# Risk stratification for stricture formation after endoscopic submucosal dissection for esophageal dysplasia

## TL;DR

This study identifies factors that increase the risk of esophageal narrowing after a procedure called endoscopic submucosal dissection for treating esophageal dysplasia.

## Contribution

The study provides a risk stratification model for stricture formation based on lesion and procedural characteristics.

## Key findings

- Stricture rates increased with the extent of circumferential defect involvement, reaching 57.7% for defects ≥90%.
- Local triamcinolone acetide injection showed varied stricture prevention depending on defect size.
- Prophylactic steroid regimens had different effectiveness, with combination therapy showing the lowest stricture rate.

## Abstract

We aimed to evaluate the demographic, clinical, procedural, and histopathologic factors associated with stricture development following esophageal endoscopic submucosal dissection (ESD). We conducted a retrospective cohort study of patients undergoing ESD for esophageal lesions from 2019 to 2024 at St. Michael’s Hospital, in Toronto, Canada. The primary outcome was stricture formation, defined as a symptomatic luminal narrowing at the ESD site confirmed on follow-up endoscopy, requiring intervention. Strictures requiring dilation developed in 24% of patients, 85% of which were impassable with a standard gastroscope (9.9 mm diameter). Stricture rates increased with defect circumferential involvement: <50% (7.7%), 50%–74% (11.5%), 75%–89% (23.1%), and ≥90% (57.7%). Intraprocedural local triamcinolone acetate (LTA) injection was administered in 40 of 108 patients (37%), with a mean defect circumferential size of 87.5%. Among patients receiving LTA, stricture rates varied based on defect size: for <50% circumferential defect involvement (n = 1) and 50%–74% (n = 3), no strictures developed; for 75%–90% (n = 17), 6 patients (35%) developed strictures, 5 of which were impassable; and for 90%–100% (n = 19), 11 patients (58%) developed strictures, all of which were impassable. Patients selectively discharged on prophylactic steroids demonstrated varied stricture rates depending on the steroid regimen: prednisone (61.5%), oral budesonide (26.9%), and combination therapy (7.7%). Independent predictors of stricture formation included defect circumferential involvement (OR 1.07, 95% CI 1.03–1.12, p < 0.001), length of hospitalization (OR 1.88, 95% CI 1.11–3.16, p = 0.018), and presence of deep mural injury (OR 6.28, 95% CI 1.10–35.88, p = 0.039). Stricture formation post-ESD is strongly associated with lesion and procedural characteristics, including defect circumferential involvement, deep mural injury, and length of hospitalization.