Gastric Outlet Obstruction (GOO) - Full Topic: General Surgery Theory & Clinical

1. DEFINITION

2. AETIOLOGY / CAUSES

Benign Causes

Malignant Causes (now the most common overall)

• Carcinoma of the antrum/pylorus - most common malignant cause
• Carcinoma of the head of pancreas / periampullary tumours
• Duodenal carcinoma
• Lymphoma
• Metastatic deposits (e.g., peritoneal carcinomatosis involving the duodenum)

Key Point (Bailey & Love 28e): With the decreasing incidence of PUD, GOO should be considered malignant until proven otherwise.

3. PATHOPHYSIOLOGY

Mechanism of obstruction

• Acute/functional: Oedema around an active peptic ulcer causing reversible outlet narrowing
• Chronic/mechanical: Progressive fibrosis and scarring of the pyloric canal from repeated ulceration/healing cycles - produces fixed, non-reversible stenosis

Metabolic Consequences - HYPOCHLORAEMIC HYPOKALAEMIC METABOLIC ALKALOSIS

1. Repeated vomiting leads to loss of HCl (gastric acid) → primary hypochloraemia and alkalosis
2. Early: Urine has low Cl⁻, high HCO₃⁻ (renal compensation for alkalosis)
3. Progressive dehydration → sodium and water conservation by kidneys → aldosterone activated
4. Aldosterone promotes Na⁺ retention with K⁺ and H⁺ excretion in distal tubule
5. Result: Paradoxical aciduria (urine becomes acidic despite systemic alkalosis) + hypokalaemia
6. Alkalosis → decreased ionised calcium → tetany (Trousseau's/Chvostek's signs)

4. CLINICAL FEATURES

Symptoms

• Vomiting - the cardinal symptom:
  • Projectile, large volume
  • Non-bilious (obstruction proximal to duodenal entry of bile duct)
  • Contains undigested food eaten hours or even days earlier
  • Characteristically occurs several hours after meals (often in the evening)
  • Vomiting may bring temporary relief of upper abdominal discomfort
• Epigastric fullness and distension
• Early satiety
• Progressive weight loss
• Anorexia
• Long history of peptic ulcer disease (in benign cases) OR short history with no prior PUD (malignant)

Signs

• Dehydration, cachexia, sunken eyes
• Signs of malnutrition

• Visible gastric peristalsis - left-to-right peristaltic waves visible in epigastrium (more common in thin patients with longstanding obstruction)
• Distended stomach visible as epigastric fullness
• Succussion splash - audible splashing sound heard with stethoscope over epigastrium when patient is gently rocked side-to-side (or by placing the ear near the epigastrium) - indicates retained gastric fluid more than 4 hours after a meal/drink - highly characteristic
• Epigastric tenderness on palpation
• Palpable epigastric mass - if underlying carcinoma

• Hard irregular epigastric mass
• Virchow's node (left supraclavicular lymphadenopathy - Troisier's sign)
• Hepatomegaly (liver metastases)
• Umbilical nodule (Sister Mary Joseph's nodule)
• Krukenberg tumour on pelvic exam
• Ascites (shifting dullness, fluid thrill)

Benign vs Malignant GOO - Clinical Distinction

5. INVESTIGATIONS

Bloods

• FBC - anaemia (chronic disease/blood loss)
• U&E - hypokalaemia, hyponatraemia (late)
• Serum Cl⁻ - low
• ABG - metabolic alkalosis (pH ↑, HCO₃⁻ ↑, BE +ve)
• LFTs - liver metastases
• Serum albumin - nutritional status
• Tumour markers - CA 19-9, CEA (if malignancy suspected)

Endoscopy (OGD) - Most Important Investigation

• Confirms diagnosis, localises obstruction
• Biopsy is mandatory to exclude malignancy (endoscopic biopsy of the area around the pylorus is essential)
• Assesses degree of narrowing
• Can be therapeutic (balloon dilatation)

Imaging

• Plain AXR - massively dilated stomach, often filling most of the upper abdomen; air-fluid level
• Erect CXR - large gastric air bubble
• Barium meal (upper GI series) - shows dilated stomach, narrowed pyloric canal ("rat-tail" appearance in carcinoma, smooth tapered narrowing in benign disease), delayed gastric emptying; the "string sign" in pyloric stenosis
• CT abdomen/pelvis with contrast - investigation of choice for malignant GOO; shows:
  • Gastric distension
  • Site and nature of obstruction
  • Lymphadenopathy
  • Liver metastases
  • Peritoneal disease
• Ultrasound - for pyloric stenosis in neonates (muscle thickness >4mm, canal length >16mm)

6. MANAGEMENT

Step 1 - Resuscitation and Correction of Metabolic Abnormalities (Preoperative)

1. Nil by mouth - stop all oral intake
2. Wide-bore nasogastric tube - gastric lavage and decompression
   • May need orogastric tube if NGT cannot cope with contents
   • Lavage until stomach is completely empty (allows subsequent investigation)
3. IV fluid resuscitation - Isotonic (0.9%) saline with potassium supplementation
   • This replaces the lost NaCl and water, allowing the kidney to independently correct the acid-base abnormality
   • Do NOT use dextrose alone or Hartmann's solution as primary fluid
4. Monitor - strict fluid balance, daily U&E, urine output
5. Nutritional support - NG/NJ feeding or TPN if prolonged period before surgery
6. Acid suppression - IV PPI (omeprazole/pantoprazole)
7. H. pylori eradication - if confirmed positive

Step 2 - Diagnosis (while resuscitating)

• OGD + biopsy, CT scan, barium meal

Step 3 - Definitive Treatment

A. BENIGN GOO (PUD)

• Aggressive PPI therapy + H. pylori eradication
• May resolve oedema-related obstruction in early/acute cases
• Medical therapy can delay surgery for 1-2 years in approximately 50% of patients

• Endoscopic balloon dilatation (EBD) - most useful in early/acute benign obstruction
  • Usually requires multiple sessions
  • Durable response in ~50% of cases
  • Preferred in high surgical-risk patients

• Peritoneum over abdominal oesophagus is incised
• Gastrohepatic ligament opened above hepatic vagal branches
• Anterior vagal trunk identified, clipped, severed - segment sent to histology
• Phrenoesophageal ligament opened along right crus
• Posterior vagus located in retroesophageal space, clipped, severed - sent to histology

• Retrocolic posterior GJ - preferred; posterior wall of distal stomach anastomosed to proximal jejunum, side-to-side, ~50cm from Treitz
• Can be done open or laparoscopically
• Laparoscopic approach allows faster return to systemic oncologic therapy

B. MALIGNANT GOO

• First-line for advanced/unresectable malignancy
• Can be placed as outpatient procedure
• ~90% of patients can tolerate soft/regular diet post-stenting
• Re-intervention possible (covered SEMS within existing uncovered stent)
• If jaundice present: biliary stenting FIRST before duodenal stenting (reverse order makes biliary access very difficult)
• Recent meta-analysis (2026) in Surg Endosc confirms EUS-guided gastroenterostomy is now competitive with stenting for malignant GOO

• Open or laparoscopic retrocolic GJ
• Better long-term patency than SEMS
• Preferred if:
  • Expected survival >3-6 months
  • Patient fit for surgery
  • Neoadjuvant therapy planned (resectable disease)
• Laparoscopic GJ allows earlier start of chemotherapy

• If resectable gastric antral carcinoma - subtotal gastrectomy (Billroth II / Roux-en-Y reconstruction)
• Pancreaticoduodenectomy for resectable periampullary/pancreatic head carcinoma
• 5-year survival in resectable cases: 15-25%

Malignant GOO
  ├── Resectable → Surgical resection (± neoadjuvant)
  ├── Locally advanced, planned neoadjuvant → Laparoscopic GJ + biliary drainage
  ├── Advanced/metastatic, good PS → Duodenal SEMS
  └── Advanced/metastatic, poor PS → Venting gastrostomy / conservative

• Creating a gastrojejunal anastomosis under EUS guidance using a lumen-apposing metal stent (LAMS)
• Systematic review and meta-analysis (Canakis et al, 2026 J Clin Gastroenterol, PMID 39761155) supports its use for both benign and malignant GOO
• Lower re-intervention rates compared to conventional SEMS for malignant GOO

7. COMPLICATIONS OF UNTREATED GOO

• Severe dehydration and electrolyte imbalance
• Malnutrition and cachexia
• Aspiration pneumonia (from vomiting)
• Tetany (from alkalosis-induced hypocalcaemia)
• Renal failure
• Death (in neglected/elderly patients)

8. COMPLICATIONS OF SURGERY

9. SPECIAL SCENARIO - INFANTILE HYPERTROPHIC PYLORIC STENOSIS (IHPS)

• Presents at 2-4 weeks of age (male:female = 4:1)
• Projectile non-bilious vomiting immediately after feeding
• "Olive-shaped" pyloric mass palpable in right epigastrium
• Visible left-to-right gastric peristalsis
• Same metabolic derangement: hypochloraemic hypokalaemic metabolic alkalosis
• Diagnosis: Ultrasound (muscle thickness >4mm, canal length >16mm)
• Treatment: Medical resuscitation FIRST, then Ramstedt's pyloromyotomy (open or laparoscopic)

10. SUMMARY BOX (Exam Rapid Revision)