Carcinoma stomach sb-rubel

CarcinomaCarcinoma Stomach Stomach

Professor Professor AMSM SharfuzzamanAMSM Sharfuzzaman

Professor of SurgeryProfessor of Surgery

Sher-e-Bangla Medical College Sher-e-Bangla Medical College

April 11, 2023April 11, 2023 11DR. RUBEL,SBMCDR. RUBEL,SBMC

Introduction

Gastric cancer is the second most common cause of cancer-related death 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 and the third leading cause of cancer deaths in women in the early 1940s.

Gastric cancer remains a difficult disease to cure in Western countries, primarily because most patients present with advanced disease. Even patients who present in the most favorable condition and who undergo curative surgical resection often die of recurrent disease.


Introduction-contd.Adenocarcinoma of the stomach is the second most common cancer

worldwide. In 2001, stomach cancer affected 850,000 people, of which 522,000 men and 328,000 women died of stomach cancer.

Tremendous geographic variation exists in the incidence of this disease around the world. The highest death rates are recorded in Chile, Japan, South America, and the former Soviet Union. Over the past half century or so, there has been a steady decline in gastric cancer incidence and gastric cancer deaths in men and women in the United States. Most of this decrease has occurred in the intestinal type of gastric cancer. In addition, the incidence of gastric cardia adenocarcinoma has actually gradually increased.

The decrease in gastric cancer incidence may be attributed in part to the adoption of diets high in vegetables and fruit. The widespread use of refrigeration contributes to the decline in incidence by reducing the intake of salt, which had been used as a food preservative, and decreasing the contamination of food by carcinogenic compounds arising from the decay of unrefrigerated meat products.

Salt and salted foods may cause damage to the gastric mucosa with resultant inflammation associated with increase in DNA synthesis and cell proliferation.


EpidemiologyRace

The rates of gastric cancer are higher in Asian and South American countries than in the United States.

Japan, Chile, and Venezuela have developed a very rigorous early screening program that detects patients with early stage disease (ie, low tumor burden). These patients appear to do quite well.

In fact, in many Asian studies, patients with resected stage II and III disease tend to have better outcomes than similarly staged patients treated in Western countries. Some researchers suggest that this reflects a fundamental biologic difference in the disease as it manifests in Western countries.

In the United States, Asian and Pacific Islander males and females have the highest incidence of stomach cancer, followed by black, Hispanic, white, American Indian, and Inuit populations.


Epidemiology-contd.SexGastric cancer affects slightly more men than women.

AgeMost patients are elderly at diagnosis. The median age for gastric cancer in the United States is 70 years for males and 74 years for females. The gastric cancers that occur in younger patients may represent a more aggressive 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 with stage III disease. Because these patients have a high likelihood of local and systemic relapse, some physicians offer them adjuvant therapy. The operative mortality rate for patients undergoing curative surgical resection at major academic centers is less than 3%.


Surgical anatomy

The stomach begins at the gastroesophageal junction and ends at the duodenum. The stomach has 3 parts. The uppermost part of the stomach is the cardia, and the largest and middle part is called the body. The distal portion of the stomach, the pylorus, connects to the duodenum.

These anatomic zones have distinct histologic features. The cardia contains predominantly mucin-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, the submucosa, 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 the lesser sac drapes posteriorly over the stomach. The gastroesophageal junction has limited or no serosal covering.

The right portion of the anterior gastric surface is adjacent to the left lobe of the liver and the anterior abdominal wall. The left portion of the stomach is adjacent to the spleen, the left adrenal gland, the superior portion of the left kidney, the ventral portion of the pancreas, and the transverse colon.

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% in Approximately 40% of cancers develop in the lower part, 40% in the middle part, and 15% in the upper part, and 10% involve more than one part of the organthe upper part, and 10% involve more than one part of the organ..


CausesSeveral factors are implicated in the development of gastric cancer, including diet, Helicobacter pylori infection, previous gastric surgery, pernicious anemia, adenomatous polyps, chronic atrophic gastritis, prior radiation exposure or inherited syndromes. Gastric cancer may often be multifactorial involving both inherited predisposition and environmental factors.

DietA diet rich in pickled vegetables, salted fish, excessive dietary salt, and smoked meats correlates 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.


Helicobacter pylori infectionChronic bacterial infection with H pylori is the strongest risk factor for stomach cancer.

H pylori may infect 50% of the world's population, but much less than 5% of infected individuals develop cancer. It may be that only a particular strain of H pylori, one which is capable of producing the greatest amount of inflammation, is especially associated with the risk of malignancy. The full malignant transformation of affected parts of the stomach may require that the human host have a particular genotype of interleukin-Iβ to cause the increased inflammation and an increased suppression of gastric acid secretion.

H pylori infection is associated with chronic atrophic gastritis, and patients with a history of prolonged gastritis have a 6-fold increase in their risk of developing gastric cancer. Interestingly, this association is particularly strong for tumors located in the antrum, body, and fundus of the stomach but does not seem to hold for tumors originating in the cardia.

Causes-contd.April 11, 2023April 11, 2023 88DR. RUBEL,SBMCDR. RUBEL,SBMC

Previous gastric surgery

Previous surgery is implicated as a risk factor. The rationale is that surgery alters the normal pH of the stomach which may in turn lead to metaplastic and dysplastic changes in luminal cells.

Retrospective studies demonstrate that a small percentage of patients who undergo gastric polyp removal have evidence of invasive carcinoma within the polyp. This discovery has led some researchers to conclude that polyps might represent premalignant conditions.

Causes-contd.


Genetic factorsSome 10% of stomach cancer cases are familial in origin.

Genetic factors involved in gastric cancer remain poorly understood, though specific mutations have been identified in a subset of gastric cancer patients. For example, germ-line truncating mutations of the E-cadherin gene are detected in 50% of diffuse-type gastric cancers and families that harbor these mutations have an autosomal dominant pattern of inheritance with a very high penetrance.

Other hereditary syndromes with a predisposition for stomach cancer include hereditary nonpolyposis colorectal cancer, Li-Fraumeni syndrome, familial adenomatous polyposis, and Peutz-Jeghers syndrome.

Ebstein-Barr virus: The Epstein-Barr virus may be associated with an unusual form of stomach cancer (<1%), lympho-epitheliomalike carcinoma.

Pernicious anemia: Pernicious anemia associated with advanced atrophic gastritis and intrinsic factor deficiency is a risk factor for gastric carcinoma.


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.


Premalignant conditions;H. pylori infectionAtrophic gastritis and pernicious anemiaGastric polypsGastric ulcerHypergastrinemiaBlood group APrevious gastric resectionMénétrier’s disease


Factors associated with increased risk of developing stomach cancerNutritional

Low fat or protein consumptionSalted meat or fishHigh nitrate consumptionHigh complex-carbohydrate consumption

EnvironmentalPoor food preparation (smoked, salted)Lack of refrigerationPoor drinking water (well water)Smoking

SocialLow social class

MedicalPrior gastric surgeryHelicobacter pylori infectionGastric atrophy and gastritisAdenomatous polypsMale gender


Correa mode of the pathogenesis of human gastric adenocarcinoma


HistopathologyAdenocarcinoma 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, Lauren

Tuesday, April 11, 2023Tuesday, April 11, 2023 1515Dr. RUBEL, SBMCDr. RUBEL, SBMC

Borrmann Classification

5 categoriesType I: polypoid or fungatingType II: ulcerating lesions with elevated bordersType III: ulceration with invasion of wallType IV: diffuse infiltrationType V: cannot be classified


Borrmann types

Borrmann I

Borrmann II

Borrmann III

Borrmann IV


Lauren systemLauren systemThe intestinalThe intestinal typetype Expansive epidemic type gastric cancer is associated Expansive epidemic type gastric cancer is associated

with atrophic gastritis, retained glandular structure, with atrophic gastritis, retained glandular structure, little invasiveness, sharp margins. It would be a little invasiveness, sharp margins. It would be a Borrmann I or II, carries better prognosis, shows no Borrmann I or II, carries better prognosis, shows no family historyfamily history

The diffuse typeThe diffuse type Infiltrative, endemic, is poorly differentiated, with Infiltrative, endemic, is poorly differentiated, with

dangerously deceptive margins, invades large areas dangerously deceptive margins, invades large areas of stomach. Younger patients, genetic factors, blood of stomach. Younger patients, genetic factors, blood groups, and family history.groups, and family history.


Lauren systemThe most useful classification of gastric cancer is the Lauren Classification System. The Lauren system classifies gastric cancer pathology as either

Type I (intestinal) Type II (diffuse).

Intestinal type - expansive, epidemic, gastric cancer is associated with chronic atrophic gastritis, retained glandular structure, little invasiveness, with sharp margin, associated with most environmental risk factors, carries a better prognosis, and shows no familial history.

Diffuse type - infiltrative, endemic cancer, consists of scattered cell clusters with poor differentiation and dangerously deceptive margins. The endemic-type tumor invades large areas of the stomach. This type of tumor is also not recognizably influenced by environment or diet, is more virulent in women, and occurs more often in relatively young patients. This pathologic entity is associated with genetic factors (such as E-cadherin), blood groups A, and a family history of gastric cancer.

Intestinal DiffuseEnvironmental FamilialGastric atrophy, intestinal metaplasia Blood type AMen > women Women > menIncreasing incidence with age Younger age groupMicroscopic Microscopic

Gland formation Poorly differentiated signet ring cellsHematogenous spread Transmural/lymphatic spreadMicrosatellite instability Decreased E-cadherinAPC gene mutations APC gene mutationsp53, p16 inactivation p53, p16 inactivation


According to the clinical presentation & According to the clinical presentation & treatment planning gastric cancer are grossly treatment planning gastric cancer are grossly classified as follows:classified as follows:

A. Early Gastric Cancer (EGC)A. Early Gastric Cancer (EGC)B. Advanced Gastric Cancer (AGC)B. Advanced Gastric Cancer (AGC)


.

Early Gastric CancerEarly Gastric CancerThe term 'early gastric cancer' is used to describe tumours confined to the gastric mucosa and submucosa, irrespective of nodal status, and was elaborated in 1962 by the Japanese Society of Gastroenterological Endoscopy

Type I Exophytic lesion Type I Exophytic lesion extending into the gastric lumen Type II Superficial variantType II Superficial variant

II A Elevated lesions with a height no more than the thickness of the adjacent mucosa

II B Flat lesions II C Depressed lesions with an

eroded but not deeply ulcerated appearance Type III Excavated lesionsType III Excavated lesions that may extend into the muscularis propria without invasion of this layer by actual cancer cells


Advanced gastric cancer:Advanced gastric cancer: The vast majority of gastric cancer are of advanced which The vast majority of gastric cancer are of advanced which

deeply penetrate the stomach wall, invade the adjacent deeply penetrate the stomach wall, invade the adjacent structures with lymphatic & haematogenous metastasis.structures with lymphatic & haematogenous metastasis.

Advanced gastric cancer classified according to the Advanced gastric cancer classified according to the

Bormann's morphologic descriptionBormann's morphologic description as as - - Borrmann IBorrmann I: : FungatingFungating

Borrmann II: Borrmann II: CarcimatousCarcimatous ulcer without ulcer without infiltratinginfiltrating surrounding mucosasurrounding mucosa

Borrmann III:Borrmann III: Carcimatous ulcer with infiltration Carcimatous ulcer with infiltration of surrounding mucosaof surrounding mucosa

Borrmann IV: Borrmann IV: Diffuse infiltrating carcinomaDiffuse infiltrating carcinoma


Advanced Gastric Cancer - Morphological Types;

Borrmann I

Borrmann II

Borrmann III

Borrmann IV

PPolypoidoid

Ulcerating

Ulcerating/infiltrating

Diffuse infiltrating


Borrmann's morphologic description


SpreadPathophysiology;

Understanding the vascular supply of the stomach allows understanding of the routes of hematogenous spread. The vascular supply of the stomach is derived from the celiac artery. The left gastric artery, a branch of the celiac artery, supplies the upper right portion of the stomach. The common hepatic artery branches into the right gastric artery, which supplies the lower portion of the stomach, and the right gastroepiploic branch, which supplies the lower portion of the greater curvature.

Understanding the lymphatic drainage can clarify the areas at risk for nodal involvement by cancer. The lymphatic drainage of the stomach is complex. Primary lymphatic drainage is along the celiac axis. Minor drainage occurs along the splenic hilum, suprapancreatic nodal groups, porta hepatis, and gastroduodenal areas.


Lymphatic drainage


Lymphatic drainage


Gastric LymphaticsNumbering of the gastric and upper abdominal node stations Station no. Anatomical location 1, 2 Adjacent to the cardia (perigastric)3, 4 Adjacent to lesser and greatercurve 5 Suprapyloric (right gastric artery) 6 Infrapyloric 7 Left gastric artery 8 Common hepatic artery 9 Coeliac artery 10 Hilum of the spleen 11 Splenic artery 12 Hepaticoduodenal ligament 13 Behind pancreatic head 14 At the root of the mesentery

(superior mesenteric artery) 15 Middle colic artery 16 Para-aortic

Tuesday, April 11, 2023Tuesday, April 11, 2023 Dr. RUBEL, SBMCDr. RUBEL, SBMC 2929

Gastric Lymphatics

Spread patternsCancer of the stomach can spread directly, via lymphatics, or hematogenously and transperitonialy.

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.April 11, 2023April 11, 2023 3030DR. RUBEL,SBMCDR. RUBEL,SBMC

ClinicalHistory

In the United States, about 25% of stomach cancer cases present with localized disease, 31% present with regional disease, and 32% present with distant metastatic disease; the remainder of cases surveyed were listed as unstaged.

Early disease has no associated symptoms; however, some patients with incidental complaints are diagnosed with early gastric cancer. Most symptoms of gastric 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 after surgery; intrahepatic jaundice caused by hepatomegaly; extrahepatic jaundice; and inanition resulting from starvation or cachexia of tumor origin.


Clinical-contds.Physical

All physical signs are late events, and almost invariably the signs develop too late for curative procedures.

Signs may include a palpable enlarged stomach with succussion splash; hepatomegaly; periumbilical metastasis (Sister Mary Joseph nodule); enlarged lymph nodes such as: Virchow’s nodes (ie, left supraclavicular), Irish node (anterior axillary); and Blumer shelf (ie, shelflike tumor of the anterior rectal wall).

Some patients experience weight loss and others may present with melena or pallor from anemia.

Paraneoplastic syndromes such as dermatomyositis, acanthosis nigricans, and circinate erythemas are poor prognostic features.

Other associated abnormalities also include peripheral thrombophlebitis and microangiopathic hemolytic anemia.


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 about 30% 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 metastatic manifestations like jaundice, enlarged left supraclavicular lymph nodes(Virchow’s gland),ascites, rectal shelf of Blummer(Metastatic nodule on the rectal wall),Sister Joseph’s nodules(Metastatic nodule on the umbilicus),Krukenberg’s tumors(Metastasis on ovary).


Lab StudiesThe 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 patient's

clinical state.

Carcinoembryonic antigen (CEA) is increased in 45-50% of cases.

Cancer antigen (CA) 19-9 is elevated in about 20%of cases.


Imaging StudiesEsophagogastroduodenoscopy has a diagnostic accuracy of 95%. This relatively safe and simple procedure provides a permanent color 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 barium swallows may be helpful in delineating the extent of disease when obstructive symptoms are present or when bulky proximal tumors prevent passage of the endoscope to examine the stomach distal to an obstruction (more common with gastroesophageal [GE]-junction tumors). These studies are only 75% accurate and should for the most part be used only when upper GI endoscopy is not feasible.


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.


Histologic FindingsAdenocarcinoma of the stomach constitutes 90-95% of all gastric malignancies. The second most common gastric malignancies are lymphomas. Gastrointestinal stromal tumors formerly classified as either leiomyomas or leiomyosarcomas account for 2% of gastric neoplasms, Carcinoids (1%), adenoacanthomas (1%), and squamous cell carcinomas (1%)

Adenocarcinoma of the stomach is subclassified according to histologic description as follows: tubular, papillary, mucinous, or signet-ring cells, and undifferentiated lesions.

Pathology specimens are also classified by gross appearance. In general, 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 either Type I (intestinal) or Type II (diffuse). An appealing feature of classifying patients according to the Lauren system is that the descriptive pathologic entities have clinically relevant differences.


TNM Classification of Carcinoma of the Stomach

Primary tumor (T)TX Primary tumor cannot be assessed

T0 No evidence of primary tumor

Tis Carcinoma in situ: intraepithial tumor withoutinvasion of the lamina propria

T1 Tumor invades lamina propria or submucosa

T2 Tumor invades muscularis propria or subserosa

T2a Tumor invades mucularis propria

T2b Tumor invades subserosa

T3 Tumor penetrates serosa (visceral peritoneum)without invasion of adjacent structures

T4 Tumor invades adjacent structures


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 assessedM0 No distant metastasisM1 Distant metastasis

Lymph node station numbers as defined by the Japanese Gastric Cancer Association


Surgical TreatmentSurgical resection provides the only hope for curing gastric cancer. Even then, some patients show criteria of inoperability at the time of presentation. These include the presence of Virchow’s node, obvious liver 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 of tumor for at least 4 to 6 cm. When the resection required is distal gastrectomy, 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 that the transverse colon has to be resected en bloc.

Surgical Treatment-contd.April 11, 2023April 11, 2023 4040DR. RUBEL,SBMCDR. RUBEL,SBMC

Surgical Treatment-contd.Surgical Treatment-contd.

The main controversy relates to the extent of lymph node dissection. Types of resective surgery have been classified 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.


A-Subtotal gastrectomy with a Billroth II anastomosis.B-Total gastrectomy with a Roux-en-Y anastomosis.

A

B


Surgical Treatment


Endoscopic ResectionThe Japanese have demonstrated that some patients with early

gastric cancer can be adequately treated by an endoscopic mucosal resection.

Small tumors (<3 cm) confined to the mucosa have an extremely low chance of lymph node metastasis (3 percent) which approaches the operative mortality rate forgastrectomy.

If the resected specimen demonstrates no ulceration, no lymphatic invasion, and size less than 3 cm, the risk of lymph node metastases is less than 1 percent.

Thus some patients with early gastric cancer might be better treated with the endoscopic technique. Currently this should be limited to patients with tumors less than 2 cm, which on EUS are node-negative and confined tothe mucosa.


PALLIATIVE TREATMENTPALLIATIVE TREATMENTBecause 20% to 30% of gastric cancer patients present with stage IV

disease, clinicians must be familiar with different methods of palliative treatment. The goal of palliative treatment is the relief of symptoms with minimal morbidity.

Surgical palliation of advanced gastric cancer may include resection or bypass alone or in conjunction with percutaneous, endoscopic, or radiotherapeutic techniques.

Complete staging is necessary to determine the appropriate method of palliation for individual patients.

In the presence of peritoneal disease, hepatic metastases, diffuse nodal metastases, or ascites, palliation of bleeding or proximal gastric obstruction would preferably be obtained nonoperatively.

Nonoperative therapies include laser recanalization and endoscopic dilation, with or without stent placement. Patients who undergo stent placement for gastric outlet obstruction are frequently able to tolerate solid foods and may not require additional interventions.


Adjuvant TherapyAdjuvant TherapyAdjuvant treatment with chemotherapy (5 FU and leucovorin) and

radiation (4500 cGy) has demonstrated a survival benefit in resected patients with stageII and III adenocarcinoma of the stomach.

There is no indication for the routine use of radiation alone in the adjuvant setting, but in certain patients it can be very effective palliation for bleeding or pain.

In patients with gross unresectable, metastatic, or recurrent disease, palliative chemotherapy has not been demonstrated to conclusively prolong 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.


Five-Year Survival Rate of Patients with Stomach Cancer

Tumor stage % SurvivalR1 resectionR1 resection R2 resectionR2 resection

IA 88 91IB 56 85II 39 58IIIA 7 30IIIB 0 12


Survival rates for all patients with gastric carcinoma stratified by combined American Joint Committee on Cancer

OUTCOMES


Survival rates for gastric cancer patients undergoing gastrectomy Survival rates for gastric cancer patients undergoing gastrectomy as stratified by combined American Joint Committee on Canceras stratified by combined American Joint Committee on Cancer

OUTCOMES-contd.


RecurrenceRecurrence rates after gastrectomy remain high, ranging from

40% to 80%, depending on the series. Most recurrences occur within the first 3 years.

The locoregional failure rate ranges from 38% to 45%, whereas peritoneal dissemination as a component of failure occurs in 54% of patients in several series.

Isolated distant metastases are uncommon, because most patients with distant failure also have locoregional recurrence as well.

The most common sites of locoregional recurrence are the gastric remnant at the anastomosis and in the gastric bed and the regional nodes. Hematogenous spread occurs to the liver, lung, and bone.


SURVEILLANCEAll patients should be followed up systematically. Because

most recurrences occur within the first 3 years, surveillance examinations are more frequent in the first several years. Follow-up should include a complete history and physical examination every 4 months for 1 year, then every 6 months for 2 years and then annually thereafter.

Laboratory examinations including complete blood counts and liver function tests should be obtained as clinically indicated. Many clinicians obtain chest radiographs as well as CT scans of the abdomen and pelvis routinely, wheresas others obtain studies only when clinically suspicious of a recurrence. Yearly endoscopy should be considered in patients who have undergone a subtotal gastrectomy.


Screening for Gastric CancerIn Japan it has clearly been shown that patients participating in gastric cancer screening programs have a significantly decreased risk of dying from gastric cancer. Thus screening is effective in a high risk population.

Certainly screening the general population in a low-risk country does not make sense, but patients clearly at risk for gastric cancer should probably have periodic endoscopy and biopsy. This includes patients with FAP, HNPCC, gastric adenomas, Menetrier disease, intestinal metaplasia, dysplasia, and remote gastrectomy or gastrojejunostomy.


SummarySummaryDefinitionMalignant lesion of the stomach epithelium.

Key points• The majority of tumours are unresectable at presentation.• Tumours considered candidates for resection should be staged withCT and laparoscopy to reduce the risk of an ‘open and shut’ laparotomy.• Most tumours are poorly responsive to chemotherapy.

EpidemiologyMale/female 2 : 1, peak incidence 50+ years. Incidence hasdecreased in Western world over last 50 years. Still common inJapan, Chile and Scandinavia.

AetiologyThe following are predisposing factors.• Diet (smoked fish, pickled vegetables, benzpyrene,nitrosamines).• Atrophic gastritis.• Pernicious anaemia.• Previous partial gastrectomy.• Familial hypogammaglobulinaemia.• Gastric adenomatous polyps.• Blood group A.

Pathology• Histology: adenocarcinoma.• Advanced gastric cancer (penetrated muscularis propria) maybe polypoid, ulcerating or infiltrating (i.e. linitus plastica).• Early gastric cancer (confined to mucosa or submucosa).


Spreadlymphatic (e.g. Virchow’s node); haematogenous toliver, lung, brain; transcoelomic to ovary (Krukenberg tumour).

Clinical features• History of recent dyspepsia (epigastric discomfort, postprandialfullness, loss of appetite).• Anaemia.• Dysphagia.• Vomiting.• Weight loss.• The presence of physical signs usually indicates advanced(incurable) disease.

Investigations• FBC.• U+E.• LFTs.• OGD (see the lesion and obtain biopsy to distinguish frombenign gastric ulcer).• Barium meal (space-occupying lesion/ulcer with rolled edge).Best for patients unable to tolerate OGD.• CT scan (helical): stages disease locally and systemically.• Laparoscopy: used to exclude undiagnosed peritoneal or liver secondaries prior to consideration of resection.

Essential management• Palliation (metastatic disease or gross distal nodal disease atpresentation):gastrectomy: local symptoms, e.g. bleeding;gastroenterostomy: malignant pyloric obstruction;intubation: obstructing lesions at the cardia.• Curative treatment (resectable primary and local nodes).• Surgical excision with clear margins and locoregional lymph nodeclearance (D2 gastrectomy).• Other treatment: combination chemotherapy with etoposide,adriamycin and cisplatin may induce regression.PrognosisFollowing ‘curative’ resection, 5-year survival rates are approximately 20%, but overall 5-year survival (palliation and resection) is only 5%.



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