Gastric outlet obstruction

Gastric outlet obstruction (GOO) is a mechanical blockage at the pylorus or proximal duodenum that prevents normal gastric emptying. Malignancies such as pancreatic and gastric cancer are the most common causes, while peptic ulcer disease (PUD) is the leading benign etiology. GOO manifests with postprandial nonbilious vomiting, early satiety, epigastric pain, and weight loss. A characteristic physical examination finding is a succussion splash after ≥ 3 hours of fasting. Diagnostic evaluation includes cross-sectional imaging (e.g., contrast-enhanced CT) and esophagogastroduodenoscopy (EGD). Initial management focuses on fluid resuscitation, electrolyte repletion, and gastric decompression using a nasogastric tube. Subsequent management is cause-specific and may include endoscopic therapy or surgical bypass (e.g., gastrojejunostomy).

Malignant ^[1][2][3]

• Pancreatic cancer ^[3]
• Gastric cancer
• Duodenal cancer
• Biliary tract cancer (e.g., cholangiocarcinoma, ampullary cancer)
• Lymphoma
• Metastases (e.g., from colon or ovarian cancer)

Malignancy (e.g., pancreatic cancer, gastric cancer) is the most common cause of GOO.

Benign ^[1][2][3]

• PUD ^[3]
• Strictures due to:
  • Chronic pancreatitis
  • Crohn disease
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Caustic ingestion
  • Postsurgical scarring or adhesions
  • Radiation
• Mechanical obstruction (intraluminal or extrinsic) due to:
  • Acute pancreatitis
  • Pancreatic pseudocyst
  • Gallstone obstruction (Bouveret syndrome)
  • Gastric bezoar
  • Foreign bodies
  • Gastrointestinal polyps or benign tumors (e.g., gastric leiomyoma)
  • Gastic volvulus
  • Eosinophilic gastritis
  • Ladd band
  • Hypertrophic pyloric stenosis
  • Tuberculosis

PUD may cause GOO via two mechanisms: inflammation and edema in acute ulcers, and scarring and fibrosis from chronic ulcers. ^[4]

Inflammation, edema, scarring, fibrosis (e.g., from PUD), or luminal encroachment/extrinsic compression (e.g., from malignancy) → mechanical or functional obstruction at the distal stomach, pylorus, or proximal duodenum → failed or delayed passage of gastric contents → gastric distention resulting in nausea, nonbilious vomiting, early satiety, and weight loss

• Establish NPO status.
• Obtain abdominal x-ray and initial labs (e.g., BMP).
• Consider nasogastric tube placement for gastric decompression.
• Administer IV fluid therapy and replete electrolytes as needed.
• Administer IV proton pump inhibitor (PPI), e.g., pantoprazole, to reduce gastric secretions.
• Provide analgesics and antiemetics as needed.
• Consider nutritional support if required.

Focused history ^[1][2]

• Symptoms that suggest GOO
  • Postprandial nausea, nonbilious vomiting
  • Early satiety
  • Epigastric pain
  • Bloating or abdominal distention
• Constitutional symptoms (e.g., weight loss)
• Medications (e.g., NSAIDs)
• Past medical history: PUD, gallstone disease, prior malignancy

Focused examination ^[1][2]

• General examination: signs of significant dehydration and malnutrition
• Abdominal examination
  • Succussion splash: a splashing sound created by the movement of gastric contents
    • Elicited by placing a stethoscope over the epigastrium of a patient in the supine position and gently rocking the upper abdomen
    • Physiological immediately after a meal; pathological if present after ≥ 3 hours of fasting ^[2]
  • Palpable abdominal mass or lymphadenopathy

GOO should be presumed malignant until proven otherwise. ^[2]

Imaging ^[1][2]

• Abdominal x-ray
  • Initial screening modality for suspected intestinal obstruction
  • Findings
    • Enlargement of the gastric bubble
    • Dilatation of the proximal duodenum
    • Reduced distal bowel gas
• Cross-sectional imaging (e.g., contrast-enhanced CT or MRI)
  • Preferred imaging modality to evaluate intestinal obstruction and identify the underlying cause
  • Findings
    • Gastric distention with retained contents
    • Transition point at pylorus or proximal duodenum
    • Features of the underlying cause (e.g., infiltrative mass in malignant GOO)
• Upper gastrointestinal series
  • Targeted study to localize the level of obstruction and assess gastric emptying
  • Findings
    • Delayed gastric emptying
    • Narrowed or irregular pylorus or proximal duodenum
    • Partial or complete obstruction
  • Avoid oral contrast if EGD is planned, as it may interfere with the procedure.

EGD ^[1][2]

• Preferred modality to confirm the diagnosis
• Allows for direct visualization of the gastric outlet and enables biopsies of suspicious lesions
• Findings
  • Retained gastric contents
  • Narrowed pylorus or proximal duodenum with difficulty advancing the endoscope
  • Features of the underlying cause (e.g., edema, ulceration, scarring, mass lesion)
• Endoscopic ultrasound (EUS): assists in evaluating the underlying cause and obtaining biopsies

A nasogastric tube should be inserted before EGD to empty the stomach and reduce aspiration risk. ^[2]

Laboratory studies ^[1][2]

Nonspecific findings may support the diagnosis.

• BMP: electrolyte abnormalities (e.g., hypokalemic, hypochloremic metabolic alkalosis from vomiting)
• Decreased albumin

• Malignant causes ^[2][3]
  • Prognosis and therapeutic intent determine the treatment approach.
  • Arrange oncology or multidisciplinary team assessment to guide staging and disease-directed treatment.
  • Palliative procedures include:
    • Endoscopic enteral stenting with, e.g., self-expandable metal stents
    • EUS-guided gastroenterostomy
    • Surgical gastrojejunostomy (open or laparoscopic)
    • Percutaneous endoscopic gastrostomy (for gastric decompression) and jejunostomy tube (for nutrition)
• Benign causes ^[2][3]
  • Treat the underlying cause (e.g., H. pylori eradication therapy, NSAID discontinuation, PPI therapy).
  • Consider endoscopic balloon dilation for intrinsic strictures or GOO due to PUD.
  • Surgery (e.g., gastrojejunostomy) for refractory obstruction

• Gastroparesis ^[2]
• Gallstone ileus ^[11]
• Pancreatitis-associated ileus ^[12]
• Superior mesenteric artery syndrome ^[13]
• Functional dyspepsia ^[14]