Abstract
Background/Purpose
Enterocolitis (EC) is a common and severe complication after pull-through for Hirschsprung's
disease; its pathogenesis remains unclear, but the role of coexistent intestinal neuronal
dysplasia (IND) in the proximal colon may be relevant. This study evaluated the relationship
between postoperative EC and IND and assessed whether a surgical protocol including
resection of coexistent IND could prevent postoperative EC.
Methods
Between June 1993 and June 2002, 36 patients with aganglionosis were submitted to
definitive surgical treatment. There were 2 sequential sets of patients: group I (n
= 17), in whom the resection was confined to the aganglionic colon, and group II (n
= 19), who were additionally submitted to resection of the coexistent IND segment;
excision was restricted to the hepatic flexure in long segmental IND. The prevalence
of postoperative EC and anorectal function were evaluated and compared between the
2 groups.
Results
There was no mortality. Fifteen patients had isolated aganglionosis, and 21 presented
with aganglionosis plus proximal IND. All 6 children who developed postoperative EC
had coexistent IND. In group I, 9 patients had coexistent IND and 5 developed postoperative
EC (5/17, 29%). In group II, 12 patients had coexistent IND but only 1 patient, with
long segmental IND, developed postoperative EC (1/19, 5%). Among the patients with
proximal IND, the prevalence of postoperative EC was 29%; but it was significantly
lower in group II than in group I (1/12 or 8% vs 5/9 or 56%; P = .02). Anorectal function was excellent or good in more than 80% of the patients
in both groups.
Conclusions
Postoperative EC was associated with retained proximal IND, suggesting that coexisting
IND may be, at least, a predictive marker for this complication. Histochemical characterization
of the proximal colon with no radical resection of the IND segment seems to be an
effective and safe approach to minimize the prevalence of postoperative EC.
Index words
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© 2006 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
