INTRODUCTION

Chronic gastroduodenal symptoms pose a diagnostic and therapeutic challenge. These symptoms are commonly seen in chronic gastroduodenal disorders, including functional dyspepsia (FD), chronic nausea and vomiting syndrome (CNVS), and in gastroparesis with delayed gastric emptying (1,2). However, recent evidence shows these disorders are clinically interchangeable because of overlapping symptom profiles and tests (3). More specific diagnostic pathways are therefore required to guide targeted care (4).

Gastric Alimetry (Alimetry, Auckland, New Zealand) is a new diagnostic device, combining noninvasive gastric electrical mapping with simultaneous symptom logging in a validated App (5,6). The gastric mapping data are capable of identifying patient subgroups with neuromuscular dysfunction, while the symptom data can help determine symptom origins (5,6).

Gastric Alimetry is now being introduced into practice, challenging existing models of care. As such, this study had 2 aims; first, to develop and refine an initial framework for the implementation of Gastric Alimetry in the routine management of gastroduodenal disorders and, second, to assess its influence on diagnosis and management in a consecutive series of 50 cases.

METHODS Study design

A series of 50 consecutive patients with chronic gastroduodenal disorders investigated with Gastric Alimetry were retrospectively evaluated after ethical approval. Patients were recruited from 2 tertiary centers in the North Island of New Zealand receiving care from gastroenterologists with motility expertise (n = 2). Patients with a diagnosis of cannabinoid hyperemesis syndrome or cyclical vomiting syndrome were excluded.

All patients underwent standard Gastric Alimetry tests: 30-minute fasted test meal, followed by 4-hour postprandial recording with concurrent symptom logging (5,6). The standard test meal recommended by the manufacturer, for which validated spectral reference ranges are available, was used (approximately 480 kCal consisting of an oatmeal energy bar and nutrient drink) (7). Pretest and posttest test diagnoses were assessed, together with management changes implemented following Gastric Alimetry, to define clinical decision-making impact made on its basis. CNVS and FD were diagnosed per Rome-IV criteria (2), and gastroparesis was defined as a delayed gastric emptying test (GET) (8). Where gastric emptying data were available, all were scintigraphic studies. Gastroscopy and Helicobacter pylori testing were routine in both centers. Comorbidity data are summarized in the Supplementary Appendix (see Supplementary Digital Content 1, https://links.lww.com/CTG/A994).

The clinical impact of Gastric Alimetry was evaluated applying similar methodology and criteria previously used in a study addressing the impact of antroduodenal manometry (9). Charts were reviewed by an independent assessor, with a positive management impact defined as an outcome that established a new diagnosis or altered therapy (medication, endoscopic intervention, feeding) (9).

Gastric Alimetry test phenotypes

A Gastric Alimetry phenotype set that is currently under iterative development was used (10). This classification approach was applied clinically, as based on recent Gastric Alimetry studies (7,11,12), the gastric physiology literature (10), and experience from applying these learnings in routine clinical practice, according to the following scheme:

Gastric Alimetry spectral analysis provides the following major phenotypes (10):

Dysrhythmic phenotype: Gastric Alimetry Rhythm Index <0.25, supported by low amplitudes <22 μV (13). Managed as per gastroparesis guidelines (1), regardless of GET status. High sustained body mass index–adjusted amplitude: >70 μV (13). Consider distal obstruction and evaluate GET with consideration of pyloric therapies (13). Normal spectral activity: Request GET if required (1). If delayed, prokinetics initiated and pyloric therapies considered (1); if normal, managed per symptom profile below.

Gastric Alimetry symptom profiling provides the following major phenotypes:

Normal spectral analysis and symptoms dependent on the gastric amplitude: Sensorimotor: symptoms correlate with gastric amplitude, suggesting possible hypersensitivity/accommodation disorders. Consider therapy per postprandial distress syndrome (2). Postgastric: symptoms trending upward late in postprandial period; investigate more distal disorders (e.g., small bowel dysmotility or other pathologies). Activity relieved: increase in gastric activity is associated with reduction in symptoms, suggesting transit or accommodation disorder. Normal spectral analysis and symptoms independent of the gastric amplitude: Continuous profile: symptoms constant/do not correlate with gastric amplitude; consider therapy per epigastric pain syndrome (2). Meal induced: symptoms worse after a meal and not meeting criteria of amplitude-dependent profiles. Meal relieved: symptoms improving after a meal and not meeting criteria of amplitude-dependent profiles. Management framework

A framework was iteratively developed on the basis of clinical experience accrued through the presented series (Figure 1a). The management framework is proposed to integrate Gastric Alimetry, GET, and existing clinical guidelines. The model was applied pragmatically with reference to individual patient histories, clinical workup, and comorbidities, while accepting that gastroduodenal disorders and phenotypes may overlap (2).

Figure 1.:

(a) Flow diagram developed for the application of Gastric Alimetry in the management of gastroduodenal disorders. Patients may have more than 1 phenotype. (b–d) Examples of Gastric Alimetry spectral data, amplitude plots, and symptom burden graphs from the study cohort. (b) Normal spectral analysis; continuous symptom profile: principal gastric frequency 3.01 cpm (range 2.65–3.35); Gastric Alimetry-Rhythm Index (GA-RI) 0.88 (range ≥0.25); body mass index–adjusted amplitude 61.3 ± 17.8 μV (range 22–70 μV). (c) Dysrhythmic profile (GA-RI 0.12; 21.6 μV). (d) Dysrhythmic neuromuscular profile with a sensorimotor symptom profile (GA-RI 0.12; 21.6 μV). (e) High amplitude activity (average 72.1 μV).

Health care utilization analysis

A health care utilization and health economic analysis was also conducted in the major participating center, where follow-up data were available. The average health care utilization costs per patient were calculated before vs after Gastric Alimetry testing. Follow-up was restricted to a year before and after Gastric Alimetry testing. Pre- and post- comparisons were made using paired nonparametric Wilcoxin tests.

RESULTS

A total of 50 patients were evaluated (Wellington/North Shore Hospitals, New Zealand), 45 were women (90%); median age 30 years (interquartile range [IQR] 22–46). The median follow-up of patients was 12.6 months (IQR 10.8–17.5). Predominant presenting symptoms were nausea/vomiting (72%), upper abdominal pain (8%), other functional gastrointestinal symptoms (e.g., bloating, fullness, heartburn; 20%). No adverse events associated with Gastric Alimetry testing were observed.

Gastric Alimetry testing

Figure 1b shows representative examples of phenotypes encountered in the cohort. Nine of 50 (18%) had a dysrhythmic disorder, 2/50 (4%) had a high sustained body mass index–adjusted amplitude, and 33 (66%) had normal spectral analysis. Of those with a normal spectral analysis, 9 had symptoms related to the gastric amplitude: 6 (18%) sensorimotor pattern, 3 (9%) activity-relieved pattern; while 19 (58%) had symptoms independent of gastric amplitude (10 [53%] continuous pattern, 7 [37%] meal-induced pattern, and 2 [11%] meal-relieved pattern). The median total symptom burden score was 24.6 (IQR 14.9–31.5).

Gastric emptying

Most of the patients had a past GET (n = 36; 72%), of which 19 (53%) had delayed emptying, 3 (8.3%) had rapid emptying, and 3 (8.3%) were indeterminate. Ten had a gastric emptying study initiated after Gastric Alimetry testing (of which 8 were repeat tests).

Changes in clinical management

Primary diagnoses before Gastric Alimetry evaluation were gastroparesis/other gut motility disorder (20/50; 40%) or Rome-IV gastroduodenal disorder, 24 (48%) with CNVS, and 6 (12%) with FD. Diagnostic outcomes of the Gastric Alimetry tests are summarized in Table 1 at the patient level and presented in Figure 2a, with impact on diagnosis and management presented in Figure 2b, c. Overall, the test aided a management decision in 42/50 patients (84%). Only 5 (10%) remained unclassified by the Gastric Alimetry phenotyping system, 4 of whom had gastroparesis and 1 had CNVS. Of the 19 with normal spectral analysis, and symptoms independent of gastric amplitude, 5 (26%) had delayed gastric emptying while the remaining 14 (74%) had CNVS or FD (Table 1 and Figure 2a). Medications were de-escalated in 10 (20%). Therapeutic changes favored prokinetics in 36%, neuromodulators in 56%, with 2 patients receiving pyloric intervention, and management focused predominantly on other medications in 8% (Figure 2b).

Site Demographics (age/sex) Time-of-test dominant symptoms Total symptom burden index Diagnosis GA symptom profile GA spectral phenotype GA overall phenotype Gastric emptying result Change in investigation Change in management Site 1 19 F/20.6 Nausea, bloating 11.4 CNVS Meal induced Low rhythm stability Low rhythm stability Indeterminant — Started prokinetics, started neuromodulators Site 1 38 F/34.1 Excessive fullness, bloating, nausea, upper gut pain 25.6 Gastroparesis Meal induced High frequency High frequency Delayed OGD Started migraine medications, stopped prokinetics Site 1 36 F/32.3 Nausea, excessive fullness 23.2 Gastroparesis Meal induced Normal spectral metrics Meal induced Delayed — Increased prokinetics, started neuromodulators Site 1 28 F/23.7 Excessive fullness, bloating, nausea, stomach burn 27.1 CNVS Sensorimotor Normal spectral metrics Sensorimotor Normal — Increased neuromodulators Site 1 46 F/29.9 Nausea, bloating, excessive fullness 24.8 Gastroparesis Meal induced Low rhythm stability Low rhythm stability Delayed — Started 5-HT4 agonist Site 1 30 F/19.2 Nausea, upper gut pain, bloating, excessive fullness 41.6 Gastroparesis Sensorimotor Normal spectral metrics Sensorimotor Delayed — Increased neuromodulators, started migraine medications, stop prokinetics, health psychology input Site 1 36 F/36.7 Nausea, bloating, excessive fullness, upper gut pain 30.4 Gastroparesis Continuous Normal spectral metrics Continuous Delayed — Increased prokinetics, started neuromodulators Site 1 22 F/28.8 Nausea, upper gut pain, bloating, excessive fullness 28 CNVS Meal induced Low rhythm stability Low rhythm stability Indeterminant GET repeated Started prokinetics, started 5-HT4 agonists, started neuromodulators, PN stopped Site 1 64 M/18.5 Excessive fullness, nausea, upper gut pain, bloating 23.9 CNVS Meal induced Low amplitude Low amplitude Rapid — No change Site 1 22 F/28.1 Nausea, bloating 15 CNVS Continuous Normal spectral metrics Continuous Rapid — Increased neuromodulators Site 1 30 M/23.5 Nausea, bloating, upper gut pain, excessive fullness 27 FD Meal induced Low amplitude Low amplitude Normal — Started PPI, started muscle relaxant Site 1 19 F/19.4 Bloating, upper gut pain, excessive fullness, nausea 26.2 CNVS Meal induced Low amplitude Low amplitude Rapid — Start 5-HT4 agonist Site 1 18 F/21.5 Nausea, bloating, upper gut pain, heartburn, excessive fullness 38.6 Other motility disorder Sensorimotor Normal spectral metrics Sensorimotor Normal GET repeated Started neuromodulator, started migraine meds, health psychology input, PN stopped Site 1 30 F/18.6 Nausea, bloating, excessive fullness 27.8 Gastroparesis Sensorimotor High amplitude High amplitude Delayed GET repeated Increased neuromodulator, started migraine meds, health psychology input Site 1 30 F/15.6 Nausea, excessive fullness, stomach burn 39.1 FD Sensorimotor Low frequency Low frequency N/A GET repeated Started prokinetics, started PPI, started neuromodulator, weaned opiates Site 1 22 F/20.2 Bloating, upper gut pain 15.3 CNVS Continuous Normal spectral metrics Continuous Normal — Health psychology input Site 1 51 F/23.5 Nausea, bloating, upper gut pain, excessive fullness 28.6 Other motility disorder Meal induced Low rhythm stability Low rhythm stability Delayed — Increased prokinetics, increased neuromodulator Site 1 60 F/31.6 Excessive fullness 5.7 Gastroparesis Other Normal spectral metrics Other Delayed OGD Pyloric botox Site 1 30 F/32.7 Nausea, heartburn, bloating, excessive fullness 25.4 Gastroparesis Other Low frequency Low frequency Delayed — Started prokinetics, started neuromodulators, started 5-HT4 agonist Site 1 45 F/15.0 Bloating 6.6 Gastroparesis Other Normal spectral metrics Other Delayed — Stopped a diabetic medication Site 1 26 F/17.2 Nausea, excessive fullness 18.9 Gastroparesis Sensorimotor Normal spectral metrics Sensorimotor Delayed — Increased neuromodulator, stopped 5-HT4 agonist, started antiemetics, PN stopped Site 1 46 F/20.8 Excessive fullness, heartburn, stomach burn, bloating 34.8 FD Meal induced Normal spectral metrics Meal induced N/A — Started neuromodulator Site 1 32 F/21.9 Excessive fullness, bloating, nausea 11.9 CNVS Meal induced Normal spectral metrics Meal induced N/A GET repeated, OGD Increased neuromodulators, started prokinetics, stopped opiates Site 1 32 F/20.8 Nausea, upper gut pain 4.1 CNVS Sensorimotor Normal spectral metrics Sensorimotor Indeterminant GET repeated, OGD No change Site 1 21 F/23.0 Bloating, nausea, stomach burn, excessive fullness, heartburn, upper gut pain 24.3 CNVS Activity relieved Normal spectral metrics Activity relieved Normal — Started prokinetics Site 1 17 F/19.4 Bloating, excessive fullness, nausea 14.8 CNVS Activity relieved Normal spectral metrics Activity relieved N/A GET, OGD No change Site 1 70 M/23.4 Bloating, excessive fullness 17.6 CNVS Activity relieved Normal spectral metrics Activity relieved Normal — No change Site 1 23 M/21.4 Nausea, excessive fullness 19.4 CNVS Meal induced Normal spectral metrics Meal induced N/A OGD Started neuromodulators, start 5-HT4 agonist Site 1 46 F/23.4 Excessive fullness, nausea, upper gut pain 31.6 Gastroparesis Meal induced Normal spectral metrics Meal induced Delayed GET repeated Increased prokinetics, started neuromodulator, start 5-HT4 agonist, PN stopped Site 1 51 F/22.7 Bloating, stomach burn 6.8 FD Other High frequency High frequency Normal — Start PPI, start prokinetics, start neuromodulator Site 1 63 F/19.6 Bloating, upper gut pain 5.7 Gastroparesis Other Low rhythm stability Low rhythm stability Delayed Antroduodenal manometry Other (increase octreotide), health psychology input Site 1 19 F/25.0 Bloating, nausea, upper gut pain 23.8 CNVS Continuous Normal spectral metrics Continuous N/A — Start neuromodulators Site 1 25 F/18.9 Excessive fullness, bloating 7.1 Gastroparesis Other Normal spectral metrics Other Delayed — No change Site 1 30 F/29.5 Nausea, bloating, upper gut pain, excessive fullness 29.5 CNVS Meal induced Normal spectral metrics Meal induced Normal — Increase PPI, increase neuromodulators Site 2 26 F/22.0 Nausea, excessive fullness, upper gut pain, bloating 39.6 Gastroparesis Continuous Normal spectral metrics Continuous Normal — Started H1 receptor antagonist, started prokinetics, PN stopped Site 2 50 F/20.7 Nausea, upper gut pain, heartburn, stomach burn, bloating, excessive fullness 59.1 CNVS Continuous Normal spectral metrics Continuous Normal — Increased neuromodulator, stopped 5-HT3 antagonist Site 2 23 F/31.2 Nausea, bloating, heartburn 15.1 Gastroparesis Other Normal spectral metrics Other Delayed — No change Site 2 20 F/25.1 Stomach burn, nausea, excessive fullness 18.5 CNVS Meal relieved Normal spectral metrics Meal relieved Normal GET repeated, MRE Increased neuromodulator, stopped H2 receptor antagonist Site 2 44 F/30.1 Heartburn, stomach burn, upper gut pain, nausea, bloating, excessive fullness 31 Gastroparesis Meal induced High amplitude High amplitude Delayed GET No change Site 2 18 F/20.4 Stomach burn, heartburn, excessive fullness, upper gut pain, nausea, bloating 41.1 FD Sensorimotor High frequency High frequency N/A — Increased PPI Site 2 56 F/18.3 Bloating, excessive fullness 13.5 FD Meal induced Normal spectral metrics Meal induced N/A — Started neuromodulator, other (stopped pancreatic enzymes), health psychology input, immunology input, dietitian Site 2 34 F/29.9 Excessive fullness, bloating, nausea 13.3 CNVS Meal relieved Normal spectral metrics Meal relieved N/A — No change Site 2 53 F/39.7 Bloating, excessive fullness, upper gut pain, nausea, stomach burn 36.3 CNVS Continuous High frequency High frequency N/A — Started prokinetics Site 2 29 F/36.8 Upper gut pain, heartburn, stomach burn, excessive fullness 36.7 CNVS Meal induced Low rhythm stability Low rhythm stability N/A — Started neuromodulator Site 2 58 M/27.1 Bloating, excessive fullness, nausea 7.4 CNVS Continuous Normal spectral metrics Continuous Normal — Increased prokinetics, increased neuromodulator, increased PPI Site 2 63 F/24.5 Upper gut pain 1.6 CNVS Other Normal spectral metrics Other N/A — Increased skeletal muscle relaxants, health psychology input, diaphragmatic breathing Site 2 19 M/20.4 Nausea, bloating, heartburn 14.7 CNVS Continuous Normal spectral metrics Continuous N/A — Increased neuromodulator, increased prokinetics, started antidepressant, health psychology and psychiatry input Site 2 25 F/17.6 Excessive fullness, nausea, heartburn, bloating, upper gut pain 25.6 Gastroparesis Continuous Normal spectral metrics Continuous Delayed — Increased neuromodulator, increased prokinetics Site 2 25 F/16.6 Nausea, bloating, upper gut pain, heartburn, stomach burn, excessive fullness 51.6 CNVS Continuous Normal spectral metrics Continuous N/A — Increased neuromodulator, dietitian, health psychology and psychiatry involvement Site 2 18 F/19.9 Bloating, nausea, excessive fullness, upper gut pain 33.9 Gastroparesis Sensorimotor Normal spectral metrics Sensorimotor Delayed — Pyloric intervention recommended

5-HT, 5-hydroxytryptamine; CNVS, chronic nausea and vomiting syndrome; FD, functional dyspepsia; GA, Gastric Alimetry; GET, gastric emptying test; MRE, magnetic resonance enterography; N/A, not applicable; OGD, Oesophago-Gastro-Duodenoscopy; PN, parenteral nutrition; PPI, proton pump inhibitor.

Figure 2.: (a) Sankey diagram showing the changes in diagnoses that occurred between gastroparesis/other motility disorder and Rome-IV gastroduodenal disorders vs post–Gastric Alimetry diagnoses (right column). (b) Significant changes in management that were guided by Gastric Alimetry test data, as per the workflow in Figure 1a. (c) Significant changes in invasive (parenteral [PN] or enteral nutrition [EN]) that were achieved because of the changes instituted in Figure 2a, b in tandem with integrated clinical care. CNVS, chronic nausea and vomiting syndrome; FD, functional dyspepsia.

Changes in invasive nutritional support occurred in 9/50 cases (18%) (Figure 2c). Of 7 patients on parenteral nutrition before evaluation, 5 were successfully weaned, together with 3 patients on enteral feeding, after management changes facilitated tolerance of diet. Conversely, nasojejunal feeding was initiated in 1 patient with a neuromuscular disorder who failed to respond to medical management.

Health care utilization