Gastroparesis (GP) is a motility disorder of the stomach characterized by the presence of upper abdominal symptoms and delayed gastric emptying in the absence of organic obstruction [1]. The prevalence of gastroparesis may range between 10 and 38 per 100,000 population and is more frequent in females [2]. Two major etiologies have been identified – diabetes mellitus (both types), and GP because of vagal nerve injury during esophageal or gastric surgery. Among patients with diabetes, gastroparesis is far more prevalent in diabetes type 1 with a cumulative risk of 5.2%, compared to diabetes type 2 with a lower cumulative risk of 1.1% [3]. Approximately one third of patients have GP without identified etiology. These patients are referred to as having idiopathic gastroparesis. A minority of patients develop GP as part of their systemic disease [1,4] or following infection [5]. The symptoms include nausea, vomiting, early satiety, postprandial fullness, bloating, and abdominal pain. In severe cases, patients may suffer from significant weight loss, dehydration and nutritional deficiencies. Importantly, GP is associated with an increased mortality [6].

One cannot diagnosis GP based on symptoms alone as there is a significant overlap between GP and functional dyspepsia [7]. Moreover, significant proportion of patients with diagnosis of functional dyspepsia may latter develop GP and vice versa, patients with confirmed GP may spontaneously switch to functional dyspepsia [8].

As such, a diagnosis of GP can be made only if objective evidence of delayed gastric emptying by scintigraphy or breath test is shown [9]. Importantly, patients with confirmed delayed gastric emptying, but without symptoms are not considered as having GP.

The pathophysiology of GP is multifactorial, complex and not completely understood. Delayed gastric emptying is a defining feature, and gastric hypomotility due to several underlying mechanisms (small muscle atrophy, loss of Interstitial Cells of Cajal and several others) is believed to play a major role as well [10]. Beside this, pylorospasm (or its inadequate relaxation) has also been suggested as another important pathophysiological factor [11].

Owing to the complex and incompletely understood pathophysiology, the effective treatment for GP remains still a real clinical challenge. First-line treatment options consist of dietary measures, administration of prokinetics and antiemetics, optimization of diabetes (if present) and nutritional support. These measures are, however, often partially effective, or ineffective. Moreover, in some countries, prokinetics such as metoclopramide or erythromycin are not readily available. Gastric hypomotility and decreased gastric accommodation may also be influenced by gastric electrical stimulation – however, this method does not accelerate gastric emptying or decrease the frequency or severity of nausea and vomiting [12]. Furthermore, it requires surgical – laparoscopic – procedure to implant electrodes on the gastric surface. Unfortunately, none of these options is supported by strong scientific evidence and their efficacy varies substantially [13].

Another approach to treat GP focuses on pylorospasm as an important pathophysiological factor. “Pylorus-directed therapies” aim to decrease pyloric tone, which is believed to be increased, at least in some patients. These therapies include intrapyloric botulinum toxin injection, balloon dilation, laparoscopic pyloroplasty or myotomy and endoscopic myotomy (G-POEM = gastric per-oral endoscopic myotomy). G-POEM is a new pylorus directed therapy, consisting of purely endoscopic (scarless) myotomy.

The aim of this review is to summarize pathophysiology of gastroparesis, pylorus directed therapies and to describe the role of G-POEM in treatment of GP.