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Gastroparesis: Etiology, clinical manifestations, and diagnosis

Author
Michael Camilleri, MD
Section Editor
Nicholas J Talley, MD, PhD
Deputy Editor
Shilpa Grover, MD, MPH

INTRODUCTION

Normal gastrointestinal motor function is a complex series of events that requires coordination of the sympathetic and parasympathetic nervous systems, neurons and pacemaker cells (called interstitial cells of Cajal) within the stomach and intestine, and the smooth muscle cells of the gut. Abnormalities of this process can lead to a delay in gastric emptying (gastric stasis) [1].

This topic will review the etiology and diagnosis of gastroparesis. Our recommendations are largely consistent with guidelines by the American Gastroenterological Association (AGA) and the American College of Gastroenterology (ACG) [2,3]. The pathogenesis and treatment of gastroparesis are discussed separately. (See "Pathogenesis of delayed gastric emptying" and "Treatment of gastroparesis".)

DEFINITION

Gastroparesis is a syndrome of objectively delayed gastric emptying in the absence of a mechanical obstruction and cardinal symptoms of nausea, vomiting, early satiety, bloating, and/or upper abdominal pain [3].

EPIDEMIOLOGY

In one of the largest population-based studies that identified 3604 potential cases of gastroparesis of whom 83 fulfilled diagnostic criteria for definite gastroparesis, the age-adjusted incidence of gastroparesis was 2.4 per 100,000 person-years for men and 9.8 per 100,000 person-years for women [4]. The age-adjusted prevalence of definite gastroparesis was 9.6 per 100,000 persons for men and 38 per 100,000 persons for women. Overall survival was significantly lower than for the age- and sex-matched general population.

ETIOLOGY

Although multiple conditions have been associated with gastroparesis, the majority of cases are idiopathic, diabetic, or postsurgical (figure 1).

                         

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Literature review current through: Nov 2016. | This topic last updated: Thu Jul 14 00:00:00 GMT 2016.
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References
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