Gastroparesis - Etiology, Clinical Manifestations, and Diagnosis - UpToDate

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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, AGAF
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Aug 15, 2022.
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 of solids in the absence

of a mechanical obstruction and cardinal symptoms of nausea, vomiting, early satiety,
belching, bloating, and/or upper abdominal pain [4].
EPIDEMIOLOGY
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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, 9.8 per
100,000 person-years for women, and 6.3 per 100,000 person-years for the combined cohort
of men and women [5]. The age-adjusted prevalence of definite gastroparesis (based on
symptoms and delayed gastric emptying measured by scintigraphy) was 9.6 per 100,000
persons for men and 38 per 100,000 persons for women. In an epidemiologic study from
Europe, the estimated overall prevalence of gastroparesis was 13.8 per 100,000 persons with
an incidence of 1.9 per 100,000 person-years [6]. A systematic review of the literature
concluded that the prevalence of definite gastroparesis (symptoms plus evidence of delayed
gastric emptying) in the general population ranged from 13.8 to 267.7 per 100,000 adults,
and the incidence ranged from 1.9 to 6.3 per 100,000 person-years [7]. Across studies,
gastroparesis was more common among females. Overall survival was significantly lower in
patients with diabetes and in those with gastroparesis than for the age- and sex-matched
general population [5,6]. However, other estimates have been lower. In a United States cross-
sectional population-based study using electronic medical records and results of upper
gastrointestinal endoscopy and gastric emptying tests, the prevalence of gastroparesis in
type 1 and type 2 diabetics was 4.6 and 1.3 percent, respectively [8]. Overall, there were
about 70,000 people with gastroparesis out of the 44 million people based on the electronic
medical records, and the diagnosis was confirmed by the tests in only about 14 percent of
those with a record of gastroparesis. Overall, these data suggest a calculated prevalence of
0.16 percent.
ETIOLOGY
Although multiple conditions have been associated with gastroparesis, the majority of cases
are idiopathic, diabetic, iatrogenic (eg, medication-induced), or postsurgical ( figure 1).
Idiopathic — Idiopathic gastroparesis may be the most common form of gastroparesis. It is

estimated that no detectable primary underlying abnormality is found in approximately one-
half of patients with delayed gastric emptying [9].
Diabetes mellitus — Diabetes mellitus (DM) is the most frequently recognized systemic
disease associated with gastroparesis. Population-based studies in patients with diabetes
mellitus have reported upper gastrointestinal symptoms in 11 to 18 percent of patients [10-
13]. The estimated 10-year cumulative incidence of gastroparesis in patients with type 1 DM
and type 2 DM was estimated to be 5.2 and 1 percent, respectively [7]. In studies from
referral centers and hence potentially biased to select for patients with relatively severe
disease, 50 to 65 percent of patients with diabetes and upper abdominal symptoms had
delayed gastric emptying [14-16]. However, in a population-based cohort study, the
cumulative incidence of gastroparesis over 10 years in patients with type 1 and type 2 DM
was 5 percent and 1 percent, respectively, as compared with 0.2 percent in controls [17].
Symptoms of delayed gastric emptying are more pronounced in patients with type 1 DM as
compared with patients with type 2 DM [18]. (See "Diabetic autonomic neuropathy of the
gastrointestinal tract".)
Gastrointestinal complications of diabetes typically occur in patients who have had the
disorder for more than five years. Patients with diabetes mellitus have abnormalities at
several levels in the process of gastric emptying, including abnormal postprandial proximal
gastric accommodation and contraction, and reduced frequency of antral contractions.
These abnormalities are primarily due to autonomic dysfunction or abnormal intrinsic
nervous system (eg, nitrergic neurons, or interstitial cells of Cajal, the pacemaker system of
the gut) [19-21].
An alternative theory implicates a role for oxidative stress in the pathogenesis of diabetic
gastroparesis [22-24]. Observations based predominantly on animal models of diabetes
suggest that oxidative stress is associated with an increased number of macrophages and
up-regulation of heme-oxygenase-1 (HO1) in CD206(+) M2 macrophages. Indeed, onset of
delayed gastric emptying in these models of diabetic gastroparesis was not associated with
alteration in the total number of macrophages, but a selective loss of the protective
CD206(+)/HO1(+) M2 macrophages [23]. The clinical relevance of this oxidative stress was
explored by studying the effects of hemin in a small randomized controlled trial;
unfortunately, hemin, which was previously shown to activate HO-1 in humans, failed to
sustain increased HO1 levels beyond a week and did not improve gastric emptying or
symptoms in diabetic gastroparesis [25]. Therefore, the clinical relevance and potential to
reverse effects of oxidative stress on intrinsic neural or ICC pathways in diabetic
gastroparesis is still unclear.
Hyperglycemia (blood glucose >200 mg/dL) may also contribute to delayed gastric emptying.
Although acute hyperglycemia, associated with poorly controlled diabetes, typically has a
reversible effect on gastric emptying, chronic hyperglycemia is associated with an increased
risk of neuropathy. The pathogenesis of delayed gastric emptying in diabetes is discussed in
detail, separately. (See "Diabetic autonomic neuropathy of the gastrointestinal tract", section
on 'Pathogenesis'.)
There is increased appreciation of the impact of risk factors on gastroparesis, particularly in

urban centers [26], and these include prescriptions for narcotic medications and the
presence of comorbid risk factors, of which the most prevalent was type 2 diabetes.
Viral — A subset of patients with gastroparesis report sudden onset of symptoms after a
viral prodrome, suggesting a viral etiology. Several reports have documented the occurrence
of gastric stasis in association with prior viral infections, including Norwalk virus and
rotavirus [27-29].
Postviral gastroparesis often improves over one year [28,30,31]. However, a small proportion
of patients with infections due to viruses such as cytomegalovirus, Epstein-Barr virus, and
varicella-zoster virus may develop severe dysautonomia or even selective cholinergic
dysautonomia leading to persistent symptoms due to extrinsic autonomic denervation
[32,33].
Medications — Several medications can delay gastric emptying. These include [2]:
● Narcotics (affecting mu opiate receptors alone or combined with inhibition of

norepinephrine reuptake [eg, oxycodone and tapentadol, respectively]) [34].
● Alpha-2-adrenergic agonists (eg, clonidine).
● Tricyclic antidepressants [35].
● Calcium channel blockers.
● Dopamine agonists.
● Muscarinic cholinergic receptor antagonists.
● Octreotide [36].
● Glucagon-like peptide (GLP)-1 agonists (eg, exenatide) or analogues (eg, liraglutide) and
amylin analogues [37].
● Phenothiazines [38].
● Cyclosporine (but not tacrolimus, which is derived from macrolide molecule like
erythromycin, and does not inhibit gastric emptying).
● Immune checkpoint inhibitor therapy [39].
Postsurgical — Previous gastric and thoracic surgery can result in gastric stasis due to
intended or accidental injury to the vagus nerves (eg, with Billroth II gastrectomy,
fundoplication, lung or heart transplantation, paraesophageal hernia repair) [40,41]. Other
cases of gastroparesis have been rarely reported in patients after duodenal switch, or
biliopancreatic diversion or after Roux-en-Y gastric bypass for obesity [42,43]. Extrinsic vagal
denervation or loss of the antrum reduces the capacity of the stomach to empty
nondigestible solids during fasting, resulting in bezoar formation, and to triturate and empty
digestible food postprandially. (See "Pathogenesis of delayed gastric emptying" and "Gastric
bezoars", section on 'Pathogenesis'.)
Fundoplication is one of the most common surgical procedures leading to reversible or

permanent vagal injury. Other causes of vagal injury include variceal sclerotherapy and
botulinum toxin injection for medical treatment of achalasia [44-46] and radiofrequency
ablation for atrial fibrillation [47]. Vagal injury can be demonstrated by measurement of the
plasma pancreatic polypeptide (PP) response to modified sham feeding. With normal
physiology, sham feeding, which consists of chewing but not swallowing food, results in
cephalic vagal stimulation and thereby a rapid increase in plasma PP of at least 25 pg/mL in
the first 20 minutes followed by a return to baseline. In patients with vagal injury, sham
feeding is not associated with an increase in PP over baseline. In a generalized neuropathy
or injury to the vagus nerve between the brainstem and the level of the heart, evidence of
vagal injury can also be appraised by the heart period response to deep breathing (six times
per minute); breathing results in sinus arrhythmia through a vagally-mediated reflex. Vagal
injury or denervation results in a loss of sinus arrhythmia. This can be initially appraised on a
standard 12-lead electrocardiogram. Loss of sinus arrhythmia may be reversible (eg, over
several months after radiofrequency ablation for atrial fibrillation) [47].
Roux stasis syndrome can occur after a Roux-en-Y anastomosis. Uncoordinated contractions
in the efferent Roux limb itself causes stasis either in the gastric remnant or in the Roux limb
itself.
Neurologic disease — Several common neurologic disorders are associated with dysmotility
of the upper gastrointestinal tract and resultant gastroparesis ( figure 1).
● Extrinsic neural control (eg, the vagus nerve and lower thoracic spinal sympathetic
outflow) may be affected in disorders such as multiple sclerosis, brainstem stroke or
tumor, Parkinsonism, diabetic or amyloid neuropathy, or primary dysautonomias.
● The myenteric plexus may be involved in a degenerative, diffuse neurologic disorder

(eg, diabetes, AIDS, or parkinsonism). Focal loss of intrinsic inhibitory innervation of the
pylorus is responsible for congenital pyloric stenosis. In Parkinson disease, enteric
nervous system dysfunction has been reported to precede motor symptoms by years to
decades [48]. (See "Clinical manifestations of Parkinson disease", section on 'Cardinal
features'.)
● Medications used to treat neurologic disease can also contribute to gastric stasis (eg,
anticholinergics, dopaminergics). (See 'Medications' above.)
● Gastroparesis may be a manifestation of autonomic dysfunction. In a study of 242

patients with chronic gastroparetic symptoms, parasympathetic dysfunction was
associated with delayed gastric emptying and more severe upper gastrointestinal
symptoms [49]. Conversely, sympathetic hypofunction was associated with milder
symptoms.
Autoimmune — Delayed gastric emptying has been described in association with

autoimmune gastrointestinal dysmotility [50,51]. Autoimmune gastrointestinal dysmotility is
a dysautonomia affecting the gastrointestinal tract that occurs idiopathically or in
association with an anatomically remote neoplasm, most commonly small cell lung cancer. In
addition to delayed gastric emptying, affected patients may have slow intestinal transit, slow
colonic transit, and pelvic floor dyssynergia. The role of the autoimmune process in cases of
acquired dysautonomia manifesting with symptoms that include gastroparesis is illustrated

by the response to plasmapheresis treatment [52]. In a retrospective analysis of 11 female
patients with drug- and device-resistant gastroparesis who had coexisting positive
autoimmune profiles, treatment for 8 to 12 weeks with diverse immunomodulatory
treatment showed total symptom score improvement in 6 out of 11 patients, with maximum
gastrointestinal symptom improvement with intravenous immunoglobulin (2 out of 3
patients treated) [53]. In a subsequent open-label study, which included 14 patients (3
diabetic, 1 postsurgical, and 10 idiopathic gastroparesis) with serological and/or tissue
evidence of immunological abnormality, intravenous immunoglobulin (400 mg/kg infusion
weekly for 12 weeks) was associated with significant improvement in nausea, vomiting, early
satiety, and abdominal pain, with 9 out of 14 patients declared as responders to this open-
label treatment [54]. (See "Paraneoplastic syndromes affecting spinal cord, peripheral nerve,
and muscle", section on 'Autonomic neuropathy'.)
Other — Other causes of gastroparesis include mesenteric ischemia and diseases that result
in infiltration or degeneration of the muscle layer of the stomach (eg, scleroderma). Patients
with gastric or intestinal involvement due to scleroderma usually have clinically evident
systemic disease involving the skin, lungs, and/or the esophagus [55]. (See "Gastrointestinal
manifestations of systemic sclerosis (scleroderma)" and "Clinical manifestations and
diagnosis of systemic sclerosis (scleroderma) in adults".)
CLINICAL MANIFESTATIONS
Clinical features — Patients with gastroparesis can present with nausea (93 percent),
vomiting (68 to 84 percent), abdominal pain (46 to 90 percent), early satiety (60 to 86
percent), postprandial fullness, bloating, and, in severe cases, weight loss [9,56]. The vomitus
may contain food ingested several hours previously.
The predominant symptom may vary based on the underlying etiology. In a retrospective
study that included 416 patients with gastroparesis, patients with idiopathic gastroparesis
reported more early satiety, postprandial fullness, and abdominal pain as compared with
patients with diabetic gastroparesis. In contrast, patients with diabetic gastroparesis had
more severe retching and vomiting [18].
Bloating is common in gastroparesis and is severe in many individuals. In one study of 335
individuals with gastroparesis, bloating was at least mild in 76 percent and severe in 41
percent of individuals [57].
While abdominal pain is a frequent symptom in patients with gastroparesis, it is rarely the
predominant symptom (18 percent). In patients whose predominant symptom is abdominal
pain, other causes should be sought [58]. The pain is usually localized to the upper abdomen
and is often described as burning, vague, or crampy. Approximately 60 percent report

exacerbation of pain after eating. In one case series, pain interfered with sleep in 80 percent
of patients. However, the severity of abdominal pain did not correlate with a delay in gastric
emptying, suggesting that the cause of pain in this tertiary referral cohort may not have
been gastroparesis [59]. (See 'Differential diagnosis' below.)
In the cohort of 506 patients assessed in the National Institute of Health gastroparesis
consortium, abdominal pain was reported to be common in patients with gastroparesis, both
idiopathic and diabetic. Severe or very severe upper abdominal pain occurred in 34 percent
of the patients with gastroparesis and was associated with other symptoms of gastroparesis,
somatization, anxiety, impaired quality of life, and opiate medication use [60], as well as
cannabis use [61]. It is unclear whether this prominent and severe pain component reflects
the tertiary nature of the cohort.
Early satiety and postprandial fullness are commonly severe symptoms in both diabetic and
idiopathic gastroparesis [62,63].
Physical examination — Abdominal examination may reveal epigastric distention or

tenderness, but not guarding or rigidity. There may be a succussion splash. (See "Gastric
outlet obstruction in adults", section on 'Physical examination'.)
Patients may have signs of the underlying disorder resulting in gastroparesis. As an example,
patients with systemic sclerosis and Raynaud phenomenon may have taut skin in the hands
and chest, telangiectasia, small joint arthropathy, and crackles over the lower lung fields
from interstitial lung disease. In diabetic patients, gastrointestinal complications are often
associated with other signs of autonomic dysfunction [64,65]. These may include orthostatic
hypotension and absence of the pupillary reaction to light with persistence of the
accommodation response (the pseudo-Argyll-Robertson pupil or tonic pupil). (See "Tonic
pupil" and "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section
on 'Clinical features' and "Clinical manifestations and diagnosis of systemic sclerosis
(scleroderma) in adults".)
EVALUATION
Gastroparesis should be suspected in patients with nausea, vomiting, early satiety,

postprandial fullness, abdominal pain, or bloating. The goal of evaluation is to exclude a
mechanical obstruction and establish the diagnosis of gastroparesis by an assessment of
gastric motility. Evaluation should begin with a history and physical examination.
Exclude mechanical obstruction — All patients with suspected delayed gastric emptying
and, in particular, patients with colicky abdominal pain should undergo a careful upper
gastrointestinal endoscopy. We also perform computed tomographic (CT) enterography or

magnetic resonance (MR) enterography to exclude mechanical obstruction (eg, from a small
bowel mass or superior mesenteric artery syndrome). A barium follow-through examination
is performed if CT/MR enterography are unavailable. The presence of retained food after an
overnight period of fasting, although supportive of a diagnosis of gastroparesis, is not
diagnostic.
Assess gastric motility — In patients with suspected gastroparesis and no evidence of a

mechanical obstruction on imaging or upper endoscopy, an assessment of gastric motility is
necessary to establish the diagnosis of gastroparesis.
Scintigraphic gastric emptying — The most cost-effective, simple, and widely available
technique to confirm the presence of delayed gastric emptying of solids is scintigraphy
( figure 2). Documenting the presence of delayed gastric emptying and assessing the
severity is best achieved by evaluating the gastric emptying of solids. Since liquids often
empty from the stomach normally even when solids are abnormally retained, assessment of
liquid emptying is generally unnecessary unless dumping syndrome is suspected [66,67]. If
patients are too sick to tolerate a solid meal, a liquid nutrient meal containing radioisotope
may be used to permit scintigraphic measurement of gastric emptying [68]. However, it is
important to establish normal values for comparison as the physical characteristics and fat
content of the meal impact the rate of emptying and hence the normal values for gastric
emptying [69]. Other centers [70] utilize real eggs or omelettes with higher fat content (~300
kcal with 30 percent fat) to test for gastroparesis arguing that the higher fat content provides
an improved test for gastric motor function; the emptying profiles of different meal
substrates are reviewed elsewhere [71]. Importantly, when an optimal gastric emptying test
is conducted (solid meal, sufficient calories, assessed over at least three hours), there is a
good correlation between the delayed gastric emptying and symptoms [72].
● Pretest instructions – Medications that affect gastric emptying should be stopped at

least 48 hours before diagnostic testing [4]. Based on the pharmacokinetics of the
medication, the medication may need to be stopped more than 48 hours before
testing. Patients with diabetes should have blood glucose measured before starting the
gastric emptying test, and hyperglycemia should be treated. The test should be
performed only once blood glucose levels are <180 mg/dL.
● Test protocol – The suggested protocol involves a low fat egg-white meal with imaging
immediately after meal ingestion and again at one, two, and four hours following
ingestion. The meal composition may need to be altered depending upon the patient's
specific symptoms. Updated normal values for (99m)Tc egg or egg substitute and
consensus standards for performing and reporting gastric emptying scintigraphy have
been published [73-75].
Studies suggest that scans obtained immediately after meal ingestion and two and four
hours later are sufficient for most clinical indications [73,76,77]. Several centers limit
scans to two hours; this is suboptimal. However, it is important to note that for delayed
gastric emptying, gastric residual at four hours has a higher sensitivity for delayed
gastric emptying as compared with the two-hour measurement [76-78]. Evaluation
should be extended to four hours in patients with normal two-hour results. As an
example, in one study in which scintigraphy was performed on 129 consecutive
patients with suspected gastroparesis, the percentage of patients with delayed gastric
emptying increased from 33 percent at two hours to 58 percent using the results of the
two-, three-, and four-hour scans [78].
● Interpretation of test results – Delayed gastric emptying is defined as gastric

retention of >10 percent at four hours and/or >60 percent at two hours when using the
standard low fat, scrambled egg protein meal described above [73]. Although the
severity of symptoms do not always correlate with the rate of gastric emptying, delayed
gastric emptying has been classified based on the extent of gastric retention on
scintigraphy at four hours into the following:
• Mild – 10 to 15 percent
• Moderate – 15 to 35 percent
• Severe – >35 percent
Normal values for the percent remaining in the stomach at the key time points are 37
to 90 percent at one hour, 30 to 60 percent at two hours, and 0 to 10 percent at four
hours. It should be noted that each institution's nuclear medicine department may
have different normal values, which vary with the nature of the meal and isotope used.
Normal data have also been reported for a higher (30 percent) fat-containing "real egg"
test meal with higher caloric content (298 kcl). With such a meal, gastroparesis is
diagnosed when there is >75 percent retained in the stomach at two hours and >25
percent retained in the stomach at four hours [70].
Alternatives to scintigraphy — Alternative approaches for assessment of gastric emptying

include wireless motility capsule testing and 13C breath testing using octanoate or spirulina
incorporated into a solid meal [3].
Wireless motility capsule – A wireless motility capsule (WMC) can simultaneously

measure phasic pressure amplitudes, temperature, and pH as it traverses different
segments of the gastrointestinal tract [79]. The characteristic change in pH between
stomach and small intestine provides an indication of the gastric emptying time for a
nondigestible solid >1 cm long [80]. A systematic review that included seven studies
found that for the diagnosis of gastroparesis, as compared with gastric scintigraphy,
WMC had a sensitivity of 59 to 86 percent and specificity of 64 to 81 percent [81].
When the WMC is given with a meal, it often emptied after five hours as it requires
fasting migrating motor complex (MMC) to be emptied. In about 30 percent of
occasions in healthy adults, it emptied with coordinated postprandial antral
contractions; in the other healthy adults, the WMC emptied when there was a return of
fasting MMCs [82]. The amplitude of contractions immediately before emptying from
the stomach can provide useful information to exclude a myopathic disorder (eg,
scleroderma, amyloidosis) which are associated with low amplitude distal antral
contractions (<40 mmHg) [83].
● 13C breath testing – C13-labeled acetate, octanoic acid breath tests, or spirulina (a
plant-based protein source) have been used to assess gastric emptying [84-86]. After
ingestion of the stable isotope labeled test meal, the expiratory 13-CO2 concentration is
measured (eg, by mass spectrometry or infrared spectroscopy). The test is noninvasive
and, unlike scintigraphy, avoids radiation exposure. Most studies suggest that the
accuracy of these breath tests in normal and pathologic conditions is less than that of
scintigraphic measurements of gastric emptying [85,87,88]. The spirulina 13C breath
test was approved by the US Food and Drug Administration to diagnose gastroparesis
in April 2015 [89]. Approval was based on the observation in a study of 115 patients
who underwent simultaneous scintigraphy and spirulina 13C breath test. At 80 percent
specificity, the 13C-spirulina breath test samples at 150 and 180 minutes had a
combined sensitivity of 89 percent for delayed gastric emptying [88]. (See "Diabetic
autonomic neuropathy of the gastrointestinal tract".)
DIAGNOSIS
Gastroparesis is suspected in patients with nausea, vomiting, early satiety, postprandial

fullness, abdominal pain, or bloating. A mechanical obstruction is excluded with imaging (eg,
computed tomography or magnetic resonance enterography) or upper endoscopy as
discussed in the evaluation approach above (see 'Evaluation' above). The presence of delayed
gastric emptying on scintigraphy establishes the diagnosis of gastroparesis.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of gastroparesis includes other causes of chronic nausea and
vomiting. This is discussed in detail, separately. (See "Approach to the adult with nausea and
vomiting", section on 'Chronic disorders'.)
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● Psychiatric disease – Vomiting, anorexia, and other clinical symptoms of gastroparesis

may be the presentation of psychiatric diseases (eg, depression or anxiety neurosis),
classical eating disorders (eg, anorexia nervosa, bulimia), psychogenic vomiting, or a
side effect of a psychotropic medication.
The differentiation between an intrinsic gastric stasis syndrome and an eating disorder
that includes vomiting can be very difficult. A thorough history may help (eg, in
bulimia); however, physiologic abnormalities of the stomach such as gastric emptying
delays or dysrhythmias have been documented in anorexic patients, rendering the
distinction difficult. A high index of suspicion of an eating disorder is essential,
particularly in young women with significant weight loss and an altered body
perception or indifference towards weight loss. (See "Anorexia nervosa in adults and
adolescents: Medical complications and their management", section on
'Gastroparesis'.)
● Rumination syndrome – Rumination syndrome is a behavioral disorder that is most

commonly identified among mentally disadvantaged children, although it is
increasingly recognized among adolescents and adults of normal mental capacity,
particularly among those who are highly stressed, high achievers, or perfectionists [90-
92]. The behavior consists of daily, effortless regurgitation of undigested food within
minutes of starting or completing ingestion of a meal. Regurgitation is not preceded by
nausea or retching. Unlike patients with gastroparesis, patients with rumination
syndrome have normal gastric emptying. (See "Rumination syndrome", section on
'Clinical manifestations'.)
● Functional dyspepsia – Symptoms of gastroparesis overlap with those of functional

dyspepsia. However, early satiety, postprandial fullness, and epigastric pain or burning
are the predominant symptoms in patients with functional dyspepsia and, in contrast,
nausea, vomiting, and weight loss are the predominant symptoms in patients with
gastroparesis. In contrast to patients with gastroparesis, gastric emptying is normal in
patients with functional dyspepsia, but one-third of patients with functional dyspepsia
have slow emptying. The National Institutes of Health (NIH) gastroparesis consortium
data also identified overlap of diagnosis during follow-up, as patients originally
diagnosed as gastroparesis subsequently fulfilled criteria for functional dyspepsia and
vice-versa [63]. Therefore, a gastric emptying test with definite cut-off criteria for
diagnosing gastroparesis (eg, 300 kcal, 30 percent fat egg meal and >25 percent
retained in the stomach at four hours, and/or >75 percent retained at two hours) is
recommended based on normal value data acquired in 319 healthy adults [70]. It is
unclear whether "chronic unexplained nausea and vomiting" included as a subcategory
in Rome IV criteria is an entity distinct from gastroparesis or functional dyspepsia. (See
"Functional dyspepsia in adults".)
● Cyclic vomiting syndrome – Cyclic vomiting syndrome (CVS) refers to recurrent

episodes of intense nausea and vomiting lasting hours to days separated by symptom-
free periods of variable lengths. CVS is mimicked by cannabinoid hyperemesis [93].
Gastric emptying is rapid in some patients with CVS during symptom-free periods. (See
"Cyclic vomiting syndrome", section on 'Clinical manifestations' and "Cyclic vomiting
syndrome", section on 'Diagnosis'.)
ESTABLISHING THE ETIOLOGY
Once the diagnosis of gastroparesis is established, the underlying etiology should be

determined. In patients with gastroparesis in whom there is a known underlying disease, no
further investigation is necessary. In patients with gastroparesis and no known underlying
disease, we perform laboratory testing. We perform gastroduodenal manometry in patients
without an identifiable etiology despite laboratory testing. Autonomic testing is useful in
patients with evidence of neuropathic dysmotility on manometry, but without a known
underlying neurologic disorder ( algorithm 1).
Laboratory studies — Laboratory testing may help to identify diseases associated with
delayed gastric emptying. We obtain the following tests: hemoglobin, fasting plasma
glucose, serum total protein, albumin, thyrotropin (TSH), and an antinuclear antibody (ANA)
titer. In patients with diabetes, we obtain an HbA1c to assess their glycemic control. In
patients with a long-standing history of smoking, we test for ANNA-1 or anti-Hu antibody in
search for paraneoplastic gastroparesis. In patients with multiple symptoms suggesting
other neurological or autonomic (including bladder, sweating, postural dizziness), we
perform additional laboratory tests for evidence of viral infection or autoimmune process
directed to nicotinic acetyl choline receptors. (See 'Viral' above.)
Gastroduodenal manometry — Manometry can help differentiate a myopathic process (eg,

amyloid and scleroderma) from a neuropathic process (eg, diabetes mellitus, amyloid
neuropathy, and idiopathic autonomic neuropathy), if this distinction cannot be achieved by
other tests (eg, gastric emptying, blood tests or tissue diagnosis). Myopathic disorders are
typically associated with low amplitude contractions (mean <40 mmHg in antrum), whereas
in neuropathic disorders the amplitude of contractions is typically normal, but the
organization of the contractile response is abnormal and there is a persistence of fasting
motor patterns after meal ingestion [94]. High resolution water-perfused
antropyloroduodenal and jejunal manometry may identify antral, pyloric, or small intestinal
dysmotility that may aid in selection of therapy (eg, pharmacologic stimulation or
pyloromyotomy) [95,96].
Identification of pylorospasm or reduced pyloric compliance — Multilumen manometry

or Endoflip can identify pylorospasm [97] or reduced diameter or compliance or distensibility
of the pylorus [98]. Evaluation for pylorospasm or reduced compliance is increasingly

relevant as gastric per-oral endoscopic myotomy or laparoscopic pyloroplasty is being
offered as a treatment for gastroparesis. It is important to note that opioid stimulation
results in pylorospasm as well as gastroparesis with antral hypomotility [99]. (See "Treatment
of gastroparesis".)
Autonomic testing — Autonomic testing may be useful in patients with a neuropathic

pattern on manometry to further define the etiology of gastric stasis ( table 1). These tests
permit differentiation of a preganglionic or central lesion from a peripheral neuropathy
associated with autonomic dysfunction. In patients in whom a central lesion is suspected,
brain and spinal cord magnetic resonance imaging (MRI) should be performed. In patients
with a peripheral dysautonomia, further screening for a toxic (eg, lead poisoning), metabolic
(eg, porphyria), or paraneoplastic process (eg, lung cancer) should be performed
( algorithm 1).
Other tests — Several other tests have been used in patients with gastroparesis but are
predominantly research tools. Their role in clinical practice has not been defined.
● Electrogastrogram – Cutaneous electrogastrogram (EGG), involves placement of

surface electrodes to record the electrical control activity or "pacemaker" of the
stomach ( figure 3) [100,101]. Alterations in frequency (bradygastria, tachygastria, or
mixed) and reduction in the amplitude ("power") of the postprandial electrical signal are
seen in patients with idiopathic and diabetic gastroparesis, anorexia nervosa,
vector/motor sickness, and nausea of pregnancy. Dysrhythmias have also been
described in patients with nonulcer dyspepsia, with or without evidence of gastric
stasis. The precise role of EGG in the clinical evaluation and management of patients
with gastroparesis is the subject of ongoing research [100,101].
● Single photon emission computed tomography (SPECT) – The accommodation

response is related to early satiety and bloating postprandially. SPECT has been used to
characterize postprandial accommodation in a variety of upper gut dysmotilities [102-
104]. SPECT may help to identify subgroups of patients with gastroparesis that are
candidates for more selective pharmacotherapy. MRI measurements have also been
used to measure gastric accommodation [105]. In a cohort of approximately 100
patients with diabetes and upper gastrointestinal symptoms (16.7 percent with a
history of opioid use), there were almost equal numbers with abnormal gastric
emptying, abnormal gastric accommodation, both abnormal or neither abnormal [106].
Increased gastric accommodation volume is associated with slower gastric emptying
rate [107], and this may explain the potential benefit of sleeve gastrectomy in patients
with significant gastro-esophageal reflux reported in an uncontrolled study [108]. It is
important to note that the results of sleeve gastrectomy require confirmation with
sham-controlled trials in patients with gastroparesis, including documentation of the

gastric fasting and post-meal or accommodation volume.
● Full thickness gastric and small intestinal biopsy – Pathological examination of full
thickness gastric and small intestinal biopsies may provide confirmation of the organic
nature of the gastric stasis and may provide prognostic information [109]. Full thickness
biopsy should not be performed outside of research studies [3]. In the largest series of
101 patients in a referral practice with refractory and unexplained nausea and vomiting,
a high incidence of small bowel morphologic abnormalities (primarily neuropathies)
was reported [110]. The histologic abnormalities in gastroparesis are heterogeneous
and include myenteric inflammation, decreased innervation, reduced number of
interstitial cells of Cajal (ICC), and rarely muscle fibrosis [111,112]. Absence of ICCs was
associated with abnormalities of gastric slow waves, worse symptoms of gastroparesis,
and less improvement with gastric electrical stimulation [20].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Gastroparesis".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Upper endoscopy (The Basics)" and "Patient
education: Gastroparesis (delayed gastric emptying) (The Basics)")
● Beyond the Basics topics (see "Patient education: Upper endoscopy (Beyond the
Basics)")
SUMMARY AND RECOMMENDATIONS
● 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. (See 'Definition' above.)
● Etiology – Although multiple conditions have been associated with gastroparesis, the
majority of cases are idiopathic, diabetic, or postsurgical. (See 'Etiology' above.)
● Clinical manifestations – Patients with gastric stasis present with nausea, vomiting,
abdominal pain, early satiety, postprandial fullness, bloating, and, in severe cases,
weight loss. While abdominal pain is a frequent symptom in patients with
gastroparesis, it is rarely the predominant symptom. (See 'Clinical manifestations'
above.)
● Diagnosis – Gastroparesis should be suspected in patients with nausea, vomiting, early

satiety, abdominal pain or bloating. We perform upper endoscopy followed if clinically
indicated by computed tomography/magnetic resonance enterography to exclude
mechanical obstruction or mucosal disease as a cause of impaired gastric emptying.
Delayed gastric emptying on scintigraphy is required to establish the diagnosis of
gastroparesis ( algorithm 1).
On scintigraphy, delayed gastric emptying is defined as gastric retention of >10 percent

at four hours and/or >60 percent at two hours when using the 250 kcal, 2 percent fat
egg protein meal. Alternatively, the cut-offs are >75 percent at two hours and >25
percent at four hours when using the 300 kcal, 30 percent fat "real egg" meal. (See
'Evaluation' above and 'Diagnosis' above.)
● Routine evaluation to determine the underlying etiology – Once the diagnosis of

gastroparesis is established, the underlying etiology should be determined. In patients
with gastroparesis and no known underlying disease, we obtain the following
laboratory tests: hemoglobin, fasting plasma glucose, serum total protein, albumin,
thyrotropin (TSH) concentrations, and antinuclear antibody titer. (See 'Laboratory
studies' above.)
● Additional evaluation in patients without a clear etiology – In patients with

gastroparesis without an identifiable cause despite laboratory testing, we perform
gastroduodenal manometry provided that the expertise is available. Manometry can
help differentiate a myopathic process from a neuropathic process. We perform
autonomic testing in patients with a neuropathic pattern on manometry to further
define the etiology of gastric stasis ( algorithm 1). (See 'Gastroduodenal manometry'
above and 'Autonomic testing' above.)
Use of UpToDate is subject to the Terms of Use.
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Topic 2640 Version 31.0
GRAPHICS
Neurologic disorders that affect gastrointestinal motility
Neurologic disorders known to affect gastrointestinal motility. These disease processes involve
craniosacral parasympathetic pathways (left), sympathetic pathways (middle), and/or primary enteric
nerves or smooth muscle (right).
ENS: enteric nervous system; MNGIE: mitochondrial neurogastrointestinal encephalomyopathy.
Used with permission of American Society for Clinical Investigation, from: Camilleri M. Gastrointestinal motility disorders in
neurologic disease. J Clin Invest 2021; 131:e143771. Copyright © 2021; permission conveyed through Copyright Clearance
Center, Inc.
Graphic 139600 Version 1.0
Scintigraphic gastric emptying assessment in gastric stasis and gastric

dumping
Scintigraphic study in gastric stasis (left panel) and gastric dumping (right panel) at two and four
hours; the blue hatched lines at two and four hours refer to normal gastric retention. Compared with
normals, the tracer is removed more slowly at two and four hours with gastric stasis, and more rapidly
at two hours with gastric dumping.
Data from: Thomforde GM, Camilleri M, Phillips SF, et al. J Nucl Med 1995; 36:93.
Clinical and basic laboratory tests for gastroparesis
CT: computed tomography; MRI: magnetic resonance imaging.
Commonly performed tests of autonomic function
Test Principle Nerves assessed
Sweat test Heat stimulates Central sympathetic adrenergic

thermoregulatory center and peripheral sympathetic
cholinergic
BP lying, standing Postural BP control by Sympathetic adrenergic

adrenergic nerves
RR interval with deep breathing Vagal reflux bradycardia Cardiac vagus
Plasma pancreatic polypeptide Sham feeding stimulates vagal Efferent vagus to abdomen
response to modified sham center and efferents
feeding
Tachygastria
Electrogastrography of the gastric antrum shows a brief period of tachygastria between six and seven
minutes, followed by a compensatory pause, and then return of normal pacemaker function with
three contractions per minute.
Adapted from: Chen JD, Pan J, McCallum RW. Clinical significance of gastric myoelectrical dysrhythmias. Dig Dis Sci 1995;
13:275.

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23/2/24, 16:15 Gastroparesis: Etiology, clinical manifestations, and diagnosis - UpToDate

Official reprint from UpToDate®

Gastroparesis: Etiology, clinical manifestations, and

Literature review current through: Jan 2024.

Normal gastrointestinal motor function is a complex series of events that requires

Gastroparesis is a syndrome of objectively delayed gastric emptying of solids in the absence

Idiopathic — Idiopathic gastroparesis may be the most common form of gastroparesis. It is

There is increased appreciation of the impact of risk factors on gastroparesis, particularly in

● Narcotics (affecting mu opiate receptors alone or combined with inhibition of

Fundoplication is one of the most common surgical procedures leading to reversible or

● The myenteric plexus may be involved in a degenerative, diffuse neurologic disorder

● Gastroparesis may be a manifestation of autonomic dysfunction. In a study of 242

Autoimmune — Delayed gastric emptying has been described in association with

acquired dysautonomia manifesting with symptoms that include gastroparesis is illustrated

and is often described as burning, vague, or crampy. Approximately 60 percent report

Physical examination — Abdominal examination may reveal epigastric distention or

Gastroparesis should be suspected in patients with nausea, vomiting, early satiety,

gastrointestinal endoscopy. We also perform computed tomographic (CT) enterography or

Assess gastric motility — In patients with suspected gastroparesis and no evidence of a

● Pretest instructions – Medications that affect gastric emptying should be stopped at

● Interpretation of test results – Delayed gastric emptying is defined as gastric

• Severe – >35 percent

Alternatives to scintigraphy — Alternative approaches for assessment of gastric emptying

Wireless motility capsule – A wireless motility capsule (WMC) can simultaneously

Gastroparesis is suspected in patients with nausea, vomiting, early satiety, postprandial

● Psychiatric disease – Vomiting, anorexia, and other clinical symptoms of gastroparesis

● Rumination syndrome – Rumination syndrome is a behavioral disorder that is most

● Functional dyspepsia – Symptoms of gastroparesis overlap with those of functional

● Cyclic vomiting syndrome – Cyclic vomiting syndrome (CVS) refers to recurrent

ESTABLISHING THE ETIOLOGY

Once the diagnosis of gastroparesis is established, the underlying etiology should be

Gastroduodenal manometry — Manometry can help differentiate a myopathic process (eg,

Identification of pylorospasm or reduced pyloric compliance — Multilumen manometry

of the pylorus [98]. Evaluation for pylorospasm or reduced compliance is increasingly

Autonomic testing — Autonomic testing may be useful in patients with a neuropathic

● Electrogastrogram – Cutaneous electrogastrogram (EGG), involves placement of

● Single photon emission computed tomography (SPECT) – The accommodation

sham-controlled trials in patients with gastroparesis, including documentation of the

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

● Definition – Gastroparesis is a syndrome of objectively delayed gastric emptying in the

● Diagnosis – Gastroparesis should be suspected in patients with nausea, vomiting, early

On scintigraphy, delayed gastric emptying is defined as gastric retention of >10 percent

● Routine evaluation to determine the underlying etiology – Once the diagnosis of

● Additional evaluation in patients without a clear etiology – In patients with

Use of UpToDate is subject to the Terms of Use.

6. Ye Y, Jiang B, Manne S, et al. Epidemiology and outcomes of gastroparesis, as

30. Naftali T, Yishai R, Zangen T, Levine A. Post-infectious gastroparesis: clinical and

33. Lobrano A, Blanchard K, Abell TL, et al. Postinfectious gastroparesis related to

64. KASSANDER P. Asymptomatic gastric retention in diabetics (gastroparesis diabeticorum).

74. Cremonini F, Mullan BP, Camilleri M, et al. Performance characteristics of scintigraphic

83. Thumshirn M, Bruninga K, Camilleri M. Simplifying the evaluation of postprandial antral

Neurologic disorders that affect gastrointestinal motility

ENS: enteric nervous system; MNGIE: mitochondrial neurogastrointestinal encephalomyopathy.

Graphic 139600 Version 1.0

Scintigraphic gastric emptying assessment in gastric stasis and gastric

Graphic 69354 Version 2.0