Gastric Outlet Obstruction

Etiology

The etiology of GOO can be broadly classified into 2 categories:

• Mechanical obstruction: This can result from either benign or malignant conditions.
• Motility disorders

Benign Mechanical Obstruction

Benign causes of mechanical GOO include:

• Peptic ulcer disease: This affects the antropyloric region of the stomach or duodenum and is the most common benign cause of GOO. This condition may occur idiopathically or result from Helicobacter pylori infection or nonsteroidal anti-inflammatory drug (NSAID) use.[3]
• Inflammatory gastric or duodenal polyps.
• Ingestion of corrosive or caustic substances.
• Gastric tuberculosis, Cytomegalovirus (CMV), Strongyloides, or other infections.
• Crohn disease.
• Hypertrophic pyloric stenosis.
• Gastric wall infiltrative disorders.
• Gastric bezoars.
• Gastric volvulus.
• Eosinophilic gastroenteritis.
• Bouveret syndrome: Gallstone impaction in the pylorus or proximal duodenum.
• Annular pancreas.
• Acute and chronic pancreatitis.
• Pancreatic pseudocyst.
• Iatrogenic causes: Scarring or anastomotic strictures after surgery, endoscopic mucosal resection, or endoscopic submucosal dissection.
• Pediatric causes: Diaphragms, webs, or luminal obstruction due to mucosal valves or heterotrophic pancreatic tissue affecting children and adolescents.[3]

These conditions primarily affect the distal stomach and duodenum, although more distal small bowel obstructions can also be responsible.[1][2][4]

Malignant Mechanical Obstruction

Malignant mechanical GOO can result from intrinsic cancers of the distal stomach and duodenum. Gastric adenocarcinoma is the most common malignancy, responsible for up to 35% of GOO cases, followed by lymphoma, gastrointestinal stromal tumors (GIST), and carcinoid tumors. Extrinsic compression of the gastric outlet may occur due to pancreatic adenocarcinoma, which accounts for 15% to 25% of cases. Other causes of extrinsic GOO include locally advanced gallbladder carcinoma, ampullary cancer, cholangiocarcinoma, and metastatic disease.[5]

Motility Disorders

Gastroparesis is the most common motility disorder that causes GOO.[6][7] In many cases of gastroparesis, although the underlying cause remains elusive, diabetes mellitus remains the leading cause. Certain viral infections (eg, Norwalk virus) and medications (eg, opiates and anticholinergics) may contribute to delayed gastric emptying. Additionally, intraoperative vagus nerve injury during gastric fundoplication or bariatric surgery can lead to gastroparesis. Solid organ and hematologic malignancies may also cause gastroparesis and small bowel dysmotility through paraneoplastic or infiltrative processes, such as amyloidosis or carcinomatosis.[5][6]

Epidemiology

The exact incidence of GOO remains unknown. Historically, peptic ulcer disease was the leading cause of GOO before the introduction of proton pump inhibitors.[2] However, with more effective treatment of H pylori infections and the use of proton pump inhibitors, the incidence of GOO due to peptic ulcer disease has decreased to around 5%. Currently, 50% to 80% of GOO cases are related to malignant mechanical obstruction, with peripancreatic malignancies accounting for 15% to 20% of these cases.[1][2] Men are more commonly affected than women, with a ratio of approximately 3:1 to 4:1 for both malignant and benign causes.[2][8]

Hypertrophic pyloric stenosis (HPS) is a common cause of GOO in neonates, with an incidence of 1.5 to 3 per 1000 live births. HPS is more prevalent in males, occurring at a ratio of 1:150 in males and 1:750 in females. HPS is rare in older children and adolescents. The condition results from diffuse hypertrophy and hyperplasia of the pyloric smooth muscle, leading to antral narrowing and subsequent GOO. HPS is one of the most common indications for surgery within the first 6 months of life.[9]

History and Physical

The onset and spectrum of symptoms in GOO vary depending on the underlying cause of the obstruction. Patients typically present with epigastric abdominal pain or postprandial nausea and vomiting as their chief complaints.[3][10] Acute onset of symptoms may raise suspicion for gallstones, pancreatitis, peptic ulcer disease, or volvulus as the underlying cause. Benign causes of GOO most commonly present with early satiety (53%) and bloating (50%),[2] while malignant obstruction more frequently causes abdominal pain, vomiting, weight loss, and resulting malnutrition.[9] A thorough drug history, including the use of aspirin, other NSAIDs, opioids, and anticholinergic medications, is crucial for diagnosis.

The physical examination may reveal signs of hypovolemia and weight loss. Abdominal distension, tenderness, and a succussion splash are present in approximately 25% of patients, indicating retained gastric material. If a succussion splash is heard more than 4 hours after a meal, it suggests GOO, with a sensitivity of about 50%.[2][9]

Evaluation

Blood studies often reveal hypokalemia and hyperchloremic metabolic alkalosis in patients with recurrent vomiting. Hypoalbuminemia may also develop as a result of malnutrition.[10] Additionally, increased serum gastrin levels can be observed, as abdominal distension stimulates gastrin release. Plain radiography may show distended gastric air bubbles that do not cross the midline, and the small bowel may not be visible in cases of high-grade obstruction.

Fluoroscopic studies using barium or water-soluble contrast can provide more detailed information on the underlying cause of the obstruction. If the contrast fails to pass into the small bowel, it suggests complete obstruction. Plain abdominal x-rays may show an enlarged stomach, a gastric air-fluid level, and the absence of air in the small bowel. A computed tomography (CT) scan can reveal additional findings, such as a thickened pylorus or gastric wall, and this technique may help identify the presence of malignancy or lymph nodes in or around the distal stomach or the duodenum.[10]

Endoscopy is generally required to confirm and establish the specific cause of the obstruction. Nasogastric or orogastric suction should be applied before endoscopy to reduce the risk of aspiration. Following gastric decompression, a saline load test can be useful in further evaluating mechanical outlet obstruction. In this test, a nasogastric tube empties 750 mL of saline load into a patient’s stomach. The test is positive if more than 400 mL of gastric contents are aspirated within 30 minutes. Biopsies performed during endoscopy can help confirm or exclude a malignant cause of GOO.[2][9] 

Endoscopic ultrasound (EUS) is performed if a malignant cause of GOO is suspected, allowing for fine-needle aspiration of tumors that are difficult to access and providing locoregional staging.[10] Gastroparesis is diagnosed when a nuclear gastric emptying scan shows delayed gastric emptying over 4 hours after structural GOO has been excluded through endoscopy, imaging, or both.[10][11]

Treatment / Management

The management of GOO depends on the underlying cause and the extent of the obstruction.

Benign Mechanical Obstruction

In benign GOO caused by peptic ulcer disease, the first step is conservative management aimed at eradicating the ulceration. This includes acid suppression, testing for and treating H pylori infection, and discontinuing NSAIDs if they were used at the time of ulcer diagnosis. If conservative management is unsuccessful or results in a stricture, endoscopic balloon dilatation (EBD) should be considered.[1] Before the introduction of EBD in the 1980s, surgical intervention was the primary treatment for GOO.[4] 

Endoscopy is first performed to visualize the ulcer within the narrowed portion of the stomach or duodenum. A contrast study may be used to assess the anatomy before intervention. Once a stricture is identified, EBD is performed. This involves inserting a balloon dilator through the endoscope's working channel or positioning a balloon over a guidewire under fluoroscopic guidance. Generally, very tight strictures require stepwise dilation over multiple endoscopic sessions, whereas less severe strictures may be managed in a single session. As sufficient dilation is achieved, the frequency of these sessions decreases.[1]

Caustic strictures are generally tighter with a smaller diameter and require several sessions of endoscopic dilatation to achieve resolution. These strictures are more likely to be refractory to EBD compared to noncaustic strictures. Additionally, perforation rates are higher in caustic strictures than in those caused by peptic ulcer disease. Caustic ingestion causes deeper tissue damage, leading to fibrosis, which makes the management of EBD more challenging.[4] EBD provides short-term success with rapid symptom relief. Postponing dilation beyond 15 mm until after a period of medical management may be beneficial. Once adequate dilation is achieved, approximately 70% to 80% of patients experience a sustained clinical response.[1] Predictors of EBD failure include caustic strictures as well as strictures that are multiple, long, or tortuous.[4] Stent placement with or without surgery should be considered if the stricture remains refractory after at least 2 dilatation sessions.[4][12]

Limited evidence supports the efficacy of self-expandable metal stents (SEMSs) for benign GOO, but they may be considered when EBD fails.[1] Studies comparing covered and uncovered SEMSs have not demonstrated a clear preference, as uncovered stents are more flexible and less prone to migration but have a higher risk of tumor ingrowth than covered stents.[13] In select cases, needle-knife incision of the pylorus may be an option, although this technique is seldom used. Surgical management is an option for treating benign GOO if the pylorus cannot safely be dilated or when obstruction persists despite endoscopic and medical treatment.[1] GOO resulting from extrinsic compression, such as chronic pancreatitis, is less likely to respond to EBD and should be considered for early surgical intervention.[4](A1)

Malignant Mechanical Obstruction

Treatment options for malignant obstruction include resection, percutaneous decompressive gastrostomy, gastrojejunal bypass surgery, endoscopic stenting, and EUS-guided gastroenterostomy. Surgery is considered the optimal approach when resection is potentially curative.[1][14] Diagnostic laparoscopy or exploratory laparotomy can be used to assess the extent of disease before performing a surgical bypass, which is typically done as a palliative measure. If no distal obstruction is present, an SEMS can be placed to alleviate obstructive symptoms,[3] particularly in patients with a life expectancy of less than 6 months. These patients often have concomitant biliary obstruction, so a biliary SEMS should be placed before the duodenal stent, as a duodenal stent may compress the biliary tree.[10] (B3)

A pancreaticoduodenal groove with jejunal extension facilitates decompression and provides access to enteral nutrition.[1][14] A newer treatment option involves the placement of an EUS-guided gastrojejunostomy using a lumen-apposing metal stent (LAMS), which creates a bypass from the stomach to the small bowel distal to the obstruction. A LAMS is useful for both malignant and benign GOO.[1][14] Patients with multiple areas of obstruction often require palliative decompressive gastrostomy along with concurrent placement of a jejunal feeding tube.[1][14] Total parenteral nutrition in malignant GOO should be considered only as a temporary measure, typically when a cure is anticipated.

Motility Disorders

Gastroparesis is the most common motility disorder causing GOO. This is often associated with advanced diabetes mellitus but can also be idiopathic. Other causes include medication use (such as opioids, anticholinergics, and glucagon-like peptide-1 agonists), the Norwalk virus, paraneoplastic syndromes, connective tissue disorders, ischemia, certain inflammatory or neurologic conditions, and complications from surgeries such as hiatal hernia repair, Nissen fundoplication, bariatric surgery, and lung transplantation.

The most effective treatment for medication-induced gastroparesis is discontinuing the causative drug. When gastroparesis is linked to an underlying condition, management should focus on treating the primary cause. Additionally, cigarette smoking can reduce blood flow to the stomach, leading to mucosal damage and impaired gastric motility, so smoking cessation is recommended for patients with gastroparesis.[1]

Metoclopramide, a prokinetic drug, is the only approved treatment by the US Food and Drug Administration (FDA) for gastroparesis, but its use is limited due to a black box warning for tardive dyskinesia. Although this adverse effect is rare, metoclopramide is approved for use only up to 12 weeks to minimize the risk. Domperidone, another prokinetic drug, has similar effectiveness in the gastrointestinal tract but does not cross the blood-brain barrier, avoiding the neurological risks associated with metoclopramide. However, it is associated with QT interval prolongation and an increased risk of ventricular tachycardia. In the United States, domperidone is available only through an FDA investigational drug application.[1] 

Due to its pro-motilin effect, oral or intravenous erythromycin can provide short-term relief for some patients with gastroparesis. Various medications, including antiemetics, tricyclic agents, serotonin and norepinephrine reuptake inhibitors, and certain anticonvulsants, may also offer symptomatic benefits.[15] Many patients with gastroparesis are often recommended to follow a diet consisting of multiple small, low-fat, low-fiber meals, with the avoidance of spicy foods, carbonated beverages, and alcohol.

Several options are available for medically refractory gastroparesis, including:

• Liquid diet or jejunostomy tube feedings
• Hypnotherapy
• Cannabidiol (CBD) or medical marijuana
• Endoscopic pyloric botulinum toxin injection
• Gastric electrical stimulation ("gastric pacemaker") (if approved under a Humanitarian Device Exemption) [16]
• Gastric peroral endoscopic myotomy (G-POEM) [17]
• Surgical procedures, including pyloroplasty, sleeve gastrectomy, partial or total gastrectomy (rarely indicated when all other options have failed) [15]
(B3)

Differential Diagnosis

GOO is a symptom that can result from various underlying etiologies, as previously mentioned. The differential diagnoses for symptoms of GOO or conditions that may clinically mimic gastroparesis include:

• Small bowel obstruction
• Hiatal hernia
• Ileus
• Functional dyspepsia
• Celiac artery syndrome due to arterial compression
• Superior mesenteric artery syndrome
• Cannabinoid hyperemesis syndrome
• Cyclical vomiting syndrome
• Rumination syndrome
• Intestinal pseudo-obstruction
• Narcotic bowel syndrome [15]

Prognosis

Early surgery is recommended for patients with GOO that does not respond to conservative therapy. Without surgical intervention, the likelihood of persistent or recurrent obstruction, hemorrhage, and perforation remains high. Early treatment of peptic ulcer disease generally has a favorable prognosis.[1] However, the prognosis of GOO due to malignant causes is poor compared to other etiologies.

Complications

Patients undergoing endoscopic treatment with either balloon dilation or stenting are at risk for perforation. While perforation rates associated with endoscopic balloon therapy (EBT) in benign peptic stenosis range from 3% to 6%, higher rates are observed with balloon diameters greater than 15 mm.[1] Minor bleeding and pain, which are typically self-resolving, may also occur with EBT.[2] Malnutrition is a significant complication of GOO, and optimizing the nutritional status of patients before surgery is essential.