Gastric Outlet Obstruction

Etiology

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

1. Mechanical obstruction (from either benign or malignant causes)
2. Motility disorders

Benign Mechanical Obstruction

Benign mechanical GOO can be cause by a number of factors, including:

• Peptic ulcer disease
• Nonsteroidal anti-inflammatory drug (NSAID) use
• Helicobacter pylori (H. pylori)—related inflammation
• Polyps
• Ingestion of corrosive substances
• Gastric tuberculosis
• Anastomotic strictures
• Crohn disease
• Gastric bezoars
• Gastric volvulus
• Eosinophilic gastroenteritis
• Bouveret syndrome (impaction of gall stones in the pylorus or proximal duodenum)
• Annular pancreas
• Pancreatitis (acute and chronic)

Thes causes typically involve the distal stomach and duodenum; however, the distal small bowel can also be affected.[1][2][3]

Malignant Mechanical Obstruction

Malignant mechanical GOO can occur with cancers in the pylorobulbar area, the antropyloric zone, and the descending duodenum. Distal gastric cancer is the most common malignancy, accounting for up to 35% of cases of GOO. The pancreatic adenocarcinoma with duodenal or gastric extension accounts for 15% to 25% of cases. Less common causes are neoplasms of the proximal duodenum and ampulla, gastric lymphoma, metastatic or primary duodenal malignancy, gastric carcinoid, and locally advanced gallbladder carcinoma or cholangiocarcinoma.[4]

Motility Disorders

Gastroparesis is the most common motility disorder that causes GOO. In many cases of gastroparesis, the underlying cause remains elusive. Among the recognized cases, diabetes mellitus remains the leading cause. Some viral illnesses (eg, Norwalk) and medications (opiates, anticholinergics) may lead to gastroparesis. Damage to the vagus nerve intraoperatively (fundoplication, bariatric procedures) can result in gastroparesis. Some solid organ and hematologic cancers can have complications through a paraneoplastic or infiltrative process (eg, amyloidosis, carcinomatosis), which can induce gastroparesis and small bowel dysmotility.[4][5][6][7]

Epidemiology

The precise incidence of GOO is not known. Before the advent of proton pump inhibitors (PPIs), peptic ulcer disease (PUD) was the major cause of GOO cases. With the better treatment of H. pylori infections and the use of PPIs, the incidence of GOO from PUD has declined to 5%. More recently, 50% to 80% of cases of GOO are related to underlying cancers. The incidence of peripancreatic malignancy causing GOO is 15% to 20%.[1][2] Males are more commonly affected than females, with a ratio of about 3 to 4:1 for both malignant and benign causes.[2][8][9]

Hypertrophic pyloric stenosis (HPS) is a frequent cause of GOO in neonates. It occurs in 1.5 to 3 per 1000 live births and is more common in males (1:150 male and 1:750 female). Its occurrence is rare in older children and adolescents. HPS is caused by diffuse hypertrophy and hyperplasia of the pyloric smooth muscles that narrow the antrum, resulting in GOO. It is one of the most common indications of surgery during the first 6 months of life.[9][10]

History and Physical

The onset and spectrum of symptoms in GOO depend on the underlying etiology of the obstruction. The patients often present with nausea and vomiting as their chief complaint. Acute onset of symptoms may lead a health care provider to suspect gallstones, pancreatitis, peptic ulcer disease, volvulus, or migration of PEG-tubes in specific cases. Benign causes of GOO most commonly present with early satiety (53%) and bloating (50%), while more malignant causes include pain, vomiting, weight loss, and malnutrition.[2][9]

The physical examination may reveal evidence of hypovolemia and weight loss. Abdominal distension and a succussion splash occur in about 25% of patients and are a reflection of retained gastric material. If a succussion splash is noted more than 4 hours after a meal, it is suggestive of GOO with a 50% sensitivity.[2][9]

A detailed drug history to elucidate the use of NSAIDs, aspirin, opioids, and anticholinergic medications is important. The patients who smoke should be educated and advised against the use.[3]

Evaluation

Hypokalemia and hypochloremic metabolic alkalosis are often present from severe vomiting. Increased serum gastrin levels can be seen as abdominal distension induces gastrin release. Plain radiography may show distended gastric air bubbles that do not cross the midline. If the obstruction is large, the small bowel may not be visualized. Studies with barium or water-soluble contrast can provide more information on the underlying cause of the blockage. If the contrast fails to pass into the small bowel, it is suggestive of complete obstruction. The CT scan may also give additional details, such as the thickness of the pylorus or gastric wall, and it can also reveal if lymph nodes or pancreatic lesions are present. Endoscopy is generally needed to confirm and establish the specific cause of the obstruction. A nasogastric tube should be inserted, and suction should be done before endoscopy to reduce the risk of aspiration. Following gastric decompression, to further evaluate mechanical outlet obstruction, a saline load test can be helpful. The saline load (750 ml) is emptied into a patient’s stomach through a nasogastric tube. If more than 400 mL of gastric contents are aspirated after 30 minutes, it is considered a positive test. Biopsies done during endoscopy can confirm or exclude a malignant cause of GOO.[2][9]

Treatment / Management

The management of gastric outlet obstruction depends on the cause and extent of the obstruction.

Benign Mechanical Obstruction

In benign GOO caused by PUD, conservative management should be tried first, including acid suppression, NSAID avoidance, and testing for and treating H. pylori. If conservative management fails, dilation via endoscopy or surgery should be attempted.[1]

Endoscopic balloon dilation (EBD) was introduced in the 1980s, and prior to this, GOO was managed with a surgical approach.[3] First, endoscopy is done to visualize the ulcer in the narrowed portion of the stomach or duodenum. A water-soluble contrast study can be done to help identify the anatomy prior to intervention. Once a stricture is visualized, endoscopic balloon dilation is performed. A balloon dilator is inserted through the working channel of the scope, or a balloon is placed over a guidewire under fluoroscopic guidance. The extent of the stricture determines the amount of dilation. Generally, narrow strictures require a stepwise dilation, which is carried out over several sessions. After adequate progress, these sessions become less frequent.[1] For example, strictures caused by caustic injury generally have a smaller diameter and require more dilatations. There is a higher percentage of caustic strictures refractory to EBD compared to noncaustic strictures. The rates of perforation are higher in caustic strictures compared to strictures from peptic ulcer disease. Caustic ingestion causes deeper damage to the tissue in contact, resulting in fibrosis, making it more challenging to manage with EBD.[3] EBD is successful in the short term, and almost instant symptom improvement is seen. It may be beneficial to postpone dilation beyond 15 mm until after a period with medical management. After a sufficient dilation is reached, sustained clinical response is seen in around 70% to 80% of patients.[1] The predictors of failure of EBD include caustic causes of strictures, multiple, long, or tortuous strictures.[3] If the stricture is refractory to dilation, stent placement with or without surgery should be considered.[3][11]

Stent placement with self-expandable metal stents (SEMSs) has been used as an alternative to surgery. However, there is limited literature evidence in the efficacy of using SEMSs in benign GOO. Nevertheless, they should be considered when EBD has failed.[1][3]

Surgical management is also an option for treating benign GOO if the pylorus cannot safely be dilated due to obstruction or if the obstruction remains in spite of endoscopic and medical management.[1] Additionally, GOO, caused by extrinsic compression such as chronic pancreatitis, is less likely to respond to EBD and should be considered early for surgery.[3]

Malignant Obstruction

For malignant obstruction, resection, decompressive gastrostomy, bypass surgery, endoscopic stenting, and endoscopic ultrasound-guided gastroenterostomy are some of the treatment options. Surgery is the optimal choice when resection is potentially curative.[1][12]

Diagnostic laparoscopy or exploratory laparotomy can be done to evaluate the degree of disease before a surgical bypass is performed, which is usually done as a palliative measure. If there is no obstruction distal to the site a stent would be placed, an endoscopic stent should be used. Those with several areas of obstruction should undergo decompressive gastrostomy and enteral or parenteral feeding options should be considered.[1][12]

SEMS can be done as a palliative measure for malignant GOO to provide relief from obstructive symptoms and to improve patients’ quality of life. Patients with a life expectancy of fewer than 6 months should be considered for this intervention. It is common for these patients to have a concomitant biliary obstruction, and a biliary SEMS should be placed before placing one in the duodenum because it could be difficult to assess the biliary tract once a duodenal stent has been placed. Surgery, including gastrojejunostomy, can also be considered for GOO. When malignant GOO is not amenable to surgery or SEMS placement, a percutaneous decompressive gastrostomy (PDG) can be used. A PDG with jejunal extension allows for decompression and access to enteral nutrition.[1][12]

Another treatment modality is endoscopic ultrasound (EUS) guided gastrojejunostomy using lumen-apposing metal stents (LAMS), where a bypass is created by inserting a stent from the stomach to the small bowel distal to the obstruction under EUS and fluoroscopic guidance. This approach is useful for both malignant and benign GOO.[1][12]

Differential Diagnosis

The differential diagnosis for gastric outlet obstruction depends on the age of the patient.[1][2][9][10][13][14] For adolescent patients presenting with suspected GOO, the differential should include congenital sources of obstruction like diaphragms, webs, or luminal obstruction with mucosal valves or heterotrophic pancreas. Other differentials should include:

• Neoplasm
• Chemical injury
• Chronic granulomatous disease
• Hiatal hernia
• Brunner gland adenoma
• Congenital duodenal webs
• Pancreatic pseudocysts
• Gallstone obstruction
• Strongyloides hyperinfection

Prognosis

For patients with GOO secondary to chronic PUD, early surgery is recommended. Without surgery, the likelihood of recurrent obstruction, hemorrhage, and perforation remains high. Early treatment of PUD has a good prognosis.[15] The prognosis of GOO due to malignant causes is poor as compared to other causes of GOO.

Complications

Patients undergoing endoscopic treatment with either balloon dilatation or stenting are at risk for perforation. Although EBD-associated perforation rates in benign peptic stenosis are 3% to 6%, higher rates are seen with a balloon diameter greater than 15 mm.[1] Minor bleeding and pain that are usually self-resolving, can happen during EBD.[2] Malnutrition is a major complication of GOO, and patients who are undergoing surgery should be optimized with total parenteral nutrition for at least 1 week before surgery.