Endoscopic Approaches to Gastroparesis

Renato V. Soares and Lee L. Swanstrom


Curr Opin Gastroenterol. 2015;31(5):368-373. 

In This Article

Abstract and Introduction


Purpose of review This review covers the cause, evaluation and treatment options for gastroparesis. Symptoms of delayed gastric emptying are increasingly seen by gastroenterologists and gastrointestinal surgeons. Endoscopy – both laparoscopic and flexible – is increasingly important in treatment algorithms for this problem.

Recent findings Gastroparesis is increasingly being seen in clinical practice. A progressive algorithm needs to be followed in these challenging cases: starting with medical treatment and diet modification, progressing through endoscopic treatments including new ones such as per-oral pyloromyotomy, and finally laparoscopic treatments including gastrectomy.

Summary Endoscopic interventions are effective treatments for certain gastroparesis patients. New procedures offer a minimally invasive alternative to more radical options and should probably be more widely adopted.


Gastroparesis is a chronic disorder defined by a delay in emptying of the stomach without mechanical obstruction to the gastric outlet. The presenting symptoms of this disease are variable and range from none to disabling to the point of not being able to take anything orally. Clinicians are often asked to see patients when they present with nausea, vomiting, abdominal pain, early satiety and bloating. The severity of each symptom varies widely among patients.[1–3] Objective documentation of abnormal gastric emptying is required for diagnosis, since the clinical picture is similar to diverse clinical and psychological entities such as functional dyspepsia, bulimia and atypical biliary colic.[4] Scintigraphic gastric emptying of solids is commonly used to document gastroparesis.[5] Other diagnostic methods include the motility-pH pill (Smart pill, Given Imaging, Yoquean, Israel)[6] and 13C breath test.[7] Upper endoscopy can be normal, but the presence of undigested food or bezoar in the gastric chamber after an overnight fasting indicates gastroparesis.

There are three main causes of the disorder: idiopathic, diabetes mellitus (type I and II) and postsurgical. In both diabetic and idiopathic gastroparesis, the most common problem at cellular level is depletion on the interstitial cells of Cajal.[8] Parkinson's disease, collagen vascular disorders and hypothyroidism have also been associated with the syndrome.[9] Several medications can delay gastric emptying, including narcotics, anticholinergic agents, glucagon-like peptide-1 (GLP-1) and amylin among diabetic patients. These drugs should be stopped before scintigraphy to avoid a false-positive result.[7]

The female sex is most frequently affected. The annual incidence of gastroparesis has been calculated as 2.4 per 100 000 for men and 9.8 per 100 000 for women.[10] The number of hospitalizations due to gastroparesis in the United States has tremendously increased in the past decades and reached more than 10 000 in 2004.[11] Gastroparesis can be a highly morbid disease and the estimated 5-year survival of the cohort of patients with gastroparesis was 67%, compared with an expected 81% in the age and sex-matched general population.[10]

Up to 50–60% of gastroparesis patients have no identifiable underlying cause (idiopathic gastroparesis).[3,9,10,12] About 20% of these develop symptoms after a viral prodrome.[12] The so-called 'postinfectious' gastroparesis may have a more benign natural history, with spontaneous regression of symptoms after several months or years.[9]

The association between diabetes and delayed gastric emptying has long been recognized and was first described in 1945 by Rundles.[13] In a population-based cohort, 5.2% of the patients with type 1 diabetes mellitus and 1.0% in type 2 diabetes mellitus developed gastroparesis during 10 years of follow-up.[14] Poor glycemic control has been associated with worsening of symptoms.

Incidental or intentional vagal lesions have been linked to the development of postsurgical gastroparesis.[15] Gastric atony may also occur for a variable time period after gastric surgery without vagal injury. It is also possible that some postsurgical patients had gastric emptying problems before the index operation.[16,17] Surgical procedures that can negatively impact gastric motility include vagotomy with antrectomy or pyloroplasty for peptic ulcer disease, gastric bypass and fundoplications.[16] Our group adds a pyloroplasty for patients with gastroesophageal reflux disease (GERD) who also have documented delayed gastric emptying, at the moment of fundoplication, in order to decrease postoperative symptoms and complications related to gastric distention.[17]

The chronic and often debilitating symptoms of gastroparesis, the complex pathophysiology of the disease and also the frequent overlapping with other gastrointestinal and psychiatric disorders make gastroparesis a challenging clinical entity.[1,7] Also, there is no treatment available that changes the disease process itself; thus the focus of treatment is alleviating symptoms.[7]

The usual medical treatments are gastric prokinetics, antiemetics and dietary manipulation.[1] In case of persistent symptoms, more invasive therapies are indicated; ranging from ablation of the pylorus (chemical or surgical), gastric electrical stimulation (GES) or even a total or near-total gastrectomy. In this review, we will emphasize the evolving role of endoscopy for the treatment of gastroparesis, among various treatment options, with attention to the recently described per-oral pyloromyotomy (POP).[18,19]