Carcinoma Stomach: Causes, Symptoms, Diagnosis and Treatment

 Carcinoma Stomach

Carcinoma Stomach Introduction: Carcinoma stomach is more common in men compared to women.

• Rare below 40 average age is 63 years.
• Worldwide, it is the fourth most common cancer and second leading cancer of death.
• North Eastern part of India, the district of Aizawl in the state of Mizoram has recorded the highest incidence in the country as per NCRP 2013 (64.2/ 100,000 population). The highest incidence of gastric cancer in Mizoram has been attributed to smoking local cigarettes like maizol and Taibur-tobacco smoke infused water. This is followed by a Southern Indian state, namely Tamil Nadu, where the incidence is 12.2/100,000 population in men.
• Incidence of proximal gastric carcinoma is increased— may be due to obesity and in rich socioeconomic status patients (Key Box 41.19).
• Carcinoma distal stomach is more commonly associated with H. pylori.
• Proximal carcinomas are more advanced at the time of presentation than distal carcinomas.
• D2 gastrectomy is currently the recommended surgical choice for cases of resectable advanced disease.
• The 5-year overall survival for resectable GC is approximately 20 to 30% worldwide, but it is 70% in Japan and in other eastern countries.

Carcinoma Proximal Stomach (Cardia)

• Incidence is increasing. Obesity and high socio-economic group o More aggressive
• Thin muscularis mucosa. Hence, submucosal invasion is seen early
• Diagnosis may also get delayed as endoscopy needs technical expertise
• Signet ring carcinoma is common here
• Surgical resection involves oesophageal anastomosis which is technically demanding. Leak rates are high
• Hence, prognosis is poor

Carcinoma Stomach Risk factors

1. Environmental and dietary factors
   • The incidence is increased in persons who consumes red meat, cabbage, spices, spirits, salf-fish
   • Smoked salmon fish was responsible for increased incidence of carcinoma stomach in the Japanese population. Probably, it is related to relase in polycyclic hydrocarbons and auromatic amino acids. Somoking, spicy food and alochol consumned over a period of mnany years produce chronic gastructus which may change into carcinona of stomach.
   • Food Products which may be Carcinogenic
     • Smoked food
     • Spirits
     • Smoking
     • Salted food—salt based preservatives and lack of refrigration
     • Soil
     • Diet low in carbohydrate
     • Animal protein
     • Rich fatty food
     • High in complex carbohydrates
     • H. pylori in contaminated water
2. Precancerous Conditions
   • Atrophic gastritis: This may be due to smoking, spicy food, continuous ingestion of drugs, reflux of bile into the stomach, etc.
   • Pernicious anaemia: Patients have increased risk (four to six times) of development of carcinoma when compared to general population. It causes atrophic gastritis and precipitates carcinoma of fundus of the stomach. Lesions are polypoidal and multicentric
   • Patients with hypogammaglobulinaemia (50-fold increase) are at high-risk.
   • H. pylori infection results in atrophic gastritis, followed by the intestinal type of gastric mucosa, metaplasia and then dysplasia. Eventually, it leads to intestinal type of gastric cancer.
     • H. pylori can also cause proliferation of gastric cancer cells and decrease secretion of vitamin C. Cytotoxin associated gene A (Cag A) is associated with increased risk.
     • Also both type A and type B gastritis can pre-dispose to carcinoma stomach. Type A—proximal stomach, type B—distal stomach. It is an important modifiable risk factor.
   • Adenomatous polyps which occur in the antrum have highest risk of malignant transformation (larger polyps, i.e. more than 2 cm—10 to 20% malignant transformation). Polyp more than 2 cm, pedunculated polyp can be removed by endoscopically. Higher chances of malignancy is seen in sessile polyps.
   • Menetrier’s disease is a protein-losing enteropathy, along with giant hypertrophy of gastric mucosal folds. It is a precancerous condition.
   • Gastric ulcer (benign): Incidence of malignancy is 2% (0.5 to 5%). Carcinoma arising in a gastric ulcer is called ” Ulcer Cancer of the Stomach”.
   • Previous GJ or gastric resection predisposes to development of carcinoma of the stomach after a period of 15-20 years. Such a carcinoma is described as stump carcinoma. Pathogenesis is related to development of atrophic gastritis, achlorhydria and duodenogastric bile reflux.
3. Genetic and Familial Factors
   • Carcinoma stomach can run in families. However, only 10% of patients give family history of carcinoma stomach.
   • Carcinoma stomach is more common in patients with blood group A. These patients have different muco¬polysaccharide secretion in the stomach and greater susceptibility to ingested carcinogens. They develop diffuse type of carcinoma.
   • Several genetic alterations have been identified such as activation of oncogenes, inactivation of tumour suppressor genes p53 and p16, reduction or loss in the cell adhesion molecule E-cadherin (met proto-oncogene).

Chronic H.Pylori Infection:

Carcinoma Stomach Familial Gastric Cancer

• Only 10% of patients give family history of carcinoma stomach
• Associated with mutation of E-cadherin gene o Bonaparte (Napoleon) appears to have this gene o It is also called hereditary diffuse gastric cancer (HDGC)
• Diagnosis is made when carcinoma is detected below the age of 40 years
• E-cadherin mutation results in a lifetime risk of gastric cancer by 60-90%.
• Hence prophylactic gastrectomy is recommended
• Familial diffuse gastric cancer (FGC)—at least 3 relatives in 2 generations are affected, one of them before 50 years of age.
• Hereditary nonpolyposis colon cancer carries—10% risk of gastric cancer
• Mutation of E-cadherin gene causes hereditary diffuse gastric cancer. Defective DNA mismatch repair (MLH1 or MSH2 mutation) causes Lynch syndrome. They have increased risk of gastric and colon cancer.

Carcinoma Stomach Gross Types

1. Cauliflower-like growth with friable tissue. This variety can give rise to melaena or bleeding causing anaemia.
2. Infiltrative type of lesion (diffuse) with dense sub-mucosal fibrosis which converts the stomach into a small contracted, functionless stomach—linitis plastica or leather bottle stomach. Mucosa may appear normal.
3. Ulcerative variety, with classical everted edges with central slough.
4. Ulcer cancer refers to carcinoma arising in a pre-existing gastric ulcer. In this variety, complete destruction of the muscle coat is present.
5. Colloid carcinoma: In this condition, malignant cells are separated by colloid material. This is the type which is common in women and gives rise to Krukenberg’s tumour—bilateral, bulky ovarian metastasis common in premenopausal women (signet ring carcinoma produces this).

Carcinoma Stomach Pathology

• Ninety-five percent of all malignant gastric neoplasms are adenocarcinomas.
• The Lauren system separates gastric adenocarcinoma into intestinal or diffuse types based on histology.
• Other histologic types include squamous cell carcinoma, adenoacanthoma, carcinoid tumours, GI stromal tumours, and lymphoma.

Early Gastric Cancer

Early gastric cancer is defined as adenocarcinoma limited to the mucosa and submucosa of the stomach, regardless of lymph node status. The entity is common in Japan, where gastric cancer is the number one cause of cancer death, and where aggressive surveillance programs have been established.

• Approximately 10% of patients with early gastric cancer will have lymph node metastasis. Approximately 70% of early gastric cancers are well differentiated and 30% are poorly differentiated.
• The overall cure rate with adequate gastric resection and lymphadenectomy is 95%. In some Japanese centres, 50% of the gastric cancers treated are early gastric cancers. In the US, less than 20% of resected gastric adenocarcinomas are early gastric cancers.

Early Gastric Cancer (Japanese Classification)

• Type 1 Exophytic lesion extending into the gastric lumen
• Type 2 Superficial variant
  • 2A Elevated lesions with a height no more than the thickness of the adjacent mucosa
  • 2B Flat lesions
  • 2C Depressed lesions with an eroded but not deeply ulcerated appearance
• Type 3 Excavated lesions that may extend into the muscularis propria without invasion of this layer by actual cancer cells

Advanced Gastric Cancer: It refers to involvement of muscularis mucosa and/or serosa with or without involvement of lymph nodes.

• The Borrmann classification system was developed in 1926 and remains useful today for the description of endoscopic findings.
• The Borrmann system divides gastric carcinoma into five types depending on the lesion’s macroscopic appearance.
  • Type 1 represents polypoid or fungating lesions
  • Type 2 ulcerating lesions surrounded by elevated borders
  • Type 3 ulcerating lesions with infiltration into the gastric wall
  • Type 4 diffusely infiltrating lesions
  • Type 5 lesions that do not fit into any of the other categories.
• Linitis plastica is the term to describe type 4 carcinoma when it involves the entire stomach.
• The original histologic classification system was developed by Borders in 1942.
• Borders classified gastric carcinomas according to the degree of cellular differentiation, independent of morphology, and ranged from 1 (well-differentiated) to 4 (anaplastic).

Early Gastric Cancer WHO Classification: Five Main Categories

1. Adenocarcinoma 95%
   • Papillary, tubular
   • Mucinous
   • Signet ring
2. Adenosquamous cell carcinoma
3. Squamous cell carcinoma
4. Undifferentiated carcinoma
5. Unclassified carcinoma

Early Gastric Cancer The Diffuse Form of Gastric Adenocarcinoma—Linitis Plastica

• Poorly differentiated
  • Lacks gland formation
  • Composed of signet ring cells
  • Consists of tiny clusters of small uniform cells
  • Tends to spread submucosally
  • Has less inflammatory infiltration
• Metastases occur early
  • Intraperitoneal metastases are frequent
  • Route of spread is generally by transmural extension and through lymphatic invasion
  • Does not generally arise in the setting of prior gastritis
• More common in women
  • Affects a slightly younger age group
  • Association with blood type A and familial occurrences, suggesting a genetic aetiology
  • The prognosis is less favourable for patients with diffuse-subtype histology.

Early Gastric Cancer Clinical Features (SOLID)

• Very often patients would have vague symptoms— early satiety, flatulence, discomfort, pain in the upper abdomen.
• Early satiety is due to decreased distensibility of the stomach.
• Anaemia is due to many factors
• Silent: Growth is silent but manifests as secondaries in the liver, ascites, Virchow’s node, rectovesical deposits, (Blumer’s shelf), umbilical nodule (Sister Mary Joseph’s nodule), left axillary nodes (Irish nodes), palpable ovarian mass (Krukenberg tumour).
• Obstruction at pylorus (pyloric antrum) producing pyloric obstruction with features of vomiting with/ without blood. Visible gastric peristalsis can also be present. Obstruction at the cardio-oesophageal junction produces dysphagia.

Early Gastric Cancer Anaemia 

• This is one of the common presentations. Often patients get investigated for anaemia by the physician only to discover carcinoma stomach.
• Achlorhydria results in poor conversion of ferrous to ferric which causes anaemia.
• 1 5% of patients may also develop haematemesis as in ulcerative lesions or proliferative lesions. GI blood loss also accounts for anaemia.
• Early satiety, loss of appetite and poor intake also con¬tribute to anaemia (minor role).
• 40% of carcinoma stomach patients have anaemia.
• Lump in the abdomen which is hard and irregular. Clinically, stomach mass is differentiated from liver mass by features mentioned below.
  1. Stomach moves with respiration.
  2. Upper border of the stomach mass can be made out.
  3. Anatomical location of the mass: Right hypochon- drium in a pyloric mass, epigastrium and left hypo- chondrium in a mass arising from body of the stomach.
  4. Knee elbow position: The mass falls forwards, unless fixed.
  5. The mass may have intrinsic mobility.
• I Insidious in onset: Anaemia, anorexia and asthenia of short duration.
• D Dyspepsia in a man over the age of 40: Carcinoma stomach should be ruled out. Early gastric cancer presents as dyspepsia.

Nonmetastatic conditions such as thrombophlebitis (Trousseau’s sign) and deep venous thrombosis can occur due to change in thrombotic and haemostatic mechanisms.

Early Gastric Cancer Strong Suspicion

• New onset dyspepsia in men >50 years of age
• Unexplained anaemia
• Unintentional weight loss
• GI bleeding
• Iron deficiency anaemia
• Progressive dysphagia

Early Gastric Cancer Clinical Signs of Inoperability

• Ascites
• Secondaries in the liver
• Para-aortic lymph nodes
• Krukenberg tumours
• Sister Mary Joseph nodule
• Blummer shelf deposits
• Supraclavicular nodes—Virchow node
• Irish node

Early Gastric Cancer Paraneoplastic Manifestations

• Sudden appearance of diffuse seborrhoeic keratoses (sign of Leser-Trelat) or acanthosis nigricans—velvety and darkly pigmented patches on skin folds.
• Hypercoagulable states (Trousseau’s syndrome)
• Polyarteritis nodosa

Early Gastric Cancer Staging: New clinical stage includes prognostic groups, cTNM, postneoadjuvant therapy pathologic stage groupings, ypTNM—new prognostic information change to anatomic boundary for staging carcinoma at oesophagogastric junction and changes to pathologic stage grouping. Refer NCCN guidelines for more details.

TNM STAGING AJCC 8th Edition

• Primary tumour (T)
  • TX Primary tumour cannot be assessed
  • T0 No evidence of primary tumour
  • Tis Carcinoma in situ. Intraepithelial tumour without invasion of the lamina propria
  • T1 Tumour invades lamina propria, muscularis mucosa or submucosa
  • T1a Tumour invades lamina propria or muscularis mucosa
  • T1b Tumour invades submucosa
  • T2 Tumour invades muscularis propria
  • T3 Tumour penetrates subserosal connective tissue without invasion of serosa or adjacent structures
  • T4 Tumour invades serosa (visceral peritoneum) or adjacent structures
  • T4a Tumour invades serosa (visceral peritoneum)
  • T4b Tumour invades adjacent structures
• Regional lymph nodes (N)
  • NX Regional lymph nodes (S) cannot be assessed
  • N0 No regional lymph node metastasis($)
  • N1 Metastasis in 1-2 regional lymph nodes
  • N2 Metastasis in 3-6 regional lymph nodes
  • N3 Metastasis in 7 or more regional lymph nodes
  • N3a Metastasis in 7 to 15 regional lymph nodes
  • N3b Metastasis in 16 or more regional lymph nodes
• Distant metastasis (M)
  • M0 No distant metastasis
  • M1 Distant metastasis
• Histologic grade (G)
  • GX Grade cannot be assessed
  • G1 Well-differentiated
  • G2 Moderately differentiated
  • G3 Poorly differentiated
  • G4 Undifferentiated

Early Gastric CancerSpread

1. Penetration of gastric serosa: This is the most important progonstic indicator. When serosa is NOT penetrated, 50% survive for 5 years aftewr resection. When serosa is penetrated, this this figure drops to 20%. Once serosa is involved, adjacent organs such as liver, pancreas, spleen, omentum, transverse colon get involved. Endoscopic ultrasound is the best investigation to detect the layers involvement in carcinoma of the stomach.
   
2. Lymphatic spread: More than 400 lymph nodes have
   been identified. Lymph node involvement is a poor
   prognostic indicator. 4 lymphatic zones have been
   described.
   1. Zone 1: In the gastrocolic omentum along the right gastroepiploic vessels. This drains the pyloric antrum and lower half of greater curvature.
   2. Zone 2: It lies in the gastrocolic omentum and gastrosplenic ligament along the left gastroepiploic vessels. This drains upper half of the greater curvature.
   3. Zone 3: It lies in the lesser omentum draining proximal two-thirds of the stomach. From here, lymph drains into peri oesophageal lymph nodes.
   4. Zone 4: It is from distal portion of the lesser curve and pylorus along the hepatic artery and right gastric artery into para-aortic nodes.
   5. Lymph nodes have been given separate numbers. They are discussed under resections.
3. Hematogenous spread: The most common sites are the liver and lungs. It produces extensive secondaries. They are signs of inoperability.
4. Transcoelomic spread results in ascites, Krukenberg tumour—bilateral bulky ovarian and rectovesical deposits (Blumer’s shelf).

Early Gastric Cancer Investigations

1. Complete blood picture: 20% of early gastric cancer patients have iron deficiency (microcytic, hypo-chromic) anaemia. A preoperative blood transfusion may be necessary before endoscopy.

2. Blood sugars, ECG and Echo, renal function, liver function are assessed and an ECOG score is given so that whether these patients can undergo radical surgery/ preoperative-neoadjuvant chemotherapy/radio-therapy can be given or not. Preoperative optimization is done by normalizing blood sugars or renal functions or cardiac functions so as to get the best results.

3. Flexible oesophagogastroduodenoscopy

• Diagnosis of malignancy by ulcerated lesion with elevated edges, obliterated gastric rugae.
• To know the extent of the lesion
• To confirm the diagnosis
• To take multiple biopsies—6 to 8 pieces
• Also, to aid brush cytology
• Biopsy is sent not only for histopathology but also for immune histochemistry. Overexpression of HER-2 neu receptors is found in about 13 to 20% of gastric cancers.

4. Ultrasound of the abdomen

• To rule out secondaries in the liver.
• To look for enlarged coeliac nodes.
• Can detect ascites-guided fluid tap and cell cytology.
• To detect Krukenberg tumour (pelvic CT).
• Useful in detecting metastatic disease.

5. CECT of the abdomen, pelvis and chest should be done.

• It is superior to ultrasound because it is objective and more specific.
• Respectability—especially infiltration into the pancreas, large fixed nodes at the origin of the left gastric artery retroperitoneal structures are better appreciated.
• However, detection of peritoneal disease sensibility is only around 30-35%.

6. Endoscopic ultrasonography can detect advanced tumours in 80% of patients. Overall staging accuracy is about 75%, however, it has significant limitations for staging mucosal disease. To know the T status— layers of the stomach involvement, it is the most sensitive and ideal investigation.

7. Laparoscopy: CT cannot detect liver or peritoneal metastasis (small <5 mm) and small lymph nodes. Laparoscopy is an ideal investigation. Almost 20 to 30% of so-called operable cases become inoperable. Laparoscopic peritoneal lavage for cytology is best test.

8. Role of PET scan

• PET scanning is not routinely used in staging gastric cancer.
• Gastric cancers have low avidity for 18F-fluoro-2- deoxyglucose.
• In advanced cases, before doing a resection for controlling the locoregional disease, a PET scan is done to rule out metastatic disease.

9. CEA: Carcinoembryonic antigen is elevated in about 60-70% of patients. It indicates the extensive spread of the disease. Also, CA 19-9 (carbohydrate antigen) and alpha-fetoprotein can be done.

10. Barium meal has become obsolete.

Early Gastric Cancer Histopathology: It is an adenocarcinoma of the stomach. There are basically two types of gastric carcinomas as per Lauren’s classification.

1. Diffuse is more common in young, females and carries poor prognosis. The leather-bottle stomach or linitis plastica is poorly differentiated with anaplastic cells. Signet-ring cell carcinoma and other poorly cohesive carcinomas are under diffuse variety as per WHO classification.
2. Intestinal is more common in elderly males. It shows areas of intestinal metaplasia. It has better prognosis. Papillary adenocarcinoma, tubular adenocarcinoma and mucinous adenocarcinoma are subtypes as per WHO classification.
   • There are so many other varieties which are grouped under indeterminate type (WHO classification). Few of them are mixed, example, adenosquamous, carcinoma with lymphoid type, etc.
3. HER-2 neu receptors to be checked by immuno- histochemistry.

Treatment Of Carcinoma Stomach

Surgery is the main modality of the treatment. Adjuvant chemotherapy has been found to be beneficial in a few patients only. Operable means cure is possible by doing radical surgery. Resectable means the growth can be removed. Inoperable means there are no chances of cure but growth may be resectable.

Carcinoma Stomach Signs of Inoperability at Surgery

• Growth infiltrating into pancreas, engulfing pedicle of left gastric vessels to pancreas or posterior abdominal wall.
• Rectovesical deposits, due to peritoneal seedings which are felt during per rectal examination.
• Enlarged, fixed coeliac nodes, para-aortic nodes.
• Ascites, peritoneal deposits.

Carcinoma Stomach Types of Resection

• Curative resection (R0) should be done whenever possible. Minimum 5 cm margin is required proximally. If serosa is involved, it qualifies for T3/ T4 and not for curative resection
• Stage IA: Regionally confined disease should undergo primary surgical R-0 resection—radical subtotal gastrectomy.
• Stage T1a: Endoscopic resection for tumours less than 2 cm—curative.
• Stage 2 and 3: Neoadjuvant therapy followed by radical resection. Curative but about 20%.
• Stage 4 or inoperable patient with vomiting, if facilities are available, endoscopic stenting can be offered. Majority of these patients succumb to the disease by 3-6 months. Gastrojejunostomy is also another option provided some part of body of the stomach is healthy to consider anastomosis.
• Stage 4 patient with bleeding, if fit for surgery: Pallia¬tive gastrectomy can be done to remove a fungating, ulcerative, bleeding mass. It gives better palliation.

Carcinoma Stomach Terminology

• Japanese Research Society for Gastric Cancer advocates very aggressive resection including lymphadenectomy. Hence, more details of lymph node station are given in Table. However, the rest of the cancer research groups were not able to produce the same results as the Japanese.
• D1 resection refers to the removal of primary group of nodes such as nodes along the lesser and greater curvature, and juxtapyloric nodes. If tumour and N1 nodes (group 1) resected = D1 gastrectomy. This will become curative resection when lymph nodes are clinically not enlarged (N0) but they are removed
• D2 resection refers to the removal of lymph nodes such as left gastric, common hepatic, splenic, retropancreatic nodes, etc. If tumour and N2 nodes (group 2) resected = D2 gastrectomy.
• This will become curative resection when lymph nodes are clinically enlarged (N1). So one step higher lymph nodes are cleared. Carcinoma stomach often causes local recurrence at the tumour site or in the locoregional lymph nodes. So aggressive approach of clearance of lymph nodes have been recommended.
• D3 resection refers to D2 resection followed by the removal of lymph nodes such as para-aortic, porta hepatis nodes, behind the head of the pancreas, etc. (not done).
• Pathological Basis for D2 Dissection
  • Gastric cancer has a great propensity to spread through the rich plexus of lymphatics of the stomach to local or regional lymph nodes. Hence, the need to remove stomach and lymph nodes.
  • Gastric cancer, unlike breast cancer, remains for a long time as a locoregional disease.
  • It is striking too, that when gastric cancer recurs it often does so locoregionally rather than more widespread dissemination.
  • It is very rare for gastric cancer to recur 5 years after surgery, whereas for breast cancer, disseminated micrometastases continue to take their toll some 10-20 years after surgery.

1. Right pericardial;
2. left pericardial;
3. lesser curvature;
4. greater curvature;
5. supra pyloric;
6. infra pyloric

Carcinoma Stomach Curative Resections: A. Gastrectomy and B. Endoscopic mucosal resections. The term R status was first described by Hermanek in 1994 and is used to describe the tumour status after resection. If no disease is identified in the lymph nodes, N0 nomenclature is used.

• A. Gastrectomy: The extent of the gastrectomy is site-dependent and focuses on complete removal of the gastric carcinoma with preferably a 5 cm margin from the gross edge of the tumour. Clearly, anatomic limitations influence this margin because in antral lesions close to or involving the pylorus, only a limited portion of the duodenum can be removed. In patients with a distal lesion, essentially a distal subtotal gastrectomy is performed regardless of T stage.
  • For proximal gastric cancers (fundic), total gastrectomy is required.
  • For midbody or more extensive lesions, total gastrectomy is required.
  • For more distal lesions, a subtotal gastrectomy is the preferred approach.
• R-Resections
• R0 describes a microscopically margin-negative resection, in which no gross or microscopic tumour remains in the tumour bed.
• R1 indicates removal of all macroscopic disease but microscopic margins are positive for tumour.
• R2 indicates gross residual disease. Since the extent of resection can influence survival, some authors include this R designation to complement the TNM system.
• Long-term survival can be expected only after a R0 resection therefore, a significant effort should be made to avoid R1 or R2 resections.
• Extended organ resection is reserved for patients with apparently node-negative T4 lesions, in which complete resection requires resection of the invaded portions of the diaphragm, pancreas, spleen, adrenal gland or colon.
• These patients usually are pretreated with chemotherapy.

Carcinoma Stomach Curative Resections Example:

• Surgery: A standard D2 resection for gastric cancer involves:
  • Removing part or whole of the stomach.
  • The N1 (groups 1-6) and N2 (groups 7-11) lymph nodes. Minimum of 15 lymph nodes need to be removed. More centers are recommending more lymph nodes removal.
  • The greater and lesser omentum and omental bursa.
  • The spleen and tail of the pancreas are removed if infiltrated by the tumours of the proximal stomach in order to remove groups 10 and 11 lymph nodes. All attempts should be made to preserve these structures but remove lymph nodes.
  • The hepatoduodenal nodes—level 12—in antral tumours.
  • The splenic hilum and other nodes—level 10, 11, 12.
• Reconstruction
  • Carcinoma of pyloric antrum and distal body of the stomach: Radical subtotal gastrectomy—D2. Recons-truction is done by gastrojejunal anastomosis. Popularly called Polya gastrectomy or Billroth II anastomosis.
  • Carcinoma of proximal stomach and diffuse carcinoma: Radical oesophagogastrectomy: Removal of the entire stomach, lower end of oesophagus, with regional lymph nodes N2, followed by oesophagojejunal anastomosis.

Carcinoma Stomach Endoscopic/Endoluminal mucosal resection

• This is indicated in early gastric cancer confined to mucosa. The cancer should be less than 2 cm and there should not be node enlargement. Small, high up lesions are ideal.
• Here, laparoscopic instrumentation is done under endoscopic guidance.
• The stomach is suitable for endoluminal surgery because it can be distended, and contents are sterile.
• Ideally cancer should be elevated variety and well differentiated.
• Normal saline is injected into submucosal plane and lesion gets elevated.
• It is excised with 1 cm margin up to muscularis propria at a deeper plane.

Carcinoma Stomach Palliative Resections

1. Carcinoma pyloric antrum (inoperable): Palliative anterior GJ  is done to relieve vomiting, by anastomosing a jejunal loop to the stomach in the prepyloric region. If posterior GJ is done, the growth may involve the GJ stoma early resulting in stomal obstruction. With anterior GJ, entero-enterostomy can be added to prevent bilious vomiting.
2. Palliative gastrectomy to get rid of ulcerated, necrotic or bleeding lesion.

Carcinoma Stomach Key points of carcinoma stomach

1. Carcinoma antrum and body—radical subtotal gastrectomy.
2. Carcinoma proximal stomach—radical total gastrectomy.
3. Inoperable carcinoma distal stomach—palliative anterior GJ.
4. Radical refers to removal of lymph nodes, fat, fascia greater and lesser omentum.
5. When level 1 to 6 (N1) nodes are removed along with stomach, it is D1 gastrectomy.
6. When level 7-11 (N2) lymph nodes are also removed along with 1-6 nodes and stomach, it is called D2 gastrectomy.
7. Early gastric cancer without lymph nodes can be treated with endoscopic mucosal resection or endo¬luminal gastric resection.
8. Palliative gastrectomy (subtotal) is worth considering in appropriate cases of obstruction/bleeding.

Carcinoma Stomach Role of Chemotherapy

1. The Adjuvant Treatment

• The Adjuvant Treatment Postoperative chemotherapy:
  • Now it is understood that gastric cancers partially respond to chemotherapy—in about 30% of cases given at advanced stage (results are better than cancer colon). Injection 5-FU (fluorouracil) 500 mg IV daily for five days, every 28 days. It can be given by IV infusion or IV bolus over 15 minutes.
  • Mechanism of action: It is an antimetabolite and acts by interfering with DNA synthesis. Side effects are myelosuppression, mucositis, excessive lacrimation, nausea, vomiting, etc.
  • Combination of 5-FU with adriamycin, mitomycin and cisplatin has also been tried. However, toxicity is more with these drugs. FAM (5-fluorouracil, adriamycin and mitomycin C) and ECF (epirubicin, cisplatin and 5-FU) are popular agents.
  • Intraperitoneal mitomycin and mitomycin C— impregnated charcoal have also been used (target the recurrence site—gastric bed).
• The Adjuvant Treatment Indications:
  • R0 resection (free margins): Any tumour greater than T2 including selected T2 cases should be considered for adjuvant therapy that includes 1 cycle of 5-FU+/- leucovorin OR capecitabine chemotherapy followed by 5-FU+/- leucovorin OR capecitabine based chemoradiation 3-4 more cycles of 5-FU+/- leucovorin OR capecitabine chemotherapy.
  • R1 (microscopic margin positive) and R2 (grossly positive margins) regardless of the TMN stage should receive chemoradiation followed by further cycles of adjuvant chemotherapy.
  • If the patient has received preoperative chemotherapy/chemoradiation then:
    • Adjuvant treatment is usually recommended beyond T2N0M0 which is usually 5-FU+/- leucovorin OR capecitabine based.
    • If patient has received ONLY preoperative chemotherapy and the resection was R1/R2, then postoperative chemoradiation is advised.

2. Neoadjuvant Chemoradiation: It is advised in medically fit unresectable—locally advanced diseases which generally includes concurrent 5-FU/capecitabine-based chemotherapy.

• Chemotherapy alone may also be used as a neoadjuvant modality.
• Recommended radiotherapy dose is 45-50.4 Gy (at 1.8 Gy/fraction).
• Trastuzumab (Herceptin) can be used in metastatic or locally advanced gastric adenocarcinomas which are overexpressing HER-2 neu receptors in about 13 to 20% of gastric cancers.

Carcinoma Surgery Role of Radiotherapy: External beam radiotherapy can also be used in metastatic cases as a part of palliation, especially when there is tumour bleed, gastric outlet obstruction due to the tumour pain. Dose for palliative radiotherapy is generally 30 Gy in 10 fractions over 2 weeks.