Gastroparesis--current concepts and considerations.

Gastroparesis presents with symptoms of gastric retention and nongastrointestinal manifestations, with objective evidence of delayed gastric emptying in the absence of mechanical obstruction. Diabetic, idiopathic, and postsurgical gastroparesis are the most common forms, although many other conditions are associated with symptomatic delayed gastric emptying (Table 1). Gastroparesis is estimated to affect up to 4% of the US population[1] and may produce either mild, intermittent symptoms of nausea, early satiety, and postprandial fullness with little impairment of daily function, or relentless vomiting with total disability and frequent hospitalizations. A recent report estimated that inpatient costs for patients with severe gastroparesis approach $7000/month.[2] Table 1 Etiologies of Gastroparesis Clinical Manifestations Gastroparesis presents with a constellation of symptoms. In one study, nausea was reported by 93% of patients whereas early satiety and vomiting were noted by 86% and 68%, respectively.[3] In another series, nausea, vomiting, bloating, and early satiety were reported by 92%, 84%, 75%, and 60% of patients, respectively.[4] Many patients in both case series (89% and 46%) also reported abdominal pain (Table 2). Others experience heartburn from acid reflux into the esophagus that is facilitated by fundic distention which increases the rate of transient lower esophageal sphincter relaxations.[5] Although some gastroparetics with frequent vomiting lose weight and develop malnutrition, most patients were overweight or obese in one series, indicating that the disorder does not necessarily restrict food intake.[6] Phytobezoars are organized concretions of indigestible food residue that are retained within the stomach. These may increase gastroparesis symptoms or produce a palpable epigastric mass, gastric ulceration, small intestinal obstruction, or gastric perforation.[7] Bezoars are eliminated by endoscopic disruption and lavage, enzymatic digestion (papain, cellulose, or N-acetylcysteine), and dietary exclusion of high-residue foods. Variably delayed gastric emptying may cause unpredictable food delivery in diabetics with gastroparesis, affecting glycemic control and increasing risks of both severe hypo- and hyperglycemia.[8] Table 2 Characteristics of Pain in 28 Gastroparesis Patients[3] Quantification of the severity and nature of gastroparesis symptoms has been facilitated by the introduction of validated surveys. The most widely used questionnaire for this purpose is the Gastroparesis Cardinal Symptom Index (GCSI), a symptom score validated in 7 university-based clinical practices in the United States that correlates well with patient and physician ratings of gastric symptom severity.[9] The GCSI comprises 3 subscales (postprandial fullness/early satiety, nausea/vomiting, and bloating) and represents a subset of the comprehensive Patient Assessment of Gastrointestinal Symptoms (PAGI-SYM) survey.[10] The Patient Assessment of Upper Gastrointestinal Disorders-Quality of Life (PAGI-QOL) survey quantifies quality of life in dysmotility syndromes such as gastroparesis.[11] Using these questionnaires, investigators have begun to stratify patients with gastroparesis into different subgroups on the basis of symptom severity and predominant symptom profiles. Although these surveys currently are most useful for research trials, in the near future they may serve a clinical role similar to the Rome criteria for functional gastrointestinal disorders in terms of helping healthcare providers to select symptom-based management approaches.