Gastric outlet obstruction

Section: UGI Sub-section: Gastric

Definition

• The consequence of any disease that mechanically impedes gastric emptying, at the level of the pylorus

Classification

• Benign
  • Previously more common, due to frequency of PUD, now decreasing due to PPIs
• Malignant
  • Now 60% of gastric outlet obstruction cases are due to malignancy
• Clinical Presentation
  • Early satiety
  • Vomiting food (not bile) – usually within 1 hour of a meal
  • Often progressive symptoms
  • Weight loss
  • Epigastric pain / tenderness / fullness
  • Succussion splash
• Differential diagnosis
  • Gastroparesis (e.g. associated with diabetes)
  • More distal obstruction

Aetiology

• Congenital cause:
  • Infantile hypertrophic pyloric stenosis (1:500 births M>F)
  • Annular Pancreas – D2 surrounded by abnormal ring of pancreatic tissue
  • Adult hypertrophic pyloric stenosis
  • Occurs due to chronic antral gastritis / PUD
• Inflammatory
  • PUD (5%)
  • Usually due to duodenal ulceration, causes oedema, muscular spasm, fibrosis
  • Pancreatitis (chronic) or pancreatic pseudocyst
  • Caustic injury
• Infiltrative
  • Infections – eg gastric Tb
  • Crohn’s
  • Amyloidosis
• Iatrogenic
  • PEG tube migration
  • Post-surgery (e.g sleeve gastrectomy, pylorus preserving whipples)
  • Bezoars
  • Gallstone obstruction (Bouveret’s syndrome)
• Neoplasms
  • Benign Polyps
  • Peripancreatic malignancy, Gastric carcinoma, cholangiocarcinoma, GIST, lymphoma

Bouveret’s Syndrome

• Rare cause of gastric outlet obstruction
• Large gallstone impacts on pyloric channel or duodenum
• Need biliary enteric fistula for this to occur
• Formed in the setting of cholecystitis and pericholecystic inflammation
• Similar to gallstone ileus
• More common in females, old and comorbid
• Clinical Presentation
  • Most with gastric outlet obstruction
  • Prolonged obstruction only occurs in 15% after stone passed into duodenum
• Investigations
  • AXR may show Rigler’s triad
  • Dilated stomach
  • Pneumobilia
  • Extra-biliary shadowing suggestive of gallstone
• Management
  • Endoscopic – consider first in old/comorbid patients
    • Retrieval with nets/basket
    • Could use mechanical lithotripsy if this fails
  • Surgical
    • Try to milk stone into stomach or jejunum then remove via gastrotomy or jejunotomy
    • Consider definitive surgical management at a later date if fit/young

Pathophysiology

• Intrinsic / extrinsic obstruction → vomiting
• Leads to
  • Hypokalaemic hypochloraemic metabolic alkalosis
    • With paradoxically acidic urine
  • Loss of HCl (and Na & K) causes↑HCO3
  • Leads to increased renal excretion of HCO3
  • Alkalosis shifts intracellular K to the extracellular compartment
  • Total body K low, even if serum K normal
  • Lost sodium leads to ↑ aldosterone →
  • Resulting in ↓ renal sodium excretion
  • At the expense of K & H renal loss
  • Results in a paradoxically acid urine

Investigations

• Bloods & ABG:
  • Hypokalemia Hypochloraemic Metabolic Alkalosis
• X-rays
  • Gastric dilatation
  • ±contrast study
  • ± Scintigraphic gastric emptying study
• Gastroscopy
  • Need to decompress stomach with NG first!
• CT may give clues as to aetiology

Management

• Resuscitation
  • Replacement of NaCl, K+ & fluid losses
  • NGT decompression
• PPIs
• Remember Nutrition (may need TPN)
• Endoscopy
  • Balloon dilatation → 50% recurred by 3yrs
  • Stenting – especially for palliative tumours
• If not settling with medical therapy or if resectable malignancy consider surgery
• Resection - distal gastrectomy
• Gastrojejunostomy as a ‘bypass’

Prognosis / Natural Hx

• If DU related, symptoms often improve with PPIs
• Oedema settles