Gastroparesis, Postprandial Distress

© Springer International Publishing AG 2018
Eytan Bardan and Reza Shaker (eds.)Gastrointestinal Motility Disorders

24. Gastroparesis, Postprandial Distress

Henry P. Parkman 

Gastroenterology Section, Temple University School of Medicine, Philadelphia, PA, USA



Henry P. Parkman

A book chapter for “Gastrointestinal Motility Disorders: A Point-of-Care Clinical Guide”. Editors: Eytan Bardan, MD and Reza Shaker, MD.


Common Patient Asked Questions

My Recent Gastric Emptying Test Was Normal, Though It Was Delayed in the Past and I Was Told I Had Gastroparesis. What Do I Have?

Gastric emptying testing is needed to diagnose gastroparesis. The standard gastric emptying test is gastric emptying scintigraphy, which uses a radiolabeled isotope bound to solid food to image the meal emptying. However, there is variable methodology used at different centers. Standardization of gastric emptying among different centers has been suggested using a 4 h imaging protocol with scans taken 0, 1, 2, 4 h after ingestion of a radioactive Tc-99m-labeled low-fat egg white with jam and two pieces of toast. The shorter duration tests lasting 60–90 min using different meals are not as helpful. Relatively high variability in gastric emptying constitutes another limitation of gastric motor testing. Unfortunately, gastric emptying rates measured by gastric motor testing do not correlate well with symptoms of gastroparesis. Patients can have severe nausea and vomiting with normal gastric emptying. These patients also represent a significant medical problem and are, for the most part, indistinguishable from those with gastroparesis. These findings suggest that factors in addition to slow gastric emptying contribute to symptoms.

My Abdominal Pain Is Still Present and Getting Worse. My Prior Gastroenterologist Gave Me Percocet for the Abdominal Pain. What Will You Do?

Abdominal pain in gastroparesis is a difficult symptom and a difficult symptom to treat. The classic teaching is to look for other causes of abdominal pain in patients with gastroparesis who have abdominal pain. This can entail evaluation for gallbladder or pancreatic causes of abdominal pain. Other causes may include functional dyspepsia, irritable bowel syndrome, and visceral hyperalgesia. Nevertheless, some studies show that moderate to severe abdominal pain is prevalent in gastroparesis (66% of patients), impairs quality of life, and is associated with idiopathic etiology. The abdominal pain does not correlate with the delayed gastric emptying. Pain has largely been ignored in gastroparesis; its cause is unknown. The presence of abdominal pain unfortunately is a poor predictor of a good improvement in overall gastroparesis symptoms. Abdominal pain can be difficult to treat. Narcotic analgesics can delay gastric emptying as well as also provoke symptoms of nausea and vomiting. They are best to be avoided. Symptom modulators, such as low dose tricyclic antidepressants, are often tried.

Can My Gastroparesis Be Cured?

Symptoms of gastroparesis may be constant or they may fluctuate with worsening periods. The medications used for gastroparesis are designed to bring the symptoms under better control. Controlling glucose in diabetic gastroparesis may also help improve symptoms. In all patients, dietary management is important and nutritional consultation may be helpful. It has been suggested that idiopathic gastroparesis of acute onset with infectious prodrome could constitute postviral or viral injury to the neural innervation of the stomach or the interstitial cells of Cajal in the stomach. In some series, patients with postviral gastroparesis improve over time, generally several years.

I Have Joined an Online Chat Room for Gastroparesis. Many of the Patient Have Received Botox for Their Gastroparesis with Good Results. Is This Something That Will Help Me?

Several studies have tested the effects of pyloric injection of botulinum toxin in patients with diabetic and idiopathic gastroparesis. Endoscopic treatment entails injection of botulinum toxin (Botox; Allergan, Inc) into the pyloric sphincter. Initial studies were unblinded in small numbers of patients from single centers and observed mild improvements in gastric emptying and modest reductions in symptoms for several months. Two double-blind studies have been reported; these show an improvement in gastric emptying, but no effect on symptoms compared to placebo. Thus, botulinum toxin injections do not result in sustained improvement in symptoms of gastroparesis. Some patients though do seem to improve. Identifying who these patients are is the subject of current research. If botox injection helps symptoms, it generally lasts 3–6 months. Other treatments such as pyloromyotomy may be longer lasting.

My Doctor Told Me Not to Take Metoclopramide Due to Its Side Effects and Referred Me to You for Treatment. What Will You Do?

Metoclopramide (Reglan) is a dopamine type 2 receptor antagonist both in the CNS and in the stomach. Metoclopramide exhibits both prokinetic and antiemetic actions. It has been the mainstay of treatment of gastroparesis. The prokinetic properties of metoclopramide are limited primarily to the stomach. Reglan can cause both acute and chronic CNS side effects in some patients. These side effects should be discussed with the patient prior to treatment and documented in the patient’s medical record. In the United States, metoclopramide is approved for diabetic gastroparesis for up to 12 weeks duration. Patients with gastroparesis have chronic nausea and often need longer periods of treatment. If used, the dose is usually limited to 10 mg four times a day, for several months. Domperidone has similar effects to metoclopramide and has less central side effects than Reglan. Domperidone may well help symptoms of gastroparesis. It does have some cardiac side effects. Since it is not fully approved, patients need to pay themselves for this medication.


Gastroparesis is a chronic symptomatic disorder of the stomach manifested by delayed emptying without evidence of mechanical obstruction [15]. This classic motility disorder of the stomach can lead to marked dysfunction in patients with poor quality of life. Although in many patients symptoms can be controlled with medical therapy, some patients remain markedly symptomatic with progressive weight loss. This chapter provides an overview of gastroparesis and updates the present status of our understanding of this disorder and the treatments available.


Gastroparesis occurs more often in women than men. Interestingly, this is true for each of the three main forms of gastroparesis: idiopathic, diabetic, and even postsurgical. The epidemiology of gastroparesis, however, has not been well systematically studied. This stems from the fact that for proper diagnosis, a gastric emptying test is needed, one that is difficult in population studies. Data from the Rochester Epidemiology Project, a database of linked medical records of residents of Olmsted County, Minnesota, show that the age-adjusted incidence of definite gastroparesis per 100,000 person-years for the years 1996–2006 was 9.8 for women and 2.4 for men [16]. Definite gastroparesis was defined as diagnosis of delayed gastric emptying by standard scintigraphy and symptoms of nausea and/or vomiting, postprandial fullness, early satiety, bloating, or epigastric pain for more than 3 months. The age-adjusted prevalence of definite gastroparesis per 100,000 persons was 37.8 for women and 9.6 for men. More recent estimates have suggested that these prevalence of gastroparesis were an underestimation and the prevalence is greater, being approximately 1.8% of the general population [17].

The prevalence of gastroparesis might be increasing. Data from the US Healthcare Cost and Utilization Project (HCUP) Nationwide Inpatient Sample (NIS), a nationally representative sample of 5–8 million hospitalizations per year, show that, from 1995 to 2004, hospitalizations with gastroparesis as the primary diagnosis increased by 158% and those with gastroparesis as the secondary diagnosis increased by 136% compared with a 13% increase in all hospitalizations [18]. The increase in hospitalization rate for gastroparesis has occurred since the year 2000, and could reflect increasing prevalence and/or the effects of heightened awareness about and better identification of gastroparesis [18]. This increase in gastroparesis hospitalizations may also be due, in part, to the increasing rate of diabetes leading to more cases of diabetic gastroparesis, withdrawal of some gastroparesis treatments from the market (cisapride, tegaserod) with hospitalizations for symptoms not adequately being treated, and hospitalizations needed for insertion of the gastric electric stimulator.


Common symptoms of gastroparesis include nausea (>90% of patients), vomiting (84% of patients), and early satiety (60% of patients) [19]. Other symptoms include postprandial fullness and abdominal pain [20, 21]. Symptoms can be persistent or can manifest as episodic flares. Weight loss, malnutrition, and dehydration may be prominent in severe cases. Although weight loss is classically described in gastroparesis, some patients can be overweight, especially patients with T2DM. In diabetics, gastroparesis may adversely affect glycemic control with both hypoglycemia and hyperglycemia.

Symptom profile can be established and symptom severity assessed with the Gastroparesis Cardinal Symptom Index (GCSI), a subset of the Patient Assessment of Upper Gastrointestinal Symptoms (PAGI-SYM) [22]. The GCSI comprises three subscales (nausea and vomiting, postprandial fullness and early satiety, and bloating) that the patient scores with reference to the preceding 2 weeks [22]. A variant on the GCSI, the GCSI daily diary (GCSI-DD) can be used to record symptoms on a daily basis and may be more accurate in recording symptoms [23]. The daily diary assesses severity of nausea, early satiety, postprandial fullness, and upper abdominal pain as well as records the number of episodes of vomiting. A composite score can be calculated for overall severity of gastroparesis. This GCSI can be used to assess individual symptoms which may then be individually targeted for treatment. Single symptom approaches to treatment may be more feasible than attempts at global symptom improvement for gastroparesis.

Although it has been a common assumption that the gastrointestinal symptoms can be attributed to delay in gastric emptying, most investigations have observed only weak correlations between symptom severity and the degree of gastric stasis. In general, the symptoms that appear to be best correlated with a delay in gastric emptying include nausea, vomiting, early satiety, and postprandial fullness [24, 25]. Some symptoms that have been present in patients with gastroparesis such as bloating and upper abdominal pain are not correlated with delayed gastric emptying and might be related to sensory alterations that might also be present in patients with gastroparesis. Accelerating gastric emptying by itself may not lead to successful treatment of all gastroparesis symptoms.


Major etiologies of gastroparesis are diabetic, postsurgical, and idiopathic [15, 26, 27]. Less common causes of gastroparesis include connective tissue disease, neurologic disease such as Parkinson’s disease, eating disorders, metabolic or endocrine conditions (hypothyroidism), critical illness, and medications such as opiates and anticholinergics [26]. In addition, GP-1 analogs, such as exenatide, used for treatment of type 2 diabetes mellitus can delay gastric empting [15].

Gastroparesis is a relatively common complication of diabetes: delayed gastric emptying has been found to occur in approximately 40% of patients with long-standing type 1 diabetes and approximately 20% of patients with type 2 diabetes [26, 27]. These estimates though are from academic medical centers and true estimates appear to be lower in the general population in patients seeing primary care physicians. In the Rochester Epidemiology project, cumulative incidence of developing gastroparesis was found to be 5.1% in type 1 diabetes mellitus (T1DM) and 1.0% in type 2 diabetes mellitus (T2DM) patients [28].

In diabetic patients in the NIH Gastroparesis Consortium Registry, baseline symptoms were similar in T1DM and T2DM patients, even though T1DM patients had worse gastric emptying delays and higher HbA1c [29]. Diabetic gastroparesis is often attributed to chronic hyperglycemia-induced damage to the vagus nerve, and is frequently observed in association with other diabetic complications such as neuropathy, retinopathy, and nephropathy. Enteric pathology may also exist in diabetic gastroparesis including loss of interstitial cells of Cajal (the pacemaker cells), loss of nitric oxide-containing nerves, and presence of an inflammatory infiltrate. Glucose can modify gastric emptying tests and symptoms: hyperglycemia can delay gastric emptying and worsen symptoms of gastroparesis, whereas hypoglycemia may accelerate gastric emptying.

Postsurgical gastroparesis can occur with many types of operations but is most often observed after upper abdominal procedures because of injury or sectioning to the vagus nerve [15]. In the past, surgery for peptic ulcer disease such as antrectomy with vagotomy was associated with the development of gastroparesis. However, this type of surgery is less often being performed due to the use of proton pump inhibitor treatments of ulcers and treatment for helicobacter pylori. Presently, Nisson fundoplication is probably the more common surgical procedure associated with gastroparesis [30]. Bariatric surgeries and pancreatic surgery have also been associated with gastroparesis.

Idiopathic gastroparesis, with no obvious cause for the gastroparesis, is a common classification for gastroparesis. Characteristics of 243 patients with idiopathic gastroparesis enrolled in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry were recently characterized based on medical histories, symptoms questionnaires, and gastric emptying scintigraphy [31]. Patients’ mean age was 41 years, and the majority (88%) were female. Half (50%) had acute onset of symptoms. The most common presenting symptoms were nausea (34%), vomiting (19%), and abdominal pain (23%). Severe delay in gastric emptying (>35% retention at 4 h) was present in 28% of patients. Severe delay in gastric emptying was associated with more severe symptoms of nausea and vomiting and loss of appetite compared with patients with mild or moderate delay. 86% of these patients with idiopathic gastroparesis met criteria for functional dyspepsia, predominately postprandial distress syndrome. Thus, idiopathic gastroparesis is a heterogeneous syndrome that primarily affects young women and often affects overweight or obese individuals.

A minority of patients with idiopathic gastroparesis (19% in the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry study above (17)) report an initial infectious prodrome such as gastroenteritis or respiratory infection. It has been suggested that idiopathic gastroparesis of acute onset with infectious prodrome could constitute postviral or viral injury to the neural innervation of the stomach or the interstitial cells of Cajal in the stomach. In some series, patients with postviral gastroparesis improve over time, generally several years.


Gastric emptying is mediated by the vagus nerve, which helps regulate fundic accommodation, antral contraction, and pyloric relaxation [15]. These regional gastric motility changes with food ingestion are then mediated through smooth muscle cells, which control stomach contractions; interstitial cells of Cajal, which regulate gastric pacemaker activity; and enteric neurons, which initiate smooth muscle cell activity [15]. The pathophysiology of gastroparesis has not been fully elucidated but appears to involve abnormalities in functioning of several elements including autonomic nervous system, smooth muscle cells, enteric neurons, and interstitial cells of Cajal. Histologic studies demonstrate defects in the morphology of enteric neurons, smooth muscle cells, and interstitial cells of Cajal and increased concentrations of inflammatory cells in gastric tissue [15, 26, 31].


Differential diagnosis of gastroparesis entails excluding other possible causes including peptic ulcer disease, gastric outlet obstruction, neoplasm, and small bowel obstruction [26]. For evaluation of these, an upper endoscopy is performed.

For evaluating gastric emptying, the standard test is gastric emptying scintigraphy, which uses a labeled isotope bound to solid food to image gastric emptying [26, 32]. There is variable methodology used at different centers. Standardization of gastric emptying among different centers has been suggested using a 4 h imaging protocol with scans taken 0, 1, 2, 4 h after ingestion of a radioactive Tc-99m-labeled low-fat egg white with jam and two pieces of toast [33].

Use of the wireless motility capsule to quantify luminal pH and pressure is an alternative to gastric emptying scintigraphy [26]. Gastric emptying is manifested by a sharp increase in pH representing the capsule passing from the acidic stomach to the alkaline small intestine [34]. Using a 5 h cutoff for gastric emptying, the capsule discriminated between normal or delayed gastric emptying with a sensitivity of 0.87 and a specificity of 0.92. This test also measures whole-gut transit—that is, gastric emptying, small bowel transit, and colonic transit. Colonic transit abnormalities has been reported in 18% of patients with gastroparesis, possibly suggesting a more diffuse GI motility disorder and it could be contributing to symptom presentation [35].

Breath tests for gastric emptying, another alternative to gastric emptying scintigraphy, measure labeled nonradioactive 13-CO2 in exhaled breath samples after ingestion of a 13-CO2-labeled meal. Breath samples are obtained periodically over several hours. The exhaled 13-CO2 represents the gastric emptying, duodenal absorption, hepatic metabolism, and pulmonary excretion where gastric emptying is the rate limiting step [32]. Findings generally correlate well with results of gastric emptying scintigraphy. This test has been used clinically in Europe for years, whereas in the United States, a breath test for gastroparesis had been generally used for research studies, but is now available for clinical practice [36].

Gastric emptying testing is useful in diagnosing gastroparesis. There are several drawbacks. First, gastric emptying rates measured by gastric motor testing generally correlate poorly with symptoms and quality-of-life impact of gastroparesis [37, 38]. Patients can have severe nausea and vomiting with normal gastric emptying [38]. These patients also represent a significant medical problem and are, for the most part, indistinguishable from those with gastroparesis. Chronic nausea from any gastrointestinal cause is a large unmet need regardless of the cause. These findings suggest that factors in addition to slow gastric emptying contribute to symptoms. Relatively high interindividual and intraindividual variability in gastric emptying rates measured with gastric motor testing constitutes another limitation of gastric motor testing [26]. The relative contributions to these variabilities of gastric motor testing methodology and biologic inconsistency in gastric emptying are not currently known.


Management of gastroparesis is guided by the goals of correcting fluid, electrolyte, and nutritional deficiencies; identifying and treating the cause of delayed gastric emptying (e.g., diabetes); and suppressing or eliminating symptoms [15]. Care of patients generally relies on dietary modification, medications that stimulate gastric motor activity, and antiemetic drug therapy.

The outcome of patients with gastroparesis has not been well characterized. It is often felt by clinicians to be a difficult disorder to treat, reflecting the paucity of medications that are available for this condition. The outcome of gastroparesis patients were assessed in the NIH Gastroparesis Consortium in patients with either diabetic or idiopathic gastroparesis [39]. Surprisingly, only 28% of 262 patients symptomatically improved at 48 weeks as determined by a decrease GCSI ≥1. This illustrates the chronic nature of gastroparesis and that the disease burden remains high. Predictors for improvement included more severe gastroparesis symptoms, more severe delay in gastric emptying, and an initial infectious prodrome. Predictors for a poor improvement included moderate/severe abdominal pain and being overweight.

Dietary Treatment

Dietary measures entail adjustment to meal composition and frequency [15, 26]. Eating small meals is recommended as patients often have early satiety, that is feeling full when eating a normal size meal; in addition, larger meals may alter gastric emptying times. Consuming mainly liquids such as soups can be useful as gastric emptying of liquids is often preserved in patients with gastroparesis [15]. Avoidance of fats and indigestible fibers is recommended because they delay gastric emptying [15, 26]. When small meals are used in the gastroparesis diet, more frequent meals, 3 meals per day plus 2 snack-type meals, are often needed to maintain caloric intake. These dietary recommendations have often been made empirically as to effects on gastric emptying [40, 41]. Recently, these have been looked at in respect to symptom generation. A high-fat solid meal significantly increased overall symptoms among individuals with gastroparesis, whereas a low-fat liquid meal had the least effect [42]. With respect to nausea, low-fat meals were better tolerated than high-fat meals, and liquid meals were better tolerated than solid meals. These data provide support for recommendations that low-fat and increased liquid content meals are best tolerated in patients with symptomatic gastroparesis. Another study assessed patient tolerances to foods [43]. Foods provoking symptoms were generally fatty, acidic, spicy, and roughage-based. Foods worsening symptoms included: orange juice, fried chicken, cabbage, oranges, sausage, pizza, peppers, onions, tomato juice, lettuce, coffee, salsa, broccoli, bacon, and roast beef. The foods that were generally tolerable were generally bland, sweet, salty, and starchy. Saltine crackers, jello, and graham crackers moderately improved symptoms. Twelve additional foods were tolerated by patients (not provoking symptoms): ginger ale, gluten-free foods, tea, sweet potatoes, pretzels, white fish, clear soup, salmon, potatoes, white rice, popsicles, and applesauce.

Many patients with gastroparesis have diets deficient in calories, vitamins, and minerals. Unfortunately, nutritional consultation is obtained infrequently but this is suggested for dietary therapy and to address nutritional deficiencies [44].

Glucose Control in Diabetic Patients

Diabetic patients with gastroparesis frequently exhibit labile blood glucose concentrations with prolonged periods of significant hyperglycemia. Hyperglycemia itself can delay gastric emptying. Hyperglycemia can counteract the accelerating effects of prokinetic agents on gastric emptying. Improvement of glucose control increases antral contractility, corrects gastric dysrhythmias, and accelerates emptying. To date, there have been no long-term studies confirming the beneficial effects of maintenance of near euglycemia on gastroparetic symptoms. Nevertheless, the consistent findings of physiologic studies in healthy volunteers and diabetic patients provide a compelling argument to strive for near-normal blood glucose levels in affected diabetic patients. Generally, patients give their meal time insulin after ingesting the meal, to ensure that the entire anticipated meal is actually consumed and without vomiting.

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Jan 31, 2018 | Posted by in ABDOMINAL MEDICINE | Comments Off on Gastroparesis, Postprandial Distress

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