cdp

Awlsctw

td

rdp

iwebea

a

ritamc

N

Enteral Feeding in Prostaglandin-Dependent Neonates:Is It a Safe Practice?

LISA WILLIS, MD, PATTI THUREEN, MD, JONATHAN KAUFMAN, MD, ERICA WYMORE, MD, HEATHER SKILLMAN, MS, RD, CSP, CNSD,AND EDUARDO DA CRUZ, MD

In many centers presurgical term neonates with prostaglandin-dependent cardiac lesions experience nutritional defi-iency because of postponed enteral feeds. We recently adopted early enteral feeding in these infants. This retrospective studyemonstrates feeding tolerance in 33 of 34 neonates fed enterally while receiving prostaglandin, suggesting the safety of thisractice. (J Pediatr 2008;153:867-9)

lthough the physiological and nutritional benefits of early enteral feeding (particularly human milk) in neonates are awell-studied subject in the premature and term infant populations, it has yet to be investigated in presurgical termneonates with ductal-dependent congenital heart disease. There is little agreement among centers that care for infants

ith congenital heart disease with regard to the safety or risks of early enteral feeding in infants with ductal dependent cardiacesions requiring continuous prostaglandin (PGE1) therapy. After careful review of the literature, we were unable to find anytudies in support of or refuting early enteral feeding in this population of infants. Therefore it is not surprising to find itommon practice to refrain from enteral feeding until these patients have been surgically corrected because of the concern thathey may have development of necrotizing enterocolitis (NEC). The risks of PGE1-related feeding intolerance have not beenell defined.

In contrast to the current varied practice in the United States, many European pediatric intensive care units enterally feedhese ductal-dependent infants who are awaiting surgery. In our previous experience, there have been no significant orocumented complications from this strategy. However, outcomes from this practice have not been published.

At our Children’s Hospital we recognize the importance of optimized presurgical nutrient intake, which is reflected in theecently instituted practice of early enteral feeding in infants receiving intravenous PGE1 therapy. This retrospective study wasesigned to assess enteral feeding tolerance in PGE1-dependent neonates awaiting surgical repair since the inception of thisractice at our institution.

METHODSAfter receiving Institutional Review Board approval, we reviewed records of all

nfants greater than 35 weeks gestation and less than 28 days of age who were admittedith PGE1-dependent cardiac defects between March 2007 and December 2007. We

lected to enroll only near-term and term infants so that gastrointestinal maturity woulde relatively consistent among patients. Infants less than 35 weeks gestation were notnrolled because even modestly preterm infants commonly demonstrate feeding intoler-nce in the first weeks of life.1-3

Clinical and radiographic patient information was gathered. Feeding type, delivery,nd caloric density were determined.

Feeding intolerance was defined as (1) clinically, per chart documentation ofecurrent large volume (greater than 2/3 of prior feed) or bilious emesis, an increasen abdominal girth of 3 cm over an 8-hour period, or hemoccult positive stools leadingo feeding cessation and (2) radiographically, as bowel dysmotility, pneumatosis,bnormal bowel distention, pneumoperitoneum, portal venous air, or gasless abdo-en. Additional patient information gathered included the presence of umbilical

atheters and the use of antibiotics, steroids, and vasopressors (Table I).

From the Heart Institute (L.W., J.K., E.D.), theService of Neonatology (P.T., E.W.), theCardiac Intensive Care Unit (J.K., E.D.), andthe Nutrition Services (H.S.), Departmentof Pediatrics, The Children’s Hospital ofDenver, University of Colorado at Denver& Health Sciences Center, Denver, CO.

The authors declare no sponsorship in-volvement or potential conflicts of interest,real or perceived.

Submitted for publication Feb 7, 2008; lastrevision received Apr 2, 2008; acceptedApr 30, 2008.

Reprint requests: Eduardo da Cruz, MD,Cardiac Intensive Care Unit, The Children’sHospital of Denver, University of Coloradoat Denver & Health Sciences Center,13123 E 16th Ave, B100, Aurora CO80045. E-mail: dacruz.eduardo@tchden.org.

0022-3476/$ - see front matter

Copyright © 2008 Mosby Inc. All rightsreserved.

EC Necrotizing enterocolitis PGE1 Prostaglandin

10.1016/j.jpeds.2008.04.074

867

Mctwfheitfp

nftl(twptksoud

anotmrdtdIctPtowwansp

nfinrdetpvr

Tfw

P

F

TBFBC

UURRR

Tii

PP

PHICCTT

SEH

8

RESULTSFrom a total of 412 admissions to the Cardiac ICU from

arch 2007 to December 2007, 67 children met the inclusionriteria; 56 of these neonates required PGE1 therapy, and ofhose, 34 patients were enterally fed. Twenty-two eligible infantsere not enterally fed while receiving PGE1 therapy for the

ollowing reasons: 14 infants underwent surgery in the first 48ours of life and therefore were not fed, 2 infants were consid-red clinically unstable to be fed because of low cardiac output, 3nfants with transposition of the great arteries were on PGE1 forransport and were not fed during that time and in 3 cases,eeding was withheld, according to the preference of attendinghysician.

We identified a total of 34 PGE1-dependent termeonates, 21 male and 11 female. Background cardiac mal-ormations were varied. Nineteen patients (56 %) had a right-o-left shunt through the ductus arteriosus, 11 (32 %) had aeft-to-right shunt, and 4 (12 %) had a bidirectional shuntTable II). All but 1 patient exhibited normal enteral feedingolerance while receiving PGE1 therapy. The only patientho exhibited feeding intolerance had the diagnosis of trans-osition of the great arteries with bidirectional shunt throughhe ductus arteriosus. While receiving PGE1 at 0.0125 �g/g/min via an umbilical venous catheter and feeding as de-ired, this infant demonstrated clinical and radiographic signsf feeding intolerance necessitating cessation of enteral feedsntil surgery. This infant progressed favorably and was later

able I. Clinical information for 33 infants enterallyed and without evidence of feeding intolerancehile receiving PGE1 infusion

Clinical parameter Number of infants

GE dose (�g/kg/min)0.0125 190.025 120.05 2

eeding methodOral demand as desired 22Gavage 7Oral demand as desired � gavage 4

ype of feedreast milk 24ormula 3reast milk � formula 6aloric density of feeds (kcal per ounce)20 2522 324 426 1

mbilical artery catheter 9mbilical venous catheter 16eceiving antibiotics 10eceiving steroids 1eceiving vasopressors 2

ischarged home after surgical repair. P

68 Willis et al

DISCUSSIONThe benefits of early enteral feeding in critically-ill term

nd pre-term infants have been widely recognized. However,eonates with PGE1-dependent congenital cardiac defects areften kept on parenteral nutrition and intestinal rest. Likelyhis practice is due to lack of objective evidence leading mostedical caregivers to the conservative practice of feeding

estraint in this unique population,4 independent of the arterialuctal flow direction. Nevertheless, the effects of such a nutri-ional strategy in neonates and infants with congenital heartisease who require continuous PGE1-therapy are not known.nfants are consequently maintained on parenteral nutrition be-ause of the presumed complications associated with feeding inhis fragile population, namely necrotizing enterocolitis (NEC).revious studies have endeavored to define the relationship be-

ween NEC and congenital heart disease. A retrospective reviewf 643 neonates with heart disease identified factors associatedith an elevated risk of NEC.5 The factors that were recognizedere premature birth, hypoplastic left heart syndrome, truncus

rteriosus, and episodes of poor systemic perfusion or shock. Ofote, neonates with heart disease in whom NEC developedupposedly experienced intestinal ischemia either by their patho-hysiology or by an episode of decreased systemic perfusion.

Balance between the hypothetical complications of feedingeonates on PGE1 infusions and the clear advantages of enteraleeding motivated the medical caregivers in our Institution tonitiate presurgical enteral feeding in PGE1-dependent termeonates, beginning in March 2007. We were encouraged by theesults of this practice, with 33 of 34 neonates with PGE1-ependent cardiac lesions exhibiting normal enteral feeding tol-rance while awaiting surgical repair. Enteral feeding was well-olerated independent of cardiac malformation or ductal-flowattern and did not appear to be affected by the use of umbilicalenous or arterial catheters. Because this is a small retrospectiveeview, conclusions regarding the safety of enteral feeding in

able II. Type of cardiac malformations among 33nfants enterally fed and without evidence of feedingntolerance while receiving PGE1 infusion

Cardiac diagnosis No. of infants

ulmonary atresia, VSD, MAPCAs 2ulmonary atresia, VSD, PDA-dependent branchpulmonary arteries

2

ulmonary atresia with intact ventricular septum 4ypoplastic left heart syndrome 8

nterrupted aortic arch “B” and VSD 3oarctation of the aorta 5ritical aortic stenosis 1ransposition of the great arteries 3etralogy of Fallot; ductal-dependentdiscontinuous branch pulmonary arteries

1

hone syndrome 2bstein anomaly and pulmonary atresia 1eterotaxy, severe pulmonary artery stenosis 1

GE1-dependent neonates are speculative. However, we believe

The Journal of Pediatrics • December 2008

tt

Th

1i

2a23w4Vs5

E

his study points toward safely providing improved nutrition inhis population through early initiation of enteral feeding.

he authors would like to thank Dr Suzanne Osorio, DVM forer support in the elaboration of this manuscript.

REFERENCES

. Berseth CL. Gestational evolution of small intestine motility in preterm and termnfants. J Pediatr 1989;115:646-51.

No

nteral Feeding in Prostaglandin-Dependent Neonates: Is It a Safe Practi

. Tyson JE, Kennedy KA. Minimal enteral nutrition for promoting feeding tolerancend preventing morbidity in parenterally fed infants. Cochrane Database Syst Rev000;(2):CD000504.. Neu J, Zhang L. Feeding intolerance in very-low-birth weight infants: what is it andhat can we do about it? Acta Paediatr Suppl 2005;94:93-9.. Johnson BA, Mussatto K, Uhing MR, Zimmerman H, Tweddell J, Ghanayem N.ariability in the preoperative management of infants with hypoplastic left heart

yndrome. Pediatr Cardiol 2007; E-pub ahead of print.. McElhinney D, Hedrick H, Bush D, Pereira G, Stafford P, Gaynor W, et al.

ecrotizing enterocolitis in neonates with congenital heart disease: risk factors and

utcomes. Pediatrics 2000;106:1080-7.

ce? 869