludging of the bile salts, due to toxins and sepsis; and so mannitol should be given intravenously for 3 days prior to surgery to flush the kidney (200 ml IV twice a day).
  • 80. Preoperative smoking and alcohol consumption •For alcohol abusers, 1 month of abstinence before surgery is beneficial and should be attempted. •For daily smokers, 1 month of abstinence before surgery is beneficial. •For appropriate groups, both should be attempted.
  • 81. Preoperative nutrition Routine use of preoperative artificial nutrition is not warranted, but significantly malnourished patients should be optimized with oral supplements or enteral nutrition preoperatively
  • 83. Perioperative oral immunonutrition (IN) The balance of evidence suggests that IN for 5-7 days perioperatively should be considered because it may reduce the rate of infectious complications in patients undergoing major open abdominal surgery.
  • 84. Oral bowel preparation Extrapolation of data from studies on colonic surgery and retrospective studies in PD show that MBP has no proven benefit. MBP should not be used.
  • 87. Preoperative fasting and preoperative treatment with carbohydrates •Intake of clear fluids up to 2 h before anaesthesia does not increase gastric residual volume and is recommended before elective surgery. •Intake of solids should be withheld 6 h before anaesthesia. •Data extrapolation from studies in major surgery suggests that preoperative oral carbohydrate treatment should be given in patients without diabetes.
  • 89. Anti-thrombotic prophylaxis •LMWH reduces the risk of thromboembolic complications, and administration should be continued for 4 weeks after hospital discharge. •Concomitant use of epidural analgesia necessitates close adherence to safety guidelines. •Mechanical measures should probably be added for patients at high risk
  • 91. Antimicrobial prophylaxis and skin preparation •Antimicrobial prophylaxis prevents surgical-site infections, and should be used in a single-dose manner initiated 30-60 min before skin incision. •Repeated intraoperative doses may be necessary depending on the half-life of the drug and duration of procedure.
  • 93. Epidural analgesia Mid-thoracic epidurals are recommended based on data from studies on major open abdominal surgery showing superior pain relief and fewer respiratory complications compared with intravenous opioids.