Gastric Cancer
A slow-growing cancer of the stomach lining often linked to chronic bacterial infections or dietary factors, presenting late with vague symptoms.
Emergency Management: Gastric perforation of a malignant ulcer causing acute peritonitis and septic shock. Massive upper GI hemorrhage requiring emergency endoscopy or embolization.
Gastric cancer is a malignancy arising from the lining of the stomach. Over 90% of cases are adenocarcinomas, which are further divided histologically into intestinal and diffuse types (Lauren classification).
Detailed Overview
The intestinal type is strongly associated with environmental factors, specifically Helicobacter pylori infection, and progresses through a well-defined cascade from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and finally carcinoma. The diffuse type is poorly differentiated, highly infiltrative (linitis plastica), and often associated with genetic mutations (CDH1). Because early gastric cancer is typically asymptomatic, most cases in Western countries are diagnosed at advanced stages with a poor prognosis.
Epidemiology & Demographics
It is the 5th most common cancer worldwide. Incidence is highly variable geographically, being extremely high in East Asia (Japan, Korea) and Eastern Europe. It is twice as common in men as in women.
Etiological Mechanism
The predominant etiology for the intestinal type is chronic infection with Helicobacter pylori. Other causes include dietary factors, autoimmune gastritis, and genetic syndromes.
Primary Causes
Helicobacter pylori Infection
Dietary Factors (high salt, smoked foods, nitrates)
Epstein-Barr Virus (EBV) (10% of cases)
Hereditary Diffuse Gastric Cancer (CDH1 mutation)
Correa's cascade describes the development of the intestinal type: H. pylori causes chronic active gastritis. Over decades, this leads to loss of gastric glands (atrophic gastritis). The stomach lining is replaced by intestinal-type epithelium (intestinal metaplasia) as a defense mechanism. DNA damage accumulates, leading to dysplasia and adenocarcinoma. Diffuse gastric cancer lacks intercellular adhesions due to loss of E-cadherin expression (often due to CDH1 mutation). This allows signet-ring cells to diffusely infiltrate the gastric wall, causing marked thickening and rigidity (linitis plastica or 'leather bottle' stomach).
Diagnostic Criteria & Guidelines
Diagnosis requires Esophagogastroduodenoscopy (EGD) with multiple biopsies of suspicious lesions or ulcers. Any gastric ulcer requires biopsy to rule out malignancy (unlike duodenal ulcers). Staging requires CT of the chest, abdomen, and pelvis, and Endoscopic Ultrasound (EUS) to assess depth.
For locally advanced disease: Perioperative chemotherapy (FLOT regimen: Fluorouracil, Leucovorin, Oxaliplatin, and Docetaxel for 4 cycles before and 4 cycles after surgery) combined with Subtotal or Total Gastrectomy and D2 lymph node dissection.
Second-Line & Adjunctive Therapy
For metastatic or unresectable disease: Palliative systemic chemotherapy (FOLFOX). Add Trastuzumab if HER2-positive. Add Nivolumab if PD-L1 CPS >= 5.
Surgical & Procedural Management
Gastrectomy. Distal tumors require subtotal gastrectomy with Roux-en-Y reconstruction. Proximal or diffuse tumors require total gastrectomy with esophagojejunostomy. D2 lymphadenectomy is the standard of care for curative intent.
Patient Counseling & Advice
Warn the patient about 'dumping syndrome' after stomach removal—rapid emptying of food into the intestine causing cramps, sweating, and diarrhea. Emphasize that dietary habits must permanently change.
Follow-Up & Monitoring Schedule
History and physical, CEA/CA 19-9 testing, and CT scans every 3-6 months for the first 2 years, then every 6-12 months up to 5 years. Endoscopy is usually repeated at 1 year post-op.
Preventive Strategies
Eradication of H. pylori with antibiotic therapy. Mass endoscopic screening in high-risk countries (e.g., Japan, South Korea) has dramatically reduced mortality by catching Stage I disease. Prophylactic total gastrectomy is recommended for patients with confirmed CDH1 genetic mutations.
Highly dependent on stage. 5-year survival for localized stage I is >70%. However, overall 5-year survival in the US is around 32% because most cases present at Stage III or IV.