Index and converted gastric bypass surgery involve reconstruction of the gastrointestinal tract with exclusion of a gastric remnant. Postoperative symptoms can be persistent, including nausea, vomiting, pain and dumping; however, the pathophysiology may be unclear with normal endoscopy or imaging [2]. The results of this study show that over one-third of patients experienced moderate to severe symptoms with worse QoL compared to matched controls. Remnant gastric stomach function was also found to be highly degraded in the patient cohort, with these changes found to be correlated to worse symptom burdens and lower quality of life scores.

The associations between remnant stomach degeneration, foregut symptoms, and quality of life in this study are novel. Degradation of the gastric pacemaker system in the bypassed stomach is expected due to disuse degeneration, as pacemaker system degeneration has also been described in animal stomachs after marked calorie restriction, thought to be mediated by reduced local production of IGF-1 [31]. Gastric bypass in itself could also conceivably modify the gastric electrical conduction system through disconnection of the stomach and partial denervation [32]. It is plausible that the gastric dysrhythmias could contribute to upper gastrointestinal symptoms in bypass patients, as post-surgical gastric dysrhythmias have been linked to symptoms in previous postoperative populations [14, 15, 33, 34].

The GA-RI was reduced in the conversion group compared to the bypass-only group, which neared significance (p = 0.07) despite the small number of conversion patients in this subgroup (n = 6). This is likely a true finding, reflecting the effect of the previous vertical sleeve gastrectomy, which definitively removes the native pacemaker and will have already caused underlying gastric rhythm disturbances [14]. The adjusted amplitude and the ff-AR reductions compared to the matched control cohort are explained by pacemaker degeneration, smooth muscle atrophy, a reduced volume of electrically active functioning gastric tissue, and the lack of food content stimulating the gastric remnant [32].

While there have been previous studies assessing the effects of surgical techniques on the postoperative outcomes and quality of life in bypass, along with manometric assessments of the gastric pouch and the Roux limb, studies of the remnant gastric conduction system have been sparse prior to this study [35, 36]. This is likely due to the lack of adequately high-resolution techniques to assess the electrophysiology of the stomach. Recent technological advances in the form of invasive and non-invasive high-resolution gastric mapping techniques have now significantly improved our understanding of gastric electrophysiology in health and disease [9, 24, 37]. Legacy techniques including electrogastrography (EGG) have previously been attempted to assess the electrical activity of the stomach following surgery; however, this is limited by low resolution and high sensitivity to noise. Gastric Alimetry overcomes these problems by employing an HR array together with sophisticated signal processing algorithms [26, 27], to non-invasively assess the electrophysiology of the gastric remnant and to also simultaneously record symptom development and progression. Previously, Gastric Alimetry has been exclusively performed in patients with normal gastric anatomies, in whom reference intervals were developed [20, 30, 37]. As this study now involves a modified Gastric Alimetry protocol to account for the effect of surgery on the stomach, the authors used both the validated reference intervals and a cohort of matched control patients (with a similar calorie load meal challenge) as a comparison.

The strengths of this study include the recruitment of symptomatic and asymptomatic patients in the patient population, and the use of a matched control cohort for comparison. The recruitment of the patient who had a resectional gastric bypass (which is rare) also allowed the confirmation that all the data captured in this study arose from the gastric remnant, as there was minimal post-meal activity identified in the gastric pouch (former fundus), which is an area of the stomach known to be electrically quiescent [10, 38]. The main limitation of this study was its dominant focus on remnant gastric motility, such that other potential sources of symptoms such as pouch and Roux limb function, together with other contributing disorders, were not systematically evaluated. A causal association should not be inferred from our results, particularly because the remnant stomach is excluded from GI continuity and symptoms had a post-prandial character. Therefore, it is highly likely that symptom genesis post-bypass is multi-factorial, with other contributing sources including gastric pouch stretch, Roux stasis syndrome, and post-surgical sequelae [32, 36]. Future work could now focus on addressing the causality of the novel finding that degradations of gastric electrophysiology correlated with symptoms, which could be approached using frameworks such as the Plausibility Criteria proposed by Tack et al. [39]Another limitation is the potential for selection bias, as those patients who are more symptomatic and/or those who are not in daytime work may have been more disposed to participate, which may explain the relatively high prevalence of symptomatic patients. Future studies performing gastric mapping pre and post operatively in a longitudinal cohort would be of further interest to define the myoelectrical consequences of bariatric procedures.

The current study does not imply a causal relationship between gastric remnant degeneration and dysrhythmia and symptoms; however, the results likely have clinical implications beyond gastric bypass. In particular, the finding that a diverted stomach develops severe degeneration of the gastric conduction apparatus may become relevant in the pathophysiology and management of other medical or surgical conditions where there is prolonged stomach disuse. Relevant conditions include prolonged illness with caloric restriction, including patients on long-term nasojejunal feeding, total parenteral nutrition, and severe anorexia, or when the stomach is surgically put out of continuity. When clinically rehabilitating these patients back onto normal oral diets after a period of gut atrophy, clinicians should be cognizant that stomach pacemaker function may have become degraded, requiring additional time for recovery with return of dietary tolerance. Recovery patterns may be variable, due to the inherent plasticity and recovery capacity of the pacemaking, enteric neural, and smooth muscle components [40, 41]; however, this requires further study.

In conclusion, a third of gastric bypass patients experienced significant long-term upper GI symptoms and a reduced quality of life. These consequences are associated with severe degradation of remnant gastric electrophysiological function, although overall symptom genesis in post-bypass patients is likely to be multi-factorial.