Carcinoma stomach sb-rubel

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  • 1. Carcinoma Stomach Professor AMSM Sharfuzzaman Professor of Surgery Sher-e-Bangla Medical CollegeJanuary 8, 2013 DR. RUBEL,SBMC 1
  • 2. Introduction Gastric cancer is the second most common cause of cancer-relateddeath in the world. Many Asian countries, including Korea China,Taiwan, and Japan, have very high rates of gastric cancer. Gastric cancer was the leading cause of cancer deaths in men andthe third leading cause of cancer deaths in women in the early 1940s. Gastric cancer remains a difficult disease to cure in Westerncountries, primarily because most patients present with advanceddisease. Even patients who present in the most favorable condition andwho undergo curative surgical resection often die of recurrent disease. January 8, 2013 DR. RUBEL,SBMC 2
  • 3. Introduction-contd. Adenocarcinoma of the stomach is the second most common cancerworldwide. In 2001, stomach cancer affected 850,000 people, of which522,000 men and 328,000 women died of stomach cancer. Tremendous geographic variation exists in the incidence of this diseasearound the world. The highest death rates are recorded in Chile, Japan,South America, and the former Soviet Union. Over the past half century orso, there has been a steady decline in gastric cancer incidence and gastriccancer deaths in men and women in the United States. Most of thisdecrease has occurred in the intestinal type of gastric cancer. In addition,the incidence of gastric cardia adenocarcinoma has actually graduallyincreased. The decrease in gastric cancer incidence may be attributed in part to theadoption of diets high in vegetables and fruit. The widespread use ofrefrigeration contributes to the decline in incidence by reducing the intakeof salt, which had been used as a food preservative, and decreasing thecontamination of food by carcinogenic compounds arising from the decayof unrefrigerated meat products. Salt and salted foods may cause damage to the gastric mucosa withresultant inflammation associated with increase in DNA synthesis and cellproliferation. January 8, 2013 DR. RUBEL,SBMC 3
  • 4. EpidemiologyRace The rates of gastric cancer are higher in Asian and South American countries thanin the United States. Japan, Chile, and Venezuela have developed a very rigorous early screeningprogram that detects patients with early stage disease (ie, low tumor burden). Thesepatients appear to do quite well. In fact, in many Asian studies, patients with resected stage II and III disease tendto have better outcomes than similarly staged patients treated in Western countries.Some researchers suggest that this reflects a fundamental biologic difference in thedisease as it manifests in Western countries. In the United States, Asian and Pacific Islander males and females have thehighest incidence of stomach cancer, followed by black, Hispanic, white, AmericanIndian, and Inuit populations. January 8, 2013 DR. RUBEL,SBMC 4
  • 5. Epidemiology-contd.SexGastric cancer affects slightly more men than women.AgeMost patients are elderly at diagnosis. The median age for gastric cancerin the United States is 70 years for males and 74 years for females. Thegastric cancers that occur in younger patients may represent a moreaggressive variant.Mortality/MorbidityThe 5-year survival rate for curative surgical resection ranges from 30-50% for patients with stage II disease and from 10-25% for patients withstage III disease. Because these patients have a high likelihood of localand systemic relapse, some physicians offer them adjuvant therapy. Theoperative mortality rate for patients undergoing curative surgicalresection at major academic centers is less than 3%. January 8, 2013 DR. RUBEL,SBMC 5
  • 6. Surgical anatomy The stomach begins at the gastroesophageal junction and ends at the duodenum. The stomachhas 3 parts. The uppermost part of the stomach is the cardia, and the largest and middle part iscalled the body. The distal portion of the stomach, the pylorus, connects to the duodenum. These anatomic zones have distinct histologic features. The cardia contains predominantlymucin-secreting cells. The fundus (ie, body) contains mucoid cells, chief cells, and parietal cells,while the pylorus is composed of mucus-producing cells and endocrine cells. The stomach wall is made up of 5 layers. From the lumen out, the layers include the mucosa, thesubmucosa, the muscularis layer, the subserosal layer, and the serosal layer. The peritoneum of the greater sac covers the anterior surface of the stomach. A portion of thelesser sac drapes posteriorly over the stomach. The gastroesophageal junction has limited or noserosal covering. The right portion of the anterior gastric surface is adjacent to the left lobe of the liver and theanterior abdominal wall. The left portion of the stomach is adjacent to the spleen, the left adrenalgland, the superior portion of the left kidney, the ventral portion of the pancreas, and the transversecolon. The site of the cancer is classified on the basis of its relationship to the long axis of the stomach.Approximately 40% of cancers develop in the lower part, 40% in the middle part, and 15% inthe upper part, and 10% involve more than one part of the organ. January 8, 2013 DR. RUBEL,SBMC 6
  • 7. CausesSeveral factors are implicated in the development of gastric cancer, including diet,Helicobacter pylori infection, previous gastric surgery, pernicious anemia, adenomatouspolyps, chronic atrophic gastritis, prior radiation exposure or inherited syndromes.Gastric cancer may often be multifactorial involving both inherited predisposition andenvironmental factors.DietA diet rich in pickled vegetables, salted fish, excessive dietary salt, and smoked meatscorrelates with an increased incidence of gastric cancer. A diet that includes fruits and vegetables rich in vitamin C may have a protective effect.SmokingSmoking is associated with an increased incidence of stomach cancer in a dose-dependent manner, both for number of cigarettes and duration of smoking. Smoking increases the risk of cardiac and noncardiac forms of stomach cancer. Cessation of smoking reduces the risk. A meta-analysis of 40 studies estimated that the risk was increased by approximately 1.5- to 1.6-fold and was higher in men. January 8, 2013 DR. RUBEL,SBMC 7
  • 8. Helicobacter pylori infectionChronic bacterial infection with H pylori is the strongest risk factor for stomach cancer. H pylori may infect 50% of the worlds population, but much less than 5% of infectedindividuals develop cancer. It may be that only a particular strain of H pylori, onewhich is capable of producing the greatest amount of inflammation, is especiallyassociated with the risk of malignancy. The full malignant transformation of affectedparts of the stomach may require that the human host have a particular genotype ofinterleukin-Iβ to cause the increased inflammation and an increased suppression ofgastric acid secretion. H pylori infection is associated with chronic atrophic gastritis, and patients with ahistory of prolonged gastritis have a 6-fold increase in their risk of developing gastriccancer. Interestingly, this association is particularly strong for tumors located in theantrum, body, and fundus of the stomach but does not seem to hold for tumorsoriginating in the cardia. January 8, 2013 DR. RUBEL,SBMC 8 8 Causes-contd.
  • 9. Previous gastric surgery Previous surgery is implicated as a risk factor. The rationale isthat surgery alters the normal pH of the stomach which may inturn lead to metaplastic and dysplastic changes in luminal cells. Retrospective studies demonstrate that a small percentage ofpatients who undergo gastric polyp removal have evidence ofinvasive carcinoma within the polyp. This discovery has led someresearchers to conclude that polyps might representpremalignant conditions. Causes-contd. January 8, 2013 DR. RUBEL,SBMC 9
  • 10. Genetic factorsSome 10% of stomach cancer cases are familial in origin. Genetic factors involved in gastric cancer remain poorly understood, thoughspecific mutations have been identified in a subset of gastric cancer patients. Forexample, germ-line truncating mutations of the E-cadherin gene are detected in50% of diffuse-type gastric cancers and families that harbor these mutations havean autosomal dominant pattern of inheritance with a very high penetrance. Other hereditary syndromes with a predisposition for stomach cancer includehereditary nonpolyposis colorectal cancer, Li-Fraumeni syndrome, familialadenomatous polyposis, and Peutz-Jeghers syndrome. Ebstein-Barr virus: The Epstein-Barr virus may be associated with an unusualform of stomach cancer (<1%), lympho-epitheliomalike carcinoma. Pernicious anemia: Pernicious anemia associated with advanced atrophicgastritis and intrinsic factor deficiency is a risk factor for gastric carcinoma. January 8, 2013 DR. RUBEL,SBMC Causes-contd. 10
  • 11. Gastric ulcers Gastric cancer may develop in the remaining portion of the stomach following a partial gastrectomy for gastric ulcer. Benign gastric ulcers may themselves develop into malignancy. Obesity: Obesity increases the risk of gastric cardiac cancer. Radiation exposure: Atomic bomb survivors exposed to radiation have had an increased risk of stomach cancer. Other populations exposed to radiation may also have an increased risk of stomach cancer.January 8, 2013 DR. RUBEL,SBMC Causes-contd. 11
  • 12. Premalignant conditions; H. pylori infection Atrophic gastritis and pernicious anemia Gastric polyps Gastric ulcer Hypergastrinemia Blood group A Previous gastric resection Ménétrier’s diseaseJanuary 8, 2013 DR. RUBEL,SBMC 12
  • 13. Factors associated with increased risk ofdeveloping stomach cancerNutritional Low fat or protein consumption Salted meat or fish High nitrate consumption High complex-carbohydrate consumptionEnvironmental Poor food preparation (smoked, salted) Lack of refrigeration Poor drinking water (well water) SmokingSocial Low social classMedical Prior gastric surgery Helicobacter pylori infection Gastric atrophy and gastritis Adenomatous polyps Male gender January 8, 2013 DR. RUBEL,SBMC 13
  • 14. Correa mode of the pathogenesis of human gastricadenocarcinoma January 8, 2013 DR. RUBEL,SBMC 14
  • 15. Histopathology Adenocarcinoma 95% Lymphomas 2% Carcinoids 1% Adenocathomas 1% Squamous cell 1% Adenocarcinoma is classified according to the most unfavorable microscopic element present: tubular, papillary, mucinous, signet-ring cells. Also identified by gross appearance: ulcerative, polypoid, scirrous, superficial spreading, multicentric, or Barrett ectopic. Variety of other schemes: Borrmann, LaurenTuesday, January 8, 2013 Dr. RUBEL, SBMC 15
  • 16. Borrmann Classification5 categories Type I: polypoid or fungating Type II: ulcerating lesions with elevated borders Type III: ulceration with invasion of wall Type IV: diffuse infiltration Type V: cannot be classified Tuesday, January 8, 2013 Dr. RUBEL, SBMC 16
  • 17. Borrmann types Borrmann I Borrmann II Borrmann III Borrmann IV Tuesday, January 8, 2013 Dr. RUBEL, SBMC 17
  • 18. Lauren systemThe intestinal type 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, carries better prognosis, shows no family historyThe diffuse type Infiltrative, endemic, is poorly differentiated, with dangerously deceptive margins, invades large areas of stomach. Younger patients, genetic factors, blood groups, and family history. Tuesday, January 8, 2013 Dr. RUBEL, SBMC 18
  • 19. Lauren systemThe most useful classification of gastric cancer is the Lauren Classification System. TheLauren system classifies gastric cancer pathology as either Type I (intestinal) Type II (diffuse).Intestinal type - expansive, epidemic, gastric cancer is associated with chronic atrophicgastritis, retained glandular structure, little invasiveness, with sharp margin, associatedwith most environmental risk factors, carries a better prognosis, and shows no familialhistory.Diffuse type - infiltrative, endemic cancer, consists of scattered cell clusters with poordifferentiation and dangerously deceptive margins. The endemic-type tumor invadeslarge areas of the stomach. This type of tumor is also not recognizably influenced byenvironment or diet, is more virulent in women, and occurs more often in relativelyyoung patients. This pathologic entity is associated with genetic factors (such as E-cadherin), blood groups A, and a family history of gastric cancer.Intestinal Diffuse Environmental Familial Gastric atrophy, intestinal metaplasia Blood type A Men > women Women > men Increasing incidence with age Younger age group Microscopic Microscopic Gland formation Poorly differentiated signet ring cells Hematogenous spread Transmural/lymphatic spread Microsatellite instability Decreased E-cadherin APC gene mutations APC gene mutations p53, p16 inactivation p53, p16 inactivation January 8, 2013 DR. RUBEL,SBMC 19
  • 20. According to the clinical presentation &treatment planning gastric cancer are grosslyclassified as follows: A. Early Gastric Cancer (EGC) B. Advanced Gastric Cancer (AGC) Tuesday, January 8, 2013 Dr. RUBEL, SBMC 20
  • 21. .Early Gastric CancerThe term early gastric cancer isused to describe tumours confinedto the gastric mucosa andsubmucosa, irrespective of nodalstatus, and was elaborated in 1962by the Japanese Society ofGastroenterological EndoscopyType I Exophytic lesion extending into thegastric lumenType II Superficial variant II A Elevated lesions with a heightno more than the thickness of the adjacentmucosa II B Flat lesions II C Depressed lesions with aneroded but not deeply ulceratedappearanceType III Excavated lesions that mayextend into the muscularis propria withoutinvasion of this layer by actual cancer cells Tuesday, January 8, 2013 Dr. RUBEL, SBMC 21
  • 22. Advanced gastric cancer: The vast majority of gastric cancer are of advanced which deeply penetrate the stomach wall, invade the adjacent structures with lymphatic & haematogenous metastasis. Advanced gastric cancer classified according to the Bormanns morphologic description as - Borrmann I: Fungating Borrmann II: Carcimatous ulcer without infiltrating surrounding mucosa Borrmann III: Carcimatous ulcer with infiltration of surrounding mucosa Borrmann IV: Diffuse infiltrating carcinoma Tuesday, January 8, 2013 Dr. RUBEL, SBMC 22
  • 23. Advanced Gastric Cancer - MorphologicalTypes; PPolypoidoid Borrmann I Ulcerating Borrmann II Ulcerating/ Borrmann III infiltrating Diffuse infiltrating Borrmann IV January 8, 2013 DR. RUBEL,SBMC 23
  • 24. Borrmanns morphologicdescriptionTuesday, January 8, 2013 Dr. RUBEL, SBMC 24
  • 25. SpreadPathophysiology; Understanding the vascular supply of the stomach allows understanding ofthe routes of hematogenous spread. The vascular supply of the stomach isderived from the celiac artery. The left gastric artery, a branch of the celiacartery, supplies the upper right portion of the stomach. The common hepaticartery branches into the right gastric artery, which supplies the lower portionof the stomach, and the right gastroepiploic branch, which supplies the lowerportion of the greater curvature. Understanding the lymphatic drainage can clarify the areas at risk for nodalinvolvement by cancer. The lymphatic drainage of the stomach is complex.Primary lymphatic drainage is along the celiac axis. Minor drainage occursalong the splenic hilum, suprapancreatic nodal groups, porta hepatis, andgastroduodenal areas. January 8, 2013 DR. RUBEL,SBMC 25
  • 26. Lymphatic drainage January 8, 2013 DR. RUBEL,SBMC 26
  • 27. Lymphatic drainage January 8, 2013 DR. RUBEL,SBMC 27
  • 28. Gastric LymphaticsNumbering of the gastric and upperabdominal node stationsStation no. Anatomical location1, 2 Adjacent to the cardia (perigastric)3, 4 Adjacent to lesser and greatercurve5 Suprapyloric (right gastric artery)6 Infrapyloric7 Left gastric artery8 Common hepatic artery9 Coeliac artery10 Hilum of the spleen11 Splenic artery12 Hepaticoduodenal ligament13 Behind pancreatic head14 At the root of the mesentery (superior mesenteric artery)15 Middle colic artery16 Para-aortic
  • 29. Gastric Lymphatics Tuesday, January 8, 2013 Dr. RUBEL, SBMC 29
  • 30. Spread patternsCancer of the stomach can spread directly, via lymphatics, or hematogenously andtransperitonialy. Direct extension into the omenta, pancreas, diaphragm, transverse colon or mesocolon, and duodenum is common. If the lesion extends beyond the gastric wall to a free peritoneal (ie, serosal) surface, then peritoneal involvement is frequent. The visible gross lesion frequently underestimates the true extent of the disease. The abundant lymphatic channels within the submucosal and subserosal layers of the gastric wall allow for easy microscopic spread. The submucosal plexus is prominent in the esophagus and the subserosal plexus is prominent in the duodenum, allowing proximal and distal spread. Lymphatic drainage is through numerous pathways and can involve multiple nodal groups (eg, gastric, gastroepiploic, celiac, porta hepatic, splenic, suprapancreatic, pancreaticoduodenal, paraesophageal, and paraaortic lymph nodes). The cancer also spreads hematogenously, and liver metastases are common. The cancer also spreads transperitonialy to other abdominal organs as omentum peritoneum, and especially to ovary as Krukenberg’s tumor. January 8, 2013 DR. RUBEL,SBMC 30
  • 31. ClinicalHistory In the United States, about 25% of stomach cancer cases present with localizeddisease, 31% present with regional disease, and 32% present with distantmetastatic disease; the remainder of cases surveyed were listed as unstaged. Early disease has no associated symptoms; however, some patients withincidental complaints are diagnosed with early gastric cancer. Most symptoms ofgastric cancer reflect advanced disease. Patients may complain of indigestion,nausea or vomiting, dysphagia, postprandial fullness, loss of appetite, melena,hematemesis, and weight loss. Late complications include pathologic peritoneal and pleural effusions;obstruction of the gastric outlet, gastroesophageal junction, or small bowel;bleeding in the stomach from esophageal varices or at the anastomosis aftersurgery; intrahepatic jaundice caused by hepatomegaly; extrahepatic jaundice;and inanition resulting from starvation or cachexia of tumor origin. January 8, 2013 DR. RUBEL,SBMC 31
  • 32. Clinical-contds.Physical All physical signs are late events, and almost invariably the signs develop too latefor curative procedures. Signs may include a palpable enlarged stomach with succussion splash;hepatomegaly; periumbilical metastasis (Sister Mary Joseph nodule); enlarged lymphnodes such as: Virchow’s nodes (ie, left supraclavicular), Irish node (anterioraxillary); and Blumer shelf (ie, shelflike tumor of the anterior rectal wall). Some patients experience weight loss and others may present with melena orpallor from anemia. Paraneoplastic syndromes such as dermatomyositis, acanthosis nigricans, andcircinate erythemas are poor prognostic features. Other associated abnormalities also include peripheral thrombophlebitis andmicroangiopathic hemolytic anemia. January 8, 2013 DR. RUBEL,SBMC 32
  • 33. Clinical presentation:There are five group of clinical presentation, which are as follows - New dyspepsia after 40 - persistent indigestion in a patient who has never had previous stomach trouble. It was one of the manifestation of our presented case. Obstructive type - carcinoma of the pyloroantrum may present with abdominal fullness & vomiting which was the predominant manifestation of our presented case. Carcinoma of the cardia may present with dysphagia & regurgitation Abdominal lump - epigastric lump is the presenting feature of about30% of cases Insidious - sometimes patient may present with only tiredness, marked anorexia, asthenia & evidence of anaemia. Silent - carcinoma of the gastric body may present with metastaticmanifestations like jaundice, enlarged left supraclavicular lymphnodes(Virchow’s gland),ascites, rectal shelf of Blummer(Metastatic nodule onthe rectal wall),Sister Joseph’s nodules(Metastatic nodule on theumbilicus),Krukenberg’s tumors(Metastasis on ovary). January 8, 2013 DR. RUBEL,SBMC 33
  • 34. Lab Studies The goal of obtaining laboratory studies is to assist in determining optimal therapy. A complete blood cell count can identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition. Approximately 30% of patients have anemia. Electrolyte panels and liver function tests also are essential to better characterize the patients clinical state. Carcinoembryonic antigen (CEA) is increased in 45-50% of cases. Cancer antigen (CA) 19-9 is elevated in about 20%of cases.January 8, 2013 DR. RUBEL,SBMC 34
  • 35. Imaging StudiesEsophagogastroduodenoscopy has a diagnostic accuracy of95%. This relatively safe and simple procedure provides a permanentcolor photographic record of the lesion. This procedure is also the primary method for obtaining a tissue diagnosis of suspected lesions. Biopsy of any ulcerated lesion should require at least 6 biopsies taken from around the lesion because of variable malignant transformation. In selected cases, endoscopic ultrasound may be helpful in assessing depth of penetration of the tumor or involvement of adjacent structures.Double-contrast upper gastrointestinal series and bariumswallows may be helpful in delineating the extent of disease whenobstructive symptoms are present or when bulky proximal tumorsprevent passage of the endoscope to examine the stomach distal to anobstruction (more common with gastroesophageal [GE]-junctiontumors). These studies are only 75% accurate and should for the mostpart be used only when upper GI endoscopy is not feasible. January 8, 2013 DR. RUBEL,SBMC 35
  • 36. Imaging Studies-contd. Chest radiograph is done to evaluate for metastatic lesions. CT scan or MRI of the chest, abdomen, and pelvis assess the local disease process as well as evaluate potential areas of spread (ie, enlarged lymph nodes, possible liver metastases). Endoscopic ultrasound allows for a more precise preoperative assessment of the tumor stage. Endoscopic sonography is becoming increasingly useful as a staging tool when the CT scan fails to find evidence of T3, T4, or metastatic disease. Institutions that favor neoadjuvant chemoradiotherapy for patients with locally advanced disease rely on endoscopic ultrasound data to improve patient stratification.January 8, 2013 DR. RUBEL,SBMC 36
  • 37. Histologic FindingsAdenocarcinoma of the stomach constitutes 90-95% of allgastric malignancies. The second most common gastricmalignancies are lymphomas. Gastrointestinal stromal tumorsformerly classified as either leiomyomas or leiomyosarcomasaccount for 2% of gastric neoplasms, Carcinoids (1%),adenoacanthomas (1%), and squamous cell carcinomas (1%)Adenocarcinoma of the stomach is subclassified according tohistologic description as follows: tubular, papillary, mucinous, orsignet-ring cells, and undifferentiated lesions.Pathology specimens are also classified by gross appearance. Ingeneral, researchers consider gastric cancers ulcerative, polypoid,scirrhous (ie, diffuse linitis plastica), superficial spreading,multicentric, or Barrett ectopic adenocarcinoma.The Lauren system classifies gastric cancer pathology as eitherType I (intestinal) or Type II (diffuse). An appealing feature ofclassifying patients according to the Lauren system is that thedescriptive pathologic entities have clinically relevant differences. January 8, 2013 DR. RUBEL,SBMC 37
  • 38. TNM Classification ofCarcinoma of the StomachPrimary tumor (T)TX Primary tumor cannot be assessedT0 No evidence of primary tumorTis Carcinoma in situ: intraepithial tumor without invasion of the lamina propriaT1 Tumor invades lamina propria or submucosaT2 Tumor invades muscularis propria or subserosaT2a Tumor invades mucularis propriaT2b Tumor invades subserosaT3 Tumor penetrates serosa (visceral peritoneum) without invasion of adjacent structuresT4 Tumor invades adjacent structures January 8, 2013 DR. RUBEL,SBMC 38
  • 39. TNM Classification of Carcinoma of the Stomach-contd.Regional lymph nodes (N)NX Regional lymph node(s) cannot be assessedN0 No regional lymph node metastasisN1 Metastasis in 1 to 6 regional lymph nodes(perigastric groups)N2 Metastasis in 7 to 15 regional lymph nodes(coeliac groups)N3 Metastasis in more than 15 regional lymph nodes(para-aortic groups) Distant metastasis (M) MX Distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasisLymph node station numbers as defined by the January 8, 2013 DR. RUBEL,SBMC 39Japanese Gastric Cancer Association
  • 40. Surgical TreatmentSurgical resection provides the only hope for curing gastric cancer.Even then, some patients show criteria of inoperability at the time ofpresentation. These include the presence of Virchow’s node, obviousliver metastasis, rectal shelf, and ascites.The type of gastric resection needed depends on location of the tumor.In all cases, proximal and distal surgical margins should be clear oftumor for at least 4 to 6 cm. When the resection required is distalgastrectomy, the following surgical strategies should also be employed: 1. Resection of the duodenal bulb and Bilroth II reconstruction. 2. Division of left and right gastric arteries at their origin, and 3. Removal of the greater omentum.It is always useful to do preoperative bowel preparation in the event thatthe transverse colon has to be resected en bloc. January 8, 2013 DR. RUBEL,SBMC 40 Surgical Treatment-contd.
  • 41. Surgical Treatment-contd.The main controversy relates to the extent of lymphnode dissection. Types of resective surgery have beenclassified based on this criterion as follows: 1. R1: complete removal of perigastric lymph nodes; 2. R2: resection of perigastric nodes and those along the left gastric, splenic, and right hepatic arteries; 3. R3: R2 with dissection of celiac axis nodes; 4. R4: R3 with dissection of paraaortic nodes.January 8, 2013 DR. RUBEL,SBMC 41
  • 42. A-Subtotal gastrectomy with a Billroth II anastomosis.B-Total gastrectomy with a Roux-en-Y anastomosis. A B January 8, 2013 DR. RUBEL,SBMC 42
  • 43. Surgical Treatment January 8, 2013 DR. RUBEL,SBMC 43
  • 44. Endoscopic Resection The Japanese have demonstrated that some patients with earlygastric cancer can be adequately treated by an endoscopicmucosal resection. Small tumors (<3 cm) confined to the mucosa have anextremely low chance of lymph node metastasis (3 percent) whichapproaches the operative mortality rate forgastrectomy. If the resected specimen demonstrates no ulceration, nolymphatic invasion, and size less than 3 cm, the risk of lymphnode metastases is less than 1 percent. Thus some patients with early gastric cancer might be bettertreated with the endoscopic technique. Currently this should belimited to patients with tumors less than 2 cm, which on EUS arenode-negative and confined tothe mucosa. January 8, 2013 DR. RUBEL,SBMC 44
  • 45. PALLIATIVE TREATMENT Because 20% to 30% of gastric cancer patients present with stage IVdisease, clinicians must be familiar with different methods of palliativetreatment. The goal of palliative treatment is the relief of symptoms withminimal morbidity. Surgical palliation of advanced gastric cancer may include resection orbypass alone or in conjunction with percutaneous, endoscopic, orradiotherapeutic techniques. Complete staging is necessary to determine the appropriate method ofpalliation for individual patients. In the presence of peritoneal disease, hepatic metastases, diffuse nodalmetastases, or ascites, palliation of bleeding or proximal gastricobstruction would preferably be obtained nonoperatively. Nonoperative therapies include laser recanalization and endoscopicdilation, with or without stent placement. Patients who undergo stentplacement for gastric outlet obstruction are frequently able to toleratesolid foods and may not require additional interventions. January 8, 2013 DR. RUBEL,SBMC 45
  • 46. Adjuvant Therapy Adjuvant treatment with chemotherapy (5 FU and leucovorin) andradiation (4500 cGy) has demonstrated a survival benefit in resectedpatients with stageII and III adenocarcinoma of the stomach. There is no indication for the routine use of radiation alone in theadjuvant setting, but in certain patients it can be very effectivepalliation for bleeding or pain. In patients with gross unresectable, metastatic, or recurrent disease,palliative chemotherapy has not been demonstrated to conclusivelyprolong survival, but an occasional patient has a dramatic response.These patients should be considered for clinical trials. Agents that have shown activity against gastric cancer include 5 FU,cisplatin, adriamycin, and methotrexate. Neoadjuvant treatment of gastric adenocarcinoma is being evaluated.January 8, 2013 DR. RUBEL,SBMC 46
  • 47. Five-Year Survival Rate of Patientswith Stomach CancerTumor stage % Survival R1 resection R2 resectionIA 88 91IB 56 85II 39 58IIIA 7 30IIIB 0 12January 8, 2013 DR. RUBEL,SBMC 47
  • 48. OUTCOMESSurvival rates for all patients with gastric carcinomastratified by combined American Joint Committee on CancerJanuary 8, 2013 DR. RUBEL,SBMC 48
  • 49. OUTCOMES-contd.Survival rates for gastric cancer patients undergoing gastrectomyas stratified by combined American Joint Committee on Cancer January 8, 2013 DR. RUBEL,SBMC 49
  • 50. Recurrence Recurrence rates after gastrectomy remain high, ranging from40% to 80%, depending on the series. Most recurrences occurwithin the first 3 years. The locoregional failure rate ranges from 38% to 45%, whereasperitoneal dissemination as a component of failure occurs in 54%of patients in several series. Isolated distant metastases are uncommon, because mostpatients with distant failure also have locoregional recurrence aswell. The most common sites of locoregional recurrence are thegastric remnant at the anastomosis and in the gastric bed andthe regional nodes. Hematogenous spread occurs to the liver,lung, and bone. January 8, 2013 DR. RUBEL,SBMC 50
  • 51. SURVEILLANCE All patients should be followed up systematically. Because mostrecurrences occur within the first 3 years, surveillanceexaminations are more frequent in the first several years.Follow-up should include a complete history and physicalexamination every 4 months for 1 year, then every 6 months for2 years and then annually thereafter. Laboratory examinations including complete blood counts andliver function tests should be obtained as clinically indicated.Many clinicians obtain chest radiographs as well as CT scans ofthe abdomen and pelvis routinely, wheresas others obtainstudies only when clinically suspicious of a recurrence. Yearlyendoscopy should be considered in patients who haveundergone a subtotal gastrectomy. January 8, 2013 DR. RUBEL,SBMC 51
  • 52. Screening for Gastric CancerIn Japan it has clearly been shown that patients participating ingastric cancer screening programs have a significantly decreasedrisk of dying from gastric cancer. Thus screening is effective in ahigh risk population.Certainly screening the general population in a low-risk countrydoes not make sense, but patients clearly at risk for gastric cancershould probably have periodic endoscopy and biopsy. This includespatients with FAP, HNPCC, gastric adenomas, Menetrier disease,intestinal metaplasia, dysplasia, and remote gastrectomy orgastrojejunostomy. January 8, 2013 DR. RUBEL,SBMC 52
  • 53. Summary AetiologyDefinition The following are predisposingMalignant lesion of the stomach factors.epithelium. • Diet (smoked fish, pickled vegetables, benzpyrene,Key points nitrosamines).• The majority of tumours are • Atrophic gastritis.unresectable at presentation. • Pernicious anaemia.• Tumours considered candidates for • Previous partial gastrectomy.resection should be staged with • Familial hypogammaglobulinaemia.CT and laparoscopy to reduce the risk of • Gastric adenomatous polyps.an ‘open and shut’ laparotomy. • Blood group A.• Most tumours are poorly responsive tochemotherapy. Pathology • Histology: adenocarcinoma.Epidemiology • Advanced gastric cancerMale/female 2 : 1, peak incidence 50+ (penetrated muscularis propria) mayyears. Incidence has be polypoid, ulcerating or infiltratingdecreased in Western world over last 50 (i.e. linitus plastica).years. Still common in • Early gastric cancer (confined toJapan, Chile and Scandinavia. mucosa or submucosa).January 8, 2013 DR. RUBEL,SBMC 53
  • 54. Spreadlymphatic (e.g. Virchow’s node); haematogenous to Essential managementliver, lung, brain; transcoelomic to ovary • Palliation (metastatic disease or(Krukenberg tumour). gross distal nodal disease at presentation):Clinical features gastrectomy: local symptoms, e.g.• History of recent dyspepsia (epigastric discomfort, bleeding;postprandial gastroenterostomy: malignant pyloricfullness, loss of appetite). obstruction;• Anaemia. intubation: obstructing lesions at the• Dysphagia. cardia.• Vomiting. • Curative treatment (resectable• Weight loss. primary and local nodes).• The presence of physical signs usually indicates • Surgical excision with clear marginsadvanced and locoregional lymph node(incurable) disease. clearance (D2 gastrectomy). • Other treatment: combinationInvestigations chemotherapy with etoposide,• FBC. adriamycin and cisplatin may induce• U+E. regression.• LFTs. Prognosis• OGD (see the lesion and obtain biopsy to Following ‘curative’ resection, 5-yeardistinguish from survival rates are approximately 20%,benign gastric ulcer). but overall 5-year survival (palliation• Barium meal (space-occupying lesion/ulcer with and resection) is only 5%.rolled edge).Best for patients unable to tolerate OGD.• CT scan (helical): stages disease locally andsystemically.• Laparoscopy: used to exclude undiagnosedperitoneal or8, 2013 January liver secondaries prior to consideration DR. RUBEL,SBMC 54
  • 55. January 8, 2013 DR. RUBEL,SBMC 55