Pancreas lecture1
Upcoming SlideShare
Loading in...5
×
 

Like this? Share it with your network

Share

Pancreas lecture1

on

  • 2,616 views

ใช้ สอนน้อง นศพ.ครับ แต่ค่อนข้างลึก resident ศัลย์เอาไว้ reviewได้ครับ

ใช้ สอนน้อง นศพ.ครับ แต่ค่อนข้างลึก resident ศัลย์เอาไว้ reviewได้ครับ

Statistics

Views

Total Views
2,616
Views on SlideShare
2,616
Embed Views
0

Actions

Likes
3
Downloads
189
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Pancreas lecture1 Presentation Transcript

  • 1. THE PANCREAS PONGSATORN TANGTAWEE HPB DIVISION, DEPARTMENT OF SURGERY RAMATHIBODI HOSPITAL
  • 2. OUTLINEAnatomy and PhysiologyHistology and PhysiologyAcute PancreatitisChronic PancreatitisPancreatic Neoplasm • Neoplasm of The Endocrine Pancreas • Neoplasm of The Exocrine Pancreas • PCN • lymphomaCongenital abnormality
  • 3. ANATOMYANDPHYSIOLOGY
  • 4. RELATED STRUCTURE
  • 5. REGIONS OF THE PANCREAS
  • 6. ARTERIAL SUPPLY
  • 7. Variation of Hepatic Vein (Precaution during Resection of Pancreas) A. LHA CHA
  • 8. VENOUS DRAINAGE
  • 9. VENOUS DRAINAGE Gastrocolic Trunk
  • 10. LYMPHATIC DRAINAGE
  • 11. LYMPHATIC DRAINAGE1 : Rt Cardiac 8 : Common Hepatic 15 : Middle Colic2 : Lt Cardiac 9 : Celiac 16 : Para-aortic3 : Lesser Curvature 10 : Splenic Hilum 17 : Anterior PD4 : Greater Curvature 11 : Splenic Art. 18 : Inferior5 : Suprapyloric 12 : Hepatoduodenal Lig. Pancreatic6 : Infrapyloric 13 : Posterior PD body.7 : Lt Gastric 14 : SMA
  • 12. INNERVATION
  • 13. DEVELOPMENT OFPANCREATIC DUCT (PD)
  • 14. VARIATION OF PD M = Main PD S = Duct of Santorini W = Duct of Wirsung About 2cm
  • 15. VARIATION OF PD Pancreatic Divisum
  • 16. NORMALITY OF PD
  • 17. 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 = ???????
  • 18. 50-60% Resection(Devision at neck =60-70% resection)
  • 19. ACINUS
  • 20. EXOCRINE1-2 L/dayClear, watery, alkaline (pH 8.0-8.3)> 20 different digestive enz.Isoosmotic to plasmaPrincipal cations : Na & K (~165 mmol/L)Principal anions : bicarb & Cl - secrete min : Cl high, bicarb low - secrete max : Cl low, bicarb high activetransportPassive exchange of intraductal bicarb forinterstitial Cl at larger pancreatic duct
  • 21. Digestive enz. are synthesized and stored in thepancreatic acinar cells, and released in response toCCK(cholecystokinin) and vagal cholinergicstimulation - proteolytic(trypsin, chymotrypsin, carboxypeptidase, ribonuclease, deoxyribonuclease, and elastase) - lipolytic (lipase, colipase, phospholypase A2) - amylolytic (amylase)
  • 22. Trypsin converts the other zymogens to active forms
  • 23. EXOCRINE PANCREATICINSUFFICIENCY (EPI)m/c cause in human : cystic fibrosis(1st), Shwachman-DiamondSyndrome(2nd)fairly common in diabetes - both type 1 and type 2symptoms of malabsorption, malnutrition, vitamindeficiencies, and weight loss or inability to gain weight inchildren and is often associated with steatorrheaTreatment : Pancreatic Enzyme Products PEPs , such aspancrelipase (mixture of three digestiveenzymes, amylase, protease (peptidase), and lipase)
  • 24. 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 andbicarbonate in the pancreatic secretion
  • 25. ENDOCRINE FUNCTIONIslet of Langerhans 1-2% of pancreatic mass 20% of total pancreatic blood flowInsulin : Beta-cell : muscle, liver, fat cellsGlucagon : alpha-cell Somatostatin : delta cellPancreatic polypeptide : PP cellsacini are exposed to higher conc. of the islethormones than peripheral tissue
  • 26. ACUTEPANCREATITIS
  • 27. DEFINITION AND INCIDENCEDefinition • An inflammatory disease of the pancreas than is associated with little or no fibrosis of the glandIncidence • About 300,000 case/yr in US • 10-20% = severe • about 4,000 Deaths/yr + more than $2billion cost
  • 28. 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
  • 29. ETIOLOGY : BILIARY TRACTDISEASEMost comonMech. not entirely clear • Common-Channel hypothesis • Incompetent Sphincter of Oddi (after passing GS) • PD blockage : Helminth , Tumor • Colocalization theory
  • 30. ETIOLOGY : ALCOHOLAt least 2yr drink , commonlyDx : Hx expose ethanol + absence of other causeMechanism • “Secretion with Blockage” Mechanism • Inc. Ductal Permeability • Improper enz. Leaking to surrounding tissue • Dec. Pancreatic Blood flow
  • 31. ETIOLOGY : TUMOR1-2% of Pancreatitis found Pancreatic carcinomaPeriampullary TumorMechanism : • Blockage of secreted juice
  • 32. ETIOLOGY : IATROGENICPancreatic Biopsy , Biliary exploration , Distal gastrectomy, SplenectomyB2 Gastrectomy & Jejunostomy • Inc. intraduodenal P. cause backflow of enz.Any Sugery than cause Low Sys. PerfusionERCP (most common) 2-10% • Direct Inj. or Intraductal Hypertension
  • 33. ETIOLOGY : DRUGS
  • 34. ETIOLOGY : INFECTIONMumps , Coxsackievirus , MycoplasmapneumoniaeFound from rising of Antibody titer in about 30%of Pt with pancreatitis with No other causeNo direct evi. that isolated from diseasesdpancreas
  • 35. ETIOLOGY : HYPERLIPIDEMIAcaused by hypertriglyceridemia but not byhypercholesterolemiaSerum triglycerides must rise above 1000 mg/dLPrimary Hypertriglyceridemia • Types I, IV, and V are associated with acute pancreatitisSecondary Hypertriglyceridemia • Alcohol • Diabetes • Pregnancy • Drugs : loop and thiazide diuretics, tamoxifen, retinoids, beta-blockers etc.
  • 36. ETIOLOGY : MISCELLANEOUSCAUSES•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
  • 37. PATHOPHYSIOLOGY :ACUTE PANCREATITIS Primary Insult : “start from (acinar) cell” Cathepsin B Hypothesis
  • 38. 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
  • 39. PATHOPHYSIOLOGY : ACUTEPANCREATITIS Systemic Metabolic Pulmonary Pleural effusion Hyperglycemia Atelectasis Hypertriglyceridemia Mediastinal abscess Pneumonitis Hypocalcemia Adult respiratory distress syndrome Encephalopathy Cardiovascular Hypotension Sudden blindness Hypovolemia (Purtschers 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
  • 40. ACUTE PANCREATITIS :DIAGNOSISClinical 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
  • 41. 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
  • 42. 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 CameronALT >3 times normal : Ac GS Pancreatitis • Found in 50% of case
  • 43. 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
  • 44. ACUTE PANCREATITIS :IMAGINGUltrasound • 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
  • 45. 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.
  • 46. ACUTE PANCREATITIS :DIFFERENTIAL DIAGNOSISBowel obstructionCholecystitis or cholangitisMesenteric ischemia or infarctionPerforated hollow viscus
  • 47. ACUTE PANCREATITIS :SEVERITYThe Atlanta classification (1992)
  • 48. SUMMARY OF THE INTERNATIONALSYMPOSIUM 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
  • 49. 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
  • 50. 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)
  • 51. 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)
  • 52. APACHE-II(ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION) Benefit : Immediate Evaluation Better in Eva. Prog. than Ranson Weak : Complex
  • 53. IMRIE/GASGLOW SCORE
  • 54. SEQUENTIAL ORGAN FAILUREASSESSMENT (SOFA) SCORE INACUTE PANCREATITIS
  • 55. CTSI Mild Pancreatitis Severe Pancreatitis
  • 56. ACUTE PANCREATITIS :PRINCIPLE OF TREATMENT1. Adequate Monitoring : Admit to ICU or not2. Adequate Resuscitation : Fluid & Electrolyte – Not too much/too low – Hypocalcemia , Met. Acidosis , Hypoalbuminemia , HypoMg.3. Pancreatic Rest : NPO4. Adequate Pain Control : dec. cholinergic n. stimuli – Avoid MO
  • 57. 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
  • 58. SEVERE PANCREATITIS APACHE-II (Acute Physiology And Chronic Health Evaluation)
  • 59. SEVERE PANCREATITISDx when : 1. Ranson score ≥ 3 2. APACHE-2 ≥ 8 3. Dev. Local/Systemic complication • MOF • Pseudocyst , necrosis , abscess 4. ceCT : necrosis >33% (???)
  • 60. TX OF BILIARY PANCREATITISControversial point : Timing (48-72hr , >72hr)ERCP , Cholecystectomy with CBD clearanceIndication : for Early ERCP • Obstructive Jx with Cholangitis • Severe pancreatitis • Pancreatitis with obstructive Jx >24hrRoutine Early ERCP : not recommended
  • 61. PANCREATIC NECROSISOccur about 20% of Pancreatitis pt.Severe Necrotizing PancreatitisSterile vs Infected : ceCT with FNA • “Air Bubble” found 20% of Infected PN (IPN) • Mortality • <1% in sterile PN • About 40% in IPNClinical : • Fevere , Leukocytosis , clinical not imp. In 72hrTreatment • Antibiotic • Drainage • Catheter-bases Therapy • Surgical Debridement • For Life-Thretening only
  • 62. OPENED NECROSECTOMYIndication • 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
  • 63. CHRONICPANCREATITIS
  • 64. DEFINITIONIncurable , Chronic inflammatory conditionMultifactorial in etiologyPermanent loss of pancreatic exocrine &endocrine function • Leading to pancreatic insufficiency
  • 65. ETIOLOGY
  • 66. 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
  • 67. ETIOLOGYHyperthyroidism • Caused Hypercalcemia • Induced Pancreatic Hypersecretion + calcium secretion • Caused Chronic calcified pancreatitis • Calculus formation and Obstructive Pancreatopathy • Tx : correct HyperparathyroidismHyperlipidemia & Hypertrigleceridemia • Worsen in women with Estrogen replacement Tx • Tx : Control Keep Fasting TG < 300 mg/dL
  • 68. ETIOLOGYTropical (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
  • 69. CLASSIFICATION
  • 70. PATHOLOGYHistology • 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
  • 71. PATHOLOGYStone 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
  • 72. 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
  • 73. 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
  • 74. • 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
  • 75. PRESENTATIONMalabsorption & Wt loss • Occur when exocrine capacity <10% • Diarrhear & Steatorrhea • Bulky , foul-smell ,float , with Oily water • Lipase def.  Trypsin Def.  dec. Bicarb. SecretionApancreatic (pancreatogenic) Diabetes (type IIIDM)
  • 76. INVESTIGATIONMeasurement of pancreatic products in blood • A. Enzymes • B. Pancreatic polypeptideMeasurement 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
  • 77. III. Imaging techniques • Plain film radiography of abdomen • Ultrasonography • Computed tomography • Endoscopic retrograde cholangiopancreatography • Magnetic resonance cholangiopancreatography • Endoscopic ultrasonography
  • 78. PROGNOSISDepend on • Etiology of disease • Complication • Age • Socioeconomic statusProgressive , cumulative inc. risk of CA
  • 79. COMPLICAITON ANDMANAGEMENT
  • 80. COMPLICATION : PSEUDOCYSTNatural 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)
  • 81. COMPLICATION : PSEUDOCYSTInvestigation • 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
  • 82. 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
  • 83. COMPLICATION : PSEUDOCYST
  • 84. CYSTOGASTROSTOMY
  • 85. R-E-Y CYSTOJEJUNOSTOMY
  • 86. R-E-Y CYSTOJEJUNOSTOMY
  • 87. 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
  • 88. 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
  • 89. COMPLICATION : PANCREATICO-ENTERICFISTULAMost common site • Transverse Colon , Splenic FlexureTx • Fistula to stomach / Duodenum • No Mx : solve spont. , leave Fistula • Fistula to Colon • Needed Surgical Correction
  • 90. 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%
  • 91. 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
  • 92. COMPLICATION : HEAD-OF-PANCREAS MASSInflammatory massFound up to 30%Symptom : pain , stenosis (Duo. , stoma, CBD) Thrombosis (compress PV)Tx : • DPPHR : Duodenal-preserving Pancreatic Head resection
  • 93. COMPLICATION :SPLENIC / PORTAL V THROMBOSISOccur 4 to 8% of caseSplenic 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
  • 94. 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
  • 95. 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 ManagementSurgical Therapy
  • 96. ALGORITHM IN TX OF CHRONIC PANCREATITISPAIN
  • 97. TREATMENT : ENDOSCOPIC MXRole • pancreatic duct obstruction • stone disease • pseudocyst formation • pancreatic duct leak • In acute pancreatitis : found 37% • The Dx and Mx of associated pancreatic tumors
  • 98. 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
  • 99. TRANSPAPILLARY DRAINAGE
  • 100. TREATMENT : SURGICAL THERAPYType of Surgery • Sphincteroplasty • Drainage Procedure • Duvals caudal pancreaticojejunostomy. • Puestow and Gillesbys 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
  • 101. • 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
  • 102. 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
  • 103. TREATMENT : SURGICALTHERAPY•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
  • 104. 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
  • 105. 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
  • 106. •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
  • 107. 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
  • 108. DUVALS CAUDALPANCREATICOJEJUNOSTOMY.(1954) Problem Fail due to Segmental Obstruction of PD “Chain of lakes” Recurrence due to Restenosis & scarring
  • 109. ORIGINAL PUESTOW PROCEDURE (1958)
  • 110. PARTINGTON AND ROCHELLE PROCEDUREMOD. PUESTOW PROCEDURE (ABOUT 1960) Pain Control rate First Few yr = 75-85% Recur >20% after 5 yr
  • 111. DISTAL PANCREATECTOMY (40-80%)SPLEEN-SPARING DISTALPANCREATECTOMY 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
  • 112. PROXIMAL PANCREATECTOMY PPPD : Pylorus-Preserving Whipple ProcedureLong term pain relief rate = 71- Pancreaticoduodenectomy89%Mortality 1.5-3%Maj. Complication =25-38%25-48 % dev. Endocrine&Exocrine insufficiency
  • 113. TOTAL PANCREATECTOMYOccurred 1944For Tx of InsulinomaUsed 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
  • 114. BEGER PROCEDURE : DPPHR (1980) Pain Relief rate = 91% Mortality <1% Dev. DM 21%  reversible 11% Major Complicaiton : Pancreatic Leakage , Intra-abdominal collection
  • 115. FREY PROCEDURE : LR-PJ(1987) F/U 7yr Pain relief rate = 87%pt No mortality 22% Maj. complication
  • 116. TREATMENT : DENERVATIONPROCEDURESChoice • operative celiac ganglionectomy • Transhiatal splanchnicectomy • Transthoracic splanchnicectomy • with or without vagotomy • Videoscopic transthoracic splanchnicectomy
  • 117. PANCREATICNEOPLASMS
  • 118. 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
  • 119. Cystic Neoplasms of the Pancreas • Pseudocysts • Cystadenoma • Mucinous Cystadenoma and Cystadenocarcinoma • Intraductal Papillary Mucinous Neoplasm • Solid-Pseudopapillary Tumor • Other Cystic NeoplasmsPancreatic Lymphoma
  • 120. NEOPLASM OF ENDOCRINEPANCREAS•1% of Pancreatic Tumor•Most common PETs = Insulinoma•Related to MEN1 – pituitary tumors – parathyroid hyperplasia – pancreatic neoplasms (Gastrinoma)•amine precursor uptake and decarboxylationcells•Benign vs Malignancy –Present of Local invasion , lymph. or Hepatic metastases –Most are Malignant • But prognosis is far better than CA exocrine pancreas
  • 121. Key of management • Clinical Syndrome • Laboratory confirmation • Localization • Surgery • For complete surgical resection • Debulking Tumor for symphtomatic control • Unresectable disease : Chemoembolization
  • 122. 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
  • 123. 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
  • 124. 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
  • 125. INSULINOMAManagement •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
  • 126. •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
  • 127. 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
  • 128. 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
  • 129. 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
  • 130. 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
  • 131. 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
  • 132. GASTRINOMATreatment • 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
  • 133. •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 Passaros triangle • the worst prognosis.
  • 134. 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
  • 135. 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
  • 136. 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
  • 137. SOMATOSTATINOMARare TypePresentation • 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 MetastasesDx : Serum Somatostatin Level >10 ng/mlTx : • Resection if possible • Debulking Tumor • Cholecystectomy
  • 138. NONFUNCTIONING ISLET CELLTUMORSThe most 2nd islet cell tumorClinical silent  mostly Metastasesstain positive for pancreatic polypeptide (PP), and elevated PP levelsRelated to Other Multiple neoplasia synd • VHL : von Hippel-Lindau syndromeSlowly Growth • 5yr survival is common
  • 139. PANCREATIC CYSTIC NEOPLASM (PCNS)•inc incidence as inc. of CT using•Most of these lesions are benign or slowgrowing –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
  • 140. 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
  • 141. OPERATION VS OBSERVATION Consider Risk&benefit ratio Life expectancy Comorbidities Malignant potential Location Hospital M&M
  • 142. PCNPathological Classification • Serous Cystic Neoplasm (SCN) • Mucinous Cystic Neoplasm (MCN) • Intrapapillary Mucinous Neoplasm (IPMN) • Solid Pseudopapillary Neoplasm (SPN)
  • 143. 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
  • 144. 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
  • 145. Mx • Observation : F/U with CT or MRI q6mo in first 2yr , then annually • Surgery when indication • Not Enucleation , Splenectomy not needed • Resection
  • 146. MUCINOUS CYSTIC NEOPLASM(MCN)Most common PCNsMiddle age , femaleBody & tailAsymptomaticFinding on CT • Cyst >2cm (macrocyst) • Thick wall • Intracystic septation • +ve solid compartmentClassical finding : • Rim Calcification (peripheral) • No PD communication
  • 147. Cystic Fluid • Clear , mucus , “string sign” •Mucin stain +ve • Cyto :Mucinous cell •Low Amylase , High CEA , High CA 15-3High risk for MalignatTx • Surgical resection , if possible
  • 148. INTRADUCTAL PAPILLARYMUCINOUS NEOPLASMIPMN•Prolifaration of mucinous cell in pancreatic duct , formingPapillary stroma•Asymp. 60%•Often cause Pancreatitis (40%) , from mucin plug•Jx (rare)•Male , elderly , Head of Pancreas
  • 149. Risk Malignancy : as MCN • With other site CA : CRC , Stomach , LungClassification • Main Duct Type : found 75% , risk CA 70% • Branch Duct type : found 15-20% , risk CA 25% • Combined type : found 10-15%
  • 150. 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
  • 151. INTRADUCTAL PAPILLARY MUCINOUSNEOPLASM IPMN•Treatment – Nonoperative : for BD type • Asymptomatic • Size < 3cm • No mural nodule , no thick septum • No PD dilatation • -ve on Cytology
  • 152. • Operative Mx : Problem = Margin ? • Frozen section of Transected margin • Intraoperative Pancreatoscopy • Intraductal US • Total Pancreatectomy
  • 153. SOLID PSEUDOPAPILLARYNEOPLASM (SPN)Solid Cystic Tumor , Franz Tumor , Hamoudi TuVery rareFemale , 20-25 yrHead , Body , tailGross & CT finding : • Multiloculated mass : Cystic – Solid massFNA • Necrotic tissue • Low CEA , Low Amylase • Histo. = Papillary elemetTx • Complete Resection • If Metastases : Metastasectomy
  • 154. EXOCRINEPANCREATICTUMOR
  • 155. 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
  • 156. 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 timesOncogenesis : • Likely initiated with Mutation of K-ras oncogene
  • 157. 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
  • 158. SYNDROME RELATEDFound 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
  • 159. PATHOLOGYPrecursor 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
  • 160. PATHOLOGYLocation • 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
  • 161. PATHOLOGYCell type • Ductal Adenocarcinoma 75% • Adenosquamous Carcinoma • Poor Prog. Too • Acinar cell carcinoma • Uncommon • Usually present at large Tumor (>10cm) • Better Prognosis
  • 162. DIAGNOSIS & STAGINGStaging • T1-4 • Size cutoff at 2 cm (T1) / or more(T2) • beyond Pancrease resectable (T3) / Unresectable (T4) • N0 vs N1 • M0 vs M1AJCC 6th same as AJCC 7thUnresectable Dz Poorer prog. than N+,resectable Dz
  • 163. 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%
  • 164. DIAGNOSISAsymptomaticSymptomatic • 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%
  • 165. DIAGNOSISCA 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
  • 166. DIAGNOSIS : IMAGING STUDYChoose • 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
  • 167. 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
  • 168. DIAGNOSIS : IMAGING STUDYPET • 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
  • 169. 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
  • 170. 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 effectIndication 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)
  • 171. 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/pstent –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.
  • 172. 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
  • 173. DOUBLE BYPASSPALLIATIVE SX FOR CAPANCREAS Not Vagotomy Most Dependece part of Greater Curvature 50 cm length Closed all Mesentery’s AnteColic Defect , if possible
  • 174. PALLIATIVE CHEMOTHERAPY& RADIATIONChemotherapy • 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.
  • 175. PANCREATICODUODENECTOMY : PREPERATIVEPREPARATION -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)
  • 176. PANCREATICODUODENECTOMY•3 Phase 1. Assessment of resectability 2. Resection phase 3. Reconstruction phase• Incision : – upper Midline incision / Bilat Subcostal incision
  • 177. COMPLICATIONMortality rate <5% in High Vol. center • Surgeon perform >15 case/yr • From Sepsis , Hemorrhage , Cardiovas. EventPost-op. complication • Delay Gastric Emptying time • Pancreatic Fistula / Leakage • Hemorrhage
  • 178. 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
  • 179. COMPLICATION : MANAGEMENT• Hemorrhage – Intraop. Hemorrhage • Compress PV and SMV – Postop. Hemorrhage • Inadq.Ligation of vessel. • Bilary-Pancreatic leakage • Stress ulcer , Marginal ulcer – Tx : PPI
  • 180. OUTCOMEMedian survival after Pancreaticoduodenectomy • 22 mo.Maj. Cause of death : Recurrence TumorStill Needed • Only 1 modality to inc. survival • Best for palliative symptom • Tell Pt and his/her relative before Sx
  • 181. ADJ TX5-Fu combination + radiationGemcitabine combination • Better but more toxicNeeded more study
  • 182. 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
  • 183. 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
  • 184. 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
  • 185. 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
  • 186. 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
  • 187. CONGENITALABNORMALITY
  • 188. HETEROTOPIC PANCREASRest of Pancreatic tissueCommon at Stomach & Duodenum • May found at Meckel diver.Finding : • Nodule , yellow , firm , central umbilication • Histo : exocrine + endocrine gl.No risk CAMostly asymp.
  • 189. Tx : • Indication : Symp. Or Incidental found • Mx : • Local excision
  • 190. ??
  • 191. ANNULAR PANCREASCongenital anomalyBand 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 signMx • Band • Duodenoduodenotomy 1st  DuodenoJejunostomy 2nd  Gastrojej. 3rd
  • 192. 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
  • 193. THANK YOU