Gastroparesis is characterized by a constellationof upper gastrointestinal (GI) symptoms in as-sociation with delayed gastric emptying (GE) inthe absence of mechanical outlet obstruction from the stomach. Cardinal symptoms are nausea, vomit-ing, early satiety or postprandial fullness, bloating, and abdominal or epigastric pain (1). Gastric retention may be asymptomatic in some, possibly due to afferent dysfunc-tion in the setting of vagal denervation (2,3), and delayed GE may be associated with recurrent hypoglycemia in patients without upper GI symptoms (4,5). In these indi-viduals, the term “delayed GE ” is preferred to gastropa-resis (1), although others have used terms such as “gastric hypoglycemia ” (6). Thus, clinical manifestations of im-paired GE may include anorexia, weight loss, malnutrition, phytobezoar formation, poorer quality-of-life, or impaired glycemic control due to erratic delivery of nutrients to the small bowel for absorption, and these may occur in-
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Shin et al. (2013) studied this question.
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