Gastric Cancer

Epidemiology

• Most common Asian countries – Japan, China, Mongolia
• More common in males
• Incidence increases with age

Etiology

• Diet – high salt diet, smoked food, preservatives containing nitrites

Familial – associated with e-cadherin mutation

• Inactivation of p53
• HNPCC

Pathology

Gross types

• Cauliflower type
• Ulcerative type
• Leather-bottle (Linitis plastica)

Lauren’s classification

• Intestinal type – favourable prognosis
  • H.pylori is the most common cause
  • Gland formation and definite cellular architecture
  • Gastric mucosa replaced with epithelium that resembles small intestinal mucosa
  • Most common in men and the elderly
  • Hematogenous spread
• Diffuse type – poor prognosis
  • Most common in blood group A, familial type
  • Poorly differentiated, signet type
  • Early gastric wall penetration
  • Lymphatic spread
  • Most common in females and young people
  • Linitis plastica, ulcerative growth

Depending on depth of invasion

• Early gastric cancer –  Japanese Classification
  • Involvement of mucosa and/or submucosa only – with or without lymph node involvement
  • TNM – T1 + any N
• Advanced gastric cancer – Borrmann’s classification
  • Involvement of muscularis and/or serosa – with or without lymph node involvement

WHO histological classification

• Adenocarcinoma (from mucous secreting cells) – Papillary, tubular, mucinous, signet-ring
• Adenosquamous carcinoma
• Squamous cell carcinoma
• Undifferentiated carcinoma

Common site of occurrence

• Prepyloric and pyloric region – most common site
• Body
• Fundus, oesophago-gastric junction

Spread

• Direct spread
  • Horizontal submucosal spread along stomach wall
  • Vertical spread by invasion to adjacent structures – pancreas, colon, liver
• Lymphatic spread
  • Occurs by permeation and embolisation through lymphatics to subpyloric, pancreaticoduodenal, splenic, celiac, aortic lymph nodes
  • Later spreads to left supraclavicular lymph node (Virchow’s lymph node)
• Haematogenous spread
  • Most often to the liver – causes multiple liver secondaries
  • Later to the lungs and bones
• Transperitoneal spread
  • Can cause peritoneal seedings – leads to ascites
  • Can cause Krukenberg’s tumours in ovaries

Clinical Presentation

• Recent onset of loss of appetite and weight loss, early satiety, fatigue
• Upper abdominal pain and vomiting
• Abdominal mass – nodular, hard, moves with respiration
• Dysphagia
• Jaundice and palpable liver
• Ascites
• (+) Troisier’s sign – palpable Virchow’s node
• (+) Trousseau sign – migrating thrombophlebitis
• Anaemia, cachexia
• Metastatic disease – liver secondaries, ascites, secondaries in ovaries, umbilicus, supraclavicular nodes, lungs and bones

Investigations

• Hb%, haematocrit
• Barium meal – irregular filling defect
  • Shows irregular filling defect , loss of rugae, delayed emptying
• Gastroscopy with biopsy
• Endosonography
• US abdomen – liver secondaries, ascites, nodes, ovaries
• FNAC from Virchow’s node
• Laparoscopy – to stage disease
• CT abdomen and thorax – to see size, extent, infiltration, lymph node status, operability
• CA 72-4 (evaluates relapse), CEA, CA 19-9, CA 12-5

Treatment

• Surgery – only curative option
• Preoperative – correction of anaemia, nutrition, fluids and electrolytes
• Growth in pylorus (A) – lower radical gastrectomy with removal of greater and lesser omentum, all lymph nodes, spleen, tail of pancreas and later Billroth II anastomosis (gastrojejunostomy)
• Growth in oesophago-gastric junction (B) – upper radical gastrectomy with removal of spleen, both omentums, lymph nodes and later oesophagogastric anastomosis
• Growth in body or linitis plastica (C) – total gastrectomy with oesophagojejunal anastomisis