Distal Radical Gastrectomy - Indications, Steps, and Complications

INDICATIONS [3 marks]

1. Gastric adenocarcinoma of the distal third - the most common indication. Distal gastrectomy is performed when the tumor is in the distal stomach and an adequate proximal margin can be achieved.
   • NCCN recommends subtotal gastrectomy for T1b-T3 tumors when microscopic-free margins plus lymphadenectomy can be achieved
   • Japanese guidelines extend this to cT2-T4a tumors (with or without node positivity) when a satisfactory proximal resection margin can be obtained
   • Required margins: >4 cm (NCCN) or 3 cm for Borrmann type 1/2 and 5 cm for type 3/4 (Japanese/Chinese guidelines); 2 cm for T1 tumors
2. Gastric MALT lymphoma confined to distal stomach (after failure of H. pylori eradication)
3. Gastrointestinal stromal tumor (GIST) originating from Cajal cells in the distal stomach

1. Complicated peptic ulcer disease - surgery is now reserved for peptic stenosis (gastric outlet obstruction), penetrating or perforated ulcers, and bleeding refractory to medical and endoscopic therapy (peptic ulcer disease has largely been replaced by H. pylori eradication therapy)
2. Other benign lesions in the distal stomach: leiomyoma, gastric lipoma, adenomyoma, juvenile polyposis

STEPS OF DISTAL RADICAL GASTRECTOMY [4 marks]

Preoperative Preparation

• Upper GI endoscopy (EGD) + CT triphasic scan for staging; FDG-PET/CT for >T2 or node-positive disease
• Correct electrolyte imbalances (CBC + CMP); pre-operative optimization
• Prophylactic antibiotics at skin incision; DVT prophylaxis (IPC devices + pharmacologic)
• Nasogastric tube for gastric decompression; 12-hour fast (longer if gastric outlet obstruction)

Positioning and Access

• Supine position; midline laparotomy (or laparoscopic/robotic ports)
• Diagnostic laparoscopy first to exclude peritoneal spread in all patients undergoing potentially curative resection
• Inspect abdomen for ascites and metastatic deposits before committing to resection

Step 1 - Greater Omentum and Greater Curvature Dissection

• The transverse colon is completely separated from the greater omentum
• The gastrocolic ligament is divided; the greater omentum is removed en bloc with the specimen
• The right gastroepiploic vessels are identified, divided, and ligated at their origin

Step 2 - Subpyloric and Infrapyloric Lymph Node Dissection

• Subpyloric (station 6) lymph nodes are dissected
• The right gastric artery is divided at its origin from the proper hepatic artery
• Suprapyloric (station 5) nodes along the hepatic artery are cleared

Step 3 - Division of the Duodenum

• The first part of the duodenum is divided just beyond the pylorus, usually with a linear surgical stapler
• The duodenal stump is secured; if necessary, the duodenum is Kocherized to allow tension-free anastomosis

Step 4 - Left Gastric Artery and D2 Lymphadenectomy

• Dissection along the lesser omentum toward the celiac axis
• D1 dissection: perigastric nodes (stations 1-6)
• D2 dissection (standard for curative intent): additionally clears nodes along the left gastric artery (station 7), common hepatic artery (station 8), celiac axis (station 9), and splenic artery (station 11)
• The left gastric artery is divided at its origin from the celiac trunk
• NCCN: goal of examining >16 lymph nodes; D2 recommended at high-volume centers

Step 5 - Proximal Gastric Transection

• The stomach is divided proximally with a linear stapler at least 4 cm (NCCN) or 3-5 cm (Japanese) from the gross tumor edge
• Frozen section analysis of the proximal margin is performed if margin clearance is in doubt

Step 6 - Reconstruction

COMPLICATIONS [3 marks]

Intraoperative

• Hemorrhage - injury to right gastric, right gastroepiploic, or left gastric vessels; splenic injury during mobilization
• Pancreatic injury during lymph node dissection (D2 dissection along the superior border of the pancreas)
• Bile duct injury during hepatic hilar dissection

Early Postoperative

• Anastomotic leak - the most feared early complication; presents with fever, tachycardia, peritonitis; duodenal stump blowout (Billroth II) is particularly dangerous
• Duodenal stump leak (after Billroth II) - can cause bile peritonitis, sepsis
• Intra-abdominal abscess - subphrenic or sub-hepatic
• Postoperative hemorrhage - intraluminal (anastomotic) or intra-abdominal
• Delayed gastric emptying / gastroparesis - especially after vagotomy or in patients with pre-existing gastric outlet obstruction
• Pancreatitis - from traction or dissection trauma to the pancreas
• Pulmonary complications - pneumonia, atelectasis (common in elderly; >70% have ≥2 comorbidities)
• DVT / Pulmonary embolism - moderate-to-high risk; requires prophylaxis

Late Postoperative

• Anastomotic stricture - causing dysphagia or outlet obstruction
• Marginal (stomal) ulceration - at the gastrojejunal anastomosis (Billroth II/Roux-en-Y), especially without adequate acid reduction
• Dumping syndrome - early (vasomotor symptoms from rapid gastric emptying) or late (reactive hypoglycemia)
• Alkaline reflux gastritis - bilious reflux into gastric remnant, particularly with Billroth II; presents with postprandial epigastric pain and bilious vomiting; treated by conversion to Roux-en-Y
• Afferent loop syndrome (Billroth II) - obstruction of the afferent limb leads to pain and bilious vomiting
• Nutritional deficiencies - vitamin B12 deficiency (loss of intrinsic factor), iron deficiency anemia, calcium/vitamin D malabsorption, folate deficiency
• Remnant gastric cancer - increased risk >15-20 years post-gastrectomy; requires surveillance endoscopy
• Roux stasis syndrome - poor emptying of the Roux limb

• Fischer's Mastery of Surgery 8e, Chapter: Distal Gastrectomy (Open and Minimally Invasive Techniques), pp. 2938-2947
• Bailey & Love's Short Practice of Surgery 28e, Chapter 67, pp. subtotal/total gastrectomy sections

Surgical Anatomy of the Stomach & Bleeding Duodenal Ulcer

1. SURGICAL ANATOMY OF THE STOMACH [2 marks]

Parts and Surfaces

• Cardia - the junction with the oesophagus at the gastro-oesophageal junction
• Fundus - the dome-shaped part above the cardia; lies in contact with the left hemidiaphragm
• Body (corpus) - the largest part, containing parietal (acid-secreting) and chief (pepsinogen-secreting) cells in gastric crypts
• Antrum - the distal part containing G cells (gastrin-producing) and mucus-secreting pyloric glands
• Pylorus - the sphincteric junction with the duodenum

Blood Supply (clinically critical)

• Lesser curvature: Left gastric artery (from coeliac axis) anastomoses with right gastric artery (from common hepatic artery)
• Greater curvature: Right gastroepiploic artery (from gastroduodenal artery) anastomoses with left gastroepiploic artery (from splenic artery)
• Fundus: Vasa brevia (short gastric arteries) from the splenic artery
• Gastroduodenal artery (GDA): Passes behind the first part of the duodenum - directly clinically relevant to bleeding duodenal ulcer. It divides into the superior pancreaticoduodenal artery (anastomoses with the inferior pancreaticoduodenal from SMA) and the right gastroepiploic artery

Venous Drainage

Nerve Supply

• Intrinsic: Myenteric plexus of Auerbach (motility) and submucosal plexus of Meissner (secretion)
• Extrinsic: Vagus nerves (CN X) - anterior and posterior trunks condense from the oesophageal plexus as they pass through the oesophageal hiatus. Efferent fibres mediate receptive relaxation, gastric motility, and acid secretion. The sympathetic supply derives from the coeliac ganglia.

Microscopic Anatomy (surgical relevance)

2. CLINICAL FEATURES OF BLEEDING DUODENAL ULCER [2 marks]

• Haematemesis - vomiting of bright red blood or coffee-ground material (blood altered by gastric acid)
• Melaena - passage of black, tarry, offensive stools; indicates upper GI bleeding proximal to the ligament of Treitz
• Haematochezia - fresh rectal bleeding; implies massive bleeding (>1000 mL) with rapid transit
• Previous dyspeptic history - epigastric pain, heartburn, use of NSAIDs/aspirin, prior PUD, H. pylori infection
• Syncope or presyncope - indicates significant haemodynamic compromise

• Haemodynamic instability: Tachycardia (pulse >100/min), hypotension (SBP <100 mmHg), postural hypotension, pallor, cold clammy peripheries - indicating >20-30% blood volume loss
• Epigastric tenderness on examination
• Signs of shock in massive bleeding: altered consciousness, oliguria, metabolic acidosis
• Stigmata of chronic liver disease should be sought to exclude variceal bleeding

• Posteroinferior location of ulcer (erodes GDA)
• Age >60 years
• Hypovolemic shock at presentation
• Haematemesis with fresh blood
• Active bleeding at endoscopy (arterial jet)
• Ulcer size >2 cm
• Comorbid illness

3. EVALUATION (INVESTIGATION) [2 marks]

Initial Assessment and Resuscitation (concurrent)

• Two large-bore IV cannulae; aggressive fluid resuscitation with crystalloids/colloids
• Blood for: FBC, U&E, LFTs, coagulation screen, group & crossmatch (at least 4-6 units)
• ABG if haemodynamically compromised
• Urinary catheterisation - monitor urine output as marker of renal perfusion
• Nasogastric tube - to confirm blood in stomach, decompress, and monitor further bleeding

Risk Stratification Scores

• Clinical Rockall score (pre-endoscopy) of 0 = low risk; complete score ≤2 = low risk for rebleeding/death
• Glasgow-Blatchford Score (GBS): uses BUN, Hb, SBP, pulse, melaena, syncope, hepatic disease, cardiac failure; score 0 = safe for outpatient management

Endoscopy (EGD) - the key investigation

• Should be performed within 24 hours of presentation (within 12 hours if haemodynamically unstable after resuscitation)
• Confirms the source of bleeding (rules out varices, Mallory-Weiss tear)
• Forrest Classification guides endoscopic management:

Other Investigations

• CT angiography - if endoscopy fails to identify source or control bleeding; detects active bleeding at rates >0.5 mL/min
• Formal angiography - if CT angiography positive; allows therapeutic embolisation
• ECG and chest X-ray - baseline cardiac/pulmonary assessment

4. MANAGEMENT [4 marks]

A. Initial Resuscitation

• Airway protection (consider intubation if active haematemesis and altered consciousness)
• Restore circulating volume: IV crystalloids initially, then blood products (target Hb ≥7-8 g/dL; ≥9-10 g/dL in cardiac disease)
• Correct coagulopathy: FFP, platelet transfusions if required
• IV Proton Pump Inhibitor: Omeprazole/pantoprazole 80 mg IV bolus then 8 mg/hr infusion - reduces rebleeding by maintaining intragastric pH >6 and stabilising clot
• Withhold anticoagulants/antiplatelet agents where possible; reverse if life-threatening bleeding
• Surgical consultation is mandatory from the outset

B. Endoscopic Therapy (first-line haemostatic treatment)

• Injection therapy: Dilute adrenaline (epinephrine 1:10,000) injected around the vessel - causes tamponade and vasoconstriction; used as adjunct, not alone
• Thermal coagulation: Bipolar electrocoagulation (BICAP) or heater probe - achieves coaptive coagulation; reduces rebleeding rates
• Mechanical clips: Haemoclips applied across the bleeding vessel; Over-the-scope clips (OTSC) are superior for recurrent/refractory bleeding
• Dual therapy (injection + thermal/clip) is superior to monotherapy
• A second attempt at endoscopic haemostasis for rebleeding is as effective as surgery with fewer complications and is recommended

C. Medical Management post-endoscopy

• Continue high-dose IV PPI for 72 hours, then oral PPI
• H. pylori eradication (triple therapy): rebleeding reduced from 20% to 3% after successful eradication
• Stop NSAIDs; if unavoidable, use COX-2 inhibitor + long-term PPI
• Long-term PPI if chronic aspirin/anticoagulants required

D. Interventional Radiology

• Transcatheter arterial embolisation (TAE) - salvage option when endoscopic control fails; embolises the gastroduodenal artery or its branches; avoids surgical risk in high-risk patients

E. Surgical Management

• Massive haemorrhage unresponsive to initial endoscopic control
• Recurrent haemorrhage after two attempts at endoscopic therapy
• Ongoing bleeding requiring >4 units blood in 24 hours or >8 units in 48 hours
• Haemodynamic instability/shock unresponsive to resuscitation
• Concomitant perforation or obstruction

1. Oversewing (suture ligation) of the bleeding vessel - the most commonly performed emergency procedure:
   • Longitudinal pyloroduodenotomy or duodenotomy for exposure
   • Kocher maneuver first - reduces tension and allows manual haemorrhage control with the left hand (fingers behind pancreatic head, thumb anterior)
   • U-stitch or figure-of-eight sutures placed in the ulcer base using heavy material - controls the GDA, its superior pancreaticoduodenal branch, and the transverse pancreatic branch (important to include all three)
   • Closure of pylorotomy as a pyloroplasty (Heineke-Mikulicz)
   • Higher rebleeding rate but lower operative mortality than resection; 30-day mortality ~27%
2. Oversewing + Vagotomy and Drainage (V+D) - preferred definitive operation if patient is haemodynamically stable and surgeon experienced:
   • Truncal vagotomy + pyloroplasty
   • 30-day postoperative mortality ~12% (NSQIP data)
   • Reduces acid secretion and rebleeding risk
3. Vagotomy and Antrectomy (V+A) - lowest rebleeding rate but highest operative morbidity:
   • Reserved for haemodynamically stable, low-risk patients
   • Billroth II gastrojejunostomy for reconstruction
   • Large posterior duodenal ulcers may need to be left in the duodenal stump with suture haemostasis and secure stump closure + omental buttress + duodenostomy decompression
   • 30-day mortality ~23%; rarely performed today

F. Postoperative Management

• High-dose PPI in early postoperative period (reduces rebleeding)
• Early rebleeding evaluated with EGD + CT/formal angiography
• H. pylori eradication if not yet treated
• Long-term smoking cessation; avoid NSAIDs
• If NSAIDs medically necessary: COX-2 inhibitor + PPI

• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, pp. 1170-1172
• Schwartz's Principles of Surgery 11e, Ch. 26, pp. 1154-1161
• Mulholland & Greenfield's Surgery 7e, Ch. 45, pp. 2262-2263
• Current Surgical Therapy 14e, Ch: Surgery for Bleeding Duodenal Ulcer, pp. 132-133

Surgical Anatomy of the Stomach & Bleeding Duodenal Ulcer

1. SURGICAL ANATOMY OF THE STOMACH [2 marks]

Parts and Curvatures

• Cardia - oesophagogastric junction
• Fundus - dome above the cardia, in contact with the left hemidiaphragm
• Body (corpus) - largest part; contains parietal cells (HCl via H+/K+-ATPase) and chief cells (pepsinogen)
• Antrum - distal part; contains G cells (gastrin) and mucus-secreting pyloric glands
• Pylorus - sphincteric junction with the duodenum

Blood Supply (surgically critical)

Venous Drainage

Nerve Supply

• Intrinsic: Myenteric plexus of Auerbach (motility) and submucosal plexus of Meissner (secretion)
• Extrinsic: Vagus nerves (CN X) - the oesophageal plexus condenses into anterior and posterior trunks passing through the oesophageal hiatus. Efferent fibres mediate receptive relaxation, gastric motility, and acid secretion (cephalic phase). Sympathetic supply from the coeliac ganglia.

Microscopic Anatomy

2. CLINICAL FEATURES OF BLEEDING DUODENAL ULCER [2 marks]

• Haematemesis - vomiting of fresh red blood (brisk bleeding) or coffee-ground material (blood altered by gastric acid, slower bleed)
• Melaena - black, tarry, foul-smelling stools; characteristic of upper GI bleeding proximal to the ligament of Treitz
• Haematochezia - fresh rectal bleeding; indicates massive haemorrhage (>1000 mL) with rapid transit
• Prior dyspeptic history, NSAID/aspirin use, known H. pylori infection, smoking
• Syncope or presyncope - indicates significant haemodynamic compromise

• Haemodynamic instability: Tachycardia (>100/min), hypotension (SBP <100 mmHg), postural hypotension, pallor, cold clammy peripheries - indicating >20-30% blood volume loss
• Epigastric tenderness
• Signs of shock in massive bleeding: altered consciousness, oliguria
• Stigmata of chronic liver disease should be sought to exclude variceal bleeding as the source

• Posterior duodenal location (erodes GDA)
• Age >60 years
• Haemodynamic shock at presentation
• Active arterial bleeding at endoscopy
• Ulcer size >2 cm
• Significant comorbidity

3. EVALUATION [2 marks]

Resuscitation (simultaneous with evaluation)

• Two large-bore IV cannulae; aggressive IV fluid resuscitation
• Blood: FBC, U&E, LFTs, coagulation screen, group & crossmatch (4-6 units)
• Urinary catheter to monitor urine output
• Nasogastric tube to confirm blood in stomach, decompress, and monitor ongoing bleeding

Risk Stratification

• Clinical (pre-endoscopy) Rockall score = 0 → low risk; complete score ≤2 → low risk for rebleeding/death
• Glasgow-Blatchford Score (GBS): incorporates BUN, Hb, SBP, pulse, melaena, syncope, hepatic/cardiac disease; GBS = 0 is safe for outpatient management

Endoscopy (OGD) - the key investigation

• Performed within 24 hours of presentation (within 12 hours if haemodynamically unstable after resuscitation)
• Confirms bleeding source, excludes varices
• Forrest Classification guides endoscopic treatment decision:

Further Investigations

• CT angiography - detects active bleeding >0.5 mL/min; used when endoscopy fails or is non-diagnostic
• Formal angiography - if CT positive; allows therapeutic embolisation
• ECG and chest X-ray for baseline cardiopulmonary assessment

4. MANAGEMENT [4 marks]

A. Resuscitation

• Airway protection (consider intubation if active haematemesis + altered consciousness)
• Restore circulating volume: IV crystalloids initially, then blood (target Hb ≥7 g/dL; ≥9-10 g/dL in cardiac disease)
• Correct coagulopathy: FFP, platelets as needed
• IV PPI: Omeprazole/pantoprazole 80 mg IV bolus then 8 mg/hr infusion - maintains intragastric pH >6, stabilises clot, reduces rebleeding
• Withhold/reverse anticoagulants and antiplatelet agents in life-threatening bleeding
• Mandatory early surgical consultation

B. Endoscopic Haemostasis (first-line treatment for Forrest Ia, Ib, IIa, IIb)

• Injection therapy: Dilute adrenaline (1:10,000) injected around the vessel - tamponade + vasoconstriction; used as adjunct only (not monotherapy)
• Thermal coagulation: Bipolar electrocoagulation (BICAP) or heater probe - coaptive coagulation of vessel
• Mechanical clips: Haemoclips or over-the-scope clips (OTSC) - superior for recurrent/refractory bleeding; OTSC shown to be more effective than standard haemoclipping in randomised trials
• Dual therapy (injection + thermal or clip) is superior to monotherapy
• A second attempt at endoscopic haemostasis for rebleeding is recommended before surgery - equally effective with fewer complications

C. Medical Management (post-endoscopy)

• High-dose IV PPI for 72 hours, then oral PPI
• H. pylori eradication (triple therapy - PPI + amoxicillin + clarithromycin): reduces rebleeding from 20% to 3%
• Discontinue NSAIDs; if unavoidable, use COX-2 inhibitor + long-term PPI
• Long-term PPI if chronic aspirin or anticoagulants required; smoking cessation

D. Interventional Radiology (salvage after failed endoscopy)

• Transcatheter arterial embolisation (TAE) of the GDA or its branches
• Avoids surgical risk in high-risk/elderly patients; preferred in centres with 24-hour IR availability

E. Surgical Management

• Massive haemorrhage unresponsive to initial endoscopic control
• Recurrent haemorrhage after two attempts at endoscopic therapy
• Ongoing bleeding requiring >4 units blood in 24 hours or >8 units in 48 hours
• Haemodynamic shock unresponsive to resuscitation
• Concurrent perforation or obstruction

• Longitudinal pyloroduodenotomy or duodenotomy for exposure
• Kocher manoeuvre first - reduces tension and allows manual haemorrhage control (left hand: long fingers behind pancreatic head, thumb anterior)
• U-stitch or figure-of-eight sutures with heavy material in the ulcer base, securing the GDA proximally, distally, and the transverse pancreatic branch (3-point ligation)
• Abrade ulcer bed with sucker tip to confirm secure haemostasis
• Close pylorotomy as a Heineke-Mikulicz pyloroplasty
• Operative mortality ~27% (NSQIP); higher rebleeding rate but lowest operative morbidity

• Truncal vagotomy + pyloroplasty
• Reduces acid secretion and rebleeding risk
• 30-day operative mortality ~12% (NSQIP data) - significantly lower than oversewing alone

• Reserved for haemodynamically stable, low-risk patients where exposure is straightforward
• Billroth II gastrojejunostomy for reconstruction
• Large posterior ulcers may need to be left in duodenal stump with suture haemostasis + secure stump closure + omental buttress + duodenostomy decompression tube
• 30-day mortality ~23%; rarely performed today given availability of PPIs and H. pylori treatment

F. Postoperative Management

• High-dose PPI in early postoperative period
• H. pylori eradication if not yet completed
• Early rebleeding: evaluate with OGD + CT/formal angiography
• Long-term smoking cessation; avoid NSAIDs

• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, pp. 1170-1172
• Schwartz's Principles of Surgery 11e, Ch. 26, pp. 1154-1161
• Mulholland & Greenfield's Surgery 7e, Ch. 45, pp. 2262-2263
• Current Surgical Therapy 14e, Surgery for Bleeding Duodenal Ulcer, pp. 132-133

Differentiation Between Gastric Ulcer and Duodenal Ulcer

Johnson Classification of Gastric Ulcers (surgical relevance)

Key Points for Exam

• "No acid, no ulcer" - both require acid but the mechanism differs: GU has defective defence; DU has excess acid
• Duodenal ulcers are more common, occur in younger patients, cause night pain relieved by food, and are never malignant
• Gastric ulcers occur in older patients, cause food-related pain, are associated with NSAIDs, and must always be biopsied to exclude malignancy
• Both are principally caused by H. pylori, and eradication is the cornerstone of treatment
• A perforated anterior DU spills into the peritoneal cavity (surgical emergency); a perforated posterior DU penetrates into the pancreas

• Sabiston Textbook of Surgery 21e, Ch. 86, pp. 1771-1800
• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, pp. 1173-1177
• S. Das Manual on Clinical Surgery 13e, Ch. 34, pp. 491-495

Causes of Gastric Outlet Obstruction (GOO)

A. MALIGNANT CAUSES (50-80% of GOO in developed countries - now the commonest overall)

1. Carcinoma of the stomach (antral/pyloric carcinoma) - commonest single malignant cause
2. Carcinoma of the pancreas - local extension into the duodenum/pyloric region
3. Gastric lymphoma (primary)
4. Proximal duodenal carcinoma (D1/D2)
5. Ampullary carcinoma (carcinoma of the ampulla of Vater)
6. Gallbladder/biliary tree carcinoma - local extension
7. Gastric carcinoid tumour
8. Metastatic disease to the gastric antrum or duodenum (e.g., from breast, lung, melanoma)

B. BENIGN CAUSES

1. Peptic Ulcer Disease (~5% in developed countries; still 50-60% in low/middle-income countries)

• Chronic duodenal ulcer with fibrosis and scarring of D1 (the classical cause)
• Pyloric channel ulcer with oedema + fibrosis
• Gastric ulcer of the antrum/prepyloric region

2. Inflammatory and Infiltrative Conditions

• Crohn's disease involving the stomach or duodenum (~5% of GOO)
• Chronic pancreatitis with fibrosis compressing the duodenum (1-5%)
• Large pancreatic pseudocyst - external compression of the duodenum
• Acute severe pancreatitis - oedema and inflammation
• Cholecystitis - adjacent inflammation (rare)
• Eosinophilic gastroenteritis - submucosal infiltration
• Gastric tuberculosis - granulomatous inflammation and stricture
• Sarcoidosis / amyloid infiltration of the gastric wall
• Strongyloides infection (in endemic areas)

3. Congenital Causes

• Infantile hypertrophic pyloric stenosis (IHPS) - hypertrophy of the pyloric musculature; commonest surgical emergency in infancy
• Adult hypertrophic pyloric stenosis - rare adult form
• Annular pancreas - encircles the second part of the duodenum, may present in adulthood
• Duodenal webs / membranes - congenital obstruction
• Duodenal atresia - complete obstruction (neonatal)
• Ectopic pancreas in the pyloric/duodenal wall

4. Vascular

• Superior mesenteric artery (SMA) syndrome (Wilkie's syndrome) - compression of D3 by the SMA

5. Mechanical / Miscellaneous

• Bouveret syndrome - impaction of a gallstone in the pyloric channel or duodenum following migration through a cholecystoduodenal/cholecystogastric fistula
• Gastric bezoars - phytobezoar, trichobezoar causing pyloric/antral obstruction
• Large pedunculated gastric polyp prolapsing into the pylorus
• Gastric volvulus - organoaxial or mesenteroaxial rotation causing obstruction
• Caustic ingestion - stricture formation after acid/alkali ingestion
• Migration of a PEG tube (buried bumper syndrome) causing intraluminal obstruction
• Post-surgical complications - anastomotic stricture, stomal stenosis, afferent loop obstruction after Billroth II
• Duodenal haematoma - after blunt abdominal trauma (especially in children)
• Radiation stricture - after radiotherapy to the upper abdomen

Summary by Mechanism

Key Clinical Points

• In the current era, malignancy (especially pancreatic and gastric carcinoma) is the commonest cause of GOO in developed countries and must be assumed until excluded by endoscopic biopsy
• Benign pyloric stenosis from chronic PUD should be a diagnosis of exclusion
• The characteristic metabolic abnormality of benign GOO (repeated vomiting of HCl-rich fluid) is hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria
• Zollinger-Ellison syndrome is associated with GOO in ~10% of cases (severe acid hypersecretion causing multiple, refractory duodenal ulcers)

• Yamada's Textbook of Gastroenterology 7e, Table 49.8, p. 1042
• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, p. 1190
• Current Surgical Therapy 14e, Gastric Outlet Obstruction, p. 132

Investigations to Diagnose Gastric Outlet Obstruction (GOO)

I. LABORATORY INVESTIGATIONS

1. Serum electrolytes (Na+, K+, Cl-) - the hallmark is hypochloraemic, hypokalaemic metabolic alkalosis due to repeated vomiting of HCl-rich gastric contents; low chloride and low potassium
2. Arterial blood gas (ABG) - confirms metabolic alkalosis (raised pH, raised HCO3-, raised base excess); paradoxical aciduria in late stages as kidneys excrete H+ to conserve Na+
3. Serum urea and creatinine - elevated if pre-renal acute kidney injury from dehydration
4. Serum calcium - may be low (alkalosis reduces ionised calcium → tetany)
5. Full blood count (FBC) - anaemia from chronic blood loss or malnutrition; raised WCC if infective cause
6. Liver function tests + serum albumin - hypoalbuminaemia reflects chronic malnutrition; LFTs relevant if biliary/hepatic malignancy suspected
7. Serum amylase/lipase - if pancreatitis is a suspected cause
8. Tumour markers - CA 19-9 (pancreatic cancer), CEA, CA 72-4 (gastric cancer) - useful when malignancy is suspected, though not diagnostic alone
9. H. pylori testing (when stable) - urea breath test or stool antigen; serology for prevalence assessment

II. BEDSIDE / CLINICAL TESTS

1. Succussion splash (clinical) - auscultate over the epigastrium while rocking the patient side-to-side; audible splash >3 hours after last oral intake confirms large volume gastric residue
2. Saline load test (historical/occasionally used) - 750 mL of normal saline instilled via NGT; aspiration of >400 mL at 30 minutes suggests mechanical obstruction; aspiration <200 mL suggests resolution after treatment

III. IMAGING INVESTIGATIONS

A. Plain X-rays

1. Erect chest X-ray - may show a massively dilated stomach; also rules out pneumoperitoneum (perforation) and pulmonary pathology
2. Plain abdominal X-ray (erect + supine) - shows a large gastric shadow with a fluid level in the left upper quadrant; distended stomach; absence of gas in small bowel distal to obstruction

B. Contrast Studies

1. Barium meal (upper GI series) / water-soluble contrast study (Gastrografin) - demonstrates:

• Dilated, atonic stomach with large gastric residue
• Narrowing at the pylorus or D1
• "Rat-tail" or "apple-core" deformity suggests malignant stricture
• Mucosal pattern of duodenal scarring (cloverleaf deformity) in benign PUD
• Delayed gastric emptying
• Note: Water-soluble contrast preferred if perforation is suspected

C. Ultrasound

1. Abdominal ultrasound - useful initial investigation; shows a distended fluid-filled stomach; can identify pancreatic mass, pseudocyst, gallstones (Bouveret syndrome), hepatic metastases, lymphadenopathy; limited by bowel gas

D. Cross-sectional Imaging (most important for staging and cause)

1. CT scan of abdomen and pelvis (with IV + oral contrast) - the investigation of choice for determining the cause of GOO:

• Identifies the site and level of obstruction
• Shows pancreatic carcinoma, gastric carcinoma, lymphoma
• Demonstrates lymphadenopathy, liver metastases, peritoneal disease (staging)
• Identifies pancreatic pseudocysts, annular pancreas, aortic/SMA compression
• Guides decision between curative and palliative management

1. CT angiography / MRI - if SMA syndrome suspected; demonstrates reduced aortomesenteric angle
2. PET-CT - for staging of malignancy if surgery is being considered

IV. ENDOSCOPIC INVESTIGATIONS (most important for definitive diagnosis)

1. Upper GI endoscopy (OGD) - the key investigation; performed after gastric decompression with NGT:

• Directly visualises the antrum, pylorus, and duodenum
• Identifies the cause: ulcer disease, malignant mass, web, Crohn's stricture
• Biopsy is mandatory - multiple biopsies from the stricture edge to exclude malignancy (gastric cancer can mimic benign pyloric stenosis)
• Can be therapeutic (balloon dilatation, stent insertion)

1. Endoscopic ultrasound (EUS) - when CT and OGD biopsies are inconclusive:

• Gives detailed imaging of the gastric wall layers and peri-gastric/peripancreatic structures
• Enables EUS-guided fine needle aspiration (FNA/FNB) of a mass for histology
• Particularly useful for submucosal lesions, GIST, and lymphoma

1. Gastric emptying scintigraphy (radionuclide study) - useful to distinguish mechanical GOO from functional gastroparesis (diabetic, postsurgical); not required if mechanical cause is obvious on imaging/endoscopy

Summary: Stepwise Approach

• Yamada's Textbook of Gastroenterology 7e, Ch. 49, p. 1041-1042
• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, p. 1190
• Current Surgical Therapy 14e, Gastric Outlet Obstruction, p. 132

Management of Pyloric Stenosis

PART A: INFANTILE HYPERTROPHIC PYLORIC STENOSIS (IHPS)

Background

• Incidence: ~1 in 300 live births; presents at 3-6 weeks of age
• Male predominance: M:F = 5:1
• Caused by progressive hypertrophy of the pyloric musculature → complete GOO
• Presents with projectile, non-bilious vomiting, hunger, dehydration, weight loss

Step 1: Resuscitation and Metabolic Correction (ALWAYS before surgery)

• IV fluid resuscitation: 5% dextrose + 0.45% normal saline + KCl (2-4 mEq/kg over 24 hours) at ~150-175 mL/kg/24 hours
• Monitoring: Urine output >2 mL/kg/hour confirms adequate rehydration
• Criteria for safe anaesthesia:
  • Serum chloride >100 mEq/L
  • Serum bicarbonate <30 mEq/L
  • Serum potassium >3.5 mEq/L
  • Normal urine output
• NGT for gastric decompression during resuscitation period

Step 2: Definitive Surgery - Fredet-Ramstedt Pyloromyotomy

1. Deliver the pylorus into the wound (or into the laparoscopic field)
2. Make a longitudinal seromuscular incision from just proximal to the pyloric vein of Mayo (marks the pyloroduodenal junction - critical landmark to avoid duodenal perforation) extending proximally 1-2 cm onto the gastric antrum
3. Spread the incised muscle down to the submucosal plane using a spreader/haemostat until the mucosa bulges freely through the entire length of the incision
4. Check for mucosal perforation - insufflate air via NGT and look for bubbles; perform duodenal milking test
5. If perforation occurs: repair mucosa with absorbable suture; reapproximate serosa; leave NGT 24 hours; rotate the pyloromyotomy 180° and repeat if needed (or close and allow healing)

• IV fluids for several hours post-op
• Start oral Pedialyte/electrolyte solution, then escalate to formula/breast milk
• Target 60 mL every 3 hours; most infants tolerate ad lib feeds
• Discharge: 24-48 hours post-operatively

• Mucosal perforation (1-3%) - commonest; usually at duodenal end
• Inadequate myotomy → recurrent symptoms
• Wound infection
• Bleeding
• Incomplete division → persistent GOO requiring re-operation

PART B: ADULT PYLORIC STENOSIS (Benign - Peptic Ulcer Disease)

Step 1: Initial Assessment and Resuscitation

• Hypochloraemic, hypokalaemic metabolic alkalosis - correct with IV isotonic (0.9%) saline + KCl
• Replacing NaCl and water allows the kidney to auto-correct the acid-base abnormality
• Monitor electrolytes, urine output, renal function
• Correct nutritional deficits: enteral (nasojejunal tube) or parenteral nutrition in severely malnourished patients

• Large-bore nasogastric or orogastric tube with lavage until stomach is completely emptied (may require repeated washes - the stomach can hold litres of stagnant food)
• This allows subsequent endoscopy and contrast imaging

• Test (urea breath test or antral biopsy at endoscopy)
• Eradicate if positive: triple therapy (PPI + amoxicillin + clarithromycin × 14 days)
• IV/high-dose oral PPI to reduce acid secretion and allow oedema to resolve

Step 2: Medical Trial

• Duration of medical trial: typically 5-7 days of NGT decompression + PPI
• Serial saline load tests can monitor improvement (<200 mL residual at 30 min = resolution)

Step 3: Endoscopic Management

• Performed via OGD using through-the-scope (TTS) balloon catheters
• Serial dilatations (typically to 12-15 mm) may be required
• Effective in ~50% of patients with benign pyloric stenosis; may delay surgery for 1-2 years
• Best suited to early, predominantly oedematous stenosis; less effective in fibrotic strictures
• Must be combined with anti-ulcer therapy and H. pylori eradication

• Self-expanding metallic stent (SEMS)
• Reserved for malignant GOO as palliation (unresectable pancreatic/gastric cancer) or as bridge to surgery
• Not appropriate for benign stenosis long-term (stent migration, overgrowth)

Step 4: Surgical Management

• Medical therapy and EBD fail or are inappropriate
• Fibrotic/organic obstruction on imaging or endoscopy
• Malignancy cannot be excluded
• Recurrent obstruction after dilatation

• Removes the obstructing antrum/pylorus + eliminates acid drive
• Reconstruction: Billroth II gastrojejunostomy (antecolic, isoperistaltic)
• Advantages: lowest ulcer recurrence, confirms benign pathology by specimen histology
• Disadvantage: higher operative mortality (~2%), technically demanding with difficult duodenal stump
• Chronically obstructed stomach has thick walls - use larger staple cartridges
• If duodenal stump closure is difficult: lateral duodenostomy, nasogastric/retrograde jejunostomy for decompression; omental buttress

• Truncal vagotomy + posterior gastrojejunostomy (drainage procedure without resection)
• Advantages: lower operative mortality, reversible if severe dumping, readily laparoscopic
• Disadvantages: obstructing cancer may be missed; risk of marginal ulceration
• Suitable when duodenal dissection is hazardous (densely adherent, inflamed)

• Preserves antral innervation; lower dumping/diarrhoea rates
• Reserved for elective, fit patients with minimal operative risk

• For functional/early stenosis with minimal scarring; rarely used in true fibrotic stenosis
• Often combined with truncal vagotomy

PART C: MALIGNANT PYLORIC STENOSIS

• Resectable disease: Curative resection - distal gastrectomy (gastric cancer) or Whipple's procedure (pancreatic/duodenal cancer)
• Unresectable/metastatic disease - Palliation:
  • Endoscopic duodenal stent (SEMS): Quicker symptom relief; preferred in patients with poor performance status or short expected survival
  • Surgical gastrojejunostomy (palliative bypass): More durable; preferred in patients with better performance status and longer expected survival; can be done laparoscopically
  • Chemotherapy ± radiotherapy per oncology protocol

Summary Algorithm

PYLORIC STENOSIS
├── INFANT (IHPS)
│   ├── Correct metabolic alkalosis (IV saline + KCl)
│   └── Fredet-Ramstedt pyloromyotomy (open/laparoscopic)
│
└── ADULT
    ├── Correct alkalosis + NGT decompression + IV PPI + H. pylori Rx
    ├── Medical trial (5-7 days) → resolve? → long-term PPI
    ├── Not resolved → Endoscopic balloon dilatation (serial)
    └── Failed/fibrotic/malignant → SURGERY
        ├── Benign: V+A (gold standard) or V+GJ (high-risk)
        └── Malignant: Resection OR palliation (stent/GJ bypass)

• Schwartz's Principles of Surgery 11e, Ch. 39, pp. 1749-1750 (IHPS)
• Current Surgical Therapy 14e, Surgery for Obstructing Duodenal Ulcer, pp. 132-134
• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, p. 1190

Stage II Carcinoma of the Stomach: Clinical Presentation, Investigations, and Management

TNM STAGING - WHAT IS STAGE II?

• T1a: Invades lamina propria or muscularis mucosae
• T1b: Invades submucosa
• T2: Invades muscularis propria
• T3: Involves subserosa (without serosa breach)
• T4a: Perforates serosa (visceral peritoneum)
• T4b: Invades adjacent structures

• N0: No nodal metastasis
• N1: 1-2 regional nodes
• N2: 3-6 regional nodes
• N3a: 7-15 nodes; N3b: ≥16 nodes

1. CLINICAL PRESENTATION

Symptoms (in order of frequency):

• Epigastric pain or discomfort - persistent, often dull, not relieved by antacids or food
• Dyspepsia / indigestion - may be indistinguishable from peptic ulcer disease early on
• Early satiety - due to loss of gastric compliance (diffuse infiltration) or tumour bulk reducing reservoir capacity
• Anorexia - common; often precedes significant weight loss
• Nausea and vomiting - especially with antral/pyloric tumours causing partial GOO
• Dysphagia - if tumour is at or near the gastro-oesophageal junction (GOJ)
• Haematemesis / melaena - from tumour ulceration and bleeding; may present as iron deficiency anaemia

• Weight loss - significant, often >10% body weight; due to anorexia, malabsorption, cancer cachexia
• Fatigue - from anaemia (chronic blood loss) or systemic effects of malignancy

Signs (may be absent in early stage II):

• Epigastric mass - may be palpable in thin patients with larger tumours
• Epigastric tenderness on palpation
• Succussion splash - if pyloric involvement causing partial GOO

• Troisier's sign / Virchow's node - palpable left supraclavicular lymph node (Troisier's sign); indicates involvement of the thoracic duct → technically N+ but distant nodal spread is M1
• Sister Mary Joseph's nodule - umbilical nodule from peritoneal spread (more advanced)

• Trousseau's sign - migratory thrombophlebitis (hypercoagulable state from malignancy)
• Pallor (anaemia), cachexia
• Acanthosis nigricans - black velvety skin in flexures (rare paraneoplastic)

2. INVESTIGATIONS

A. To Confirm Diagnosis

1. Upper GI endoscopy (OGD) - key investigation
   • Visualises tumour: ulcerating, polypoid, infiltrating (linitis plastica)
   • Multiple biopsies (≥8) from the edge and floor of the lesion - mandatory for histological confirmation
   • Biopsies of adjacent antral mucosa for H. pylori
   • Endoscopic classification: Borrmann types I-IV (macroscopic); Japanese early gastric cancer types
2. Biopsy and histopathology - confirms adenocarcinoma; Lauren classification:
   • Intestinal type (well-differentiated, glandular; H. pylori-related; better prognosis)
   • Diffuse type (poorly differentiated, signet ring cells; worse prognosis; CDH1 mutation in hereditary diffuse GC)

B. Staging Investigations

1. CT scan of chest, abdomen and pelvis (with IV contrast - triphasic) - primary staging tool:
   • Assesses T stage (wall invasion depth), N stage (lymphadenopathy), M stage (liver metastases, lung, peritoneal disease)
   • Distinguishes resectable from metastatic disease
2. PET-CT (FDG-PET) - recommended for T2 or above:
   • Detects occult distant metastases not seen on CT
   • Assesses response to neoadjuvant chemotherapy
   • Note: FDG-PET has limited sensitivity for diffuse/signet ring cell type (low FDG uptake)
3. Endoscopic ultrasound (EUS) - most accurate for local T and N staging:
   • Assesses depth of wall invasion (T stage) and perigastric node involvement
   • EUS-FNA of suspicious nodes for cytological confirmation
   • Particularly important when surgical planning depends on precise T stage
4. Diagnostic laparoscopy (with peritoneal washings):
   • Recommended for all patients with locoregional (potentially resectable) disease (T1b or above) before curative surgery
   • Detects peritoneal metastases not visible on CT (~20-30% of "stage II/III" patients on CT have peritoneal disease at laparoscopy)
   • Positive peritoneal cytology = M1 disease (stage IV)

C. Haematological and Biochemical Investigations

1. FBC - microcytic anaemia (chronic blood loss); baseline
2. Serum albumin and total protein - nutritional assessment; hypoalbuminaemia indicates poor nutritional status
3. LFTs + bilirubin - baseline; may indicate liver involvement
4. Urea and electrolytes, creatinine - baseline renal function; important pre-chemotherapy
5. Coagulation studies - pre-operative
6. Blood group and crossmatch - pre-operatively

D. Tumour Markers

1. CEA (carcinoembryonic antigen) - elevated in ~30-40%; useful for monitoring response and recurrence, not diagnostic
2. CA 19-9 - may be elevated; useful in combination with CEA
3. CA 72-4 - more specific for gastric cancer than CEA; useful in monitoring
4. HER2 testing (IHC/FISH) on biopsy - mandatory: ~15-20% of gastric adenocarcinomas overexpress HER2; determines eligibility for trastuzumab (ToGA regimen)
5. PD-L1 (CPS score) - important for immunotherapy eligibility (pembrolizumab)
6. Microsatellite instability (MSI) testing - MSI-H tumours respond to checkpoint inhibitors

E. Cardiopulmonary Assessment (pre-operative)

1. ECG, chest X-ray - baseline
2. Echocardiogram / pulmonary function tests - if cardiac/respiratory comorbidity; particularly if using anthracycline-based chemotherapy (epirubicin)

3. MANAGEMENT

A. Perioperative (Neoadjuvant + Adjuvant) Chemotherapy

• Fluorouracil + Leucovorin + Oxaliplatin + Docetaxel (FLOT)
• 4 pre-operative cycles + 4 post-operative cycles
• Based on the FLOT4 trial: FLOT showed median OS of 50 months vs 35 months for the older ECF (epirubicin + cisplatin + 5-FU) regimen; significantly improved R0 resection rates and pathological response

• ECF/ECX (epirubicin + cisplatin + 5-FU or capecitabine) - based on MAGIC trial
• 3 pre-op + 3 post-op cycles; improved 5-year survival from 23% to 36%

• Downstages tumour (reduces T and N stage)
• Eliminates occult micrometastases
• Tests chemo-sensitivity
• Improves R0 resection rates
• Practical issue: <50% of patients in trials received the full post-operative component; hence emphasis on completing pre-operative cycles

B. Surgical Resection - the only curative treatment

• Proximal margin: ≥5 cm for diffuse type; ≥3 cm for intestinal type (or 2 cm for T1)
• Frozen section of margins performed intraoperatively if margin status uncertain

• D2 lymphadenectomy is the standard of care in curative-intent surgery (Japan, Korea, Europe)
• Removes perigastric nodes (stations 1-6) + nodes along the coeliac axis, left gastric, common hepatic, and splenic arteries (stations 7-11)
• Goal: ≥16 lymph nodes examined (NCCN) to ensure adequate staging
• Spleen-preserving D2 is standard; splenectomy added only if direct splenic or splenic hilar (station 10) involvement

• After subtotal gastrectomy: Billroth I (gastroduodenostomy) or Roux-en-Y gastrojejunostomy
• After total gastrectomy: Roux-en-Y oesophagojejunostomy (alimentary limb ≥50 cm to prevent bile reflux)

• Laparoscopic or robotic gastrectomy: equivalent oncological outcomes to open surgery for early and locally advanced disease; less blood loss, shorter hospital stay; increasing use globally

C. Adjuvant Therapy (post-operative)

1. Adjuvant chemotherapy (after surgery-first approach if neoadjuvant not given):
   • Capecitabine + oxaliplatin (CAPOX) for 6 months - CLASSIC trial (Asia)
   • S-1 (oral fluoropyrimidine) for 1 year - ACTS-GC trial (Japan)
2. Chemoradiotherapy (if R1 resection or D0/D1 surgery):
   • Macdonald protocol (US INT-0116 trial): 5-FU/leucovorin + 45 Gy radiotherapy post-operatively
   • Currently used mainly when D2 dissection not achieved or positive margins
3. Targeted therapy:
   • Trastuzumab (anti-HER2): added to chemotherapy in HER2+ tumours (ToGA trial); applicable if metastatic disease develops
   • Pembrolizumab (anti-PD-1): for MSI-H tumours or high PD-L1 CPS; increasingly used in first-line and adjuvant settings

D. Summary of Management Plan for Stage II Gastric Cancer

Stage II Gastric Cancer (M0, potentially resectable)
│
├── Pre-treatment staging: CT chest/abdomen/pelvis + EUS + diagnostic laparoscopy
│
├── Peritoneal cytology negative → PROCEED WITH CURATIVE INTENT
│
├── NEOADJUVANT CHEMOTHERAPY: FLOT × 4 cycles (3 months)
│
├── Re-staging CT ± EUS after neoadjuvant
│
├── SURGERY: R0 resection + D2 lymphadenectomy
│   ├── Distal: subtotal gastrectomy
│   └── Proximal/diffuse: total gastrectomy + Roux-en-Y
│
├── ADJUVANT CHEMOTHERAPY: FLOT × 4 cycles (complete perioperative protocol)
│
└── SURVEILLANCE: CT every 6-12 months; OGD at 1 year; nutritional support

Key Points for Exam

• Stage II = locoregional disease (T1-T4a, N0-N3a, M0); potentially curable
• The FLOT4 trial established FLOT as the preferred perioperative regimen (50 vs 35 months median OS vs ECF)
• Diagnostic laparoscopy is mandatory before curative surgery; positive peritoneal cytology = M1 (stage IV) → palliative intent
• D2 lymphadenectomy with ≥16 nodes examined is the surgical standard
• HER2 testing and MSI testing are mandatory at diagnosis for targeted/immunotherapy planning
• 5-year survival for stage II: ~40-65% (varies by substage)

• Bailey & Love's Short Practice of Surgery 28e, Ch. 67, pp. 1191-1197 (Table 67.6, UICC 8th edition TNM)
• Schwartz's Principles of Surgery 11e, Ch. 26, pp. 1145-1160
• Sabiston Textbook of Surgery 21e, Ch. 49 (Gastric Cancer)