The GI tract is a tube. Any tube can be blocked by something pressing from outside (extrinsic — e.g. tumour, adhesions), something growing within the wall itself (mural — e.g. cancer, stricture), or something lodging inside the lumen (intraluminal — e.g. bezoar, foreign body, gallstone ileus).

The level of obstruction determines what is "upstream" and therefore what accumulates and what the patient vomits. Proximal obstruction presents early with vomiting and minimal distension; distal obstruction presents late with distension and constipation before vomiting.

Upper GI obstruction — the nature of the vomitus tells you the level relative to the ampulla of Vater: ^[1]

• Bile-stained vomitus → obstruction is distal to the ampulla (i.e. beyond D2 duodenum)
• Not bile-stained vomitus → obstruction is proximal to the ampulla (pyloric/gastric obstruction)

This is a crucial clinical discriminator. Bile enters the duodenum at the ampulla of Vater (D2). If obstruction is at the pylorus (e.g. gastric cancer, pyloric stenosis from chronic duodenal ulcer), no bile reaches the stomach → vomitus is non-bilious, containing undigested or partially digested food.

Bulge (distension) in epigastrium + succussion splash are the two key exam findings in upper GI obstruction ^[1]

• Epigastric distension — the stomach fills with secretions and swallowed food that cannot pass distally
• Succussion splash — when you shake the patient's abdomen from side to side, you hear a splashing sound. This indicates a stomach that is abnormally full of fluid + air. Normally the stomach empties within ~4 hours of eating; a splash > 4 hours post-prandially is pathological and suggests GOO.

Gastric adenocarcinoma: ^[1]

• Decreasing incidence worldwide (due to declining H. pylori, better food preservation)
• Remains the 3rd leading cause of cancer deaths worldwide
• Incidence varies globally — high incidence in Asia (Japan, Korea, China)
• 6th leading cause of cancer deaths in Hong Kong

At QMH, the age distribution peaks in the 60s–70s ^[1]. This is predominantly a disease of older adults.

The classic Lauren classification divides gastric adenocarcinoma into:

• Intestinal type — well-differentiated, gland-forming; associated with H. pylori, dietary factors, intestinal metaplasia; more common in high-incidence areas
• Diffuse type — poorly differentiated, signet ring cells; infiltrative growth pattern; associated with CDH1 mutation; younger patients; worse prognosis → linitis plastica

Linitis plastica: ^[1]

• 'Leather bottle' stomach
• Mucosa may appear "normal" on endoscopy — this is a trap! The tumour infiltrates the submucosa and muscularis without obvious mucosal ulceration
• Rigid, could not be distended with air — on endoscopy, the stomach won't inflate properly

4 molecular subtypes of gastric cancer are mentioned in the lecture (TCGA classification): ^[1]

1. EBV-positive — PIK3CA mutations, DNA hypermethylation, PD-L1/2 amplification
2. MSI-high — hypermutated, respond to immunotherapy
3. Genomically stable — enriched for diffuse type, CDH1/RHOA mutations
4. Chromosomal instability (CIN) — most common; intestinal type; TP53 mutations, RTK-RAS amplification

Four modes of spread: ^[1]

1. Direct invasion — into adjacent organs (pancreas, transverse colon, spleen, diaphragm)
2. Lymphatic — to perigastric nodes, then to coeliac, para-aortic nodes, and distant nodal sites
3. Transcoelomic (peritoneal seedling) — tumour cells shed into peritoneal cavity → Krukenberg tumour (bilateral ovarian metastases, classically signet ring cells)
4. Haematogenous — via portal vein to liver (most common); also lung, bone, brain

Investigations: ^[1]

• CBP — anaemia (iron deficiency from chronic blood loss)
• LFT — liver metastases
• RFT — hydronephrosis / renal impairment from ureteric obstruction
• Upper endoscopy and biopsies — the gold standard diagnostic investigation
• Chest X-ray — pulmonary metastases, pleural effusion
• (CEA, CA19-9) — used for follow-up, not diagnosis (low sensitivity/specificity for primary diagnosis)

After diagnosing gastric cancer, ask two fundamental questions: ^[1]

1. What is the stage of the disease? (determines treatment intent — curative vs palliative)
2. Is the patient fit for surgery/treatment? (comorbidities, nutritional status, performance status)

TNM staging system: ^[1]

• T staging = depth of invasion (not size!)
  • T1: mucosa (T1a) or submucosa (T1b)
  • T2: muscularis propria
  • T3: subserosa
  • T4: serosa (T4a) or adjacent structures (T4b)
• N staging = number of lymph nodes with metastasis
  • N0: 0; N1: 1–2; N2: 3–6; N3a: 7–15; N3b: ≥16
• M staging = presence/absence of distant metastasis
  • M0: no distant mets; M1: distant mets present

Note: T staging in gastric cancer is about depth, not size. This differs from some other cancers. The deeper the invasion, the higher the risk of lymph node metastasis and peritoneal seeding.

Clinical staging modalities: ^[1]

• History and physical examination — always first
• LFT — hepatic involvement
• CXR — thoracic spread
• Ultrasonography or CT scan abdomen — intra-abdominal staging (liver mets, ascites, lymphadenopathy)
• PET/CT scan — whole-body metabolic staging; may miss diffuse-type cancers and small tumours ^[2]
• Endoscopic ultrasound (EUS) — best for T and N staging (visualises layers of gastric wall)
• Laparoscopy — best for detecting peritoneal metastases often missed by imaging (e.g. omental seedlings) ^[1][2]

Treatment depends on "fitness" and clinical stage. ^[1] Currently, resection remains the only hope for cure for resectable disease. ^[1] In HK, ~70% patients present with diseases ≥ Stage III. ^[1]

This statistic is sobering — most patients in HK present late because early gastric cancer is largely asymptomatic, and there is no population-level screening programme (unlike Japan/Korea).

Early cancer treatment: ^[1]

• T1, mucosal (confined to mucosa or submucosa)
• Rare in Hong Kong — most detected in Japan through screening endoscopy programmes
• Treatment options:
  • Endoscopic mucosal resection (EMR) — lesion lifted with submucosal saline injection → snared and resected
  • Endoscopic submucosal dissection (ESD) — mucosa dissected en-bloc at the submucosa level after saline injection; allows larger and more precise resection but higher perforation risk
  • Laparoscopic gastrectomy

EMR vs ESD:

• EMR: simpler, faster, lower perforation risk; suitable for small ( < 2 cm), well-differentiated, non-ulcerated lesions
• ESD: allows en-bloc resection of larger lesions; better histological assessment of margins; higher risk of perforation and bleeding

Resectable gastric cancer: ^[1]

• Gastric resection with D2 lymph node dissection — standard of care
• Distal (subtotal) gastrectomy for distal lesions (antral/pyloric)
• Total gastrectomy for proximal lesions (body/fundus/cardia)
• Postoperative adjuvant chemotherapy — for advanced cancer (≥ Stage II)
• Preoperative neoadjuvant chemotherapy — in selected patients (e.g. locally advanced, borderline resectable)

D2 lymph node dissection = removal of perigastric nodes (N1 stations) + nodes along the coeliac axis branches (N2 stations: left gastric, common hepatic, coeliac, splenic hilum, splenic artery). This is the standard in Asian centres and has been shown to improve survival compared to D1 dissection (perigastric nodes only), though with higher morbidity.

Reconstruction after total gastrectomy:

Roux-en-Y oesophagojejunostomy ^[1] — the standard reconstruction. The jejunum is divided; the distal limb (Roux limb) is brought up to anastomose with the oesophagus; the proximal limb (carrying bile/pancreatic secretions) is joined to the Roux limb ~40–60 cm downstream. This prevents bile reflux into the oesophagus.

Surgical approaches:

Laparoscopic gastrectomy ^[1] — increasingly performed; can be laparoscopic-assisted (anastomosis through a mini-laparotomy) or totally laparoscopic (intra-corporeal anastomosis) Robotic gastrectomy ^[1] — offers 3D vision and wristed instruments; used in high-volume centres

Unresectable disease management: ^[1]

• Supportive care, pain control — palliative care involvement
• Palliative resection — for bleeding that cannot be controlled endoscopically
• Palliative bypass (gastrojejunostomy, GJ) — for outlet obstruction (food bypasses the obstructed pylorus)
• Systemic chemotherapy — for disease control and symptom palliation
• Endoscopic stenting — self-expanding metallic stent across malignant stricture for rapid palliation of GOO or dysphagia

Chemotherapy classification: ^[1]

• Primary — first-line treatment for unresectable/metastatic disease
• Adjuvant — after curative surgery to reduce recurrence
• Neoadjuvant — before surgery to downstage and improve resectability

Targeted therapy:

ToGA trial — HER2 mutation: ^[1] HER2-positive gastric cancer (~15-20% of cases) benefits from the addition of trastuzumab to chemotherapy. HER2 testing (IHC/FISH) should be performed on all advanced gastric adenocarcinomas.

• Presenting complaint: vomiting (nature — bilious vs non-bilious; timing relative to meals; volume), weight loss (quantify — percentage of body weight), appetite, abdominal distension
• Alarm features (red flags): age ≥ 45, weight loss > 10%, anaemia/bleeding, dysphagia, persistent vomiting, abdominal mass, family history of GI cancer, previous gastrectomy ^[6]
• Past medical history: H. pylori status, peptic ulcer disease, previous gastric surgery, pernicious anaemia
• Drug history: NSAIDs (peptic ulcer as a differential)
• Family history: E-cadherin mutation (HDGC), GI cancers
• Social history: smoking, diet (preserved/salted foods), occupation

• General: cachexia, pallor, jaundice, left supraclavicular node (Virchow's), left axillary node (Irish's), acanthosis nigricans, periumbilical nodule (Sister Joseph's)
• Abdomen: epigastric distension, visible peristalsis, succussion splash, epigastric mass (hard, irregular, moves with respiration), ascites, hepatomegaly
• DRE: Blumer's shelf (rectal shelf)
• Other: pleural effusion signs (stony dull percussion, decreased breath sounds)

1. Bloods: CBP (anaemia), LFT (liver mets), RFT (ureteric obstruction), albumin (nutritional status)
2. Diagnostic: OGD + biopsies (gold standard)
3. Staging: CT TAP, EUS, PET/CT, staging laparoscopy, CXR
4. Tumour markers: CEA, CA19-9 (for follow-up only)
5. HER2 testing: IHC ± FISH on biopsy (for treatment decisions in advanced disease)

• Q: ESD vs EMR → ESD allows en-bloc resection for larger lesions but higher perforation risk
• Q: Distal vs total gastrectomy → Distal for antral/pyloric tumours; Total for proximal/cardia/body tumours
• Q: D1 vs D2 dissection → D2 is the standard in Asian practice (includes coeliac axis nodes)
• Q: Adjuvant chemo vs chemoradiation → In Asian setting with adequate D2 dissection, adjuvant chemo alone (CLASSIC/ACTS-GC); chemoradiation mainly Western practice where D2 not consistently performed
• Q: T2 antral gastric cancer, PET clean → Distal radical gastrectomy (not ESD, not stent, not neoadjuvant alone) — see 2021 MCQ Q72

Stem: A 50-year-old man presented with repeated vomiting after meal for 3 days. He also complained of increasing epigastric distension and weight loss of 5 kg over the past 2 months. Physical examination showed mildly distended epigastric region with the presence of succussion splash. Which of the following would you arrange as an initial investigation to confirm your clinical suspicion? A. Abdominal X-ray B. Barium meal C. Computed tomography scan of abdomen D. Ultrasound of abdomen

Answer: A. Abdominal X-ray Rationale: The clinical picture is classic GOO (vomiting after meals, epigastric distension, succussion splash, weight loss). The initial investigation is an AXR to confirm gastric distension. CT is for staging after diagnosis. Barium meal is largely replaced by endoscopy. USG is for biliary assessment.

Stem: A 50-year-old lady presents with epigastric pain over the recent 3 months. She is otherwise asymptomatic. She does not smoke or drink. Her past health has been good. Abdominal examination is unremarkable. Upper endoscopy and biopsies show a 2 cm adenocarcinoma of the gastric antrum. Endoscopic ultrasonography shows that the lesion involves the muscularis propria. PET-CT scan does not show any hypermetabolic lesion. What is the MOST APPROPRIATE management? A. Distal radical gastrectomy B. Endoscopic stenting C. Endoscopic submucosal dissection D. Neoadjuvant chemotherapy

Answer: A. Distal radical gastrectomy Rationale: EUS shows T2 (muscularis propria involvement) — this excludes ESD (only for T1). PET-CT clean means no distant mets (M0). Distal location → distal gastrectomy with D2 dissection is appropriate. Neoadjuvant is reserved for selected locally advanced cases (typically ≥T3 or node-positive). Stenting is palliative.

Stem: A 55-year-old gentleman presented with a 4 cm ulcer in the posterior gastric antrum... After 6 months of medical therapy including a PPI, he continued to complain of intermittent epigastric pain. He was also noted to be anaemic, requiring iron supplementation. Repeated endoscopy and biopsies showed that the ulcer was of the same size and was benign on histologic examination. What is the MOST APPROPRIATE management at this stage? A. Distal gastrectomy B. Endoscopic submucosal dissection C. Life-long proton pump inhibitor D. Repeat endoscopy and biopsies every 6 months

Answer: A. Distal gastrectomy Rationale: A 4 cm gastric ulcer that is not healing after 6 months of adequate PPI therapy, with persistent symptoms and iron deficiency anaemia, is suspicious for malignancy despite benign biopsies (sampling error). Surgical excision (distal gastrectomy) is the safest approach — it provides definitive histology and treatment. Continued surveillance risks missing a cancer.

Stem: A 45-year-old taxi driver with a long history of epigastric pain presented with vomiting. The vomitus was mainly undigested food. He is a regular user of NSAIDs due to chronic pain. On examination, the upper abdomen was distended but the lower part was scaphoid. Options: A. Colorectal cancer; B. Drug-induced ileus; C. HCC; D. Hypokalaemia; E. Intestinal lymphoma; F. Intestinal perforation; G. Mesenteric ischaemia; H. Oesophageal cancer; I. Peptic ulcer disease; J. Post-operative adhesion

Answer: I. Peptic ulcer disease Rationale: Chronic NSAID use + long history of epigastric pain + vomiting undigested food + upper abdominal distension with scaphoid lower abdomen = pyloric stenosis from chronic peptic ulcer. The upper distension is the dilated stomach; the scaphoid lower abdomen indicates no distal bowel distension (obstruction is at the pylorus). Not gastric cancer because of young age and chronic NSAID history pointing to PUD.

Stem: A 45-year-old man presents with a sudden onset of epigastric pain. He has a history of cardiac disease on long-term aspirin. Physical examination reveals marked tenderness at epigastrium. What is the MOST APPROPRIATE initial diagnostic investigation? Options: A. AXR; B. Angiogram; C. CT scan; D. Contrast meal; E. Contrast swallow; F. Erect CXR; G. MRI; H. Percutaneous cholangiogram; I. PET scan; J. USG

Answer: F. Erect chest X-ray Rationale: Sudden epigastric pain on long-term aspirin → suspect perforated peptic ulcer. The initial investigation to confirm is an erect CXR looking for free gas under the diaphragm (pneumoperitoneum).

Stem: A 72-year-old man with a history of right hemicolectomy done for carcinoma of colon presents with abdominal distension. He has not had bowel opening for 10 days and started to have abdominal pain since yesterday. Physical examination reveals a distended abdomen with active bowel sound. What is the MOST APPROPRIATE initial diagnostic investigation?

Answer: A. Abdominal X-ray Rationale: Previous surgery + absolute constipation + distension + active bowel sounds = adhesive small bowel obstruction. AXR is the initial investigation (dilated loops, air-fluid levels).