Small Bowel Dilatation in Pediatric Short Bowel Syndrome Associates with Mucosal Damage, Bowel-Derived Bloodstream Infections, and Liver Injury.

Abstract

Introduction: Adaptive small bowel (SB) dilatation is common in short bowel syndrome (SBS). Whether SB dilatation predisposes to bloodstream infections (BSI) or associates with mucosal damage or liver injury remains unknown. Methods: Among SBS children (n=50), maximal SB diameter was measured in contrast series (n=179), expressed as ratio to fifth lumbar vertebra height (SB diameter ratio), and related to fecal calprotectin and plasma citrulline; markers of mucosal inflammation and mass, BSIs, liver biochemistry, and liver histology. Results: Median length of remaining SB was 38 (interquartile range 25–60) cm, age at contrast series 1.04 (0.34-3.01) years, and SB diameter ratio 2.14 (1.65-2.71). Patients with pathological SB diameter ratio >2.17 predicting prolonged PN-dependence had increased fecal calprotectin (86 vs. 22, p=0.012), plasma bilirubin (8 vs. 6, p=0.033), gamma-glutamyl transferase (52 vs. 20, p<0.001), and aminotransferase concentrations (45 vs. 30; 59 vs. 42, p<0.001-0.019) while decreased plasma citrulline (15 vs. 26, p=0.033) compared to others. All BSIs occurred during parenteral nutrition (PN) and 48% (16/33) of them were caused by intestinal bacteria, cultured 15 times more frequently when SB diameter ratio exceeded 2.17 (Figure 1). In logistic regression, SB diameter ratio was the only predictor of intestinal BSIs (odds ratio 1.88, p=0.017). Histological cholestasis grade was higher when SB diameter ratio exceeded 2.17 vs. ≤2.17 (1.15 vs. 0.21, p<0.001), while cholestasis, portal inflammation, and fibrosis grades were higher in the presence of intestinal BSIs vs. no BSIs (Figure 2). In linear regression, histological cholestasis was predicted by intestinal BSIs, SB diameter ratio, and PN (β=0.36-1.29, p<0.001-0.014), while portal inflammation by intestinal BSIs only (β=0.61, p=0.021). Conclusion: In pediatric SBS, SB dilatation relates with mucosal damage, BSIs of intestinal origin, and cholestatic liver injury, while BSIs of intestinal origin predict both histological cholestasis and portal inflammation. Results suggest the damaged mucosa of excessively dilated SB predisposes to bacterial translocation, which contributes to liver disease development.FIGURE 1: The occurrence of BSIs of intestinal origin according to small bowel (SB) diameter ratio within 6 months of contrast series (n=179).FIGURE 2: Grading of portal inflammation, cholestasis, and fibrosis (Metavir) according to the presence of BSIs of intestinal origin within 6 months of liver biopsies (n=50).