Gastric outlet obstruction
Gastric outlet obstruction is mechanical narrowing at the pylorus or proximal duodenum that blocks gastric emptying, presenting with postprandial vomiting and a succussion splash. Diagnosis rests on upper endoscopy with biopsy to exclude malignancy, and first-line treatment is nasogastric decompression, fluid and electrolyte correction, and acid suppression before definitive endoscopic dilation or stenting.
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What this article covers
- Overview
Gastric outlet obstruction (GOO) is mechanical narrowing at the pylorus or proximal duodenum that prevents the stomach from emptying into the small bowel.
- Epidemiology
Shifting etiology: peptic ulcer disease was historically the dominant cause of GOO, but Helicobacter pylori eradication and proton pump inhibitor (PPI) use have reduced benign disease, so malignancy…
- Risk factors
Peptic ulcer disease: recurrent or poorly treated duodenal and pyloric channel ulcers fibrose the channel through repeated cycles of ulceration and healing.
- Pathophysiology
Mechanical narrowing at the pylorus or duodenal bulb, from fibrotic scar after repeated peptic ulceration or an infiltrating tumor mass, raises resistance to gastric emptying.
- Clinical features
Postprandial vomiting: nonbilious vomiting of partially digested food, often within an hour of eating and sometimes containing food consumed many hours earlier.
- Differential diagnosis
Gastroparesis: same nausea, vomiting, and early satiety, but EGD is normal and a gastric emptying study, not a mechanical lesion, confirms delayed transit.
- Diagnosis
Diagnostic gold standard: the diagnosis is established by esophagogastroduodenoscopy (EGD), which directly visualizes a nonpassable or severely narrowed pyloric or duodenal channel; biopsy confirms…
- Management
First action: place an NG tube for decompression, keep the patient without oral intake, and begin 0.9% sodium chloride 1 to 2 L intravenously over the first several hours, then continue and titrate…
- Complications
Dehydration and acute kidney injury (AKI): from ongoing vomiting and poor intake, worsened by prerenal azotemia.
- Prognosis
Benign, peptic ulcer related GOO: most patients respond to acid suppression, Helicobacter pylori eradication when present, and dilation, though some need repeat dilation or eventual surgery.
- Prevention
Helicobacter pylori eradication with confirmed cure: urea breath or stool antigen test at least 4 weeks after completing antibiotics, to prevent the recurrent ulceration that scars the outlet.
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Related articles
- Peptic ulcer disease
Peptic ulcer disease is a mucosal break in the stomach or duodenum caused chiefly by Helicobacter pylori infection or NSAID use, diagnosed by upper endoscopy with biopsy of gastric ulcers to exclude malignancy. Treatment eradicates H. pylori when present, stops the ulcerogenic drug, and heals the ulcer with a proton pump inhibitor, while its complications of bleeding, perforation, and obstruction drive most of its morbidity.
- Gastric cancer
Gastric cancer is mostly adenocarcinoma, split into an H. pylori-driven intestinal type arising through chronic atrophic gastritis and intestinal metaplasia and a diffuse signet-ring type causing linitis plastica, and it typically presents late with alarm dyspepsia and weight loss. Upper endoscopy with biopsy confirms the diagnosis, TNM stage with endoscopic ultrasound, CT, and diagnostic laparoscopy sets treatment, and management ranges from endoscopic resection for early T1a disease to gastrectomy with D2 lymphadenectomy and perioperative FLOT chemotherapy for resectable disease to palliative chemotherapy for advanced disease.
- Gastroparesis
Gastroparesis is delayed gastric emptying without mechanical obstruction, most often from longstanding diabetes, prior gastric surgery, or an idiopathic postviral course, presenting with nausea, vomiting, early satiety, and postprandial fullness. Diagnosis requires upper endoscopy to exclude obstruction followed by objective gastric emptying testing, and management progresses from glycemic control and dietary change through time-limited prokinetics to device or endoscopic therapy for refractory disease.
- Dumping syndrome
Dumping syndrome follows rapid emptying of hyperosmolar gastric contents into the small bowel after gastric surgery, producing early gastrointestinal and vasomotor symptoms within 30 minutes of eating or late reactive hypoglycemia 1 to 3 hours after eating. Diagnosis is clinical from the postoperative time course, supported by an oral glucose challenge, and treatment starts with dietary modification before escalating to acarbose or octreotide.
- Acute upper gastrointestinal bleeding
Acute upper gastrointestinal bleeding arises proximal to the ligament of Treitz and presents with hematemesis or melena, most often from peptic ulcer disease or bleeding gastroesophageal varices. Management sequences resuscitation, restrictive transfusion, IV proton pump inhibitor therapy, and, when varices are suspected, octreotide plus antibiotic prophylaxis, all before upper endoscopy within 24 hours, which is both diagnostic and therapeutic.