Pancreatic Neoplasm

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Pancreatic Neoplasm. 5/24/06 Brent White Richard Barth. Facts About Brent & Georgia. Born in Durham, NC 4/8/74 My family moved to Columbus, Georgia when I was 6 weeks old Georgia is known as The Goober State Goober=Peanut - PowerPoint PPT Presentation


<ul><li><p>Pancreatic Neoplasm5/24/06Brent WhiteRichard Barth</p></li><li><p>Facts About Brent &amp; GeorgiaBorn in Durham, NC 4/8/74My family moved to Columbus, Georgia when I was 6 weeks oldGeorgia is known as The Goober StateGoober=PeanutGeorgia produces quite a few peanuts, growing 42% of peanuts grown in the US</p></li><li><p>OverviewDuring 2006, estimated 32,300 people will die in the US of pancreatic cancerFourth and fifth most common cause of cancer deaths in men and women in the US respectivelyPeak incidence in age 60-80African Americans with slightly higher incidence compared with Caucasians</p></li><li>Types of Pancreatic NeoplasmsBroadly speaking, there are three basic types:Ductal adenocarcinoma &gt;90% of pancreatic cancers with a 4% 5-year survival (worst of any cancer)Neuroendocrine tumors aka islet-cell tumors, rareCystic neoplasms account for </li><li><p>Clinical Scenario #1 Adenocarcinoma of the Pancreas70yo female with PMH of HTN who developed jaundice without significant abdominal pain, no feverBilirubin 12No significant complaints of abdominal pain</p></li><li><p>Clinical Scenario #1 Adenocarcinoma of the PancreasWhat are typical symptoms of pancreatic CA?Abdominal pain-&gt;pain can suggest neural plexus, tail lesion, unresectability, poor prognosisAnorexiaWeight lossJaundicePruritis -&gt;biliary obstructionSteatorrhea-&gt;pancreatic duct obstruction</p></li><li><p>Risk Factors for Pancreatic Cancer?Firmly linked to cigarette smokingNo clear dietary factorsIncreased BMI associated with increased riskOccupational exposures to amines (chemistry, hairdressing, rubber work) associated with increased risk</p></li><li><p>Risk Factors for Pancreatic CancerPrevious epidemiology identified chronic pancreatitis as a risk factorMay actually be EtOH, smoking, and a degree of selection bias instead of pancreatitis Familial excess of pancreatic cancer, hereditary cancer syndromes, hereditary pancreatitis, BRCA-2 mutations all associated with increased risk of pancreatic cancer</p></li><li><p>Adenocarcinoma of the Pancreas: Workup70yo female with painless jaundice...What would widely be regarded as the single most useful imaging study in this patients workup?CT</p></li><li><p>Adenocarcinoma of the Pancreas: CT scanCT can confirm pancreatic cancer with a sensitivity of 85-95% (sensitivity is limited by smaller tumor size)Other than the presence of a pancreatic mass, what else can you determine from CT scan? PRESENCE of METASTASES (along with CXR)RESECTABILITY</p></li><li><p>Adenocarcinoma of the Pancreas: CT scanWhat makes a pancreatic mass likely resectable?No evidence of extrapancreatic diseaseEvidence of nonobstructive superior mesenteric-portal vein confluenceNo evidence of direct tumor extension to the celiac axis and SMAEUS, laparoscopy are universally regarded as useful adjuncts to CT, not as essential however</p></li><li><p>Adenocarcinoma of the Pancreas: CT scanBorderline Resectable lesions include: SMV occlusion of a short segment (open vein proximally and distally)Body and tail lesions with + celiac, para-aortic nodes in the vicityTumors briefly involving the IVC may be borderline</p></li><li><p>Adenocarcinoma of the Pancreas: CT scan</p></li><li><p>Adenocarcinoma of the Pancreas: WorkupThe mass appears borderline resectable per these criteriaNow what?GI consultation for ERCP and EUS!</p></li><li><p>Pancreatic Cancer: Endoscopic AdjunctsERCP can be utilized to:detecting small tumors not visualized on CT (irregular solitary duct stenoses &gt;1cm long, abrupt cutoff of main pancreatic duct, or panc and bile duct obstruction)palliating biliary obstructionbrush cytology of the pancreatic duct has fair sensitivity (70%) but excellent specificityEUS can be utilized to:aid in diagnosis and characterization of lesionobtain tissue biopsy; may be associated with lower risk of peritoneal seeding c/w percutaneous approach</p></li><li><p>Pancreatic Cancer: Endoscopic AdjunctsERCP picture</p></li><li><p>Pancreatic Cancer: Serum MarkersIs there a role for serum markers? If so, what?CA 19-9 is a sialylated Lewis A blood group antigen commonly expressed and shed in pancreatic and hepatobiliary disease, not tumor specificThis antigen, when significantly increased, can assist in differentiating between pancreatic adenocarcinoma and inflammatory pancreatic diseasedecrease in serial CA 19-9 correlates with survival of pancreatic patients after surgery or chemotherapyDebatable as to whether this is useful as early treatment of recurrences have not been shown to improve outcomes</p></li><li><p>Pancreatic Cancer StagingThough TNM staging exists, we can roughly simplify to:local/resectable, median survival 17 monthslocally advanced and unresectable, median survival 8-9 monthsmetastatic disease, median survival of 4-6 months</p></li><li><p>Pancreatic AdenoCA Algorithm</p></li><li><p>Pancreatic Cancer: Neoadjuvant TherapyThis 70yo female has borderline resectable features, has been stented to answer obstructive jaundice via ERCP with EUS demonstrating a positive adenocarcinomaIs there any role for neoadjuvant therapy for this patient? If so, what sort of regimen and with what objectives?</p></li><li><p>Pipas, Barth et al.24 patients with pancreatic adenocarcinomaInclusion criteria: biopsy-proven adenocarcinoma of pancreas (Stage I-III), age&gt;18yo, Karnofsky of &gt;70%, Creatinine3000, Hgb &gt;10g/dL, Plts &gt;100,000No history of chemo/XRT or malignancyTreatment consisted of docetaxel 65mg/m2 IV over 1 hour and gemcitabine 4000mg/m2 IV over 30 minutes on days 1, 15, 29. On Day 43, XRT at 50.4 Gray with gemcitabine 50mg/m2 IV over 30 minutes biweekly for 12 doses</p></li><li><p>Pipas, Barth et al.All but one of 24 patients completed 12 week course of therapyGrade 3 and 4 toxicities common, but manageableNo tumor progression, 12 responded to therapy with one radiographic CR50% of patients had radiographic response, 17/24 patients underwent resection after therapy Of 17 resection patients, 13 (76%) with negative margins</p></li><li><p>Pipas, Barth et al.</p></li><li><p>Adenocarcinoma70yo female undergoes docetaxel/gemcitabine followed by gemcitabine with XRT and appreciable response is seen on repeat CTWhipple OperationUtility to pylorus preservation?Extended lymphadenectomy?Does type of pancreatic anastamosis matter?Do stents decrease pancreatic fistulas?</p></li><li><p>Case #228yo surgical resident was golfing, badly. Suddenly, according to his partners, he began acting crazy and drove the golf cart wildly around the green, through a sandtrap and into a small creek. He was incoherent when he was brought to the ER and found to have a serum glucose of 32.</p></li><li>How is insulinoma diagnosed?Whipples Triad:symptoms of hypoglycemia during fasting or exerciseserum glucose </li><li>What percent are malignant?10% are malignant, indicated by metastasesMetastases usually to regional peripancreatic lymph nodes, livergenerally sporadic, solitary, benign, </li><li><p>How are insulinomas localized?Non-invasive preoperative imaging studies fail to localize 30-35% of insulinomasCT/MRI, etc. generally reserved by most endocrine surgeons to r/o hepatic metastasesIntraoperative U/S and palpation are the GOLD standard for finding an insulinoma, 96-100% sensitivity</p></li><li><p>What is proper operation for insulinoma?Generally wide Kocher maneuver, superior and inferior pancreatic border mobilization, medial reflection of the spleenBimanual palpation with U/SEnucleation of the lesion Secretin can assist in identifying pancreatic duct leak after enucleation completedWhat about lesion in pancreatic head?Need to monitor glucose levels q15 minutes until lesion out</p></li><li><p>Case #3A patient has a gastric ulcer diagnosed endoscopically and is treated with Cimetidine. One month later, the ulcer is still present despite treatment.</p></li><li><p>How is ZE diagnosis made?Elevated serum gastrin level, elevated basal acid secretory rate both only suggest possible gastrinomaSecretin stimulation testdiscontinue acid-inhibitory medicationbasal serum gastrin levels2 U/kg of secretin IV bolus, then serum gastrin measured at 2, 5, 10, and 20 minutes laterPositive response is gastrin &gt;200pg/mL above basal level</p></li><li><p>How would you control gastric acid secretion?Proton pump inhibitor titrated to achieve non-acidic gastric pH</p></li><li>Where are gastrinomas? How would you localize it?Most are found in the duodenum, pancreas, or lymph nodes near the head of the pancreas, 10% of the time they are heart, liver, bile ducts, ovary, etc.Localization with somatostatin receptor scintigraphy (SRS) (only 30% of gastrinomas </li><li><p>At operation, what is the likelihood of finding metastatic tumor? Metastatic tumor to liver is found in 5-14% of cases, nodal metastases in 50% of patients</p></li><li><p>Where are most gastrinomas found?Gastrinoma triangle is where most tumors are found (70-90%)Tumor detection can be improved via palpation, IOUS, extended Kocher maneuver, transillumination of the duodenum, and duodenotomy</p></li><li><p>Hypercalcemia and GastrinomaIf patient has MEN-1 (hyperparathyroidism, pituitary adenoma, islet-cell tumor), can they be cured with surgery for gastrinoma?Seldom can biochemical cure be achieved due to multicentric nature of disease in MEN-193% of patient with MEN-1 alive 15 years after diagnosis, if they are on PPIs and have no liver metssome advocate surgical treatment only in sporadic form of disease; others propose operating on MEN-1 gastrinomas only when 2.5-3cm in size in order to reduce possibility of metastases</p></li></ul>