U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Gastric Outlet Obstruction

; .

Author Information and Affiliations

Last Update: September 19, 2022.

Continuing Education Activity

Gastric outlet obstruction (GOO) is a result of any disease process that causes a mechanical impediment to gastric emptying. It can be caused by mechanical causes as well as motility disorders and typically is associated with abdominal pain, postprandial vomiting, early satiety, and weight loss. This activity reviews the evaluation and management of gastric outlet obstruction and highlights the role of the interprofessional team in evaluating and improving care for patients with this condition.


  • Identify the etiology of gastric outlet obstruction.
  • Review how to evaluate a patient with gastric outlet obstruction.
  • Outline the approach to treating gastric outlet obstruction depending on the etiology of the disease.
  • Identify interprofessional team strategies for improving care coordination and outcomes in patients with gastric outlet obstruction.
Access free multiple choice questions on this topic.


Gastric outlet obstruction (GOO) is a clinical syndrome that can manifest with a variety of symptoms, including abdominal pain, postprandial vomiting, early satiety, and weight loss. It is caused by either a benign or malignant mechanical obstruction or a motility disorder interfering with gastric emptying. Anatomically, the mechanical obstruction can be at the distal stomach, pyloric channel, or duodenum; and can be intrinsic or extrinsic to the stomach.[1][2]


The etiology of gastric outlet obstruction can be broadly divided into two categories:

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


  1. Benign
    • 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
    • The above causes typically involve the distal stomach and duodenum. However, the distal small bowel can also be affected.[1][2][3]
  2. 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 (e.g., 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 (e.g., amyloidosis, carcinomatosis), which can induce gastroparesis and small bowel dysmotility.[4][5][6][7]


The precise incidence of gastric outlet obstruction (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 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 six months of life.[9][10]

History and Physical

The onset and spectrum of symptoms in gastric outlet obstruction (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 is a reflection of retained gastric material. If a succussion splash is noted more than four 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, anticholinergic medications is important. The patients who smoke should be educated and advised against the use.[3]


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 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, 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 will 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 include 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 six 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 for 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


For patients with gastric outlet obstruction (GOO) secondary to chronic peptic ulcer disease (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.


Patients undergoing endoscopic treatment with either balloon dilatation or stenting are at risk for perforation. Although endoscopic balloon dilatation (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 one week before surgery.

Deterrence and Patient Education

The presenting symptom of gastric outlet obstruction (GOO) is usually vomiting. Once GOO is suspected, timely investigations to determine the underlying etiology of the obstruction should be performed. The treatment strategies widely vary depending on the etiology.[2][9] In benign GOO caused by PUD, lifestyle modifications are the cornerstone for management including acid suppression, NSAID avoidance, smoking cessation, testing for and treating H. pylori.

Enhancing Healthcare Team Outcomes

Gastric outlet obstruction (GOO) has a variety of causes. Often, emergency medicine or primary care providers are the first to encounter patients and suspect GOO. A thorough workup to determine the cause of the obstruction must be performed that may include a CT scan and endoscopy. The gastroenterology team should be involved in care. If endoscopic treatments are unsuccessful or the etiology of the obstruction is not amenable to treatment by non-invasive strategies, the surgical team should be consulted for intervention. Emergency department, gastroenterology, and operating room nurses assist in the care of patients and keep managing providers informed of patient status.[2][9] [Level 4]

Review Questions


Tringali A, Giannetti A, Adler DG. Endoscopic management of gastric outlet obstruction disease. Ann Gastroenterol. 2019 Jul-Aug;32(4):330-337. [PMC free article: PMC6595925] [PubMed: 31263354]
Appasani S, Kochhar S, Nagi B, Gupta V, Kochhar R. Benign gastric outlet obstruction--spectrum and management. Trop Gastroenterol. 2011 Oct-Dec;32(4):259-66. [PubMed: 22696905]
McNeice A, Tham TC. Endoscopic balloon dilation for benign gastric outlet obstruction: Does etiology matter? Gastrointest Endosc. 2018 Dec;88(6):909-911. [PubMed: 30449403]
Abell TL, Bernstein RK, Cutts T, Farrugia G, Forster J, Hasler WL, McCallum RW, Olden KW, Parkman HP, Parrish CR, Pasricha PJ, Prather CM, Soffer EE, Twillman R, Vinik AI. Treatment of gastroparesis: a multidisciplinary clinical review. Neurogastroenterol Motil. 2006 Apr;18(4):263-83. [PubMed: 16553582]
Tada S, Iida M, Yao T, Kitamoto T, Yao T, Fujishima M. Intestinal pseudo-obstruction in patients with amyloidosis: clinicopathologic differences between chemical types of amyloid protein. Gut. 1993 Oct;34(10):1412-7. [PMC free article: PMC1374552] [PubMed: 8244111]
Lee HR, Lennon VA, Camilleri M, Prather CM. Paraneoplastic gastrointestinal motor dysfunction: clinical and laboratory characteristics. Am J Gastroenterol. 2001 Feb;96(2):373-9. [PubMed: 11232678]
Park MI, Camilleri M. Gastroparesis: clinical update. Am J Gastroenterol. 2006 May;101(5):1129-39. [PubMed: 16696789]
Sukumar V, Ravindran C, Prasad RV. Demographic and Etiological Patterns of Gastric Outlet Obstruction in Kerala, South India. N Am J Med Sci. 2015 Sep;7(9):403-6. [PMC free article: PMC4630733] [PubMed: 26605204]
Khullar SK, DiSario JA. Gastric outlet obstruction. Gastrointest Endosc Clin N Am. 1996 Jul;6(3):585-603. [PubMed: 8803569]
Wolf LL, Nijagal A, Flores A, Buchmiller TL. Late-onset hypertrophic pyloric stenosis with gastric outlet obstruction: case report and review of the literature. Pediatr Surg Int. 2016 Oct;32(10):1013-6. [PubMed: 27506212]
Perng CL, Lin HJ, Lo WC, Lai CR, Guo WS, Lee SD. Characteristics of patients with benign gastric outlet obstruction requiring surgery after endoscopic balloon dilation. Am J Gastroenterol. 1996 May;91(5):987-90. [PubMed: 8633593]
Irani S, Khashab M. Gastric outlet obstruction: when you cannot do an endoscopic gastroenterostomy or enteral stent, try an endoscopic duodenojejunostomy or jejunojejunostomy. VideoGIE. 2020 Mar;5(3):125-128. [PMC free article: PMC7058712] [PubMed: 32154487]
Balekuduru A, Sheik S, Prakash BS, Vilmann P. Gastric outlet obstruction-A rare cause. Indian J Gastroenterol. 2016 Mar;35(2):150. [PubMed: 27006128]
Yazdanpanah F, Saba H, Rahmani R, Schreiber ZJ, Hindy P. Strongyloides Hyperinfection Presenting as a Gastric Outlet Obstruction. Cureus. 2020 Jan 08;12(1):e6603. [PMC free article: PMC7008763] [PubMed: 32064185]
Jaffin BW, Kaye MD. The prognosis of gastric outlet obstruction. Ann Surg. 1985 Feb;201(2):176-9. [PMC free article: PMC1250637] [PubMed: 3970597]

Disclosure: Anila Kumar declares no relevant financial relationships with ineligible companies.

Disclosure: Pavan Annamaraju declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK557826PMID: 32491758


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...