Management of Gastroparesis

Abstract

Gastroparesis is a gastrointestinal motility disorder characterized by nausea, vomiting, early satiation, postprandial fullness, bloating, and upper abdominal pain. The diagnosis requires documented delay in gastric emptying with an optimal test such as scintigraphy or stable isotope gastric emptying breath test in the absence of mechanical obstruction. The pathophysiologic mechanisms of gastroparesis are multifactorial, including antroduodenal hypomotility, pylorospasm, impaired gastric accommodation, and visceral hypersensitivity. The etiologies of gastroparesis are broad, but the most common subtypes are idiopathic, diabetic, and postsurgical. Less frequent etiologies are neurodegenerative disorder (Parkinson disease), myopathies (scleroderma, amyloidosis), and neoplastic syndrome. Symptoms of gastroparesis can be refractory and challenging to manage, leading to reduced quality of life and significant health care expenditure. This article introduces the epidemiology, clinical presentation, diagnosis, and differential diagnoses of gastroparesis, followed by a focused discussion on its management, including nutritional support, prokinetic and antiemetic agents, and emerging interventions directed at the pylorus. Robust sham-controlled trials are needed to evaluate the long-term efficacy of gastric peroral endoscopic myotomy. A multidisciplinary approach with individualized strategies based on characterization of the patho-physiology is deemed necessary to enhance clinical outcomes.

Keywords: Gastric emptying; gastric accommodation; gastric peroral endoscopic myotomy; nutritional support; prokinetics; visceral hypersensitivity.

Figure 1.

Representative EndoFLIP measurements at 40 mL of inflation from a healthy volunteer (A) and from a patient with diabetic gastroparesis and altered pyloric sphincter distensibility of 4 mm/mm Hg (B).

Figure 2.

Examples of high-resolution antropyloroduodenal manometry in patients with delayed gastric emptying. Panel A shows normal fasting in the digestive migrating motor complex in the small intestine with a deficiency in the antral component of the migrating motor complex. Panel B shows the postprandial recording with the pylorus generally coordinated with antral phasic pressure activity, and a reduced frequency of distal antral contractions (less than 1 per minute). Panel C shows a short period with isolated pyloric pressure contractions unassociated with distal antral contractions in the postprandial period. Panel D shows a postprandial tracing consistent with pylorospasm from a separate patient, characterized by prominent pyloric contractility with tonic elevation of baseline pressure lasting several minutes together with superimposed phasic contractions over the elevated tone.