The document discusses the anatomy, physiology, histology, and various pathologies of the pancreas including acute and chronic pancreatitis, pancreatic neoplasms, and congenital abnormalities. It provides details on the etiology, pathophysiology, diagnosis, imaging, severity assessment, and differential diagnosis of acute pancreatitis. Key factors in assessing severity include clinical risk factors, scoring systems, biological markers, computed tomography severity index, and presence of necrosis.

1. THE PANCREAS
PONGSATORN TANGTAWEE
HPB DIVISION, DEPARTMENT OF SURGERY
RAMATHIBODI HOSPITAL

2. OUTLINE
Anatomy and Physiology
Histology and Physiology
Acute Pancreatitis
Chronic Pancreatitis
Pancreatic Neoplasm
• Neoplasm of The Endocrine Pancreas
• Neoplasm of The Exocrine Pancreas
• PCN
• lymphoma
Congenital abnormality

3. ANATOMY
AND
PHYSIOLOGY

5. RELATED STRUCTURE

7. REGIONS OF THE PANCREAS

8. ARTERIAL SUPPLY

9. Variation of Hepatic Vein (Precaution during Resection of Pancreas)
A.
LHA
CHA

10. VENOUS DRAINAGE

11. VENOUS DRAINAGE
Gastrocolic
Trunk

12. LYMPHATIC DRAINAGE

13. LYMPHATIC DRAINAGE
1 : Rt Cardiac 8 : Common Hepatic 15 : Middle Colic
2 : Lt Cardiac 9 : Celiac 16 : Para-aortic
3 : Lesser Curvature 10 : Splenic Hilum 17 : Anterior PD
4 : Greater Curvature 11 : Splenic Art. 18 : Inferior
5 : Suprapyloric 12 : Hepatoduodenal Lig. Pancreatic
6 : Infrapyloric 13 : Posterior PD body.
7 : Lt Gastric 14 : SMA

14. INNERVATION

15. DEVELOPMENT OF
PANCREATIC DUCT (PD)

16. VARIATION OF PD
M = Main PD
S = Duct of Santorini
W = Duct of Wirsung
About 2cm

17. VARIATION OF PD
Pancreatic
Divisum

18. NORMALITY OF PD

19. HISTOLOGY AND PHYSIOLOGY
•100% of Pancreatic mass
– 85% Exocrine Pancreas
– 10% Extracellular Matrix
– 4% Vessels and Duct
– 2% Endocrine Pancreas
– The remaining normal Pancreas tissue to prevent Pancreatic
Insufficiency = 20%
• Chronic Pancreatitis = ???????

20. 50-60% Resection
(Devision at neck =60-70%
resection)

21. ACINUS

22. EXOCRINE
1-2 L/day
Clear, watery, alkaline (pH 8.0-8.3)
> 20 different digestive enz.
Isoosmotic to plasma
Principal cations : Na & K (~165 mmol/L)
Principal anions : bicarb & Cl
- secrete min : Cl high, bicarb low
- secrete max : Cl low, bicarb high active
transport
Passive exchange of intraductal bicarb for
interstitial Cl at larger pancreatic duct

23. Digestive enz. are synthesized and stored in the
pancreatic acinar cells, and released in response to
CCK(cholecystokinin) and vagal cholinergic
stimulation
- proteolytic
(trypsin, chymotrypsin, carboxypeptidase, ribonuclease, deo
xyribonuclease, and elastase)
- lipolytic (lipase, colipase, phospholypase A2)
- amylolytic (amylase)

24. Trypsin converts the other zymogens to active forms

25. EXOCRINE PANCREATIC
INSUFFICIENCY (EPI)
m/c cause in human : cystic fibrosis(1st), Shwachman-Diamond
Syndrome(2nd)
fairly common in diabetes - both type 1 and type 2
symptoms of malabsorption, malnutrition, vitamin
deficiencies, and weight loss or inability to gain weight in
children and is often associated with steatorrhea
Treatment : Pancreatic Enzyme Products PEPs , such as
pancrelipase (mixture of three digestive
enzymes, amylase, protease (peptidase), and lipase)

26. Tests
- Fecal fat (fat stain)
- stool trypsin tests
- Trypsinogen (Immunoreactive trypsin)
- Elastase (in stool)
Non-laboratory tests
- ERCP
- MRCP
- Secretin test tube in duodenum : amount of certain enzymes and
bicarbonate in the pancreatic secretion

27. ENDOCRINE FUNCTION
Islet of Langerhans
1-2% of pancreatic mass
20% of total pancreatic blood flow
Insulin : Beta-cell : muscle, liver, fat cells
Glucagon : alpha-cell
Somatostatin : delta cell
Pancreatic polypeptide : PP cells
acini are exposed to higher conc. of the islet
hormones than peripheral tissue

29. ACUTE
PANCREATITIS

30. DEFINITION AND INCIDENCE
Definition
• An inflammatory disease of the pancreas than is associated with
little or no fibrosis of the gland
Incidence
• About 300,000 case/yr in US
• 10-20% = severe
• about 4,000 Deaths/yr + more than $2billion cost

31. ETIOLOGY
•Alcohol 80-90% of cases
•Biliary tract disease
•Hyperlipidemia
•Hereditary
•Hypercalcemia
•Trauma
•External
•Surgical
•Endoscopic retrograde cholangiopancreatography
•Ischemia
•Hypoperfusion
•Atheroembolic 10-20% of cases
•Vasculitis
•Pancreatic duct obstruction
•Neoplasms
•Pancreas divisum
•Ampullary and duodenal lesions
•Infections
•Venom
•Drugs
•Idiopathic

32. ETIOLOGY : BILIARY TRACT
DISEASE
Most comon
Mech. not entirely clear
• Common-Channel hypothesis
• Incompetent Sphincter of Oddi (after passing GS)
• PD blockage : Helminth , Tumor
• Colocalization theory

33. ETIOLOGY : ALCOHOL
At least 2yr drink , commonly
Dx : Hx expose ethanol + absence of other cause
Mechanism
• “Secretion with Blockage” Mechanism
• Inc. Ductal Permeability
• Improper enz. Leaking to surrounding tissue
• Dec. Pancreatic Blood flow

34. ETIOLOGY : TUMOR
1-2% of Pancreatitis found Pancreatic carcinoma
Periampullary Tumor
Mechanism :
• Blockage of secreted juice

35. ETIOLOGY : IATROGENIC
Pancreatic Biopsy , Biliary exploration , Distal gastrectomy
, Splenectomy
B2 Gastrectomy & Jejunostomy
• Inc. intraduodenal P. cause backflow of enz.
Any Sugery than cause Low Sys. Perfusion
ERCP (most common) 2-10%
• Direct Inj. or Intraductal Hypertension

36. ETIOLOGY : DRUGS

37. ETIOLOGY : INFECTION
Mumps , Coxsackievirus , Mycoplasma
pneumoniae
Found from rising of Antibody titer in about 30%
of Pt with pancreatitis with No other cause
No direct evi. that isolated from diseasesd
pancreas

38. ETIOLOGY : HYPERLIPIDEMIA
caused by hypertriglyceridemia but not by
hypercholesterolemia
Serum triglycerides must rise above 1000 mg/dL
Primary Hypertriglyceridemia
• Types I, IV, and V are associated with acute pancreatitis
Secondary Hypertriglyceridemia
• Alcohol
• Diabetes
• Pregnancy
• Drugs : loop and thiazide diuretics, tamoxifen, retinoids, beta-blockers etc.

39. ETIOLOGY : MISCELLANEOUS
CAUSES
•Hypercalcemia (both acute & chronic Pancreatitis)
– Hypersecretion & Calcified causing obstruction
•Ascaris Lumbricoides / Clonorchis sinensis
– Oriental Cholangitis , CHCA , PD obstruction
•Hereditary Pancreatitis :
– Mutation of Trypsinogen gene  Cationic Trypsinogen
(PRSS1)
•Pancreatic Divisum
•Azotemia
•Vasculitis
•Scorpion venom : surge of cholinergic n. effect
– (as same as Antiacetylcholinesterase inhibitor agent)
•Idiopathic pancreatitis

40. PATHOPHYSIOLOGY :
ACUTE PANCREATITIS
Primary Insult : “start from (acinar) cell”
Cathepsin B Hypothesis

41. PATHOPHYSIOLOGY :
ACUTE PANCREATITIS
Acute pancreatitis Review Article : The Lancet, Volume 371, Issue 9607, 12 January 2008-18 January 2008, Pages 143-152
Jean-Louis Frossard, Michael L Steer, Catherine M Pastor

42. PATHOPHYSIOLOGY : ACUTE
PANCREATITIS
Systemic Metabolic
Pulmonary
Pleural effusion Hyperglycemia
Atelectasis Hypertriglyceridemia
Mediastinal abscess
Pneumonitis Hypocalcemia
Adult respiratory distress syndrome Encephalopathy
Cardiovascular
Hypotension Sudden blindness
Hypovolemia (Purtscher's retinopathy)
Sudden death
Nonspecific ST-T changes in electrocardiogram Central nervous system
simulating myocardial infarction Psychosis
Pericardial effusion
Hematologic Fat emboli
Disseminated intravascular coagulation Fat necrosis
Gastrointestinal hemorrhage
Peptic ulcer disease Subcutaneous tissues
Erosive gastritis (erythematous nodules)
Hemorrhagic pancreatic necrosis with erosion into
major blood vessels Bone
Portal vein thrombosis, variceal hemorrhage Miscellaneous
Renal
Oliguria (mediastinum, pleura, nervo
Azotemia us system)
Renal artery and/or renal vein thrombosis
Acute tubular necrosis

43. ACUTE PANCREATITIS :
DIAGNOSIS
Clinical Diagnosis
• Pain : Epigastric (can occur any where in thoracoabdomen)
• Knifing , boring through
• Relieved by leaning forward
• N/V (later presentation) that not relieve pain
• PE
• Tachycardia
• Tachypnea
• Hypotension
• Hyperthermia
• Guarding (both Voluntary/Involuntary)
• Dec. BS / Absent
• May have abd distended with intraperitoneal fluid
• Mah have Pleural Effusion (often on Lt side)
• Cullen/s sign , Grey Turner’s sign : indicate for Necrotizing (Hemorrhagic) Pancreatitis
• Investigation
• Hemoconcentration
• Rising BUN , Cre
• Hyperglycemia
• Hypoalbuminemia
• Hypocalcemia

44. ACUTE PANCREATITIS : DIAGNOSIS
•Serum marker
– Serum Amylase
• Early rising : Peak within several Hr , remain 3-5 Days
• Not related to severity
– Urine Amylase
• May elevated 2-3 days after serum amylase
• False Positive
– P-amylase : Pancreatic specific amylase
More specific (88-93%)
– If >3 times of normal level = reliable for Dx Pancreatitis
• May False Negative
– Esp. in alcoholic pancreatitis , HyperTG pancreatitis
» Normal Serum Amylase , NOT EXCLUDE ACUTE
PANCREATITIS

45. Serum lipase
• Indicate for Highest probability of the disease
• Positive in 75-80% of case
• Persistence than Amylase
• >3 times of normal level = Diagnosis
• Normal level : vary upon the laboratory method
• Sens & Spec about 100% : from Cameron
ALT >3 times normal : Ac GS Pancreatitis
• Found in 50% of case

46. ACUTE PANCREATITIS :
IMAGING
•Plain Film Abdomen
– Finding
• Colon Cutoff sign
– abrupt termination of gas within the proximal colon at the level
of the radiographic splenic flexure
• Sentinel Loop
– Localized Bowel ileus
• Generalized Bowel ileus
• Other
– Soft tissue Density at Epigastrium
– Pancreatic Calcification
– Opaque GS
– Lt Pleural Effusion

47. ACUTE PANCREATITIS :
IMAGING
Ultrasound
• Best noninvasive for confirm GS
• Can detect Extrapancreatic duct dilatation
• Pancreatic edema , swelling & Peripancreatic Fluid collection
• 20% of pt may not give info. due to bowel gas

48. ACUTE PANCREATITIS :
IMAGING
•Contrast-Enhanced CT scan
– Gold standard
• Using in detect complication and access severity
– Indication for use
1. Suspected of Diagnosis
2. Ac. Pancreatitis , that Clinical not improved in 48-72 hr
3. Suspected of Complication from Acute pancreatitis
– Peripancreatic collection
– Pancreatic Necrosis
– Pancreatic Pseudocyst (late)
– Etc.

49. ACUTE PANCREATITIS :
DIFFERENTIAL DIAGNOSIS
Bowel obstruction
Cholecystitis or cholangitis
Mesenteric ischemia or infarction
Perforated hollow viscus

50. ACUTE PANCREATITIS :
SEVERITY
The Atlanta classification (1992)

51. SUMMARY OF THE INTERNATIONAL
SYMPOSIUM ON ACUTE PANCREATITIS.
ATLANTA , 1992
•Definition
– Acute Fluid Collections.
• Occur early
• Found 30-50% of Pt
• lack a wall of granulation or fibrous tissue
• more than half regress spontaneously
– Pancreatic and Peripancreatic Necrosis
• areas of nonviable pancreatic or peripancreatic tissue
• Either sterile / infected
• Fat necrosis +/- tissue necrosis : puttylike or pastelike
• may evolve into pseudocysts ,(late fibrosis)
– Pancreatic Pseudocyst
• collections of pancreatic juice
• enclosed by a nonepithelialized wall composed of fibrous and granulation tissue
• Intrapancreatic / Extrapancreatic (more common , esp in lesser sac)
• not present before 4 to 6 weeks after the onset of an attack
• If infected  Pancreatic abscess
• If rupture into peritoneal cavity  Pancreatic Ascites
• If rupture into pleral space  Pancreaticopleural fistula
– Pancreatic Abscess and Infected Pancreatic Necrosis

52. ACUTE PANCREATITIS :
ASSESSMENT OF SEVERITY
1. Clinical Risk factor
• Ages and Comorbidity
• Clinical sign
2. Scoring Systems
• Ranson score
• APACHE-II
• Other : Imrie/Gasglow score , SOFA
3. Biological marker (not routeinly used)
• C-reacitive Protein (CRP) : >150 at 48hr confirm Ac Severe
Pan.
• IL-6 , PMN elastase , Trypsinogen Activation Peptide (TAP)
4. CT severity Index (CTSI)
• Balthazar
• Necrosis

53. ACUTE PANCREATITIS :
ASSESSMENT OF SEVERITY
Clinical Risk factor
• Ages and Comorbidity
– Age > 70 yr
– BMI >30 kg/m2
– Cardiovascular disease
– DM
• Clinical sign
– Fever
– Shock
– respiratory failure
– Anuria
– neurologic disturbance
– Ileus
– palpable abdominal mass
– abdominal compartment syndrome > 25 mmHg
» (>15 mmHg = Abdominal Hypertension)

54. RANSON SCORE
Mortality rate
1-2 pt = <1%
3 pt = 10%
4 pt = 15%
5-6 pt = 15%
>7 pt = >50%
Recommendation
3pt up :
Admit ICU
ATB
Weak :
Delay eva. (48hr)

55. APACHE-II
(ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION)
Benefit :
Immediate
Evaluation
Better in Eva. Prog.
than Ranson
Weak :
Complex

56. IMRIE/GASGLOW SCORE

57. SEQUENTIAL ORGAN FAILURE
ASSESSMENT (SOFA) SCORE IN
ACUTE PANCREATITIS

58. CTSI
Mild Pancreatitis
Severe Pancreatitis

59. ACUTE PANCREATITIS :
PRINCIPLE OF TREATMENT
1. Adequate Monitoring : Admit to ICU or not
2. Adequate Resuscitation : Fluid &
Electrolyte
– Not too much/too low
– Hypocalcemia , Met. Acidosis , Hypoalbuminemia
, HypoMg.
3. Pancreatic Rest : NPO
4. Adequate Pain Control : dec. cholinergic n.
stimuli
– Avoid MO

60. ACUTE PANCREATITIS : ADJ.
TREATMENT
•Decompressive Nasogastric Tube
•H2-Blocker
•Secretion-inhibiting Drugs
– Atropine , Calcitonin , Somatostatin , Glucagon , Fluorouracil
•Protease-inhibiting Drugs
– Aprotinin , Gabexate masylate , Camostate , Phospholipase
A2 inh.
•Anti-inflammatory response Therapy
– Indomethacin & Prostaglandin inhibitors
– PAF (Platelet-activating factor ) antagonist : PAF
acetylhydrolase , Lexipafant
•Peritoneal Lavage

62. SEVERE PANCREATITIS
APACHE-II
(Acute Physiology And Chronic Health
Evaluation)

63. SEVERE PANCREATITIS
Dx when :
1. Ranson score ≥ 3
2. APACHE-2 ≥ 8
3. Dev. Local/Systemic complication
• MOF
• Pseudocyst , necrosis , abscess
4. ceCT : necrosis >33% (???)

65. TX OF BILIARY PANCREATITIS
Controversial point : Timing (48-72hr , >72hr)
ERCP , Cholecystectomy with CBD clearance
Indication : for Early ERCP
• Obstructive Jx with Cholangitis
• Severe pancreatitis
• Pancreatitis with obstructive Jx >24hr
Routine Early ERCP : not recommended

66. PANCREATIC NECROSIS
Occur about 20% of Pancreatitis pt.
Severe Necrotizing Pancreatitis
Sterile vs Infected : ceCT with FNA
• “Air Bubble” found 20% of Infected PN (IPN)
• Mortality
• <1% in sterile PN
• About 40% in IPN
Clinical :
• Fevere , Leukocytosis , clinical not imp. In 72hr
Treatment
• Antibiotic
• Drainage
• Catheter-bases Therapy
• Surgical Debridement
• For Life-Thretening only

68. OPENED NECROSECTOMY
Indication
• Infected Pancreatic and/or peripancreatic necrosis
• Sterile necrosis with progressive clinical deterioration under
Maximum Medical Tx : Controversial
• Massive hemorrhage or bowel perforation (colon, duodenum).
Timing : “as late as possible”
Preparation
• Empirical Antibiotic
• CT : for road map
• Prepare For massive Blood loss
• G/M PRC 4-6 u
• Invasive monitoring : Central line / Swan-Ganz catheter

69. CHRONIC
PANCREATITIS

70. DEFINITION
Incurable , Chronic inflammatory condition
Multifactorial in etiology
Permanent loss of pancreatic exocrine &endocrine function
• Leading to pancreatic insufficiency

71. ETIOLOGY

72. ETIOLOGY
•Alcohol
– 70% of Pt
– Dose and Duration related
• Varied in each individual
– Onset :
• At age 35-40 yr
• Or at 16-20 yr of alc. consumption
– Mechanism not clear
• SAPE theroy
– Pancreatic Stellate cell (PSC) activation
• Multiple-Hit Theory
– Necrosis-Fibrosis sequence
• Alcohol
– Interfere transport of Digestive enz.  Colocalization  Acinar cell inj.
– Depletion of Lithostathine  inc. Pancreatic stone formation
•Smoking
– Strong associated
– Inc. High risk for Chronic Pancreatitis and CA pancreas

73. ETIOLOGY
Hyperthyroidism
• Caused Hypercalcemia
• Induced Pancreatic Hypersecretion + calcium secretion
• Caused Chronic calcified pancreatitis
• Calculus formation and Obstructive Pancreatopathy
• Tx : correct Hyperparathyroidism
Hyperlipidemia & Hypertrigleceridemia
• Worsen in women with Estrogen replacement Tx
• Tx : Control Keep Fasting TG < 300 mg/dL

74. ETIOLOGY
Tropical (Nutritional)
• Found in Indonesia , Souther indeia , Africa
• Adolescent and young adult
• Mechnism : not clearly known
• Malnutrition
• Trace Element def.
• Toxin from Food : Cassava root ( )
Hereditary
• PRSS1 : Cationic Trypsinogen gene
• Autosomal dominant
• SPINK1 : PSTI
• Pancreatic Secretory Trypsin inibitor= Serine Protease Inhibitor
Kazal-1 (SPINK 1)
• CFTR gene : Cystic Fibrosis Transmembrane receptor

75. CLASSIFICATION

76. PATHOLOGY
Histology
• Early : induration , Nodular scarring , Lobular fibrosis
• Then : Loss of normal lobulation , Thicker fibrosis
• Then : reduce in acinar cell mass , Ductal dilatation , Ductular epithelium
dysplasia , monoNu. Cell infiltrat.
• Cystic change
• Severe Chronic Pancreatitis : Replacement of acinar tissue by Fibrosis , islet
size &number reduced

77. PATHOLOGY
Stone formation
• Pancreatic stones
• Calcium carbonate crystal
• Inh. of stone formation by
• Pancreatic Stone Protein : PSP
• Lithostathine
• Pancreatic thread protein
• Reg gene
• Sig. dec. in Alcoholic Pancreatitis
• Indicator for Advance stage disease

78. PATHOLOGY
•Radiology
– Using of Imaging for Chronic Pancreatitis
1. diagnosis
2. the evaluation of severity of disease
– Cambridge Classification
3. detection of complications
4. assistance in determining treatment options
– Choice of Imaging
• US , CT , EUS , MRCP , ERCP
• ERCP : Gold standard in Dx and staging of CP
• EUS : more sens. than ERCP

79. PRESENTATION
•Pain
– Most common symptom
– Midepigastrium but also LUQ , RUQ
– Penetrating to back
– Steady and boring pain
– Aggravated by Food , Alc.
– Relieve by : Flex abdomen , hip flex , sit

80. • Mechanism
1. Ductal (and also Parenchymal) Hypertension
2. Inflammation of Parenchyma
3. Neural involvement
• Strategies to relieve pain
1. Reducing secretion and/or decompress the secretory
compartment
2. Resecting the focus of chronic inflammatory change
3. Neural ablative procedures

81. PRESENTATION
Malabsorption & Wt loss
• Occur when exocrine capacity <10%
• Diarrhear & Steatorrhea
• Bulky , foul-smell ,float , with Oily water
• Lipase def.  Trypsin Def.  dec. Bicarb. Secretion
Apancreatic (pancreatogenic) Diabetes (type III
DM)

82. INVESTIGATION
Measurement of pancreatic products in blood
• A. Enzymes
• B. Pancreatic polypeptide
Measurement of pancreatic exocrine secretion
• A. Direct measurements : Lundh test meal
, CCK/secretin stimulation
• 1. Enzymes
• 2. Bicarbonate
• B. Indirect measurement
• Bentiromide test : PABA excretion (urine)
• Schilling test : Vit B12 absorption
• Fecal fat, chymotrypsin, or elastase concentration
• [14C]-olein absorption : Triolein Breath test

83. III. Imaging techniques
• Plain film radiography of abdomen
• Ultrasonography
• Computed tomography
• Endoscopic retrograde cholangiopancreatography
• Magnetic resonance cholangiopancreatography
• Endoscopic ultrasonography

84. PROGNOSIS
Depend on
• Etiology of disease
• Complication
• Age
• Socioeconomic status
Progressive , cumulative inc. risk of CA

85. COMPLICAITON AND
MANAGEMENT

86. COMPLICATION : PSEUDOCYST
Natural Hx :
• For acute pseudocyst (or <6wk) : 40% solve spontaneous , 20% dev. Complication
• For Chronic pseudocyst (7wk up) : about 5 % solve spon. , 50-60% dev. Complication
•No malignant potential : af <6cm/asymp. No complication : surviellance
•Indication for surgery
•Symptomatic : often occur in Pseudocyst size > 6cm.
•early satiety, gastric outlet obstruction, jaundice, pain , thrombosis
•Complication
•GI bleeding (Hemosuccus pancreaticus) , infection, rupture , erod vessel
(pseudoaneurysm)

87. COMPLICATION : PSEUDOCYST
Investigation
• ceCT : Imaging of choice
• EUS : if available
• To detect : septation , mural nodule , debris , calcified
• To aspirated collection for CEA , CA19-9 ,Amylase
• R/O Pancreatic Cystic Neoplasm (PCNs)
• Pancreatic Pseudocyst : Hi Amylase (>5000) , -ve Tu.Marker

88. COMPLICATION : PSEUDOCYST
•Treatment
– Rule
1. cystic neoplasm must not be treated as a pseudocyst
2. elective external drainage must not be done
– If not correct of downstream obstruction
– Point of consideration
• The thickness of the pseudocyst wall : after 4-6wk
• The location of the pseudocyst : near Stomach ,Duodenum
• The contents of the pseudocyst : Blood , pus
• The pancreas and the pancreatic duct need separate
consideration in planning the treatment of a pseudocyst

89. COMPLICATION : PSEUDOCYST

91. CYSTOGASTROSTOMY

92. R-E-Y CYSTOJEJUNOSTOMY

93. R-E-Y CYSTOJEJUNOSTOMY

94. TX OF PSEUDOCYST : OPEN SURGERY
•Cystogastrostomy
– If Lying posterior to stomach
•Cystojejunostomy
– Ideal for internal drainage
– If located at body and tail
– Not adhere to stomach , Bulging through T.colon
•Cystoduodenostomy
– If located at head of pancreas
•Distal pancreatectomy
– Extent of resection , depend on ERCP finding
•External Drainage
– Only if no occlusion of PD

95. COMPLICATION : PANCREATIC ASCITES
•internal pancreatic fistulae
– Pancreatic Ascites
– Pancreatic pleural effusion
• Thoracocentsis
– Prot level >25 g/L
– Marked elevated amylase level
•ERCP
– Eva. Point of leakage of PD
– +/- PD stenting
•Tx :
– Antisecretory therapy : Somatostatin , Octreotide
– Bowel reset + TPN
– ICD for Pancreatic Pleural effusion
– R-E-Y Pancreaticojejunostomy or Distal pancreatectomy
• if fail conservative Tx

96. COMPLICATION : PANCREATICO-ENTERIC
FISTULA
Most common site
• Transverse Colon , Splenic Flexure
Tx
• Fistula to stomach / Duodenum
• No Mx : solve spont. , leave Fistula
• Fistula to Colon
• Needed Surgical Correction

97. COMPLICATION : PANCREATICOCUT.
FISTULA
•Criteria Diagnosis
– Fluid > 50 cc/day
– Fluid Amylase> 3 times of Serum Amylase
– Persistence leakage >7 days
•Low Output Fistula : <200 ml/day
•High Output Fistula : >200 ml/day
•Spon. Solved about 90%

98. Tx :
• Drainage
• Confirm Pancreatic Juice , Record Vol. , Resuscitation
, Culture , Skin Protection
• Diagnosis
• ERCP
• Fistulogram / Fistuloscope (after 3 wk.)
• Decompression
• Drug : Somatostatin , Octreotide
• Definitive Surgery
• Distal Pancreatectomy vs R-E-Y Pancreaticojejunostomy

99. COMPLICATION : HEAD-OF-
PANCREAS MASS
Inflammatory mass
Found up to 30%
Symptom : pain , stenosis (Duo. , stoma, CBD)
Thrombosis (compress PV)
Tx :
• DPPHR : Duodenal-preserving Pancreatic Head resection

100. COMPLICATION :
SPLENIC / PORTAL V THROMBOSIS
Occur 4 to 8% of case
Splenic v. Thrombosis
• Lt side Portal Hypertension
• Sinistral Portal Hypertension
• Caused isolated Gastric Varices
• Bleeding complication no frequence
• Mortality rate of bleeding about 20%
• Tx : Splenectomy

101. CHRONIC PANCREATITIS :
TREATMENT
•Principle of Treatment
– Pain control , correct Malabsorption&DM
– Medical Treatment is 1st choice
•Medical Therapy
• Analgesia
– Strop Drinking : Reduce pain in 60-75% of Pt
– Analgesic drug : can up to Narcotics (Oral / Transdermal
patch)
– Analgesic Enhancing Agent : Gabapentin
• Enzyme therapy : Correct Malabsorption + Help in pain control
– Conventional (non-enteric coated) form : bind to CCK
, reduce in Pancreatic secretn.
» Duration of therapy about 1 mo.
– Enteric coated form : Help in malabsorption , little to no Help
in pain control
• Antisecretory therapy : no sig. pain relief

102. Neurolytic Therapy : Celiac Plexus Neurolytic
• Using Alcohol
• Effective in CA pancreas , but Dissapoint in pain control for
chronic Pancreatitis
• From Schwartz : under EUS-guided  Initial control
pain=55% , but Beyond 6mo=10%
Endoscopic Management
Surgical Therapy

103. ALGORITHM IN TX OF CHRONIC PANCREATITIS
PAIN

104. TREATMENT : ENDOSCOPIC MX
Role
• pancreatic duct obstruction
• stone disease
• pseudocyst formation
• pancreatic duct leak
• In acute pancreatitis : found 37%
• The Dx and Mx of associated pancreatic tumors

105. TREATMENT : ENDOSCOPIC MX :
PANCREATIC DUCT STENT
•Role
– Prox. Pancreatic duct stenosis
– Decompression of Pancreatic Leakage
– Decompression of Pseudocyst
– Prophylaxis PD stenting : Post ERCP
• esp in Sphincter of Oddi Dyskinesia
– Pancreatic Divisum
• Minor papilla Sphincterotomy with Dorsal duct stenting
– Idiopathic Pancreatitis : Dec. symp recurrence
– After Pancreatic stone Removal Procedure
•Transpapillary Drainage

106. TRANSPAPILLARY DRAINAGE

107. TREATMENT : SURGICAL THERAPY
Type of Surgery
• Sphincteroplasty
• Drainage Procedure
• Duval's caudal pancreaticojejunostomy.
• Puestow and Gillesby's longitudinal pancreaticojejunostomy.
• Modified Puestow procedure
= Partington and Rochelle Procedure
= Longitudinal Pancreaticojejunostomy : side-to-side Roux-en-Y
pancreaticojejunostomy
• Resection Procedure
• Distal Pancreatectomy
• Partial 40-80%
• Ninety-Five Percent Distal Pancreatectomy
• Proximal Pancreatectomy
• Whipple procedure
• Pylorus Preserving Pancreaticoduodenectomy (PPPD)
• Total pancreatectomy

108. • Hybrid Procedure
• Beger Procedure
= DPPHR (Duodenal-preserving Pancreatic Head resection)
• Berne modification of the DPPHR
• Frey’s Procedure
=LR-LPJ (Local resection of Pancreatic Head with Lateral
Pancreaticojejunostomy)
• Hamburg modification of the LR-LPJ

109. WHICH OPERATION??
Point of consideration
• Size of MPD
• Large PD (≥5mm) : Drainage Procedure , better outcome
• Small PD (<5mm) : Resection Procedure , Poorer outcome
• Presence of Pancreatic Head mass
• Distal CBD obstruction
• Suspicious of Malignancy

110. TREATMENT : SURGICAL
THERAPY
•Indication for surgery in Chronic Pancreatitis
1. Chronic intractable abdominal pain unresponsive to
nonsurgical treatment
2. Suspicious Pancreatic Cancer
3. Persistent CBD obstruction , unresponsive to
endoscopic Treatment
4. Duodenal Obstruction
5. Splenic v. Thrombosis with Bleeding Gastric Varice
6. Symphtomatic or enlargement pancreatic
Pseudocyst
7. Persistent Pancreatic ascites or fistula

111. Contraindication
• Occlusion of SMV and PV
• Chronic Pain from other cause
• Inadequate Medical Treatment
• For Resection Procedure & Hybrid Procedure
(Frey&Beger Procedure)
• Unable to cope Apancreatic DM (Brittle DM) : Relative
• For Drainage & Hybrid Procedure (Frey & Beger
Procedure)
• Cannot exclude Pancreatic malignancy
• For PPPD
• s/p Vagotomy
• Hx of Sever PU

112. SURGICAL THERAPY :
PREOPERATIVE INVESTIGATION
• History:
• Exclude alcohol or drug addiction, gallstones, pancreatitis-inducing
medications, hyperparathyroidism, hypercalcemia, and
hyperlipidemia
• Evaluate for steatorrhea and diabetes mellitus (glucose
intolerance), especially the need for insulin
• Severity of pain (Likert visual analog pain scale completed by
patient)
• Psychosocial stability
• Quality of life survey (optional)
• European Organization for Research and Treatment of Cancer QLQ-C30 (EORTC)
• Medical Outcomes Trust Short-Form 36 (MOS SF-36)
• Impact of pain on employment, family support, daily activities
• Clinical evaluation:
• Jaundice, ascites, nutritional status, weight, physiologic health, co-
morbidities
• Baseline pancreatic exocrine and endocrine function if indicated

113. •Laboratory tests:
• CA 19–9 (most useful if common bile duct
patent), LFTs, HbAIC, glucose tolerance test
• Fecal fat and secretin studies are only required rarely
•Imaging
• Triphasic helical CT to evaluate for
• Pancreatic masses
• Portal and left-sided hypertension or thrombosis of the splenic vein
• Involvement of adjacent organs
• Extrapancreatic causes of pancreatitis (cholelithiasis)
• ERCP to evaluate pancreatic and biliary ductal systems and
esophagogastroduodenoscopy to exclude peptic ulcer
disease
• Endoscopic or intraoperative ultrasonography to evaluate for
vascular involvement and biopsy if indicated

114. Preparation for the Procedure
• Review Infrom consent
• Chance of Pain Relieve , Chance of Recurrence
• Complication from surgery
• If plan Drainage Procedure
 inform Resection Procedure , for inpredictable introp. finding
• Broad spectrum, perioperative prophylactic antibiotic
• Full bowel preparation

115. DUVAL'S CAUDAL
PANCREATICOJEJUNOSTOMY.(1954)
Problem
Fail due to
Segmental Obstruction of PD
“Chain of lakes”
Recurrence due to
Restenosis & scarring

116. ORIGINAL PUESTOW PROCEDURE (1958)

117. PARTINGTON AND ROCHELLE PROCEDURE
MOD. PUESTOW PROCEDURE (ABOUT 1960)
Pain Control rate
First Few yr = 75-85%
Recur >20% after 5 yr

118. DISTAL PANCREATECTOMY (40-80%)
SPLEEN-SPARING DISTAL
PANCREATECTOMY
Lesser Morbidity
Poorer Pain relief rate
but good long term outcome
Laparoscopic (if
available)
Ninety-Five Percent
Distal Pancreatectomy
60-70% pain relief Pt
Longterm

119. PROXIMAL PANCREATECTOMY
PPPD : Pylorus-Preserving
Whipple Procedure
Long term pain relief rate = 71- Pancreaticoduodenectomy
89%
Mortality 1.5-3%
Maj. Complication =25-38%
25-48 % dev. Endocrine
&Exocrine insufficiency

120. TOTAL PANCREATECTOMY
Occurred 1944
For Tx of Insulinoma
Used to be Used in Chronic Pancreatitis
• Unsuccess from other operation
• But  even Do Total Pancreatectomy
• Not improve outcome
• Face “Brittle DM”
• Late death :due to Hypoglycemia

121. BEGER PROCEDURE : DPPHR (1980)
Pain Relief rate = 91%
Mortality <1%
Dev. DM 21%  reversible 11%
Major Complicaiton : Pancreatic Leakage , Intra-abdominal collection

122. FREY PROCEDURE : LR-PJ
(1987)
F/U 7yr
Pain relief rate = 87%pt
No mortality
22% Maj. complication

123. TREATMENT : DENERVATION
PROCEDURES
Choice
• operative celiac ganglionectomy
• Transhiatal splanchnicectomy
• Transthoracic splanchnicectomy
• with or without vagotomy
• Videoscopic transthoracic splanchnicectomy

124. PANCREATIC
NEOPLASMS

125. PANCREATIC NEOPLASM :
OUTLINE
•Neoplasms of the Endocrine Pancreas
– Insulinoma
– Gastrinoma : ZES
– Vasoactive Intestinal Peptide-Secreting Tumor
– Glucagonoma
– Somatostatinoma
– Nonfunctioning Islet Cell Tumors
•Neoplasms of the Exocrine Pancreas
•Ampullary and Periampullary Cancer

126. Cystic Neoplasms of the Pancreas
• Pseudocysts
• Cystadenoma
• Mucinous Cystadenoma and Cystadenocarcinoma
• Intraductal Papillary Mucinous Neoplasm
• Solid-Pseudopapillary Tumor
• Other Cystic Neoplasms
Pancreatic Lymphoma

127. NEOPLASM OF ENDOCRINE
PANCREAS
•1% of Pancreatic Tumor
•Most common PETs = Insulinoma
•Related to MEN1
– pituitary tumors
– parathyroid hyperplasia
– pancreatic neoplasms (Gastrinoma)
•amine precursor uptake and decarboxylation
cells
•Benign vs Malignancy
–Present of Local invasion , lymph. or Hepatic
metastases
–Most are Malignant
• But prognosis is far better than CA exocrine pancreas

128. Key of management
• Clinical Syndrome
• Laboratory confirmation
• Localization
• Surgery
• For complete surgical resection
• Debulking Tumor for symphtomatic control
• Unresectable disease : Chemoembolization

129. INSULINOMA
•the most common PNETs
•Whipple Triad
–symptomatic fasting hypoglycemia
–serum glucose level <50 mg/dL
– relief of symptoms with the administration of
glucose
•10% disease
– 10% malignancy (the least)
– 10% metastasis to node
– 10% multiple lesion
– 10% found in MEN1
•Best Prognosis

130. INSULINOMA
•Investigation
– Low Blood sugar
– Elevated serum insulin level
– Elevated C-peptide level
– Diagnosis :
• NPO with serial Blood exam q4-6hr
• Insulin-Glucose Ratio >0.3

131. Preoperative Localization
• ceCT : arterial Phase
• EUS = Diagnostic modality of choice (sens 70-90%)
• Laparoscopy with LUS
• Transhepatic Portal venous sampling
• Selective arterial stimulation with Hepatic venous sampling
(ASVS)
• Stimulant : Calcium (for insulinoma) , Secretin (for
gastrinoma)
• Intraoperative palpate with IOUS

132. INSULINOMA
Management
•Mostly Benign + single lesion
• Laparoscopic surgery + LUS
•Tumor < 2cm , not attach MPD : Enucleation
•Tumor >2cm , Resection
• Distal Pancreatectomy : for lesion at Body & tail
• Whipple / PPPD : for Head &uncinate process
•Attach MPD , any size : Resection
•If Metastases : Debulking Tumor

133. •If can’t localized Tumor :
• Subtotal Pancreatectomy
• Biopsy and Closed  then ASVS
•Unresectable Insulinoma
• Tx of Hypoglycemia : CHO rich diet , inc. meal.
• Medication : Diazoxide , Propanolol , Verapamil , Chropomazine
• Octreotide : dec. insulin secretion 30%
• Chemotherapy :
• Streptozotocin, Decarbazine , Doxorubicin , 5-FU
•Insulinoma in MEN-I : usual multiple
• Subtotal pancreatectomy + enucleation at Head using IOUS

134. GASTRINOMA
•Zollinger-Ellison syndrome (ZES)
– abdominal pain, peptic ulcer disease, and severe esophagitis
– Suspected if :
• multiple ulcers
• Fail response to PPI
• Ulcer in abnormal location
• Severe Esophagitis
• PU without H.pylori or Hx NSAID
• If no Hx PU , Suspected if
– +ve Hx MEN-1 in family
– + Hx PU almost whole family
– Unexplained Diarrhea (due to Hyper acidity)
– Unexplain Steatorrhea
– Hypercalcemia
– EGD : found Prominent Gastric /Duodenal fold

135. GASTRINOMA
•Clinical Presentation
– PU 90% , Diarrhea 50% , GERD 50%
•Sporadic case 75%
•MEN-1 related 25% (most common PNETs in MEN-1)
•Disease of 50%
– 50% Malignancy (may up to 90%)
– 50% Metastasis
– 50% Multiple
•Location
– 70-90% in Passaro triangle) , mostly at duodenum wall

136. PASSARO TRIANGLE
the junction of the cystic
duct and common bile
duct
The junction of the neck and
body of the pancreas
The junction of the second
and third portion of the
duodenum

137. GASTRINOMA
•Diagnostic test
– Fasting Serum Gastrin (stop PPI before test)
• >1000 pg/ml
– Secretin Sti. Test : secretin 2u/kg iv
– >200 pg/ml
– Ddx :
– pernicious anemia
– treatment with proton pump inhibitors
– renal failure
– G-cell hyperplasia
– atrophic gastritis
– retained or excluded antrum
– gastric outlet obstruction

138. GASTRINOMA
•Localization
– Preoperative
• ceCT
• SSTR (octreotide) scintigraphy : single test of choice
– Tu. <1 cm found 85%
• Octreotide scan + EUS : Best
– Tu. <1cm found 90%
• EGD
– Intraoperative Localization
• Palpation + IOUS
• Intraoperative EGD
• Duodenotomy

139. GASTRINOMA
Treatment
• R/O MEN-1  Serum Calcium + Tx HPT
• If Metastases
• Found intraop : Debulking tumor + Highly Selective
Vagotomy
• Found Befor surgery : Chemotherapy + life-long PPI
• Before surgery : PPI
• if Tumor ….
• Well capsulated , size <2cm , not attach MPD : Enucleation
• Well capsulated , size <2cm , at duodenal wall
• Full thickness resection
• Attach MPD / size>2cm / Deep in pancreas
• Resection (whipple / PPPD or Distal pancreatectomy
• Postop Octreotide

140. •ZE syndrome
– Def. of Postop Cure
• Normal Fasting Serum gastrin
• -ve on Octreotide scan
• -ve on CT
• -ve on Secretin stimulation test
•In MEN-1 : often Multiple & Metastases
– Controversial
•Prognosis :
– Depended on liver metastases
• +ve met : 5yr survival about 20%
• -ve met : 5yr survival about 80%
– Large tumors + liver metastases+ located outside of Passaro's triangle
• the worst prognosis.

141. VIPOMA
•vasoactive intestinal peptide-secreting tumor (VIPoma)
syndrome
•WDHA syndrome
– watery diarrhea , > 5L/d , tea-colored
– Hypokalemia
– Achlorhydria
•Verner Morrison syndrome
•Diagnostic test
– Multiple measure of serum VIP level
• Due to episodic secret VIP
• >200
•Localization : as other PNET
– Mostly at Tail of Pancreas & usual Metastases

142. VIPOMA
•Ddx :
– Villous Adenoma :mucus diarrhea + HypoK
– ZE : Diarrhea + PU
– Carcinoid Tumor : diarrhea + Facial Faushing
– UC : Blood diarrhea
•Tx
– Fluid and Elec. Resuscitation
– Octreotide
– Surgical Resection / Debulking Tumor

143. GLUCAGONOMA
•Diabetes
– Usually mild diabetes
•Dermatitis
– Necrolytic migratory erythema
•Diarrhea , Dementia , DVT
•Diagnostic test
– Serum Glucagon level >500 pg/ml
– Hyperglycemia
– Hypoproteinemia
•Localization
– Body and tail : same as VIPoma
•Tx
– Control DM
– Nutritional support : TPN
– Octreotide
– DVT prophylaxis
– Distal Pancreatectomy with Splenectomy or Debulking Tumor

144. SOMATOSTATINOMA
Rare Type
Presentation
• GS
• DM (inh. Insulin secretion)
• Steatorrhea (inh. Pancreatic & Bile excretion)
• abdominal pain (25%), jaundice (25%), and cholelithiasis (19%).
Localization
• Mostly Proximal , at pancreaticoduodenal groove
• Periampullary area 60%
• Often Metastases
Dx : Serum Somatostatin Level >10 ng/ml
Tx :
• Resection if possible
• Debulking Tumor
• Cholecystectomy

145. NONFUNCTIONING ISLET CELL
TUMORS
The most 2nd islet cell tumor
Clinical silent  mostly Metastases
stain positive for pancreatic polypeptide (PP), and elevated PP levels
Related to Other Multiple neoplasia synd
• VHL : von Hippel-Lindau syndrome
Slowly Growth
• 5yr survival is common

146. PANCREATIC CYSTIC NEOPLASM (PCNS)
•inc incidence as inc. of CT using
•Most of these lesions are benign or slow
growing
–Better prognosis than Exocrine pancreas tu.
•Female > male (exc. IPMN : male>female)
•Most asymptomatic
•Point of Consideration
– Cyst of pancreas , or not?
– Pseudocyst(80-90%) or PCN(10-20%)
– If PCN : Operation vs Observation

147. PSEUDOCYST VS PCN
Pseudocyst PCN
• Pancreatitis •+ •-
• Trauma •+ •-
• Serum amylase • High • Normal , except IPMN
• Imaging
• Septal /loculation • -ve • +ve
• Intracystic solid component • -ve • +ve
• Central /wall calcification
• -ve • +ve
• Ductal communication
• +ve • -ve , except IPMN
• Pressure to Pancreatic duct
• -ve • +ve
• Intraop.finding
• Well demarcation
• Normal surrounding Pancrea • -ve • +ve
• Locally adhesion • -ve • +ve
• Frozen Section cyst wall • +++ • +
• Fibous Tissue • Epithelial tissue
• Cystic fluid
• Appearance
• Cytologic feature
• Thin , dark , no Mucin • Viscus , clear , with Mucin
• Amylase
• CEA
• Inflammatory cell • Mucinous cell , except SCN
• High • Low , except IPMN
• Low • High , except SCN

148. OPERATION VS OBSERVATION
Consider
Risk&benefit ratio
Life expectancy
Comorbidities
Malignant potential
Location
Hospital M&M

149. PCN
Pathological Classification
• Serous Cystic Neoplasm (SCN)
• Mucinous Cystic Neoplasm (MCN)
• Intrapapillary Mucinous Neoplasm (IPMN)
• Solid Pseudopapillary Neoplasm (SPN)

150. SCN MCN IPMN
• Incidence (%) • 30 • 50 • 17
• Sex • F • F • M
• Age (yr) • 60 • 40-50 • Elderly >65
• Location • Head • Body • Head
• Malig.potential • Extremely rare • 30-45% • MD 75% , BD 25%
• Ass. Disease • VHL • - • CRC , stomach , Pancreas ,
lung 23-32%
• Symptom • Asymp. ,Except large • 60% • Pancreatitis 40%
• Asymptomatic 60%
• Endoscopy • Nonspecify • Nonspecify • MD type
• Bulgin ampulla
• Mucin extrution
• Gross • Single • Macrocyst • Cystic dilated duct
• Spongy • Filled with Mucous • Thin capsule
• Round • Thick Fibrous wall
• Well circum. • Septum
• Multiple Micryocyst
• Honey comb app.
• Thin Transculant wall
• Histology • Cuboidal cell • Tall columnar • Similar MCN
• Glycogen-rich Cytoplasm • Mucinous cell
• PD communication • absent
• absent • Present

151. SEROUS CYSTIC NEOPLASM
•Female 50-60yr
•Head
•Asymptomatic
•Ass. Disease : VHL
•Finding on CT :
– Group of Microcyst size <2cm , Spongy
•Classical finding
–Central calcification
• Sunburst / Radial / Stellate app.
– Fluid : clear , no color , normal Tu. Marker
&amylase
– Cell : Cuboidal , Glycogen rich cell
•Benign

152. Mx
• Observation : F/U with CT or MRI q6mo in first 2yr , then
annually
• Surgery when indication
• Not Enucleation , Splenectomy not needed
• Resection

154. MUCINOUS CYSTIC NEOPLASM
(MCN)
Most common PCNs
Middle age , female
Body & tail
Asymptomatic
Finding on CT
• Cyst >2cm (macrocyst)
• Thick wall
• Intracystic septation
• +ve solid compartment
Classical finding :
• Rim Calcification (peripheral)
• No PD communication

155. Cystic Fluid
• Clear , mucus , “string sign”
•Mucin stain +ve
• Cyto :Mucinous cell
•Low Amylase , High CEA , High CA
15-3
High risk for Malignat
Tx
• Surgical resection , if possible

156. INTRADUCTAL PAPILLARY
MUCINOUS NEOPLASM
IPMN
•Prolifaration of mucinous cell in pancreatic duct , forming
Papillary stroma
•Asymp. 60%
•Often cause Pancreatitis (40%) , from mucin plug
•Jx (rare)
•Male , elderly , Head of Pancreas

157. Risk Malignancy : as MCN
• With other site CA : CRC , Stomach , Lung
Classification
• Main Duct Type : found 75% , risk CA 70%
• Branch Duct type : found 15-20% , risk CA 25%
• Combined type : found 10-15%

158. INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM
IPMN
•Finding on CT
– Microcyst + Macrocyst
– No thick capsule
– MD : PD dilatation , may seen filling defect/mural nodule
– BD : Gr. Of cyst , no Duct dilation
•EUS + FNA
– Mucin +ve ,Mucinous cell
– If +ve Hx Pancreatitis : High Amylase
– Tumor marker : rising (except CA 15-3)
•ERCP
– Bulging Ampulla
– Mucin extrution : Fish-eye deformity
– Dilated PD

159. INTRADUCTAL PAPILLARY MUCINOUS
NEOPLASM IPMN
•Treatment
– Nonoperative : for BD type
• Asymptomatic
• Size < 3cm
• No mural nodule , no thick septum
• No PD dilatation
• -ve on Cytology

160. • Operative Mx : Problem = Margin ?
• Frozen section of Transected margin
• Intraoperative Pancreatoscopy
• Intraductal US
• Total Pancreatectomy

161. SOLID PSEUDOPAPILLARY
NEOPLASM (SPN)
Solid Cystic Tumor , Franz Tumor , Hamoudi Tu
Very rare
Female , 20-25 yr
Head , Body , tail
Gross & CT finding :
• Multiloculated mass : Cystic – Solid mass
FNA
• Necrotic tissue
• Low CEA , Low Amylase
• Histo. = Papillary elemet
Tx
• Complete Resection
• If Metastases : Metastasectomy

162. EXOCRINE
PANCREATIC
TUMOR

163. EPIDEMIOLOGY & RISK FACTOR
•the worst prognosis (5% 5-year survival rate)
•Etiology : unknown
•More common in elderly (esp. >60 years old)
•More common in African Americans
•Slightly more common in men

164. Risk Factor
• Family History : 2-3 times risk
• Cigarette smoking : atleast 2 times
• Coffee &alcohol : ??
• Other GI malignancy
• Hi-fat , Low-fiber / Fruits / vegetables
• Pre-existing type II DM
• Chronic Familial Pancreatitis : 20 times
Oncogenesis :
• Likely initiated with Mutation of K-ras oncogene

165. GENETIC OF CA PANCREAS
•K-ras mutation
– Found mutation in 90% of Pt with CA pancreas
• w/o in DNA from serum ,stool , Pancreatic Juice , Pancreatic
tissue
•HER-2/neu oncogene
– EGFr , overexpression in CA Pancreas
•Tumor-suppressor genes
– P53 , p16 & DPC4 (Smad4) , BRCA2
– Multiple mutations in above genes
•Gene related to expression of GF and GFr

166. SYNDROME RELATED
Found about 10%
• Familial cancer syndrome
• BRCA2
• Familial atypical multiple mole-melanoma syndrome
• Hereditary pancreatitis
• FAP (Fam. Adenomatous polyposis)
• HNPCC (Hereditary nonpolyposis CC)
• Peutz-Jeghers synd.
• Ataxia-telangiectasia

167. PATHOLOGY
Precursor lesion
• Pancreatic intraepithelial neoplasia
• PanIN-1A  PanIN-1B  PanIN-2  PanIN-3
• more genes mutation
, more progressive atypia &Arch. disarray
• Goal : to improved ability to detect of these lesion

168. PATHOLOGY
Location
• 66% in Head and Uncinate Process
• Dx earlier ,
• Symptomatic
• 15% in Body
• 10% in Tail
• Usually larger & more progress at time of Dx
• Asymptomaic
• Other diffuse involvement

169. PATHOLOGY
Cell type
• Ductal Adenocarcinoma 75%
• Adenosquamous Carcinoma
• Poor Prog. Too
• Acinar cell carcinoma
• Uncommon
• Usually present at large Tumor (>10cm)
• Better Prognosis

170. DIAGNOSIS & STAGING
Staging
• T1-4
• Size cutoff at 2 cm (T1) / or more(T2)
• beyond Pancrease resectable (T3) / Unresectable (T4)
• N0 vs N1
• M0 vs M1
AJCC 6th same as AJCC 7th
Unresectable Dz Poorer prog. than N+,resectable Dz

172. DIAGNOSIS & STAGING
•Stage at Diagnosis
– 7% : Localized stage
• 5yr-SR = 20.3%
– 26% : +ve Regional LN involvment / T3 up
• 5yr-SR = 8.0%
– 52% : metastasis (Distant stage)
• 5yr-SR = 1.7%
– 15% : unknown stage information
• 5yr-SR = 4.1%
• Overall 5yr-SR = 5%

173. DIAGNOSIS
Asymptomatic
Symptomatic
• Pain : often 1st symptom
• Low Threshold for CT scan
• Esp : Elderly Pt , inc. Insulin in DM , new-onset DM in elderly
• Jx : may found in Lesion at Head
• Wt loss : sign of advance Dz
• Distend / Palpable GB found 25%

174. DIAGNOSIS
CA 19-9
• Mucin-ass. Carbohydrate Ag
• Elevated in 75%
• False +ve in Obstructive Jx , Benigh HBP disezse 10%
• Fail for using as early detective screnning test
• Using for F/U : pregression & Recurrence Dz

175. DIAGNOSIS : IMAGING STUDY
Choose
• Pt with Jx
• US
• If +ve Dilatation with Stone  ERCP
• if +ve Dilatation without stone  CT
• Pt with Jx with suspected of CA Pancreas
• CT scan for 1st step

176. DIAGNOSIS : IMAGING STUDY
•ceCT scan : single most versatile &cost-eff.
– Accuracy : to predict unresectable = 90-95%
• Unresectable Dz
– Invasion to Hep. a. or SMA
– Enlarge LN outside the boundaries of resection
– +ascites
– +distance Metastasis
– Invasion of SMV or PV with not patent or Unable to
recon.
– Not accuracy in predicting resectable Dz
• Miss smll Hep. Nodule
• Miss invasion to artery

177. DIAGNOSIS : IMAGING STUDY
PET
• May help in diff. Chronic Pancreatitis vs CA pan.
EUS
• For detect small Pancreatic mass
• For Transluminal Bx : esp for Neoadj. Tx or DDx
• More sens. For PV/SMV invasion
• Less eff. in detect SMA invasion

178. DIAGNOSIS : DIAG.LAP.
About 20% of Pt with Resectable Dz on Preop.
investigation , is unresectable Dz at Op.room
( Free 20%)
Diag.Lap. : imp. Acc. For predict resectability to 98%
• Gen. Explor peritoneal surface
• Lig. of Treitz , Base of the T.colon
• Incised Gastocoloic Lig. , explor Lesser sac.
• US probe using for exam. : Liver , Porta., PV , SMA
% of +ve pt. by Lap. Dx
• 10-30% in lesion at head
• 50% in lesion at body and tail

179. DIAGNOSIS : DIAG.LAP.
Advantage of Diag.Lap.
• Less morbidity than free
• OPD case
• Recover more rapid
• Time to palliative CMTx / radiation , more rapid
• Less psychologic effect
Indication suggestive for Diag. Lap.
• Tumor >4cm
• Tumor at body or tail
• Equiocal finding of Metas or ascites on CT scan
• Marked wt loss
• Marked Elevated CA19-9 (>1,000 u/ml)

180. JX IN CA PANCREAS
•Found PreOp. , unresectable Dz
–No Bypass , DO ERCP with stenting
•Found Intraop. , unresectable Dz
–Go-on Bypass , not ERCP
•Found Intraop. , unresectable Dz with s/p
stent
–Do Bypass , if possible
•Choledochojejunostomy : procedure of choice
•Cholecystojejunostomy : may do if
– Poor performance , unable to do prolong Surgery
– Patent Cystic duct and common duct above lesion.

181. PALLITIVE SURGERY &
ENDOSCOPY
•Palliative Tx is needed in 85-90% of Pt
– Imp. QOL
– Prob : Pain , Jx , Duodenal Obstruction
oral narcotic use  Celiac plexus n.block
•Pain :
•Jx : as previous slide
•Dudenal obstuction :
– Found 20%
– Prophylaxis Gastrojejunostomy : controversial
– Con : Anas. Leakage , delay Gastric emptying time
– Procedure :
• Antecolic , prefered than retrocolic
• 50 cm distance from Gastrojej. To Bili-enteric anastomosis
– Dec. risk for Cholangitis , more easier if anastomosis leakage
• Gastrojej. Placed at most dependence part , greater Curvature
• Not do Vagotomy

182. DOUBLE BYPASS
PALLIATIVE SX FOR CA
PANCREAS
Not Vagotomy
Most Dependece
part of
Greater Curvature
50 cm length
Closed all Mesentery’s
AnteColic
Defect , if possible

183. PALLIATIVE CHEMOTHERAPY
& RADIATION
Chemotherapy
• 5-FU Gemcitabine : FDA proven for standard Tx
• imp symp. , imp. pain control , imp. Performance
• Imp. SURVIAL only 1-2 mo.
• Combination , Still in clinical research
• Gemcitabine +
• topoisomerase I inhibitors / platinums / taxanes.
• Targeted Tx :
• Antiangiogenic
• epidermal growth factor receptor agents.

184. PANCREATICODUODENECTOMY : PREPERATIVE
PREPARATION
-ve for FNA : not exclude Malignancy
Major part of Pancreatic cancer is : Fibrous tissue
, not very Cellular
Can’t Dx Chronic Pancreatitis : if FNA -ve
NEEDed if
1. NeoAdj. Tx needed , or in Trial
2. Unresectable Dz : toR/O other Dx :
such as Lymphoma , PNETs (Debulking Sx have role)

185. PANCREATICODUODENECTOMY
•3 Phase
1. Assessment of resectability
2. Resection phase
3. Reconstruction phase
• Incision :
– upper Midline incision / Bilat Subcostal incision

188. COMPLICATION
Mortality rate <5% in High Vol. center
• Surgeon perform >15 case/yr
• From Sepsis , Hemorrhage , Cardiovas. Event
Post-op. complication
• Delay Gastric Emptying time
• Pancreatic Fistula / Leakage
• Hemorrhage

189. COMPLICATION : MANAGEMENT
• Delay Gastric Emptying time
– Common
– Tx conservative : iv Erythromycin
– Mostly self-limit
• Pancreatic Fistula / Leakage : 10% of Pt
– Octreotide :
• North American : no benefit
• Europe : routine use
• Selective used if PD <3mm. (High rate complication)
– Technique : not clear.
– Duct-to-mucosa VS Invagination
• Depend on size PD and Pancreatic Texure
– Lare PD , Fibrotic Pancreas : Duct to mucosa
– Small PD , soft Pancreas : Invagination
– PD stent :
• Reduce incidence of Pancreatic fistula in some study
– PD occlusion : Permanent / Temporary : Not sig. Benefit

190. COMPLICATION : MANAGEMENT
• Hemorrhage
– Intraop. Hemorrhage
• Compress PV and SMV
– Postop. Hemorrhage
• Inadq.Ligation of vessel.
• Bilary-Pancreatic leakage
• Stress ulcer , Marginal ulcer
– Tx : PPI

191. OUTCOME
Median survival after Pancreaticoduodenectomy
• 22 mo.
Maj. Cause of death : Recurrence Tumor
Still Needed
• Only 1 modality to inc. survival
• Best for palliative symptom
• Tell Pt and his/her relative before Sx

192. ADJ TX
5-Fu combination + radiation
Gemcitabine combination
• Better but more toxic
Needed more study

193. NEOADJ. TX
•Adv.
– Dec. the tumor burden at operation
– Inc. rate of resectability
– Killing some Tu. Cell before spread intraop.
– Buying time
• Make Pt with Occult Metas.Dz , shown.
• Less Futile surgery.
– By evi. : not inc. Morbidity /mortality
• May dec. rate of Pancreatic fistula
• BUT no survival advantage

194. POST-OP SURVEILLANCE
•Most common recur.
– Hepatic Metastasis
•F/U q6mo
– PE
– Lab test : CA19-9 , LFT
– CT scan :
• after complete Chemotherapy
• rising CA19-9
• New symptoms suggest recurrence
•Surgery for recurrence Dz :
– Only for Gastric Outlet obstruction /Bowel Obstruction

195. PERIAMPULLARY CA
•Around 2 cm from ampulla of Vater
•4 type :
– CA head of pancreas
– Ampullary cancer
– Distal CBD cancer
– Duodenal Cancer
•Most AdenoCA
•Tx : Pancreaticoduodectomy

196. MX OF PERIAMPULLARY ADENOMA
•Result From endoscopic biopsy
•Mx of small Tu. (2cm or less)
– Local Excision if no malignancy
– EUS : Help in eva. of Duodenal invasion
– Endoscopic / Transduodenal excision :
• 2-3 mm margin
– If post-op. Patho. Reveal Invasive cancer
• Reop. For Whipple
– FAP
• Even patho =Duodenal Adenoma
• High recurrence rate & High CA
• Op. of choice = Standard (not PPPD) Whipple

197. LYMPHOMA
•Clinical Presentation as AdenoCA Pancreas
•Rare
•Confirm Dx
– Percut. Bx or EUR-guided Bx needed
– If fail , Explor.Lap. With Bx is indication.
•Tx
– Endoscopic Stenting
– Medication
– No role of Surgical resection

198. CONGENITAL
ABNORMALITY

199. HETEROTOPIC PANCREAS
Rest of Pancreatic tissue
Common at Stomach & Duodenum
• May found at Meckel diver.
Finding :
• Nodule , yellow , firm , central umbilication
• Histo : exocrine + endocrine gl.
No risk CA
Mostly asymp.

200. Tx :
• Indication : Symp. Or Incidental found
• Mx :
• Local excision

201. ??

202. ANNULAR PANCREAS
Congenital anomaly
Band of ventral Pancreas , engulf 2nd part Duo.
Ass. Abnormality
• Duodenal atresia / stenosis
• Down’s synd.
Presentating age :
• at infant 50%
• At >40yr : 50%
Presentation :
• Upper Gut obstruction
• Film : Double Bubble sign
Mx
• Band
• Duodenoduodenotomy 1st  DuodenoJejunostomy 2nd  Gastrojej. 3rd

203. PANCREATIC DIVISUM
•Failure in fusion of Ventral & Dorsal Pancreas
•Presentation : Pancreatitis
– Young , Recurrence Pancreatitis
•Dx
– MRCP
– ERCP : contrast local in Uncinated
•Tx :
– Endoscopic sphincterotomy
– Inserted Stent into minor papilla
– Opened Sphincteroplasty
– If Dev. Chronic Pancreatitis : Tx as CP

204. THANK YOU