Background Water-absorbent beads (WAB) may expand after ingestion and cause small-bowel obstruction in young children, but the associated intestinal injury and microbiota changes remain poorly defined. We combined pediatric case analysis with an experimental model to characterize WAB-induced ileal obstruction. Methods Ten children who underwent surgery for WAB-induced ileal obstruction were retrospectively reviewed. A non-surgical rat model was established by intragastric administration of WAB. In total, 10 rats were assigned into two groups: WAB-obstruction group ( n = 5) and sham control group ( n = 5). Tissue assessment was performed at 48 h after gavage. Clinical features, gross and histologic injury, inflammatory and barrier-related gene expression, and 16S rRNA-based microbiota changes were assessed in the ileum, cecum, and colon. Results In children, WAB were consistently impacted near the terminal ileum. Common presenting symptoms included vomiting and abdominal distension; complications such as perforation occurred only in a subset of these paediatric patients. In rats, 2–2.5 mm beads reproducibly induced ileal obstruction with weight loss, increased pain scores, ileal dilatation. Injury was segment-specific, with severe ileal mucosal damage, mild cecal changes, and relative colonic preservation. Ileal obstruction increased inflammatory cytokine expression, reduced Muc2 and Tjp1 expression, and was associated with enrichment of Pseudomonadota, Klebsiella, Proteus, and Escherichia-Shigella together with depletion of Lactobacillus and Akkermansia. Conclusions WAB ingestion causes clinically important ileal obstruction in young children. This non-surgical rat model reproduces the composite pathological state of WAB-induced ileal obstruction frequently complicated by distant secondary intussusception, but it is not fully equivalent to uncomplicated paediatric WAB-induced ileal obstruction, and generalisation to all human WAB-obstruction cases should be exercised with caution. Our findings suggest that WAB-induced injury involves segment-specific mucosal damage, altered expression of barrier-related genes, inflammation, and microbiota dysbiosis.
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