Carcinoma Head of
pancreas
CHAIRPERSON
DR. JAGADISH B
PROFESSOR AND HOD
DEPT. OF GENERAL SURGERY
KVG MEDICAL COLLEGE
PRESENTER
Dr. Veeranath reddy.v
PG Student
 Referrences:
 Bailey &love 26th edition
 Schwartz principles of surgery (10th edition)
 Sabiston first (southeast asia edition)
 Blumgarts hepatobiliary surgery
 Objectives:
 Surgical anatomy
 Epidemiology
 pathology
 Clinical features
 Management
Pancreas
Normal (50%)
Carcinoma head of pancreas
 Incidence is about 8 to 9 cases per 1,00,000
population.
 9th most common cancer in the US , but 4th in terms of
cancer deaths.
 74% of patients die within the first year after diagnosis,
with 5-year survival rate of only 6%.
Risk Factors
 Environmental
 Genetic
Risk Factors – Definitive Association
Smoking
1 – 3 times risk, Directly proportional to the
quantity and duration of smoking (i.e. pack
year).
Environmental risk Factors –
Suggested Association
 Diabetes Mellitus
 Chronic Pancreatitis
 Obesity
 Diet
Diabetes Mellitus
 Glucose intolerance in 80% of patients , 50%
overt diabetes.
 Two fold increase in chance of Ca pancreas in
patients with pre existing diabetes.
 The new onset of diabetes - may be an early
manifestation of occult pancreatic cancer.
Chronic Pancreatitis
 Patients with chronic pancreatitis especially
familial have up to a 20-fold increase in risk for
pancreatic cancer.
Obesity
 obese patients may be up to three times more likely
to develop pancreatic cancer than non-obese
individuals.
Diet
 Increased risk with increased total calorie intake, and
increased intake of carbohydrate, cholesterol, meat, salt,
dehydrated food, fried food, refined sugar, and nitrosamines.
 Fat, beta carotene, and coffee are of unproven risk.
 Consumption of dietary fibre, vitamin C, fruits, vegetables, and
unprepared food may have a protective effect, as may
pressure and microwave cooking.
Environmental risk Factors – Unproven
Association
 Alcohol
 Coffee
 Radiation
Genetic Risk Factors
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.
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.
Location of the tumour
 About two-thirds of pancreatic adenocarcinomas
arise within the head or uncinate process of the
pancreas
 15% are in the body
 10% in the tail,
 remaining tumours demonstrating diffuse
involvement of the gland.
Clinical features
 The symptoms at presentation are related to the
location of the tumour.
 Lesions occurring in or near the bile duct presents
with obstructive jaundice,
 body or tail with pain.
 Weight loss, loss of appetite, generalised weakness -
non specific
 Tumours in the head of the pancreas are typically
diagnosed earlier because they cause obstructive
jaundice.
 Tumours in the pancreatic body and tail are generally
larger at the time of diagnosis, and therefore, less
commonly resectable.
Presentation - History
 The classic constellation of symptoms in 66%-
75% of cases.
 Painless, progressive Jaundice associated with
 Pruritus
 Acholic stools
 High -coloured urine.
 Pain,( left sided tumour present with pain)
 cachexia
 Pancreatitis in the absence of cholelithiasis and ethanol
abuse.
 New onset diabetes mellitus and pancreatic exocrine
insufficiency are rare as initial presentation.
 Non specific symptoms include nausea, anorexia, weight
loss.
 Symptoms of GOO – Indicate locally advanced disease.
Clinical signs
 Anaemia
 icterus,
 hepatomegaly,
 a palpable gallbladder (Courvoisier’s sign),
 and skin excoriation from pruritus and scratching.
Signs of advanced disease
 Cachexia
 palpable nodules in the liver
 palpable metastatic disease in the left supra-
clavicular fossa (Virchow’s node),
 palpable metastatic disease in the periumbilical area
(Sister Mary Joseph’s node)
 Pelvic metastatic disease palpable anteriorly on
rectal examination (Blumer’s shelf).
Biochemical investigations
LFT
Elevated bilirubin, alkaline phosphatase and GGT
Only mild to moderate elevations in liver
transaminases
CA 19-9
 Used in cases where diagnosis is in doubt.
 Elevated in 75% of patients with pancreas cancer.
 also elevated in benign conditions of the pancreas,
liver, and bile ducts.
 To measure response to therapy or for screening for
recurrence
 Fallacy – can not be used in cases of jaundice.
Imaging
 ultrasonography
 Computed tomography (CT),
 Endoscopic ultrasound (EUS)
 Magnetic resonance imaging (MRI) with or without
magnetic resonance cholangio-pancreatography (MRCP)
 Endoscopic retrograde cholangio-pancreatography
(ERCP)
 Positron emission Tomography (PET)
Ultrasonography
 Initial investigation
 The sensitivity is low, and the absence of a
pancreatic mass by ultrasonography does not rule
out ca pancreas, Also pick up hepatic metastases,
pancreatic massesp, eripancreatic and hilar
lymphadenopathy, and ascites.
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 CT
scan
 Non Contrast CT
 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 (100 s)
 Delayed phase (6-10 minutes)
 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
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.
ENDOSCOPIC ULTRASOUND ( EUS
)
Sensitivity ranges from 69 to 94%.
Superior than CT for detecting the lesions smaller
than 2cm
It is superior to CT for the venous invasion but it is
less useful in determination of arterial involvement.
 Another advantage of EUS is the ability to obtain tissue for
biopsy via FNA.
 With EUS, the issue of needle-tract tumour seeding is
minimized, as the FNA is generally performed through a
segment of duodenal or stomach wall that will be removed as
part of a resection,
The duodenum, ampulla, head of the
pancreas, and uncinated process of the
pancreas are accessible with an
ultrasound probe positioned in the
duodenum.
The body and tail of the pancreas are
accessible with an ultrasound probe
positioned in the stomach.
Images eus
Endoscopic ultrasound (EUS) image with linear array echoendoscope demonstrating a mass in the
head of the pancreas with no vascular invasion of the superior mesenteric artery (SMA), superior
mesenteric vein (SMV), or portal vein (PORTAL).
MRI and MRCP
 MRI, MRA, and MRCP can be performed in a single
setting.
 has the potential to provide information about tumour
size and extent, biliary and pancreatic ductal
anatomy, and vascular involvement through a single,
non-invasive procedure.
 Motion artefact, lack of bowel opacification,
compromised resolution, and patient discomfort from
the longer scanning times are disadvantages.
MRI Vs CT
 There is no significant diagnostic advantage of MRI
over contrast- enhanced CT
 MRI is better at characterizing cystic lesions of the
pancreas
 has the capability to evaluate the bile ducts both
above and below a stricture, and can also identify
intrahepatic mass lesions
T1-weighted MR images with gadolinium contrast. A mass in the head
of the pancreas appears hypodense.
Single-shot spin-echo MR cholangiopancreatogram of patient with obstructive jaundice. Both the
common bile duct and the pancreatic duct are dilated. The hypointense tumor is apparent in the
periampullary region.
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
Indications for pre operative
decompression of biliary system.
 Cachexic patient for nutritional improvement.
 In patients with cholangitis
 If your plan is non operative management.
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.
Staging
 CT, EUS, MRI to detect local disease.
 Chest x-ray with SOS CT chest,
 Staging laparoscopy- varies between institutions.
AJCC Staging
Staging of Pancreatic Cancer
 TX: Primary tumor cannot be assessed
 T0: No evidence of primary tumor
 Tis: Carcinoma in situ
 T1: Limited to pancreas, ≤ 2 cm in greatest dimension
 T2: Limited to the pancreas, >2 cm in greatest dimension
 T3: Extends beyond the pancreas, without involving of the celiac
axis or the superior mesenteric artery
 T4: Involves the celiac axis or the superior mesenteric artery
(unresectable).
 Regional lymph nodes
- NX: Regional lymph nodes cannot be
assessed
- N0: No regional lymph node metastasis
- N1: Regional lymph node metastasis
present
 Distant metastasis
- MX: Distant metastasis cannot be
assessed
- M0: No distant metastasis
- M1: Distant metastasis
Stage grouping
Management
Surgical Procedures
 Head of the pancreas:
Whipple Procedure
Allen Oldfather Whipple
(1881-1963)
 Pancreatico-duodenectomy (PD)
was first performed by Kausch in
1908, and popularized by Whipple
in the 1930s (who performed 37
procedures).
—Whipple AO, Parsons WB,
Mullins CR.
Treatment of Carcinoma of the Ampulla of Vater.
Ann Surg 1935; 102: 763-769.
STEP 1 EXPOSURE OF INFRA PANCREATIC
SMV
 The lesser sac is entered,
The inferior body of the
pancreas is identified.
 The superior mesenteric
vein (SMV) is exposed at
the inferior border of the
neck of the pancreas
adjacent to the uncinate
process.
STEP 2 KOCHERS MANEUVERE
 A Kocher maneuver has been
performed by first identifying the
inferior vena cava (IVC) at the level
of the proximal portion of the
transverse segment of the
duodenum (D3).
 One can then mobilize the
duodenum and pancreatic head off
of the IVC in a cephalad direction
thereby removing all soft tissue
anterior to the IVC.
 Note that the Kocher maneuver is
continued to the left lateral border
of the aorta .
STEP 3: PORTAL DISSECTION
 Dissection of the porta hepatis begins
with identification of the common
hepatic artery (CHA), by removal of
the large lymph node which
commonly sits anterior to this vessel.
 The CHA is then followed distally to
allow identification and division of the
right gastric artery and the
gastroduodenal artery (GDA).
 This allows the CHA to be mobilized
off of the underlying anterior surface
of the portal vein (PV). The PV is
always identified prior to division of
the common hepatic duct (CHD).
STEP 4: TRANSECT STOMACH
 The antrum of the stomach is
resected with the main
specimen by dividing the
stomach at the level of the third
or fourth transverse vein on the
lesser curvature.
 Sometimes the entire stomach is
preserved; when this is done,
the operation is called a pylorus
preserving Whipple (or
pancreaticoduodenectomy).
STEP 5: TRANSECTION OF JEJUNUM
 Transection of the jejunum is
followed by ligation and division of
its mesentery. The loose
attachments of the ligament of Treitz
are taken down, and the fourth and
third portions of the duodenum are
mobilized by dividing their short
mesenteric vessels.
 The duodenum and jejunum are
then reflected underneath the
mesenteric vessels in preparation
for the final and most important part
of pancreaticoduodenectomy.
STEP 6: TRANSECT PANCREAS
 The pancreatic head and uncinate
process are separated from the
superior mesenteric-portal vein
confluence.
 The pancreas has been
transected at the level of the
portal vein and the pancreatic
head is reflected laterally, allowing
identification of small venous
tributaries from the portal vein and
superior mesenteric vein (SMV).
These tributaries are ligated and
divided.
Modified Whipple operation
—PPPD
 A more limited duodenectomy with preservation of
the stomach and antropyloric region is preferred by
some experts .
PPPD
Pylorus-preserving
pancreatico-
duodenectomy
Advantages of pyloric preservation
 Prevention of reflux of pancreaticobiliary secretions into
the stomach,
 decreased incidence of marginal ulceration,
 normal gastric acid secretion and hormone release, and
improved gastric function.
 Patients with pylorus-preserving resections have
appeared to regain weight better than historic controls.
 it is controversial whether there is any significant
improvement in long-term quality of life with pyloric
preservation.
Classic Whipple V.S. PPPD
 PPPD—protects against gastric dumping, marginal
ulceration, and bile reflux gastritis. Significant
reduction of the operation time, the intraoperative
blood loss and the consequent need for blood
substitution.
 But sufficiently radical to treat pancreatic cancer?
Similar or even better postoperative morbidity and
mortality result was debated.
Results following
Pancreaticoduodenectomy
Due to improved surgical skill and peri-operative care
 Mortality rate 20%-40% in earlier days
 During the past decades, dramatically decreased and
currently is between 0-4% in experience centers with
experience.
 Complication rate is still 30%-40%
Complications of
Pancreaticoduodenectomy
 Common
Delayed gastric emptying
Pancreatic fistula
Intra-abdominal abscess
Hemorrhage
Wound infection
Metabolic
Diabetes
Pancreatic exocrine
insufficiency
 Uncommon
Fistula (Biliary , Duodenal, Gastric )
Organ failure
Cardiac
Hepatic
Pulmonary
Renal
Pancreatitis
Marginal ulceration
CHEMOTHERAPY
Chemotherapy
 5 FU alone or combination with radiotherapy
 gemcitabine
ADJUVANT CHEMOTHERAPY
 Current recommendation for adjuvant chemotherapy
- gemcitabine
 capecitabine, a prodrug for 5-FU. It is sequentially
metabolized into active 5-FU by enzyme thymidine
phosphorylase-highly expressed in the tumour.
 This has four potential advantages:
1) systemic side effects are reduced,
2) high concentrations are achieved in the vicinity of
the tumor,
3) oral capecitabine has a pharmacokinetic profile
similar to that of a continuous systemic infusion 5-
FU, and
4) Patients tolerate it better than 5-FU.
 But clinical response in 24% and tumor response in
7% . Better responses when combined with
gemcitabine.
RADIOTHERAPY
INTRAOPERATIVE RADIOTHERAPY
 EBRT on the pancreatic bed is limited – adjascent
radiosensitive structures; so intraoperative
radiotherapy (IORT) is useful.
 Results unsatisfactory.
PALLIATIVE
CARE
Surgical Palliative procedures – Biliary
enteric bypass
Coeliac nerve block
Non operative palliation
 Nonoperative Palliation of Obstructive Jaundice
Per cutaneous drainage or endoscopic stenting
 Nonoperative Palliation of Duodenal Obstruction
Self expanding gastro duodenal stenting
PALLIATIVE CHEMOTHERAPY
 Gemcitabine is more beneficial than 5-FU when used
as monotherapy in advanced pancreatic cancer.
 Those receiving gemcitabine had a modest but
significant increase in median survival (5.56 vs. 4.41
months; P = .0025) and improved clinical benefit
(23.8% vs. 4.8%; P = .0022).
PALLIATIVE RADIOTHERAPY
 Hyper fractionation and IMRT – Better tolerance
Thank you...

Veeru ca pancreas

  • 1.
    Carcinoma Head of pancreas CHAIRPERSON DR.JAGADISH B PROFESSOR AND HOD DEPT. OF GENERAL SURGERY KVG MEDICAL COLLEGE PRESENTER Dr. Veeranath reddy.v PG Student
  • 2.
     Referrences:  Bailey&love 26th edition  Schwartz principles of surgery (10th edition)  Sabiston first (southeast asia edition)  Blumgarts hepatobiliary surgery
  • 3.
     Objectives:  Surgicalanatomy  Epidemiology  pathology  Clinical features  Management
  • 4.
  • 9.
  • 10.
    Carcinoma head ofpancreas  Incidence is about 8 to 9 cases per 1,00,000 population.  9th most common cancer in the US , but 4th in terms of cancer deaths.  74% of patients die within the first year after diagnosis, with 5-year survival rate of only 6%.
  • 11.
  • 12.
    Risk Factors –Definitive Association Smoking 1 – 3 times risk, Directly proportional to the quantity and duration of smoking (i.e. pack year).
  • 13.
    Environmental risk Factors– Suggested Association  Diabetes Mellitus  Chronic Pancreatitis  Obesity  Diet
  • 14.
    Diabetes Mellitus  Glucoseintolerance in 80% of patients , 50% overt diabetes.  Two fold increase in chance of Ca pancreas in patients with pre existing diabetes.  The new onset of diabetes - may be an early manifestation of occult pancreatic cancer.
  • 15.
    Chronic Pancreatitis  Patientswith chronic pancreatitis especially familial have up to a 20-fold increase in risk for pancreatic cancer.
  • 16.
    Obesity  obese patientsmay be up to three times more likely to develop pancreatic cancer than non-obese individuals.
  • 17.
    Diet  Increased riskwith increased total calorie intake, and increased intake of carbohydrate, cholesterol, meat, salt, dehydrated food, fried food, refined sugar, and nitrosamines.  Fat, beta carotene, and coffee are of unproven risk.  Consumption of dietary fibre, vitamin C, fruits, vegetables, and unprepared food may have a protective effect, as may pressure and microwave cooking.
  • 18.
    Environmental risk Factors– Unproven Association  Alcohol  Coffee  Radiation
  • 19.
  • 20.
    Pathology  Pancreatic cancerprobably 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.
  • 21.
    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.
  • 23.
    Location of thetumour  About two-thirds of pancreatic adenocarcinomas arise within the head or uncinate process of the pancreas  15% are in the body  10% in the tail,  remaining tumours demonstrating diffuse involvement of the gland.
  • 24.
    Clinical features  Thesymptoms at presentation are related to the location of the tumour.  Lesions occurring in or near the bile duct presents with obstructive jaundice,  body or tail with pain.  Weight loss, loss of appetite, generalised weakness - non specific
  • 25.
     Tumours inthe head of the pancreas are typically diagnosed earlier because they cause obstructive jaundice.  Tumours in the pancreatic body and tail are generally larger at the time of diagnosis, and therefore, less commonly resectable.
  • 26.
    Presentation - History The classic constellation of symptoms in 66%- 75% of cases.  Painless, progressive Jaundice associated with  Pruritus  Acholic stools  High -coloured urine.  Pain,( left sided tumour present with pain)  cachexia
  • 27.
     Pancreatitis inthe absence of cholelithiasis and ethanol abuse.  New onset diabetes mellitus and pancreatic exocrine insufficiency are rare as initial presentation.  Non specific symptoms include nausea, anorexia, weight loss.  Symptoms of GOO – Indicate locally advanced disease.
  • 28.
    Clinical signs  Anaemia icterus,  hepatomegaly,  a palpable gallbladder (Courvoisier’s sign),  and skin excoriation from pruritus and scratching.
  • 29.
    Signs of advanceddisease  Cachexia  palpable nodules in the liver  palpable metastatic disease in the left supra- clavicular fossa (Virchow’s node),  palpable metastatic disease in the periumbilical area (Sister Mary Joseph’s node)  Pelvic metastatic disease palpable anteriorly on rectal examination (Blumer’s shelf).
  • 30.
    Biochemical investigations LFT Elevated bilirubin,alkaline phosphatase and GGT Only mild to moderate elevations in liver transaminases
  • 31.
    CA 19-9  Usedin cases where diagnosis is in doubt.  Elevated in 75% of patients with pancreas cancer.  also elevated in benign conditions of the pancreas, liver, and bile ducts.  To measure response to therapy or for screening for recurrence  Fallacy – can not be used in cases of jaundice.
  • 32.
    Imaging  ultrasonography  Computedtomography (CT),  Endoscopic ultrasound (EUS)  Magnetic resonance imaging (MRI) with or without magnetic resonance cholangio-pancreatography (MRCP)  Endoscopic retrograde cholangio-pancreatography (ERCP)  Positron emission Tomography (PET)
  • 33.
    Ultrasonography  Initial investigation The sensitivity is low, and the absence of a pancreatic mass by ultrasonography does not rule out ca pancreas, Also pick up hepatic metastases, pancreatic massesp, eripancreatic and hilar lymphadenopathy, and ascites.
  • 34.
    CT Scan forpancreas  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.
  • 35.
    Phases of anpancreatic protocol CT scan  Non Contrast CT  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 (100 s)  Delayed phase (6-10 minutes)
  • 36.
     The noncontrast 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.
  • 37.
     The latearterial 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
  • 38.
    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.
  • 39.
    CT images Dilated intrahepaticducts. Double-duct sign” with dilated common bile duct and pancreatic ducts. There is a stent in the common bile duct (S)
  • 40.
    Pancreas cancer masswith 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.
  • 42.
    ENDOSCOPIC ULTRASOUND (EUS ) Sensitivity ranges from 69 to 94%. Superior than CT for detecting the lesions smaller than 2cm It is superior to CT for the venous invasion but it is less useful in determination of arterial involvement.
  • 43.
     Another advantageof EUS is the ability to obtain tissue for biopsy via FNA.  With EUS, the issue of needle-tract tumour seeding is minimized, as the FNA is generally performed through a segment of duodenal or stomach wall that will be removed as part of a resection,
  • 44.
    The duodenum, ampulla,head of the pancreas, and uncinated process of the pancreas are accessible with an ultrasound probe positioned in the duodenum. The body and tail of the pancreas are accessible with an ultrasound probe positioned in the stomach.
  • 45.
    Images eus Endoscopic ultrasound(EUS) image with linear array echoendoscope demonstrating a mass in the head of the pancreas with no vascular invasion of the superior mesenteric artery (SMA), superior mesenteric vein (SMV), or portal vein (PORTAL).
  • 46.
    MRI and MRCP MRI, MRA, and MRCP can be performed in a single setting.  has the potential to provide information about tumour size and extent, biliary and pancreatic ductal anatomy, and vascular involvement through a single, non-invasive procedure.  Motion artefact, lack of bowel opacification, compromised resolution, and patient discomfort from the longer scanning times are disadvantages.
  • 47.
    MRI Vs CT There is no significant diagnostic advantage of MRI over contrast- enhanced CT  MRI is better at characterizing cystic lesions of the pancreas  has the capability to evaluate the bile ducts both above and below a stricture, and can also identify intrahepatic mass lesions
  • 48.
    T1-weighted MR imageswith gadolinium contrast. A mass in the head of the pancreas appears hypodense.
  • 49.
    Single-shot spin-echo MRcholangiopancreatogram of patient with obstructive jaundice. Both the common bile duct and the pancreatic duct are dilated. The hypointense tumor is apparent in the periampullary region.
  • 50.
    ERCP  ERCP maybe 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.
  • 51.
    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
  • 52.
    Indications for preoperative decompression of biliary system.  Cachexic patient for nutritional improvement.  In patients with cholangitis  If your plan is non operative management.
  • 53.
    Tissue diagnosis  Atissue 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.
  • 54.
    FNA is requiredif 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.
  • 55.
    Staging  CT, EUS,MRI to detect local disease.  Chest x-ray with SOS CT chest,  Staging laparoscopy- varies between institutions.
  • 56.
  • 57.
    Staging of PancreaticCancer  TX: Primary tumor cannot be assessed  T0: No evidence of primary tumor  Tis: Carcinoma in situ  T1: Limited to pancreas, ≤ 2 cm in greatest dimension  T2: Limited to the pancreas, >2 cm in greatest dimension  T3: Extends beyond the pancreas, without involving of the celiac axis or the superior mesenteric artery  T4: Involves the celiac axis or the superior mesenteric artery (unresectable).
  • 58.
     Regional lymphnodes - NX: Regional lymph nodes cannot be assessed - N0: No regional lymph node metastasis - N1: Regional lymph node metastasis present  Distant metastasis - MX: Distant metastasis cannot be assessed - M0: No distant metastasis - M1: Distant metastasis
  • 59.
  • 60.
  • 61.
    Surgical Procedures  Headof the pancreas: Whipple Procedure
  • 62.
    Allen Oldfather Whipple (1881-1963) Pancreatico-duodenectomy (PD) was first performed by Kausch in 1908, and popularized by Whipple in the 1930s (who performed 37 procedures). —Whipple AO, Parsons WB, Mullins CR. Treatment of Carcinoma of the Ampulla of Vater. Ann Surg 1935; 102: 763-769.
  • 65.
    STEP 1 EXPOSUREOF INFRA PANCREATIC SMV  The lesser sac is entered, The inferior body of the pancreas is identified.  The superior mesenteric vein (SMV) is exposed at the inferior border of the neck of the pancreas adjacent to the uncinate process.
  • 66.
    STEP 2 KOCHERSMANEUVERE  A Kocher maneuver has been performed by first identifying the inferior vena cava (IVC) at the level of the proximal portion of the transverse segment of the duodenum (D3).  One can then mobilize the duodenum and pancreatic head off of the IVC in a cephalad direction thereby removing all soft tissue anterior to the IVC.  Note that the Kocher maneuver is continued to the left lateral border of the aorta .
  • 67.
    STEP 3: PORTALDISSECTION  Dissection of the porta hepatis begins with identification of the common hepatic artery (CHA), by removal of the large lymph node which commonly sits anterior to this vessel.  The CHA is then followed distally to allow identification and division of the right gastric artery and the gastroduodenal artery (GDA).  This allows the CHA to be mobilized off of the underlying anterior surface of the portal vein (PV). The PV is always identified prior to division of the common hepatic duct (CHD).
  • 68.
    STEP 4: TRANSECTSTOMACH  The antrum of the stomach is resected with the main specimen by dividing the stomach at the level of the third or fourth transverse vein on the lesser curvature.  Sometimes the entire stomach is preserved; when this is done, the operation is called a pylorus preserving Whipple (or pancreaticoduodenectomy).
  • 69.
    STEP 5: TRANSECTIONOF JEJUNUM  Transection of the jejunum is followed by ligation and division of its mesentery. The loose attachments of the ligament of Treitz are taken down, and the fourth and third portions of the duodenum are mobilized by dividing their short mesenteric vessels.  The duodenum and jejunum are then reflected underneath the mesenteric vessels in preparation for the final and most important part of pancreaticoduodenectomy.
  • 70.
    STEP 6: TRANSECTPANCREAS  The pancreatic head and uncinate process are separated from the superior mesenteric-portal vein confluence.  The pancreas has been transected at the level of the portal vein and the pancreatic head is reflected laterally, allowing identification of small venous tributaries from the portal vein and superior mesenteric vein (SMV). These tributaries are ligated and divided.
  • 73.
    Modified Whipple operation —PPPD A more limited duodenectomy with preservation of the stomach and antropyloric region is preferred by some experts .
  • 74.
  • 75.
    Advantages of pyloricpreservation  Prevention of reflux of pancreaticobiliary secretions into the stomach,  decreased incidence of marginal ulceration,  normal gastric acid secretion and hormone release, and improved gastric function.  Patients with pylorus-preserving resections have appeared to regain weight better than historic controls.  it is controversial whether there is any significant improvement in long-term quality of life with pyloric preservation.
  • 76.
    Classic Whipple V.S.PPPD  PPPD—protects against gastric dumping, marginal ulceration, and bile reflux gastritis. Significant reduction of the operation time, the intraoperative blood loss and the consequent need for blood substitution.  But sufficiently radical to treat pancreatic cancer? Similar or even better postoperative morbidity and mortality result was debated.
  • 77.
    Results following Pancreaticoduodenectomy Due toimproved surgical skill and peri-operative care  Mortality rate 20%-40% in earlier days  During the past decades, dramatically decreased and currently is between 0-4% in experience centers with experience.  Complication rate is still 30%-40%
  • 78.
    Complications of Pancreaticoduodenectomy  Common Delayedgastric emptying Pancreatic fistula Intra-abdominal abscess Hemorrhage Wound infection Metabolic Diabetes Pancreatic exocrine insufficiency  Uncommon Fistula (Biliary , Duodenal, Gastric ) Organ failure Cardiac Hepatic Pulmonary Renal Pancreatitis Marginal ulceration
  • 79.
  • 80.
    Chemotherapy  5 FUalone or combination with radiotherapy  gemcitabine
  • 81.
    ADJUVANT CHEMOTHERAPY  Currentrecommendation for adjuvant chemotherapy - gemcitabine  capecitabine, a prodrug for 5-FU. It is sequentially metabolized into active 5-FU by enzyme thymidine phosphorylase-highly expressed in the tumour.
  • 82.
     This hasfour potential advantages: 1) systemic side effects are reduced, 2) high concentrations are achieved in the vicinity of the tumor, 3) oral capecitabine has a pharmacokinetic profile similar to that of a continuous systemic infusion 5- FU, and 4) Patients tolerate it better than 5-FU.
  • 83.
     But clinicalresponse in 24% and tumor response in 7% . Better responses when combined with gemcitabine.
  • 84.
  • 85.
    INTRAOPERATIVE RADIOTHERAPY  EBRTon the pancreatic bed is limited – adjascent radiosensitive structures; so intraoperative radiotherapy (IORT) is useful.  Results unsatisfactory.
  • 86.
  • 87.
    Surgical Palliative procedures– Biliary enteric bypass
  • 88.
  • 89.
    Non operative palliation Nonoperative Palliation of Obstructive Jaundice Per cutaneous drainage or endoscopic stenting  Nonoperative Palliation of Duodenal Obstruction Self expanding gastro duodenal stenting
  • 90.
    PALLIATIVE CHEMOTHERAPY  Gemcitabineis more beneficial than 5-FU when used as monotherapy in advanced pancreatic cancer.  Those receiving gemcitabine had a modest but significant increase in median survival (5.56 vs. 4.41 months; P = .0025) and improved clinical benefit (23.8% vs. 4.8%; P = .0022).
  • 91.
    PALLIATIVE RADIOTHERAPY  Hyperfractionation and IMRT – Better tolerance
  • 92.

Editor's Notes

  • #5 Largest digestive gland, Salmon pink in colour Firm, lobulated smooth surface.
  • #6 The boundary between head and neck is often marked - anteriorly by a groove for the gastroduodenal artery - posteriorly by a similar but deeper groove containing the union of the superior mesenteric and splenic veins to form the portal vein The uncinate process of the pancreas extends from the inferior lateral end of the head of the gland.
  • #7 The head of the pancreas cannot be resected without devascularizing the duodenum unless a rim of pancreas containing the pancreaticoduodenal arcade is preserved.
  • #8 the veins usually superficial to the arteries. Anterior traction on the transverse colon can tear fragile branches along the inferior border of the pancreas, which then retract into the parenchyma of the pancreas. Venous branches draining the pancreatic head and uncinate process enter along the right lateral and posterior sides of the portal vein. There are usually no anterior venous tributaries, and a plane can usually be developed between the neck of the pancreas and the portal and superior mesenteric veins.
  • #9 The lymphatic drainage from the pancreas is diffuse and widespread, which explains the high incidence of lymph node metastases and local recurrence of pancreatic cancer. The pancreatic lymphatics also communicate with lymph nodes in the transverse mesocolon and mesentery of the proximal jejunum. Tumors in the body and tail of the pancreas are often unresectable because they metastasize to these lymph nodes.
  • #11 Worst prognosis of all with survival of 6%. The incidence of pancreatic cancer continues to increase, perhaps related to the increased incidence of risk factors such as obesity and diabetes
  • #14 As with other GI malignancies, diet rich in refined carbohydrates and saturated fatty acids are thought tio be associated with pancreatic cancer
  • #15 Thus, the new onset of diabetes, or a sudden increase in insulin requirement in an elderly patient with pre-existing diabetes, should provoke concern for the presence of pancreatic cancer.
  • #21 Like colonic adenoma carcinoma sequence
  • #23 PanIN1A - Replacement of the normal cuboidal, non-mucinous ductal epithelium with columnar cells that contain abundant apical mucin, but without architectural complexity (e.g., papilla formation) or cytological atypia. Cytologically similar lesions like PanIn1A that form papillae constitute PanIN1B When a substantial pseudo-stratification of the cells and some degree of cytological atypia are seen, the lesion is PanIN2 When irregular papillary architecture is present with tufting, cytologic atypia, necrosis, suprabasal mitoses, and loss of cell polarity, it is regarded as PanIN3
  • #25 Painless obstructive jaundice classical, where as pain in obstructive jaundice may point towards cbd stone and cholangitis, this classical teaching may not always true.
  • #27 Contrary to popular teaching, patients with pancreas cancer often experience pain as a part of their symptoms. Albeit early in the course of the disease, the pain is often vague and involving the upper abdomen, epigastrium, or back.
  • #31 Normochromic anemia, mild hypoalbuminemia and prolonged prothrombin time.
  • #32 CA 19–9 is neither sensitive nor specific enough to be used in population screening.
  • #34 ill-defined hypoechoic mass associated with abrupt dilation of the upstream pancreatic duct and atrophy of the more distal pancreas . Carcinomas of the pancreatic head cause biliary dilation and a “Courvoisier gallbladder.” Dilation of both the pancreatic duct and common bile duct, the “double duct sign” Adenocarcinoma in the body or tail of the pancreas is inconsistently visualized on sonography because of variables such as patient body habitus and overlying gastric or bowel gas. Colour Doppler sonography typically does not show increased vascularity within pancreatic adenocarcinoma.
  • #35 The “workhorse” in the workup of patients suspected of a pancreatic cancer.
  • #38 Weight < 75kg : 100cc Weight 75-90kg: 120cc Weight > 90kg : 150cc The late arterial phase - distinguish pancreatic neoplasms from adjacent normal pancreatic tissue by maximizing differences in contrast enhancement. It also is useful to evaluate hyper-vascular liver metastases as seen in patients with neuroendocrine tumors of the pancreas.
  • #43 EUS is of particular utility when a patient has a presentation consistent with pancreatic cancer (biliary or pancreatic duct obstruction) but no evidence of mass on cross-sectional imaging
  • #44 In a prospective study of 102 patients with suspected pancreatic cancer who had a negative CT-guided biopsy, EUS-FNA had a sensitivity of 95%, specificity of 100%, PPV of 100%, and a NPV of 92%.
  • #51 long, irregular stricture in a pancreatic duct with distal dilation or a “double duct sign” in which there is cut-off of both the pancreatic duct and distal bile duct at the level of the genu of the pancreatic duct are pathognomonic.
  • #52 long, irregular stricture in a pancreatic duct with distal dilation or a “double duct sign” in which there is cut-off of both the pancreatic duct and distal bile duct at the level of the genu of the pancreatic duct are pathognomonic.
  • #54 Radical surgeries are usually not planned in the absence of tissue diagnosis, pancreatic cancer is an exception.
  • #82 5 fu is radio sensitiser
  • #86 Preoperative chemotherapy with surgery and IORT gave a 5-year local control of 23.3%, Results showed a disappointing median survival of 9 months. similarly showed a median survival of only 12 months in patients treated with surgery or surgery and IORT.
  • #92 Shift in radiotherapy delivery techniques from fractional or low doses (e.g., 2 Gy over 6 weeks with a radiation holiday of 2 weeks in the middle) to a continuous-course fraction with a higher overall dose (e.g., 50.4 Gy compared with 40 Gy in fractionated low-dose EBRT). This has the advantage of faster completion of treatment and better overall local control. Radiation field size has decreased with the use of intensity-modulated radiation therapy (IMRT), in which smaller fields are targeted by “pencil” beams to reduce the traditional scatter effect to surrounding tissues. This has the added advantage of potentially reducing side effects of combination agents