Am J Perinatol 2015; 32(07): 633-638
DOI: 10.1055/s-0034-1390349
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Necrotizing Enterocolitis in Infants with Ductal-Dependent Congenital Heart Disease

Kristian C. Becker
1   Duke Clinical Research Institute, Durham, North Carolina
,
Christoph P. Hornik
1   Duke Clinical Research Institute, Durham, North Carolina
2   Department of Pediatrics, Duke University Medical Center, Durham, North Carolina
,
C. Michael Cotten
2   Department of Pediatrics, Duke University Medical Center, Durham, North Carolina
,
Reese H. Clark
3   Medical Group, Pediatrix-Obstetrix Center for Research and Education, Sunrise, Florida
,
Kevin D. Hill
1   Duke Clinical Research Institute, Durham, North Carolina
2   Department of Pediatrics, Duke University Medical Center, Durham, North Carolina
,
P. Brian Smith
1   Duke Clinical Research Institute, Durham, North Carolina
2   Department of Pediatrics, Duke University Medical Center, Durham, North Carolina
,
Robert W. Lenfestey
1   Duke Clinical Research Institute, Durham, North Carolina
› Institutsangaben
Weitere Informationen

Publikationsverlauf

21. April 2014

25. Juli 2014

Publikationsdatum:
08. Dezember 2014 (online)

Preview

Abstract

Objective Infants with congenital heart disease (CHD) receiving prostaglandins (PGEs) may be at an increased risk for necrotizing enterocolitis (NEC). Enteral feeding may further increase the risk of NEC in these patients. We evaluated the incidence of NEC and its association with enteral feeding in infants with ductal-dependent CHD.

Study Design We examined a cohort of infants with CHD receiving PGE in neonatal intensive care units managed by the Pediatrix Medical Group (Sunrise, FL) between 1997 and 2010. We used logistic regression to evaluate the association between NEC and enteral feeding, as well as other risk factors, including antacid medications, inotropic and ventilator support, and anatomic characteristics, controlling for gestational age.

Results We identified 6,710 infants with ductal-dependent CHD receiving PGE for 17,158 infant days. NEC occurred in 21 of the 6,710 (0.3%) infants, of whom 12/21 (57%) were < 37 weeks gestational age. The incidence of NEC was 1.2/1,000 infant days while on enteral feeds versus 0.4/1,000 infant days while not on enteral feeds (p = 0.27). Enteral feeding was not associated with a statistically significant increased odds of NEC on the day of diagnosis (odds ratio [OR] 2.08; 95% confidence interval [CI] 0.38, 11.7). Risk factors associated with a significant increased odds of NEC included a diagnosis of single-ventricle heart defect (OR 2.82; 95% CI 1.23, 6.49), although the overall risk in this population remained low (8/1,631, 0.5%).

Conclusion The incidence of NEC in our cohort of infants with ductal-dependent CHD on PGE therapy was low and did not increase with enteral feeding.