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CC BY 4.0 · Journal of Digestive Endoscopy
DOI: 10.1055/s-0045-1810094
Editorial

Benign Gastric Outlet Obstruction: Does Underlying Pathophysiology Dictate Outcomes?

Ankit Agarwal
1   Department of Gastroenterology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Chhagan Lal Birda
1   Department of Gastroenterology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
,
Ashish Agarwal 
1   Department of Gastroenterology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
› Author Affiliations

Funding None.
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Mechanical gastric outlet obstruction (GOO) is obstruction of antropyloric, bulbar, or post-bulbar segments impeding gastric emptying. Both malignant and nonmalignant etiologies contribute significantly to the disease burden. While surgery has been the primary modality of management, advent of through-the-scope endoscopic balloon dilatation (EBD) marked a new era, particularly in the management of benign GOO with low complication rates and better patient outcomes.

Use of EBD was first reported by Benjamin et al,[1] subsequently multiple studies concreted its place as a first-line therapeutic option for benign GOO. Adequate dilatation (endpoint of 15 mm) leads to a clinical response in approximately 75% of the patients.[2] EBD have been described in almost all causes of benign GOO with good clinical outcomes. In a single-center study by Rana et al,[3] EBD was successful in 84% patients, while a similar retrospective analysis with large sample size and long-term follow-up by Kochhar et al,[4] showed EBD had a clinical success of 97.3% with no recurrence during a 98-month follow-up period. In both the studies, the number of endoscopic sessions required was less in cases of peptic GOO when compared with other etiologies of GOO, particularly caustic.

This prompts the question why are caustic strictures more difficult to manage then peptic strictures? It is known that ingestion of a corrosive, both acid and alkali, causes direct tissue damage on contact. This leads to pylorospasm and prolonged contact time ultimately leading to more damage to gastric mucosa.[5] This may lead to a more fibrotic response of the underlying tissue, which in turn leads to a tighter stricture which is less responsive to EBD. Also, fibrosis from caustic ingestion is deeper then peptic strictures, resulting in more fibrosis and poorer response to dilatation.

Adjunctive therapies in the form of intralesional steroids, endoscopic incision, and placement of self-expanding metal stents (SEMS) have been tried for difficult-to-treat strictures with variable efficacy.[6] While both endoscopic incision and SEMS alleviate the symptoms by widening the luminal diameter, intralesional steroids block the cross-linking of collagen, prevent scar contracture, and inhibit stricture formation leading to better endoscopic response.[6]

Sareen et al[7]** have conducted a prospective randomized controlled trial in India on endoscopic management of GOO due to nonsteroidal anti-inflammatory drugs (NSAIDs), caustic, peptic, and opioids. Novelty of the study is the use of misoprostol as an adjunctive therapy, which has never been investigated previously. Patients were randomized to receive 2 weeks of misoprostol with proton-pump inhibitor (PPI) and EBD in one arm and PPI alone in the control arm. Procedural success was defined as achieving 15 mm dilatation and clinical success as symptomatic resolution till study duration. Misoprostol was administered via either oral or rectal route. Within the study, there were no procedure-related adverse events in the groups and both clinical and procedural success was significantly better in the misoprostol group.

In light of this, an important question arises, does misoprostol changes the behavior and underlying pathophysiology of gastric mucosa and makes it more responsive to dilatation? The pathophysiology of stricture development depends on the underlying etiology but basic pathological changes include persistent damage to mucosal lining leading to chronic inflammatory changes with subsequent development of intramural fibrosis and scarring, leading to luminal constriction. In peptic stricture, these pathophysiological changes occur due to exposure of gastric mucosa to excessive acid.[8] NSAID causes mucosal injury by generation of free radicals via COX-1 inhibition causing mitochondrial damage.[9] The authors proposed mechanism of stricture formation in opioid users is due to a combination of delayed gastric emptying causing acid stasis leading to persistent mucosal injury. Concomitant NSAID abuse may also contribute to stricture formation in this subgroup of patients. Misoprostol is a synthetic prostaglandin E1 analog that inhibits basal and nocturnal gastric acid secretion by the parietal cells in the stomach. It also helps in the secretion of mucin and bicarbonate, enhances mucosal blood flow, and preserves the mucosa's ability to regenerate new cells.[10]

Sareen et al**[7] showed a procedural success rate of 90% in the misoprostol arm, which is significantly higher than previously published data. The mean number of dilatations required was 3.85 ± 0.8. These results are encouraging as repeated EBD sessions pose a significant challenge in terms of procedural complications such as pain, bleeding, and perforation. This also significantly decreases the burden on health care resources and caregiver burden.

Eradication of Helicobacter pylori leads to better outcome in peptic stricture.[11] This suggests that there is an inflammatory component similar to inflammatory bowel disease, which should be dealt in a timely manner and may lead to decrease in the fibrosis burden leading to better EBD success. Current management options including EBD, incision, and SEMS for benign GOO address the fibrotic component of a stricture. Intralesional steroids have been tried for refractory strictures; however, there is no significant difference in terms of the number of dilatations required for clinical success or number of patients achieving procedural or clinical success. Misoprostol in this regard have opened up avenues for further research as it addresses the underlying inflammatory component and has a different mechanism of action then steroids.

There is no data from Sareen et al[7]** demonstrating the difference in outcomes in terms of individual etiologies. It is important as caustic strictures are more common in countries such as India and endoscopic management is more difficult than peptic strictures. The sample size is too small for any meaningful conclusion. There remain many other unanswered questions from the study, such as timing and optimal dosage of misoprostol and its route of administration. Studies have shown the role of PPI during the maintenance phase during EBD. Duration of misoprostol given was too short to impact the number of EBD sessions as they may go on for weeks to months, whether only 2 weeks of misoprostol therapy would impact long duration of therapy is up to debate. Even though PPI was given to both arms, additional contribution of misoprostol in addition to PPI needs further confirmation. Further, whether misoprostol can be given for long term is one of the important questions that needs discussion considering its side effect profile. This study was done in patients with new-onset strictures and as such there was a presumptive inflammatory component for misoprostol to act on. All patients were either well controlled or abstinent in terms of underlying etiology, thereby limiting its application to real-world scenario. Other factors requiring more investigation is the role of misoprostol in refractory strictures where the disease burden is primarily fibrotic and concurrent use with triamcinolone injections, radial incisions, and SEMS. Multicentric studies with large sample size would still be required to establish its definitive role in GOO management.

In conclusion, EBD is successful in ameliorating symptoms in benign GOO and should be the first-line management for benign strictures as it has relatively low rates of adverse events, addition of adjunctive therapies and addressing the underlying etiology may improve the efficacy of EBD, thereby avoiding surgery.

We believe that a slow and safe approach should be used for EBD for benign GOOs. Assessment of initial luminal diameter should guide the endoscopist for the anticipated number of attempts that may be required before considering treatment failure. Underlying etiology should also be kept in mind as the number of sessions required for a caustic stricture may be more than a peptic stricture. If the patient is clinically well and has adequate nutritional intake, persistence may be your best friend to avoid invasive surgery. Our suggested approach for management of benign GOOs is as follows: First and the most important thing is to maintain nutritional status. It can be achieved with the insertion of a nasojejunal tube or if not possible, a feeding jejunostomy. Second, ascertain whether the obstruction is extraluminal or intraluminal. Patients with extraluminal obstruction/extrinsic compression should be considered for early surgery. A detailed drug history for the use of NSAIDs and opioids should be taken. H. pylori should be eradicated and patient should be given long-term PPI. Patient should be on a 1 to 4 weekly endoscopic dilatation schedule till procedural/clinical success is achieved. Patient should be followed up clinically and if case of recurrence of symptoms, repeat dilatations may be required. Use of adjunctive therapies such as intralesional steroids and SEMS placement should be considered in case of refractory stricture.


 

Conflict of Interest

None declared.


Address for correspondence

Ashish Agarwal, MD, DM
Department of Gastroenterology, All India Institute of Medical Sciences
Jodhpur 342005, Rajasthan
India   

Publication History

Article published online:
18 July 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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