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Our aim was to investigate the feasibility of measuring antral contractions and duodenal bolus propagation (DBP) during dynamic antral contraction scintigraphy (DACS) as an assessment of antro-pyloro-duodenal coordination (APDC). Gastric emptying scintigraphy (GES) with DACS was performed with Tc-99m sulfur colloid (SC) using increasing doses of 74 MBq (2 mCi) for 10 subjects, 185 MBq (5 mCi) for 11, and 370 MBq (10 mCi) for 11. DACS was performed for 10 min after static images at 0, 30, 60, 120, 180, and 240 min in anterior and right anterior oblique (RAO) projections. Best projection and lowest dose of Tc-99m SC were assessed visually. DBP were quantified utilizing duodenal activity peaks from a region of interest in the first portion of the duodenum. DBP was better visualized in the RAO projection than anterior projection and using 185 MBq (5 mCi) and 370 MBq (10 mCi) compared with 74 MBq (2 mCi). DBP showed infrequent and irregular bolus transfers from the antrum to the duodenum. Antral activity peaks at 60 min averaged 2.91 ± 0.66 per minute and duodenum bolus peaks 0.36 ± 0.18 per minute (ratio 0.36/2.91 = 0.12). DBP activity peaks can be measured during GES with DACS but requires a 185-MBq (5 mCi) dose of Tc-99m SC radiolabeled test meal for adequate DBP signal detection and is better imaged in RAO than anterior projection. DBPs over the first 60 min postmeal ingestion are infrequent with only 12% of the antral contractions propagating into the duodenum. This methodology appears promising to assess APDC. NEW & NOTEWORTHY This study shows that duodenal bolus propagations after meal ingestion can be measured during gastric emptying scintigraphy using dynamic scintigraphy. Duodenal bolus propagation over the first 60 min postmeal ingestion are infrequent with only 12% of the antral contractions propagating into the duodenum. This methodology appears promising to assess antropyloroduodenal coordination in patients with unexplained symptoms of upper gastrointestinal dysmotility.

The SNMMI EANM Procedure Guide on Gastrointestinal Transit currently indicates that the mean of total abdominal counts of seven time points (0-360 min) are used to define the total abdominal counts for bowel transit studies. The purpose of this study was to investigate the variability of total abdominal counts during the initial six hours of bowel transit and to determine if a simplified, single time point measurement can be used. METHODS: Thirty consecutive bowel transit studies were retrospectively analyzed. Patients received an oral dose of 4.6 MBq(125 µCi) 111In-DTPA in 300 cc of water together with a standard egg white solid-phase, gastric emptying meal to measure small bowel and colon transit. 111In-DTPA geometric mean and decay corrected total abdominal counts obtained at 0, 30, 60, 120, 180, 240, 300, and 360 minutes post meal ingestion were analyzed. The coefficient of variation (CV) was used to determine the variability of the mean total abdominal counts. Slope of the regression line, Student’s t-test and a Pearson Product-Moment Correlation Coefficient (PCC) were also calculated to determine the correlation of total abdominal counts at each time point compared to the mean of all time points. RESULTS: The mean CV of total abdominal counts of each patient was 3.3% with a range of 1.1% to 6.3%. The mean of the slope of the regression line of the total abdominal counts of the patients was -0.001±0.003. There was no significant difference between the measured slope of the regression line compared to a line with a slope of 0 (p>0.05). Comparing the counts at each time to the mean counts, there was no significant difference (p>0.05). The PCC of each of the counts showed a significant and strong correlation between each interval and the mean total abdominal counts (p

Impaired fundic accommodation (FA) limits fundic relaxation and the ability to act as a reservoir for food. Assessing intragastric meal distribution (IMD) during gastric emptying scintigraphy (GES) allows for a simple measure of FA. The 3 goals of this study were to evaluate trained readers’ (nuclear medicine and radiology physicians) visual assessments of FA from solid-meal GES; develop software to quantify GES IMD; and correlate symptoms of gastroparesis with IMD and gastric emptying. Methods: After training to achieve a consensus interpretation of GES FA, 4 readers interpreted FA in 148 GES studies from normal volunteers and patients. Mixture distribution and κ-agreement analyses were used to assess reader consistency and agreement of scoring of FA. Semiautomated software was used to quantify IMD (ratio of gastric counts in the proximal stomach to those in the total stomach) at 0, 1, 2, 3, and 4 h after ingestion of a meal. Receiver-operating-characteristic analysis was performed to optimize the diagnosis of abnormal IMD at 0 min (IMD0) with impaired FA. IMD0, GES, water load testing, and symptoms were then compared in 177 patients with symptoms of gastroparesis. Results: Reader pairwise weighted κ-values for the visual assessment of FA averaged 0.43 (moderate agreement) for normal FA versus impaired FA. Readers achieved 84.0% consensus and 85.8% reproducibility in assessing impaired FA. IMD0 based on the division of the stomach into proximal and distal halves averaged 0.809 (SD, 0.083) for normal FA and 0.447 (SD, 0.132) (P < 0.01) for impaired FA. On the basis of receiver-operating-characteristic analysis, the optimal cutoff for IMD0 discrimination of normal FA from impaired FA was 0.568 (sensitivity, 86.7%; specificity, 91.7%). Of 177 patients with symptoms of gastroparesis, 129 (72.9%) had delayed gastric emptying; 25 (14.1%) had abnormal IMD0. Low IMD0 (impaired FA) was associated with increased early satiety (P = 0.02). Conclusion: FA can be assessed visually during routine GES with moderate agreement and high reader consistency. Visual and quantitative assessments of FA during GES can yield additional information on gastric motility to help explain patients’ symptoms.

Background & Aims There are few effective treatments for nausea and other symptoms in patients with gastroparesis and related syndromes. We performed a randomized trial of the ability of the neurokinin-1 receptor antagonist aprepitant to reduce symptoms in patients with chronic nausea and vomiting caused by gastroparesis or gastroparesis-like syndrome. Methods We conducted a 4-week multicenter, double-masked trial of 126 patients with at least moderate symptoms of chronic nausea and vomiting of presumed gastric origin for a minimum of 6 months. Patients were randomly assigned to groups given oral aprepitant (125 mg/day, n = 63) or placebo (n = 63). The primary outcome from the intention-to-treat analysis was reduction in nausea, defined as a decrease of 25 mm or more, or absolute level below 25 mm, on a daily patient-reported 0-to-100 visual analog scale (VAS) of nausea severity. We calculated relative risks of nausea improvement using stratified Cochran-Mental-Haenszel analysis. Results Aprepitant did not reduce symptoms of nausea, based on the primary outcome measure (46% reduction in the VAS score in the aprepitant group vs 40% reduction in the placebo group; relative risk, 1.2; 95% CI, 0.8–1.7) ( P = .43). However, patients in the aprepitant group had significant changes in secondary outcomes such as reduction in symptom severity (measured by the 0–5 Gastroparesis Clinical Symptom Index) for nausea (1.8 vs 1.0; P = .005), vomiting (1.6 vs 0.5; P = .001), and overall symptoms (1.3 vs 0.7; P = .001). Adverse events, predominantly mild or moderate in severity grade, were more common in aprepitant (22 of 63 patients, 35% vs 11 of 63, 17% in the placebo group) ( P = .04). Conclusions In a randomized trial of patients with chronic nausea and vomiting caused by gastroparesis or gastroparesis-like syndrome, aprepitant did not reduce the severity of nausea when reduction in VAS score was used as the primary outcome. However, aprepitant had varying effects on secondary outcomes of symptom improvement. These findings support the need to identify appropriate patient outcomes for trials of therapies for gastroparesis, including potential additional trials for aprepitant. ClinicalTrials.gov no: NCT01149369.