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Gastric cancer

Carcinoma stomach - its etiology classification investigations, staging and management

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Gastric cancer

  1. 1. Dr. kundan Junior Resident , Department of surgery Patna medical college
  2. 2. Anatomy The stomach J-shaped. The stomach has two surfaces (the anterior & posterior), two curvatures (the greater & lesser), two orifices (the cardia & pylorus). It has fundus, body and pyloric antrum.
  3. 3. a. The left gastric artery b. Right gastric artery c. Right gastro-epiploic artery d. Left gastro-epiploic artery e. Short gastric arteries The corresponding veins drain into portal system. The lymphatic drainage of the stomach corresponding its blood supply.
  4. 4. Histology Consist of four layers serous layer muscular layer submucous layer mucous layer
  5. 5. PHYSIOLOGY Function: 1. Digestion of food, reduce the size of food 2. Acts as reservoir 3. Absorption of Vit. 12, iron and calcium Stimulant of Gastric secretion: 1. Gastrin -----> (+) parietal cell 2. Acetylcholine (vagus) ---> (+) gastric cells 3. Histamine (mast cells) ---> parietal & chief cells
  6. 6. Carcinoma stomach Clinical Presentation Diagnosis Staging Treatment Screening
  7. 7. Spectrum of gastric cancer Proposed progression: chronic gastritis --> chronic atrophic gastritis -->  intestinal metaplasia --> dysplasia --> adenocarcinoma
  8. 8. Risk Factors for gastric cancer Diet  nitroso compounds  low fruit/vegetable, high fried foods/processed meat  High salt intake Obesity Smoking (HR 2-3) ? Alcohol H. Pylori Low socioeconomic status Hereditary diffuse gastric cancer  40-67% lifetime risk for men, 60-83% for women Immigrants from endemic areas  maintain native country risk, risk to offspring similar to new homeland
  9. 9. Precursors of Gastric Cancer Adenomatous polyps Chronic atrophic gastritis Pernicious gastritis Menetries’s disease Previous gastric surgery for non- cancerous conditions
  10. 10. Symptoms at presentation
  11. 11. Symptoms (cont’d) Dysphagia: more common with proximal gastric tumors Occult GI bleeding very common, overt bleeding <20%.
  12. 12. Signs Palpable abdominal mass: most common physical finding If cancer spreads via lymphatics… Left supraclavicular node (Virchow’s) Periumbilical node (Sister Mary Joseph) Left axillary node (Irish) Enlarged ovary (Krukenberg's tumor) Ascites
  13. 13. Investigations Routine blood examination low hemoglobin , high ESR  stool examination for occult blood  gastric function test - will reveal gross hypo / achlorhydria  Endoscopy – helpful in diagnosing early cases and taking biopsy  Ultrasonography - helps in assesing thickening of agstric wall, local invasion, peritoneal involvement , ascitis  CT scan - extent of the disease , lymph node involvement , liver metastasis  Barium studies  Staging laproscopy
  14. 14. Diagnosis Endoscopy Gold standard Single biopsy from ulcer -> sensitivity ~ 70% Seven biopsies from ulcer -> sensitivity >98% Brush cytology increases sensitivity of single biopsies, aid in multiple biopsies unclear
  15. 15. Preoperative Staging Abdominal / pelvic CT scanning Endoscopic ultrasound (EUS) Depth of the tumour Enlarged perigastric/coeliac lymph nodes
  16. 16. Endoscopic ultrasound A small, high frequency ultrasound transducer incorporated into the distal end of the endoscope. Advantages: - superior resolution. - image not compromised by intervening gases. - lesion as small as 2-3 mm in diameter can be imaged.
  17. 17. Barium studies False negative in as many as 50% of cases Sensitivity as low as 14% in early cases May be superior to EGD for linitis plastica EGD may be normal while “leather-bottle” will be apparent on radiograph
  18. 18. Staging Laparoscopy
  19. 19. Malignant Neoplasms of the Stomach Primary Adenocarcinoma (94%) Lymphoma (4%) Malignant GIST (1%) Haematogenous spread Breast Malignant melanoma Direct invasion Pancreas; Liver; colon; ovary
  20. 20. Staging of Gastric Cancer Two systems: Japanese classification (more elaborate and anatomic based) Western: developed by American Joint Committee on Cancer (AJCC) and International Union Against Cancer (UICC) -- more widely used Tumors at GE junction of in cardia of stomach within 5cm of GE junction Classified using esophageal staging
  21. 21. Gastric carcinoma CLASSIFICATION Depth of invasion EARLY GASTRIC CA - mucosa & submucosa ADVANCED GASTRIC CA - into or through muscularis propria Macroscopic growth pattern – Ming classification Expanding Infiltrative - "linitis plastica" Histologic subtype Intestinal Diffuse (gastric); poorly differentiated; "signet ring" cells
  22. 22. Gastric carcinoma CLASSIFICATION WHO Classification: 1. Adenocarcinoma: a. Papillary adenocarcinoma b. Tubular adenocarcinoma c. Mucinous adenocarcinoma d. Signet-ring cell carcinoma 2. Adenosquamous carcinoma 3. Squamous cell CA 4. Small cell CA 5. Undifferentiated CA 6. Others Lauren Classification: 1. Intestinal type (53%) 2. Diffuse type (33%) 3. Unclassified (14%) Ming Classification: 1. Expanding type (67%) 2. Infiltrative type (33%)
  23. 23. Histologic type: 1. Papillary 2. Tubular 3. Mucinous 4. Signet ring Mode of spread: 1. Direct 2. Lymphatic 3. Hematologic 4. Transcoelomic route
  24. 24. Linitis Plastica Diffuse-type gastric cancer Tumor often infiltrates the submucosa and muscularis propria Superficial biopsies may be falsely negative Combination of strip and bite biopsy needed if suspicious for linitis plastica
  25. 25. Linitis Plastica, “leather bottle stomach”
  26. 26. Staging workup Biopsy Imaging CT: evaluates for metastases (M stage)  20-30% with negative CT have intraperitoneal disease at laparatomy  Accuracy of 50-70% for T stage  Slightly worse accuracy for N stage compared to EUS EUS: most reliable nonsurgical method to evaluate depth of invasion  More accurate than CT for T stage  65-90% accurate for N stage
  27. 27. Staging workup PET More sensitive than CT for detection of distant metastases. Also useful for detecting LNs Negative PET not helpful- even large tumors can be falsely negative if metabolic activity low.  Most diffuse gastric cancers (signet ring) are not FDG avid
  28. 28. Staging workup Serologic markers CEA, CA-125, CA 19-9, CA 72-4 may be elevated but have low sensitivity/specificity None are diagnostic Preoperative elevation in markers usually pretends high risk of adverse outcome No serologic finding should exclude surgical consideration
  29. 29. AJCC Staging System
  30. 30. AJCC Staging System
  31. 31. Treatment Locoregional (stage I-III) disease Potentially curable multidisciplinary evaluation and consideration of surgery Advanced (stage IV) disease Palliative therapy Studies indicate longer survival and better quality of life with systemic treatment
  32. 32. Surgery The extent of gastric resection depends on: - tumor size - location - depth of invasion - histological type
  33. 33. Treatment Complete surgical resection with removal of LNs (only chance of cure) Possible in < 1/3 of cases Subtotal gastrectomy for distal carcinomas, total or near-total for proximal masses Reduction of tumor bulk (palliative) Chemotherapy (cisplatin + 5-FU or irinotecan)  Partial response in 30-50% of patients Radiation (for pain control, no mortality benefit with XRT alone)
  34. 34. The Japanese Research Society for Gastric Cancer The 16 lymph node locations were classified into 4 concentric groups: N1, N2, N3, N4 Periepigastric Extraepigastric
  35. 35. What is the ideal extent of lymphadenectomy ? D0- removes less than all relevant N1 nodes D1- removes N1 nodes only - Lt and Rt cardiac - Lt and Rt gastro-epiploic - Sub and Supra pyloric D2- removes all N1 and N2 nodes - Lt gastric - Common hepatic - Celiac - Splenic hilum and along splenic artery D3- removes all N2 and N3 nodes
  36. 36. The residual tumor (R) classification The absence or presence of demonstrable residual tumor after conclusion of the treatment (UICC) R0 resection -no demonstrable residual tumor R1 resection- microscopically demonstrable residual tumor (e.g. diseased residual margin) R2 resection – macroscopically visible tumor Distinction between primary palliative intervention (R1&R2) vs. potentially curative ones (R0)
  37. 37. Prognosis Stage TNM Features % of Cases* % 5-year survival* 0 TisN0M0 Node negative; limited to mucosa 1 90 IA T1N0M0 Node negative; invasion of lamina propria or submucosa 7 59 IB T2N0M0 Node negative; invasion of muscularis propria 10 44 II T1N2M0 Node positive; invasion beyond mucosa but within wall 17 29T2N1M0 T3N0M0 Node negative; extension through wall IIIA T2N2M0 Node positive; invasion of muscularis propria or through wall 21 15 T3N1-2M0 IIIB T4N0-1M0 Node negative; adherence to surrounding tissue 14 9 IV T4N2M0 Node negative; adherence to surrounding tissue 30 3 Any M1 Distant Metastases ** Data from American Cancer Society
  38. 38. Pharmacologic Therapy  Cisplatin + epirubicin & infusional 5-FU or + irinotecan  Complete remissions are uncommon.  Partial responses in 30-50% of cases are transient.  Overall influence on survival has been unclear.  Adjuvant chemotherapy alone following complete resection has only minimally improved survival.  Perioperative treatment and postoperative chemotherapy + radiation therapy reduce the recurrence rate and prolongs survival.
  39. 39. Treatment: Supportive: Nutrition (jejunal enteral feedings or total parenteral nutrition), Correction of metabolic abnormalities that arise from vomiting or diarrhea Treatment of infection from aspiration or spontaneous bacterial peritonitis. To maintain lumen patency, endoscopic laser treatment or stenting for palliation.
  40. 40. Screening Mostly barium studies, EGD is concerning findings Some use serum pepsinogen testing for high risk with EGD confirmation H. pylori: sensitivity 88%, specificity 41% (Japan)  5-year survival 74-80 in screened group, 46-56% for non- screened group.