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gastric cancer ppt.

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  1. 1. Gastric Carcinoma Vic Vernenkar, D.O. St. Barnabas Hospital Department of Surgery
  2. 2. Background <ul><li>Second most common cancer-related death. </li></ul><ul><li>Korea, Japan, China, Taiwan high rates. </li></ul><ul><li>22,000 diagnosed annually in US. </li></ul><ul><li>14 th most common cancer. </li></ul><ul><li>Difficult to cure, as advanced disease. </li></ul><ul><li>Most die of recurrent disease even after resection for cure. </li></ul>
  3. 4. Anatomy <ul><li>Stomach begins at GE junction, ends at duodenum. </li></ul><ul><li>3 parts- uppermost is cardia, largest part in middle is body, the last part is pylorus. </li></ul><ul><li>Cardia contains mucin producing cells. </li></ul><ul><li>Fundus or body mucoid cells, chief cells, parietal cells. </li></ul><ul><li>Pylorus has mucin producing cells. </li></ul>
  4. 5. Anatomy <ul><li>Five layers: Mucosa, submucosa, muscular layer, subserosal layer, serosal layer. </li></ul><ul><li>Peritoneum of greater sac covers anterior surface </li></ul><ul><li>A portion of lesser sac drapes posteriorly over stomach. </li></ul><ul><li>The GE junction has limited serosal covering. </li></ul>
  5. 6. Anatomy <ul><li>The site of the lesion is classified on basis of relationship to long axis of stomach. </li></ul><ul><li>40% lower part </li></ul><ul><li>40% middle part </li></ul><ul><li>15% upper part </li></ul><ul><li>10% more than one part </li></ul><ul><li>Recently the # of lesions proximally has increased. </li></ul>
  6. 8. Pathophysiology <ul><li>Understand vascular supply, allows for understanding of routes of spread. </li></ul><ul><li>Derived from celiac artery. </li></ul><ul><li>Left gastric supplies upper right stomach. </li></ul><ul><li>Right gastric off common hepatic- lower portion. </li></ul><ul><li>Right gastroepiploic -lower portion of greater curve. </li></ul>
  7. 9. Pathophysiology <ul><li>Understanding lymphatic drainage can clarify nodal involvement. </li></ul><ul><li>Complex drainage </li></ul><ul><li>Primarily along celiac axis. </li></ul><ul><li>Minor drainage along splenic hilum, suprapancreatic nodal groups, porta hepatis, and gastroduodenal areas </li></ul>
  8. 10. Frequency <ul><li>US: seventh leading cause of cancer deaths, with 22,000 diagnosed yearly, and 14,000 deaths. </li></ul><ul><li>Internationally: second most common cancer. Tremendous geographic variation, with highest death rates in Chile, Japan, and former USSR. </li></ul>
  9. 11. Mortality and Morbidity <ul><li>5-year survival for curative resections ranges from 30-50% for stage II disease and 10-25% in stage III. </li></ul><ul><li>High likelihood of systemic and local relapse. </li></ul><ul><li>Adjuvant therapy is offered . </li></ul><ul><li>Operative mortality is less than 3% for curative resections. </li></ul>
  10. 12. Race <ul><li>Higher in Asian countries. </li></ul><ul><li>Japanese detect patients at very early stage, patients appear to do quite well. </li></ul><ul><li>In Asian studies, patients with resected stage II and III disease have better outcomes than similar stages in the west. </li></ul><ul><li>Some believe this reflects a biologic difference between diseases in Asia and west. </li></ul><ul><li>Black race, low socioeconomic class. </li></ul>
  11. 13. Sex, Age <ul><li>Men>women </li></ul><ul><li>Most are elderly at diagnosis. Median age 65 years. The ones that present in younger patients may represent a more aggressive variant. </li></ul><ul><li>Cigarettes </li></ul>
  12. 14. History <ul><li>Early disease has no symptoms, some patients with incidental complaints get an early diagnosis. </li></ul><ul><li>If symptoms, it reflects advanced disease; These may include indigestion, nausea, dysphagia, early satiety, anorexia, weight loss. </li></ul>
  13. 15. History <ul><li>Late complications include: pleural effusions, peritoneal effusions, GOO, GE obstruction, SBO, bleeding, jaundice, cachexia. </li></ul>
  14. 16. Physical <ul><li>All physical signs are late events. </li></ul><ul><li>Too late for curative procedures. </li></ul><ul><li>Palpable stomach with succussion splash, hepatomegaly, Virchow nodes, sister MJ nodes, Blumer shelf, weight loss, pallor from bleeding and anemia. </li></ul>
  15. 17. Etiology <ul><li>Diet </li></ul><ul><li>H. Pylori </li></ul><ul><li>Previous stomach surgery </li></ul><ul><li>Pernicious anemia </li></ul><ul><li>Polyps(rarely a precursor) </li></ul><ul><li>Atrophic gastritis </li></ul><ul><li>Radiation, genetics </li></ul>
  16. 18. Diet <ul><li>Certain diets are implicated. </li></ul><ul><li>Rich in pickled vegetables, salted fish, excessive dietary salt, smoked meats. </li></ul><ul><li>A diet that includes fruits and vegetables rich in vitamin C may have a protective effect. </li></ul>
  17. 19. Helicobacter <ul><li>Implicated as precursor of gastric cancer. </li></ul><ul><li>H. Pylori associated with atrophic gastritis, and patients with a history of prolonged gastritis have a 6-fold increase in risk. </li></ul><ul><li>Particularly true of tumors of antrum, body, and fundus of stomach, but not in cardia. </li></ul>
  18. 20. Previous Surgery <ul><li>Implicated as risk factor, the rational being that previous gastric surgery alters normal pH of stomach. </li></ul><ul><li>Retrospective studies show that a small percentage of patients who have a gastric polyp removed have evidence of invasive carcinoma in the polyp. </li></ul><ul><li>Polyps may therefore be premalignant. </li></ul>
  19. 21. Genetic Factors <ul><li>Poorly understood </li></ul><ul><li>Some familial aggregation exists </li></ul>
  20. 22. Laboratory <ul><li>Assists in determining optimal therapy. </li></ul><ul><li>CBC identifies anemia, with may be caused by bleeding, liver dysfunction, or poor nutrition. </li></ul><ul><li>30% have anemia. </li></ul><ul><li>Electrolyte panels and LFTs are also essential to better characterize patients clinical state. </li></ul>
  21. 23. Imaging Studies <ul><li>EGD: safe, simple, providing a permanent color photographic record. </li></ul><ul><li>Obtains tissue for diagnosis. </li></ul><ul><li>UGI: detects large tumors, but only occasionally detects extension into esophagus or duodenum, especially if small or submucosal. </li></ul>
  22. 26. Imaging Studies <ul><li>CXR: done to evaluate for metastases. </li></ul><ul><li>CT scan or MRI of chest, abdomen, pelvis: evaluate local disease process, and areas of spread. Some tumors are deemed unresectable based on the testing. </li></ul><ul><li>Accurately predicts stage 66-77%. </li></ul><ul><li>Poor nodal status prediction. </li></ul>
  23. 27. Endoscopic Ultrasound <ul><li>Endoscopic ultrasound: becoming extremely useful as a staging tool, when CT fails to show T3, T4, or metastatic disease. </li></ul><ul><li>Used with neoadjuvant chemo to stratify pts </li></ul><ul><li>Can achieve resolution of 0.1 mm. </li></ul><ul><li>Cannot reliably distinguish between tumor and fibrosis. </li></ul><ul><li>Overall staging accuracy of 75% </li></ul><ul><li>Poor for T2 lesions (38%) </li></ul><ul><li>Better for T1(80%), T3 (90%) </li></ul>
  24. 30. Histology <ul><li>Adenocarcinoma 95% </li></ul><ul><li>Lymphomas 2% </li></ul><ul><li>Carcinoids 1% </li></ul><ul><li>Adenocathomas 1% </li></ul><ul><li>Squamous cell 1% </li></ul>
  25. 31. Histology <ul><li>Adenocarcinoma is classified according to the most unfavorable microscopic element present: tubular, papillary, mucinous, signet-ring cells. </li></ul><ul><li>Also identified by gross appearance: ulcerative, polypoid, scirrous, superficial spreading, multicentric, or Barrett ectopic. </li></ul><ul><li>Variety of other schemes: Borrmann, Lauren. </li></ul>
  26. 32. Borrmann Classification <ul><li>5 categories </li></ul><ul><li>Type I: polypoid or fungating </li></ul><ul><li>Type II: ulcerating lesions with elevated borders </li></ul><ul><li>Type III: ulceration with invasion of wall </li></ul><ul><li>Type IV: diffuse infiltration </li></ul><ul><li>Type V: cannot be classified </li></ul>
  27. 33. Lauren System <ul><li>Epidemic or endemic </li></ul><ul><li>The intestinal, expansive epidemic type gastric cancer is associated with atrophic gastritis, retained glandular structure, little invasiveness, sharp margins. It would be a Borrmann I or II. </li></ul>
  28. 34. Lauren System <ul><li>The epidemic or Borrmann I or II carries better prognosis, shows no family history. </li></ul><ul><li>The diffuse, infiltrative, endemic, is poorly differentiated, with dangerously deceptive margins, invades large areas of stomach. Younger patients, genetic factors, blood groups, and family history. </li></ul>
  29. 35. Staging <ul><li>Primary tumor </li></ul><ul><li>Tx- cannot be assessed </li></ul><ul><li>T0- no evidence </li></ul><ul><li>Tis- carcinoma in situ, no invasion of lamina </li></ul><ul><li>T1- invades lamina propria or submucosa </li></ul><ul><li>T2- invades muscularis or subserosa </li></ul><ul><li>T3- penetrates serosa, no adjacent structure </li></ul><ul><li>T4- invades adjacent structures </li></ul>
  30. 36. Regional Lymph Nodes <ul><li>NX- cannot be assessed </li></ul><ul><li>N0- no nodes </li></ul><ul><li>N1- mets in 1-6 regional nodes </li></ul><ul><li>N2- mets in 7-15 regional nodes </li></ul><ul><li>N3- mets in more than 15 regional nodes </li></ul>
  31. 37. Distant Metastases <ul><li>MX- cannot be assessed </li></ul><ul><li>M0- no distant metastases </li></ul><ul><li>M1-distant metastases </li></ul>
  32. 38. Prognostic Features <ul><li>Depth of invasion through gastric wall, presence or absence of regional lymph node involvement </li></ul><ul><li>The greater number of positive nodes, the greater the likelihood of local or systemic failure postoperatively </li></ul>
  33. 39. Spread Patterns <ul><li>Directly, via lymphatics, or hematogenously </li></ul><ul><li>Direct extension into omentum, pancreas, diaphragm, transverse colon, and duodenum. </li></ul><ul><li>If lesion extends beyond wall to a free peritoneal surface, peritoneal involvement is frequent. </li></ul>
  34. 40. Spread Patterns <ul><li>The visible gross lesion frequently underestimates true extent. </li></ul><ul><li>Abundant lymphatic channels in submucosal and subserosal layers allow for easy spread. </li></ul><ul><li>The submucosal plexus is prominent in esophagus, the subserosal plexus prominent in duodenum, which allows for proximal and distal spread. </li></ul><ul><li>Liver mets common, from hematogenous spread. </li></ul>
  35. 42. Laparoscopy <ul><li>Inspect peritoneal surfaces, liver surface. </li></ul><ul><li>Identification of advanced disease avoids non-therapeutic laparotomy in 25%. </li></ul><ul><li>Patients with small volume metastases in peritoneum or liver have a life expectancy of 3-9 months, thus rarely benefit from palliative resection. </li></ul>
  36. 43. Lymph Node Dissection <ul><li>AJCC: number rather than location of LN is prognostic. </li></ul><ul><li>Extent of dissection controversial. </li></ul><ul><li>Nodal involvement indicates poor prognosis, and more aggressive approaches to remove them are taking favor. </li></ul><ul><li>Ongoing trials regarding this in Europe. </li></ul><ul><li>Critics argue that the apparent benefit associated with extended LND reflects stage migration (each LN is reviewed more carefully). </li></ul>
  37. 44. Residual Disease R Status <ul><li>Tumor status following resection. </li></ul><ul><li>Assigned based on pathology of margins. </li></ul><ul><li>R0- no residual gross or microscopic disease. </li></ul><ul><li>R1- microscopic disease only. </li></ul><ul><li>R2- gross residual disease. </li></ul><ul><li>Long term survival only in R0 resection. </li></ul>
  38. 45. “D” Nomenclature <ul><li>Describes extent of resection and lymphadenectomy. </li></ul><ul><li>D1- removes all nodes within 3cm of tumor. </li></ul><ul><li>D2- D1 plus hepatic, splenic, celiac, and left gastric nodes. </li></ul><ul><li>D3- D2 plus omentectomy, splenectomy, distal pancreatectomy, clearance of porta hepatis nodes. </li></ul><ul><li>Current standards include a D1 dissection only. </li></ul>
  39. 46. Type of Surgery <ul><li>In general most surgeons perform total gastrectomy ( if required for negative margins), esophagogastrectomy for tumors of the cardia and GE junction, and a subtotal gastrectomy for tumors of the distal stomach. </li></ul><ul><li>Similar 5 year rates for subtotal vs. total in tumors of distal stomach. </li></ul><ul><li>Extensive lymphatics require 5cm margin. </li></ul>
  40. 47. Outcome <ul><li>5-year survival for a curative resection is 30-50% for stage II disease, 10-25% for stage III disease. </li></ul><ul><li>Adjuvant therapy because of high incidence of local and systemic failure. </li></ul><ul><li>A recent Intergroup 0116 randomized study offers evidence of a survival benefit associated with postoperative chemoradiotherapy </li></ul>
  41. 48. Complications <ul><li>Mortality 1-2% </li></ul><ul><li>Anastamotic leak, bleeding, ileus, transit failure, cholecystitis, pancreatitis, pulmonary infections, and thromboembolism. </li></ul><ul><li>Late complications include dumping syndrome, vitamin B-12 deficiency, reflux esophagitis, osteoporosis. </li></ul>
  42. 49. Adjuvant Therapy <ul><li>Rationale is to provide additional loco-regional control. </li></ul><ul><li>Radiotherapy- studies show improved survival, lower rates of local recurrence when compared to surgery alone. </li></ul><ul><li>In unresectable patients, higher 4 year survival with mutimodal tx, in comparison to chemo alone. </li></ul>
  43. 50. Chemotherapy <ul><li>Numerous randomized clinical trials comparing combination chemotherapy in the adjuvant setting to surgery alone did not demonstrate a consistent survival benefit. </li></ul><ul><li>The most widely used regimen is 5-FU, doxorubicin, and mitomycin-c. The addition of leukovorin did not increase response rates. </li></ul>
  44. 51. Advanced Unresectable Disease <ul><li>Surgery is for palliation, pain, allowing oral intake </li></ul><ul><li>Radiation provides relief from bleeding, obstruction and pain in 50-75%. Median duration of palliation is 4-18 months </li></ul>