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Gastrointestinal Morbidity After Norwood Palliation for Hypoplastic Left Heart Syndrome
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Gastrointestinal Morbidity After Norwood Palliation for Hypoplastic Left Heart Syndrome Howard E. Jeffries, MD, Winfield J. Wells, MD, Vaughn A. Starnes, MD, Randall C. Wetzel, MD, and David Y. Moromisato, MD Departments of Anesthesiology, Critical Care Medicine, and Cardiothoracic Surgery, Childrens Hospital Los Angeles, Los Angeles, California
Background. Neonates with hypoplastic left heart syndrome are at high risk for developing gastrointestinal complications after first stage palliation. These complications likely play a major role in their morbidity and mortality. The goal of this review was to examine the incidence and clinical impact of gastrointestinal morbidities in these newborns. Methods. The charts of all neonates with hypoplastic left heart syndrome who underwent stage-one palliation between January 1997 and December 2001 were reviewed to determine the incidence of gastrointestinal complications. Demographic, perioperative, and procedural variables were collected and correlated with major gastrointestinal problems. Results. There were 117 patients in our study population, and survival to discharge was 87% (102 of 117). Gastrointestinal complications occurred in 48 (41%), including 18% with necrotizing enterocolitis, 18% who required home feeding tubes, and 8% who required
prolonged hospital length of stay for nutritional support. These infants had a longer length of stay (52 days versus 22 days; p < 0.0001). Multivariate logistic regression analysis revealed that weight less than 2.5 kg and development of necrotizing enterocolitis were each independently related to death. Neonates with a birth weight less than 2.5 kg had an odds ratio for death of 5.7 (95% confidence interval: 1.14 to 28.86), and the odds ratio for death with necrotizing enterocolitis was 5.6 (95% confidence interval: 1.55 to 20.67). Conclusions. Gastrointestinal complications in infants with hypoplastic left heart syndrome are common, and necrotizing enterocolitis increases the risk of death. Measures directed at reducing the incidence of gastrointestinal complications may improve outcomes and reduce costs in this population.
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many require supplemental nutrition through a nasogastric or surgically placed gastrostomy tube. Poor nutrition leads to poor growth and impairs surgical outcome in these infants [8 –11]. To document the incidence, impact, and risk factors associated with GI morbidity in neonates with HLHS, we have performed a retrospective analysis of the incidence, impact and risk factors for gastrointestinal complications after the modified Norwood procedure, including NEC, supplemental enteral nutrition, and feeding difficulties.
ssuring adequate nutrition is often difficult in pediatric patients with congenital heart disease and may play an important role in their survival [1, 2]. Overall, more than half of children admitted with congenital heart disease are less than the third percentile for weight, and a third are less than the third percentile for height [2]. Although newborns presenting with congenital heart disease usually have normal weight for gestational age, they often remain below birth weight for weeks after surgery. Acute gastrointestinal (GI) events are of particular concern in patients with congenital heart disease, and some problems such as necrotizing enterocolitis (NEC) are known to influence hospital mortality and morbidity [3– 6]. Among neonates with congenital heart disease, those with hypoplastic left heart syndrome (HLHS) are at particular risk for NEC [7]. Neonates with HLHS who have undergone first stage palliation (Norwood) are poor feeders even if they do not have an acute GI event such as NEC. They remain in the hospital for an extended period learning to feed, and
(Ann Thorac Surg 2006;81:982–7) © 2006 by The Society of Thoracic Surgeons
Material and Methods The study population consists of 117 neonates with HLHS who survived more than 48 hours after a modified Norwood operation between January 1997 and December 2001. This retrospective chart review was approved by the Institutional Review Board at Childrens Hospital Los Angeles on May 24, 2002, and individual consent was waived.
Demographic and Clinical Variables Accepted for publication Sept 1, 2005. Address correspondence to Dr Jeffries, Children’s Hospital and Regional Medical Center, 4800 Sandpoint Way, NE, 9G-1, Seattle, WA 98105; e-mail: [email protected].
© 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
Demographic data and admission characteristics are summarized in Table 1. In addition, operative age, admission pediatric risk of mortality (PRISM) score [12] (modified for cyanotic heart disease by the omission of 0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2005.09.001
JEFFRIES ET AL GI MORBIDITY AFTER NORWOOD PALLIATION
Table 1. Demographic Data and Admission Characteristics Characteristic
117 74 43 1.4 ⫾ 1.9 days 3.1 ⫾ 0.5 kg 2.6 ⫾ 0.9 mm 6.5 ⫾ 5.8
PRISM ⫽ pediatric risk of mortality.
PaO2 data), inotrope score [13, 14], presence and duration of umbilical catheters, positive blood or urine cultures, length of stay, and hospital mortality were also recorded. This information is summarized in Table 2. It should be noted that because of concern of marginal bowel perfusion, our patients received only parenteral nutrition before their Norwood procedure.
Surgical Procedure All patients underwent a modified Norwood using a limited period of deep hypothermic circulatory arrest. The technique for arch reconstruction included augmentation with pulmonary homograft tissue. Pulmonary blood flow came from a modified Blalock-Taussig shunt, which was usually 3.5 mm in diameter. By protocol, all patients had delayed sternal closure 2 to 4 days after their Norwood procedure. Variables extracted from the surgiTable 2. Hospital Course Characteristics Characteristic Age at operation Lowest pH Umbilical artery catheter, duration Umbilical venous catheter, duration Cardiopulmonary bypass time Deep hypothermic circulatory arrest time Blalock-Taussig shunt size 3.0 mm 3.5 mm 4.0 mm Day of initiation of ACE inhibitor Infection (positive blood/or urine culture) Positive blood culture Positive urine culture Positive blood and urine culture Survival to discharge Length of hospital stay
Table 3. Mortality Odds Ratios
Value
Number of patients Sex distribution Male Female Age Weight Ascending aorta size PRISM score
Value 6.5 ⫾ 4.8 days 7.24 ⫾ 0.16 (range, 6.60–7.46) 8.2 ⫾ 4.1 days (n ⫽ 82) 6.9 ⫾ 4.6 days (n ⫽ 66) 43.5 ⫾ 13.4 minutes 42.7 ⫾ 7.9 minutes
1 patient (0.8%) 99 patients (85%) 17 patients (14.2%) 10.7 ⫾ 11.7 days
ACE ⫽ angiotension-converting enzyme.
32 patients (27%) 24 patients (20%) 5 patients (4%) 3 patients (2.5%) 102 patients (87%) 34 ⫾ 35 days
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PRISM score Weight ⬍ 2.5 kg NEC
Odds Ratio
CI (95%)
p Value
1.13 5.73 5.66
1.02–1.24 1.14–28.86 1.55–20.67
0.003 0.023 0.001
CI ⫽ confidence interval; NEC ⫽ necrotizing enterocolitis; ⫽ pediatric risk of mortality.
PRISM
cal event included cardiopulmonary bypass and deep hypothermic circulatory arrest times and size of the modified Blalock-Taussig shunt, as noted in Table 2. The occurrence of any important intraoperative complication was also extracted.
Variables Related to the GI Tract The timing of enteral feedings after the Norwood operation, days required to reach full feeds, development of the clinical features of NEC, requirement for home supplemental enteral nutrition, and additional hospital days required exclusively for nutritional issues were tabulated and are shown in Table 3. For the purpose of our analysis, a gastrointestinal complication was defined as the diagnosis of NEC, requirement for home enteral tube feedings, gastroesophageal reflux, or hospital stay prolonged longer than 1 week owing solely to nutritional needs.
Statistics Data were analyzed using standard parametric and nonparametric statistical techniques, including independent sample t test and one-way analysis of variance for comparison of means between groups, and 2 or Fisher’s exact test for comparison of categorical variables. Four outcome variables were evaluated. Patient death, GI event, and a NEC event are dichotomous variables that were analyzed using logistic regression analysis. The need for extra days was treated as a continuous variable and was analyzed using linear regression analysis. Initially, a univariate analysis was performed, and all variables that reached a statistical significance level of 0.05 or less were subsequently analyzed in a variety of multivariate models. Odds ratios are presented with 95% confidence intervals (CI). Data are given as means and standard deviation. A p value less than 0.05 was considered significant.
Results Hospital Survival Survival to hospital discharge was 87% (102 of 117 patients), with the average length of stay being 34.2 ⫾ 34.6 days. By univariate analysis, there was an increased risk of death for patients who weighed less than 2.5 kg (p ⫽ 0.02), had a higher PRISM score at admission (p ⫽ 0.0003), a higher preoperative inotrope score (p ⫽ 0.02), developed two or more infections (p ⫽ 0.006), developed NEC (p ⫽ 0.001), required a longer period to reach full feedings (p ⫽ 0.03), or had a prolonged hospital stay (p ⫽ 0.009). By multivariate analysis, weight less than 2.5 kg, high
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Table 4. Gastrointestinal/Nutritional Characteristics
complications and patients without this problem are shown in Table 5. By multivariate analysis, patients were more likely to have GI complications if they had one or two infections (p ⫽ 0.03 and p ⫽ 0.001, respectively), or had a higher postoperative inotrope score (p ⫽ 0.04). The odds ratio for a GI complication was 1.4 for each 10-point increase in postoperative inotrope score, 4 for the presence of a single infection, and 9.4 if there was a second infection. Prolonged hospital stay exclusively related to feeding problems occurred in 9 patients, and these children were found to more likely have a higher PRISM score (p ⫽ 0.002), multiple infections (p ⫽ 0.04), and female sex (p ⫽ 0.006).
Characteristic
Value
Day of enteral nutrition initiation Full feedings achieved (100 cc/kg daily) Extra hospital days due to feeding difficulties Gastroesophageal reflux Development of necrotizing enterocolitis Stage 1a Stage 1b Stage 2a Stage 3a Stage 3b Gastrostomy tube placement Discharge home with nasogastric tube feedings Jejunostomy tube placement
5.9 ⫾ 3.1 days 11.1 ⫾ 4.9 days 6.1 ⫾ 9.0 days 9 patients (9%) 21 patients (18%) 12 patients (10%) 1 patients (0.8%) 5 patients (4%) 2 patients (1.6%) 1 patients (0.8%) 17 patients (15%) 3 patients (2.5%) 1 patient (0.8%)
PRISM score, and development of NEC correlated significantly with death. For each 4-point increase in PRISM score, the odds ratio for death was 1.5. Patients weighing 2.5 kg or less had an odds ratio for death of 5.7. For those with NEC, the odds ratio for death was 5.6. Table 3 summarizes these findings.
Gastrointestinal Complications Forty-eight patients met the criteria for GI complications, including 21 with NEC, 21 who required tube feeding at discharge, 11 with gastroesophageal reflux, and 9 with a prolongation of hospital stay greater than 1 week due exclusively to feeding difficulty, as depicted in Table 4. The demographic and clinical factors for patients with GI
Necrotizing Enterocolitis Among GI complications, the development of NEC was a particularly serious event. Necrotizing enterocolitis occurred in 21 of the study patients (18%). The mortality rate among these patients was 38% (8 of 21), which is significantly higher than the 7% mortality among the 89 patients without NEC (p ⫽ 0.009). A further breakdown of those with NEC (15) showed that in 13 of the 21 cases, the event was diagnosed as mild (Bell stage 1a or 1b), whereas the remaining 8 had moderate or severe NEC (Bell stage 2 or 3). There was a marked difference in outcome between these two groups, with 85% survival (11 of 13) for those with mild NEC as compared with 25% survival (2 of 8) for the moderate to severe cohort (p ⫽ 0.006). Bacteremia was documented in 75% of the moderate to severe cases, which was significantly higher than the 23.1% for cases with mild NEC (p ⫽ 0.03), and 18.7% for cases without NEC (p ⫽ 0.002).
Table 5. Comparison of Patients With Gastrointestinal (GI) Complications Versus Patients Without GI Complications
Total patients Age at diagnosis Age at surgery Weight Ascending aorta size PRISM score Umbilical artery catheter duration Umbilical venous catheter duration Cardiopulmonary bypass time Deep hypothermic circulatory arrest time ACE inhibitor initiated Blalock-Taussig shunt size Blalock-Taussig shunt size/weight Feeds initiated Day attained full feeds “Extra” days Positive cultures Postoperative day discharged Survived ACE ⫽ angiotensin-converting enzyme;
ns ⫽ not significant;
GI Complications
No Complications
p Value
48 1.2 ⫾ 1.9 days 7.1 ⫾ 5.1 days 3.1 ⫾ 0.6 kg 2.7 ⫾ 0.8 mm 7.6 ⫾ 6.9 8.9 ⫾ 3.9 days 8.8 ⫾ 4.5 days 43.5 ⫾ 14.7 min 42.5 ⫾ 7.9 min 15.0 ⫾ 16.1 days 3.55 ⫾ 0.15 mm 1.17 ⫾ 0.23 mm/kg 7.1 ⫾ 3.7 days 13.5 ⫾ 5.1 days 12.6 ⫾ 11.0 days 20 patients (42%) 52 ⫾ 31 days 39 patients (81%)
69 1.5 ⫾ 2.0 days 6.1 ⫾ 4.5 days 3.1 ⫾ 0.4 kg 2.6 ⫾ 0.9 mm 5.6 ⫾ 4.8 8.5 ⫾ 3.5 days 6.6 ⫾ 3.8 days 43.5 ⫾ 12.6 min 42.7 ⫾ 7.9 min 7.2 ⫾ 3.8 days 3.58 ⫾ 0.20 mm 1.17 ⫾ 0.16 mm/kg 5.1 ⫾ 2.2 days 9.3 ⫾ 3.9 days 1.6 ⫾ 2.2 days 12 patients (17%) 22 ⫾ 31 days 62 patients (90%)
0.52, ns 0.29, ns 0.73, ns 0.46, ns 0.07, ns 0.57, ns 0.04 0.99, ns 0.89, ns 0.0006 0.42, ns 0.90, ns 0.0004 ⬍0.0001 ⬍0.0001 0.002 ⬍0.0001 0.2, ns
PRISM ⫽ pediatric risk of mortality.
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Table 6. Comparison of Necrotizing Enterocolitis (NEC) Versus No-NEC Patients
Total number Sex Age at diagnosis Age at operation Weight Ascending aorta size Lowest pH PRISM score Umbilical artery catheter duration Umbilical venous catheter duration Preoperative inotrope score Postoperative inotrope score Cardiopulmonary bypass time Deep hypothermic circulatory arrest time ACE inhibitor initiated Blalock-Taussig shunt size Blalock-Taussig shunt size/body weight Feeds initiated Age at full feeds No gastrostomy tube “Extra” days Positive cultures Postoperative day discharged Survived ACE ⫽ angiotensin-converting enzyme;
ns ⫽ not significant;
NEC
No NEC
p Value
21 10 M : 10 F 1.6 ⫾ 2.3 days 7.8 ⫾ 5.2 days 2.9 ⫾ 0.6 kg 2.8 ⫾ 0.9 mm 7.18 ⫾ 0.21 9.4 ⫾ 8.0 6.7 ⫾ 5.4 days 7.1 ⫾ 5.2 days 13.1 ⫾ 16.6 24.1 ⫾ 13.1 41.4 ⫾ 10.6 min 40.9 ⫾ 8.6 min 16.1 ⫾ 19.5 days 3.57 ⫾ 0.18 mm 1.28 ⫾ 0.27 mm/kg 6.6 ⫾ 3.9 days 14.5 ⫾ 6.0 days 14 patients (67%) 14.0 ⫾ 13.8 days 11 patients (52%) 59 ⫾ 36 days 13 patients (62%)
96 61 M : 32 F 1.3 ⫾ 1.9 days 6.3 ⫾ 4.7 days 3.2 ⫾ 0.5 kg 2.6 ⫾ 0.9 mm 7.25 ⫾ 0.15 5.8 ⫾ 5.0 8.4 ⫾ 3.8 days 6.8 ⫾ 4.4 days 10.6 ⫾ 9.9 20.6 ⫾ 13.1 43.9 ⫾ 13.9 min 43.0 ⫾ 7.7 min 9.3 ⫾ 8.4 days 3.57 ⫾ 0.19 mm 1.15 ⫾ 0.17 mm/kg 5.8 ⫾ 2.9 days 10.3 ⫾ 4.3 days 80 patients (83%) 4.3 ⫾ 6.5 days 21 patients (22%) 29 ⫾ 32 days 89 patients (93%)
0.21, ns 0.19, ns 0.007 0.03 0.23, ns 0.08, ns 0.009 0.16, ns 0.84, ns 0.35, ns 0.26, ns 0.44, ns 0.26, ns 0.02 0.93, ns 0.005 0.25, ns 0.0004 0.13, ns ⬍0.0001 0.001 0.0002 0.009
PRISM ⫽ pediatric risk of mortality.
The development of any form of NEC had a univariate association with lower weight (p ⫽ 0.02), later attainment of full feedings (p ⫽ 0.0004), a positive blood culture (p ⫽ 0.001), and higher PRISM score (p ⫽ 0.009). The NEC cohort also had a larger modified Blalock-Taussig shunt, when indexed to body weight (1.28 ⫾ 0.27 versus 1.15 ⫾ 0.17, p ⫽ 0.005), as depicted in Table 6. By multivariate analysis, the odds ratios of developing NEC was 3.2, if birth weight was less than 3 kg, 2.8 if the patient had bacteremia, and 8 if the patient experienced two episodes of bacteremia or sepsis.
Comment Our study was performed to identify the incidence and risk factors for GI complications after the Norwood procedure. McElhinney and colleagues [7] have suggested that HLHS is a predisposing factor for the development of NEC. Patients with HLHS were at significantly increased risk, with an odds ratio of 3.8, when compared with neonates who had other forms of congenital heart disease. Their incidence of NEC at 7.6% was much lower than the 18% we report in this series; however, we have included patients with Bell stage I disease, which they did not. We included this mild form of NEC in our study because it is our practice to delay or discontinue enteral feedings with early findings of NEC, and therefore this was thought to be an important GI event. If we include only those patients with moderate to severe NEC (Bell
stage 2 and 3), the incidence in our series of 7% is very close to the 7.6% found by McElhinney and coworkers [7]. It is also noteworthy that the development of moderate to severe NEC in our post-Norwood patients was associated with a 75% mortality rate, which is much higher than the 19% death rate among NEC cases in a population of patients with all types of congenital heart disease [7]. The development of NEC has been correlated with circulatory dysfunction related to the presence of a patent ductus [15]. With decreasing pulmonary vascular resistance, left to right shunting at the ductal level may decrease mesenteric flow, resulting in bowel ischemia. Cheung and associates [16] found disturbances in splanchnic perfusion in infants after Blalock-Taussig shunts, an integral component of the classic Norwood procedure. The finding that Blalock-Taussig shunt size normalized to body weight was larger in infants in whom NEC developed is in keeping with the hypothesis that mesenteric hypoperfusion due to left to right shunt may be a factor in the development of bowel ischemia. Doppler studies of superior mesenteric artery flow performed in a group of patients after Blalock-Taussig shunt placement from our own institution have also shown abnormal flow in response to enteral feeds [17]. Additionally, there is often right ventricular dysfunction and decreased cardiac output in the period immediately after the Norwood operation that may further compromise mesenteric perfusion. It is intriguing to postulate whether a right ventricle to pulmonary artery shunt would reduce the inci-
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dence of NEC, because of the theoretical reduction of run off in to the pulmonary vascular bed and improved splanchnic perfusion with this physiology. Although there has been concern that aggressive use of afterload reducing agents in Norwood patients might decrease systemic pressure to the point of interfering with mesenteric perfusion, we found that our NEC patients were started on these agents later and at lower doses than were patients who did not have this complication. That may have reflected our concern of hemodynamic instability in the NEC subset. Previous studies have documented a very high incidence of endotoxemia in children with congenital heart disease [18], and the presence of bacteremia or sepsis has been implicated in the development of NEC [19]. In our study, we found that infants in whom NEC developed were likely to be bacteremic. The interpretation of this finding is problematic, however, as it is difficult to know whether the occurrence of sepsis is the result of bacterial translocation from bowel ischemia, and as such is the harbinger of NEC, or whether sepsis from a nonbowelrelated source triggers hemodynamic compromise and thus the mesenteric vascular insufficiency that leads to NEC. It was not possible to sort out this dilemma in our patient population. Major feeding problems led to the need for gastrostomy tube placement in 18% of our patients, and extended hospitalization to master oral feeding in many others. We speculate that these GI problems and poor oromotor coordination observed by other investigators may be related to surgical manipulation and trauma to the left vagus nerve, which is in the area of dissection when constructing the neoaorta. Recent work presented by Skinner and coworkers [20] documented a 36% incidence of poor oromotor coordination among 25 patients routinely studied after the Norwood procedure. In addition, 24% were shown to be aspirating, although left vocal cord paralysis was found in only 8% of their patients. In our study population, 3 patients had left vocal cord paralysis (3%), and these children required gastrostomy tube placement for nutritional support. Although we attempt to avoid trauma to the nerve, avoiding it in the dissection is difficult. Other factors that could contribute to feeding problems include suboptimal cardiac function or neurologic injury. We found no evidence that these were significant contributing factors in our population. After surgical palliation, we use a nutritional support protocol in the care of our neonates with single ventricle physiology. Parenteral nutritional support is initiated in the first 24 to 48 hours after surgery. Enteral nutrition is started only after hemodynamic stability is achieved. In addition, feeding is advanced over 3 to 5 days. Then the formula concentration is incrementally increased to achieve a caloric intake of 110 to 130 kcal/kg daily as directed by our dedicated cardiac dietician. If feeding (as directed by our specialized occupational therapy team) is progressing poorly after 7 to 10 days, we proceed with a GI work-up. That includes a swallowing study, upper GI barium study, or a nuclear medicine scan to rule out important gastroesophageal reflux. We then proceed to
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either percutaneous or surgical gastrostomy tube placement depending on the child’s anatomy and the need for an antireflux procedure. The incidence of gastroesophageal reflux in our study was 9% (n ⫽ 11), and 7 of these children underwent a surgical antireflux procedure. Whereas other programs frequently discharge patients with a nasogastric tube to provide supplemental feedings, our family demographics have made us reluctant to use this method owing to concern over unrecognized tube displacement leading to aspiration with feedings. Optimally, the care of GI complications in neonates after congenital heart repair would be managed by a multidisciplinary team that includes the occupational therapy feeding specialist, the pediatric gastroenterologist, and pediatric surgeon. Early recognition and work-up of problematic feedings with appropriate action has the potential to shorten the hospital stay and conserve resources. It is hoped that such an approach will also lead to the early diagnosis of impending NEC at a point at which bowel rest and aggressive antibiotic therapy has the potential to salvage this otherwise potentially devastating problem. Finally, the creation and implementation of a nutritional support protocol may serve to further decrease the incidence of NEC. Future work will need to be done to determine whether the placement of a right ventricle to pulmonary artery conduit will reduce the incidence of NEC. In addition, the development of a feeding protocol may also serve to decrease the incidence of NEC.
The authors wish to thank Fred Dorey for providing statistical assistance.
References 1. Radtke WAK. Glenn, bi-directional Glenn, and hemi-Fontan operation. Perspect Pediatr Cardiol 1998;6:325– 44. 2. Mitchell IM, Logan RW, Pollock JC, Jamieson MP. Nutritional status of children with congenital heart disease. Br Heart J 1995;73:277– 83. 3. Cheng W, Leung MP, Tam PHK. Surgical intervention in necrotizing enterocolitis in neonates with symptomatic congenital heart disease. Pediatr Surg Int 1999;15:492–5. 4. Ostlie DJ, Spilde TL, St Peter SD, et al. Necrotizing enterocolitis in full-term infants. J Pediatr Surg 2003;38:1039 – 42. 5. Bolisetty S, Lui K, Oei J, Wojtulewicz J. A regional study of underlying congenital diseases in term neonates with necrotizing enterocolitis. Acta Paediatr 2000;89:1226 –30. 6. Kurbegov AC, Sondheimer JM. Pneumatosis intestinalis in non-neonatal pediatric patients. Pediatrics 2001;108:402– 6. 7. McElhinney DB, Hedrick HL, Bush DM, et al. Necrotizing enterocolitis in neonates with congenital heart disease: risk factors and outcomes. Pediatrics 2000;106:1080 –7. 8. Schwarz SM, Gewitz MH, See CC, et al. Enteral nutrition in infants with congenital heart disease and growth failure. Pediatrics 1990;86:368 –73. 9. Unger R, DeKleermaeker M, Gidding SS, Christoffel KK. Calories count. Improved weight gain with dietary intervention in congenital heart disease. Am J Dis Child 1992;146: 1078 – 84. 10. Cameron JW, Rosenthal A, Olson AD. Malnutrition in hospitalized children with congenital heart disease. Arch Pediatr Adolesc Med 1995;149:1098 –102.
11. Hofner G, Behrens R, Koch A, Singer H, Hofbeck M. Enteral nutritional support by percutaneous endoscopic gastrostomy in children with congenital heart disease. Pediatr Cardiol 2000;21:341– 6. 12. Pollack MM, Ruttimmann UE, Getson PR. Pediatric risk of mortality (PRISM) score. Crit Care Med 1988;16: 1110 – 6. 13. Shore S, Nelson DP, Pearl JM, et al. Usefulness of corticosteroid therapy in decreasing epinephrine requirements in critically ill infants with congenital heart disease. Am J Cardiol 2001;88:591– 4. 14. Wernovsky G, Wypij D, Jonas RA, et al. Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. Circulation 1995;92: 2226 –35. 15. Walsh MD, Kleigman RM. Necrotizing enterocolitis: treatment based on staging criteria. Pediatr Clin 1986;33:179 – 201.
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16. Cheung TF, Ho MH, Cheng VY. Mesenteric blood flow response to feeding after systemic-to-pulmonary arterial shunt palliation. Ann Thorac Surg 2003;75:947–51. 17. del Castillo SL, Moromisato DY, Ludwick J, et al. Mesenteric blood flow velocities in the newborn with single ventricle physiology: modified Blalock-Taussig shunt versus right ventricle-pulmonary artery conduit. Pediatr Crit Care Med. In press. 18. Lequier LL, Nikaidoh H, Leonard SR, et al. Preoperative and postoperative endotoxemia in children with congenital heart disease. Chest 2000;117:1706 –12. 19. Fatica C, Gordon S, Mossad E, McHugh M, Mee R. A cluster of necrotizing enterocolitis in term infants undergoing open heart surgery. Am J Infect Contr 2000;28:130 –2. 20. Skinner ML, Halstead LA, Rubinstein CS, Atz AM, Bradley SM. Laryngopharyngeal dysfunction following the Norwood procedure [Abstract]. 85th Annual Meeting of the American Association for Thoracic Surgery, April 2005:116.
Southern Thoracic Surgical Association: Fifty-Third Annual Meeting The Fifty-Third Annual Meeting of the Southern Thoracic Surgical Association (STSA) will be held November 9 –11, 2006, in Tucson, Arizona. Members wishing to participate in the Scientific Program should submit an abstract by April 7, 2006, 12:00 Midnight, Central Daylight Time. Abstracts must be submitted electronically. Instructions for the abstract submission process can be found on the STSA Web site
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Gastrointestinal Morbidity After Norwood Palliation for Hypoplastic Left Heart Syndrome Howard E. Jeffries, MD, Winfield J. Wells, MD, Vaughn A. Starnes, MD, Randall C. Wetzel, MD, and David Y. Moromisato, MD Departments of Anesthesiology, Critical Care Medicine, and Cardiothoracic Surgery, Childrens Hospital Los Angeles, Los Angeles, California
Background. Neonates with hypoplastic left heart syndrome are at high risk for developing gastrointestinal complications after first stage palliation. These complications likely play a major role in their morbidity and mortality. The goal of this review was to examine the incidence and clinical impact of gastrointestinal morbidities in these newborns. Methods. The charts of all neonates with hypoplastic left heart syndrome who underwent stage-one palliation between January 1997 and December 2001 were reviewed to determine the incidence of gastrointestinal complications. Demographic, perioperative, and procedural variables were collected and correlated with major gastrointestinal problems. Results. There were 117 patients in our study population, and survival to discharge was 87% (102 of 117). Gastrointestinal complications occurred in 48 (41%), including 18% with necrotizing enterocolitis, 18% who required home feeding tubes, and 8% who required
prolonged hospital length of stay for nutritional support. These infants had a longer length of stay (52 days versus 22 days; p < 0.0001). Multivariate logistic regression analysis revealed that weight less than 2.5 kg and development of necrotizing enterocolitis were each independently related to death. Neonates with a birth weight less than 2.5 kg had an odds ratio for death of 5.7 (95% confidence interval: 1.14 to 28.86), and the odds ratio for death with necrotizing enterocolitis was 5.6 (95% confidence interval: 1.55 to 20.67). Conclusions. Gastrointestinal complications in infants with hypoplastic left heart syndrome are common, and necrotizing enterocolitis increases the risk of death. Measures directed at reducing the incidence of gastrointestinal complications may improve outcomes and reduce costs in this population.
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many require supplemental nutrition through a nasogastric or surgically placed gastrostomy tube. Poor nutrition leads to poor growth and impairs surgical outcome in these infants [8 –11]. To document the incidence, impact, and risk factors associated with GI morbidity in neonates with HLHS, we have performed a retrospective analysis of the incidence, impact and risk factors for gastrointestinal complications after the modified Norwood procedure, including NEC, supplemental enteral nutrition, and feeding difficulties.
ssuring adequate nutrition is often difficult in pediatric patients with congenital heart disease and may play an important role in their survival [1, 2]. Overall, more than half of children admitted with congenital heart disease are less than the third percentile for weight, and a third are less than the third percentile for height [2]. Although newborns presenting with congenital heart disease usually have normal weight for gestational age, they often remain below birth weight for weeks after surgery. Acute gastrointestinal (GI) events are of particular concern in patients with congenital heart disease, and some problems such as necrotizing enterocolitis (NEC) are known to influence hospital mortality and morbidity [3– 6]. Among neonates with congenital heart disease, those with hypoplastic left heart syndrome (HLHS) are at particular risk for NEC [7]. Neonates with HLHS who have undergone first stage palliation (Norwood) are poor feeders even if they do not have an acute GI event such as NEC. They remain in the hospital for an extended period learning to feed, and
(Ann Thorac Surg 2006;81:982–7) © 2006 by The Society of Thoracic Surgeons
Material and Methods The study population consists of 117 neonates with HLHS who survived more than 48 hours after a modified Norwood operation between January 1997 and December 2001. This retrospective chart review was approved by the Institutional Review Board at Childrens Hospital Los Angeles on May 24, 2002, and individual consent was waived.
Demographic and Clinical Variables Accepted for publication Sept 1, 2005. Address correspondence to Dr Jeffries, Children’s Hospital and Regional Medical Center, 4800 Sandpoint Way, NE, 9G-1, Seattle, WA 98105; e-mail: [email protected].
© 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
Demographic data and admission characteristics are summarized in Table 1. In addition, operative age, admission pediatric risk of mortality (PRISM) score [12] (modified for cyanotic heart disease by the omission of 0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2005.09.001
JEFFRIES ET AL GI MORBIDITY AFTER NORWOOD PALLIATION
Table 1. Demographic Data and Admission Characteristics Characteristic
117 74 43 1.4 ⫾ 1.9 days 3.1 ⫾ 0.5 kg 2.6 ⫾ 0.9 mm 6.5 ⫾ 5.8
PRISM ⫽ pediatric risk of mortality.
PaO2 data), inotrope score [13, 14], presence and duration of umbilical catheters, positive blood or urine cultures, length of stay, and hospital mortality were also recorded. This information is summarized in Table 2. It should be noted that because of concern of marginal bowel perfusion, our patients received only parenteral nutrition before their Norwood procedure.
Surgical Procedure All patients underwent a modified Norwood using a limited period of deep hypothermic circulatory arrest. The technique for arch reconstruction included augmentation with pulmonary homograft tissue. Pulmonary blood flow came from a modified Blalock-Taussig shunt, which was usually 3.5 mm in diameter. By protocol, all patients had delayed sternal closure 2 to 4 days after their Norwood procedure. Variables extracted from the surgiTable 2. Hospital Course Characteristics Characteristic Age at operation Lowest pH Umbilical artery catheter, duration Umbilical venous catheter, duration Cardiopulmonary bypass time Deep hypothermic circulatory arrest time Blalock-Taussig shunt size 3.0 mm 3.5 mm 4.0 mm Day of initiation of ACE inhibitor Infection (positive blood/or urine culture) Positive blood culture Positive urine culture Positive blood and urine culture Survival to discharge Length of hospital stay
Table 3. Mortality Odds Ratios
Value
Number of patients Sex distribution Male Female Age Weight Ascending aorta size PRISM score
Value 6.5 ⫾ 4.8 days 7.24 ⫾ 0.16 (range, 6.60–7.46) 8.2 ⫾ 4.1 days (n ⫽ 82) 6.9 ⫾ 4.6 days (n ⫽ 66) 43.5 ⫾ 13.4 minutes 42.7 ⫾ 7.9 minutes
1 patient (0.8%) 99 patients (85%) 17 patients (14.2%) 10.7 ⫾ 11.7 days
ACE ⫽ angiotension-converting enzyme.
32 patients (27%) 24 patients (20%) 5 patients (4%) 3 patients (2.5%) 102 patients (87%) 34 ⫾ 35 days
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PRISM score Weight ⬍ 2.5 kg NEC
Odds Ratio
CI (95%)
p Value
1.13 5.73 5.66
1.02–1.24 1.14–28.86 1.55–20.67
0.003 0.023 0.001
CI ⫽ confidence interval; NEC ⫽ necrotizing enterocolitis; ⫽ pediatric risk of mortality.
PRISM
cal event included cardiopulmonary bypass and deep hypothermic circulatory arrest times and size of the modified Blalock-Taussig shunt, as noted in Table 2. The occurrence of any important intraoperative complication was also extracted.
Variables Related to the GI Tract The timing of enteral feedings after the Norwood operation, days required to reach full feeds, development of the clinical features of NEC, requirement for home supplemental enteral nutrition, and additional hospital days required exclusively for nutritional issues were tabulated and are shown in Table 3. For the purpose of our analysis, a gastrointestinal complication was defined as the diagnosis of NEC, requirement for home enteral tube feedings, gastroesophageal reflux, or hospital stay prolonged longer than 1 week owing solely to nutritional needs.
Statistics Data were analyzed using standard parametric and nonparametric statistical techniques, including independent sample t test and one-way analysis of variance for comparison of means between groups, and 2 or Fisher’s exact test for comparison of categorical variables. Four outcome variables were evaluated. Patient death, GI event, and a NEC event are dichotomous variables that were analyzed using logistic regression analysis. The need for extra days was treated as a continuous variable and was analyzed using linear regression analysis. Initially, a univariate analysis was performed, and all variables that reached a statistical significance level of 0.05 or less were subsequently analyzed in a variety of multivariate models. Odds ratios are presented with 95% confidence intervals (CI). Data are given as means and standard deviation. A p value less than 0.05 was considered significant.
Results Hospital Survival Survival to hospital discharge was 87% (102 of 117 patients), with the average length of stay being 34.2 ⫾ 34.6 days. By univariate analysis, there was an increased risk of death for patients who weighed less than 2.5 kg (p ⫽ 0.02), had a higher PRISM score at admission (p ⫽ 0.0003), a higher preoperative inotrope score (p ⫽ 0.02), developed two or more infections (p ⫽ 0.006), developed NEC (p ⫽ 0.001), required a longer period to reach full feedings (p ⫽ 0.03), or had a prolonged hospital stay (p ⫽ 0.009). By multivariate analysis, weight less than 2.5 kg, high
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Table 4. Gastrointestinal/Nutritional Characteristics
complications and patients without this problem are shown in Table 5. By multivariate analysis, patients were more likely to have GI complications if they had one or two infections (p ⫽ 0.03 and p ⫽ 0.001, respectively), or had a higher postoperative inotrope score (p ⫽ 0.04). The odds ratio for a GI complication was 1.4 for each 10-point increase in postoperative inotrope score, 4 for the presence of a single infection, and 9.4 if there was a second infection. Prolonged hospital stay exclusively related to feeding problems occurred in 9 patients, and these children were found to more likely have a higher PRISM score (p ⫽ 0.002), multiple infections (p ⫽ 0.04), and female sex (p ⫽ 0.006).
Characteristic
Value
Day of enteral nutrition initiation Full feedings achieved (100 cc/kg daily) Extra hospital days due to feeding difficulties Gastroesophageal reflux Development of necrotizing enterocolitis Stage 1a Stage 1b Stage 2a Stage 3a Stage 3b Gastrostomy tube placement Discharge home with nasogastric tube feedings Jejunostomy tube placement
5.9 ⫾ 3.1 days 11.1 ⫾ 4.9 days 6.1 ⫾ 9.0 days 9 patients (9%) 21 patients (18%) 12 patients (10%) 1 patients (0.8%) 5 patients (4%) 2 patients (1.6%) 1 patients (0.8%) 17 patients (15%) 3 patients (2.5%) 1 patient (0.8%)
PRISM score, and development of NEC correlated significantly with death. For each 4-point increase in PRISM score, the odds ratio for death was 1.5. Patients weighing 2.5 kg or less had an odds ratio for death of 5.7. For those with NEC, the odds ratio for death was 5.6. Table 3 summarizes these findings.
Gastrointestinal Complications Forty-eight patients met the criteria for GI complications, including 21 with NEC, 21 who required tube feeding at discharge, 11 with gastroesophageal reflux, and 9 with a prolongation of hospital stay greater than 1 week due exclusively to feeding difficulty, as depicted in Table 4. The demographic and clinical factors for patients with GI
Necrotizing Enterocolitis Among GI complications, the development of NEC was a particularly serious event. Necrotizing enterocolitis occurred in 21 of the study patients (18%). The mortality rate among these patients was 38% (8 of 21), which is significantly higher than the 7% mortality among the 89 patients without NEC (p ⫽ 0.009). A further breakdown of those with NEC (15) showed that in 13 of the 21 cases, the event was diagnosed as mild (Bell stage 1a or 1b), whereas the remaining 8 had moderate or severe NEC (Bell stage 2 or 3). There was a marked difference in outcome between these two groups, with 85% survival (11 of 13) for those with mild NEC as compared with 25% survival (2 of 8) for the moderate to severe cohort (p ⫽ 0.006). Bacteremia was documented in 75% of the moderate to severe cases, which was significantly higher than the 23.1% for cases with mild NEC (p ⫽ 0.03), and 18.7% for cases without NEC (p ⫽ 0.002).
Table 5. Comparison of Patients With Gastrointestinal (GI) Complications Versus Patients Without GI Complications
Total patients Age at diagnosis Age at surgery Weight Ascending aorta size PRISM score Umbilical artery catheter duration Umbilical venous catheter duration Cardiopulmonary bypass time Deep hypothermic circulatory arrest time ACE inhibitor initiated Blalock-Taussig shunt size Blalock-Taussig shunt size/weight Feeds initiated Day attained full feeds “Extra” days Positive cultures Postoperative day discharged Survived ACE ⫽ angiotensin-converting enzyme;
ns ⫽ not significant;
GI Complications
No Complications
p Value
48 1.2 ⫾ 1.9 days 7.1 ⫾ 5.1 days 3.1 ⫾ 0.6 kg 2.7 ⫾ 0.8 mm 7.6 ⫾ 6.9 8.9 ⫾ 3.9 days 8.8 ⫾ 4.5 days 43.5 ⫾ 14.7 min 42.5 ⫾ 7.9 min 15.0 ⫾ 16.1 days 3.55 ⫾ 0.15 mm 1.17 ⫾ 0.23 mm/kg 7.1 ⫾ 3.7 days 13.5 ⫾ 5.1 days 12.6 ⫾ 11.0 days 20 patients (42%) 52 ⫾ 31 days 39 patients (81%)
69 1.5 ⫾ 2.0 days 6.1 ⫾ 4.5 days 3.1 ⫾ 0.4 kg 2.6 ⫾ 0.9 mm 5.6 ⫾ 4.8 8.5 ⫾ 3.5 days 6.6 ⫾ 3.8 days 43.5 ⫾ 12.6 min 42.7 ⫾ 7.9 min 7.2 ⫾ 3.8 days 3.58 ⫾ 0.20 mm 1.17 ⫾ 0.16 mm/kg 5.1 ⫾ 2.2 days 9.3 ⫾ 3.9 days 1.6 ⫾ 2.2 days 12 patients (17%) 22 ⫾ 31 days 62 patients (90%)
0.52, ns 0.29, ns 0.73, ns 0.46, ns 0.07, ns 0.57, ns 0.04 0.99, ns 0.89, ns 0.0006 0.42, ns 0.90, ns 0.0004 ⬍0.0001 ⬍0.0001 0.002 ⬍0.0001 0.2, ns
PRISM ⫽ pediatric risk of mortality.
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Table 6. Comparison of Necrotizing Enterocolitis (NEC) Versus No-NEC Patients
Total number Sex Age at diagnosis Age at operation Weight Ascending aorta size Lowest pH PRISM score Umbilical artery catheter duration Umbilical venous catheter duration Preoperative inotrope score Postoperative inotrope score Cardiopulmonary bypass time Deep hypothermic circulatory arrest time ACE inhibitor initiated Blalock-Taussig shunt size Blalock-Taussig shunt size/body weight Feeds initiated Age at full feeds No gastrostomy tube “Extra” days Positive cultures Postoperative day discharged Survived ACE ⫽ angiotensin-converting enzyme;
ns ⫽ not significant;
NEC
No NEC
p Value
21 10 M : 10 F 1.6 ⫾ 2.3 days 7.8 ⫾ 5.2 days 2.9 ⫾ 0.6 kg 2.8 ⫾ 0.9 mm 7.18 ⫾ 0.21 9.4 ⫾ 8.0 6.7 ⫾ 5.4 days 7.1 ⫾ 5.2 days 13.1 ⫾ 16.6 24.1 ⫾ 13.1 41.4 ⫾ 10.6 min 40.9 ⫾ 8.6 min 16.1 ⫾ 19.5 days 3.57 ⫾ 0.18 mm 1.28 ⫾ 0.27 mm/kg 6.6 ⫾ 3.9 days 14.5 ⫾ 6.0 days 14 patients (67%) 14.0 ⫾ 13.8 days 11 patients (52%) 59 ⫾ 36 days 13 patients (62%)
96 61 M : 32 F 1.3 ⫾ 1.9 days 6.3 ⫾ 4.7 days 3.2 ⫾ 0.5 kg 2.6 ⫾ 0.9 mm 7.25 ⫾ 0.15 5.8 ⫾ 5.0 8.4 ⫾ 3.8 days 6.8 ⫾ 4.4 days 10.6 ⫾ 9.9 20.6 ⫾ 13.1 43.9 ⫾ 13.9 min 43.0 ⫾ 7.7 min 9.3 ⫾ 8.4 days 3.57 ⫾ 0.19 mm 1.15 ⫾ 0.17 mm/kg 5.8 ⫾ 2.9 days 10.3 ⫾ 4.3 days 80 patients (83%) 4.3 ⫾ 6.5 days 21 patients (22%) 29 ⫾ 32 days 89 patients (93%)
0.21, ns 0.19, ns 0.007 0.03 0.23, ns 0.08, ns 0.009 0.16, ns 0.84, ns 0.35, ns 0.26, ns 0.44, ns 0.26, ns 0.02 0.93, ns 0.005 0.25, ns 0.0004 0.13, ns ⬍0.0001 0.001 0.0002 0.009
PRISM ⫽ pediatric risk of mortality.
The development of any form of NEC had a univariate association with lower weight (p ⫽ 0.02), later attainment of full feedings (p ⫽ 0.0004), a positive blood culture (p ⫽ 0.001), and higher PRISM score (p ⫽ 0.009). The NEC cohort also had a larger modified Blalock-Taussig shunt, when indexed to body weight (1.28 ⫾ 0.27 versus 1.15 ⫾ 0.17, p ⫽ 0.005), as depicted in Table 6. By multivariate analysis, the odds ratios of developing NEC was 3.2, if birth weight was less than 3 kg, 2.8 if the patient had bacteremia, and 8 if the patient experienced two episodes of bacteremia or sepsis.
Comment Our study was performed to identify the incidence and risk factors for GI complications after the Norwood procedure. McElhinney and colleagues [7] have suggested that HLHS is a predisposing factor for the development of NEC. Patients with HLHS were at significantly increased risk, with an odds ratio of 3.8, when compared with neonates who had other forms of congenital heart disease. Their incidence of NEC at 7.6% was much lower than the 18% we report in this series; however, we have included patients with Bell stage I disease, which they did not. We included this mild form of NEC in our study because it is our practice to delay or discontinue enteral feedings with early findings of NEC, and therefore this was thought to be an important GI event. If we include only those patients with moderate to severe NEC (Bell
stage 2 and 3), the incidence in our series of 7% is very close to the 7.6% found by McElhinney and coworkers [7]. It is also noteworthy that the development of moderate to severe NEC in our post-Norwood patients was associated with a 75% mortality rate, which is much higher than the 19% death rate among NEC cases in a population of patients with all types of congenital heart disease [7]. The development of NEC has been correlated with circulatory dysfunction related to the presence of a patent ductus [15]. With decreasing pulmonary vascular resistance, left to right shunting at the ductal level may decrease mesenteric flow, resulting in bowel ischemia. Cheung and associates [16] found disturbances in splanchnic perfusion in infants after Blalock-Taussig shunts, an integral component of the classic Norwood procedure. The finding that Blalock-Taussig shunt size normalized to body weight was larger in infants in whom NEC developed is in keeping with the hypothesis that mesenteric hypoperfusion due to left to right shunt may be a factor in the development of bowel ischemia. Doppler studies of superior mesenteric artery flow performed in a group of patients after Blalock-Taussig shunt placement from our own institution have also shown abnormal flow in response to enteral feeds [17]. Additionally, there is often right ventricular dysfunction and decreased cardiac output in the period immediately after the Norwood operation that may further compromise mesenteric perfusion. It is intriguing to postulate whether a right ventricle to pulmonary artery shunt would reduce the inci-
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dence of NEC, because of the theoretical reduction of run off in to the pulmonary vascular bed and improved splanchnic perfusion with this physiology. Although there has been concern that aggressive use of afterload reducing agents in Norwood patients might decrease systemic pressure to the point of interfering with mesenteric perfusion, we found that our NEC patients were started on these agents later and at lower doses than were patients who did not have this complication. That may have reflected our concern of hemodynamic instability in the NEC subset. Previous studies have documented a very high incidence of endotoxemia in children with congenital heart disease [18], and the presence of bacteremia or sepsis has been implicated in the development of NEC [19]. In our study, we found that infants in whom NEC developed were likely to be bacteremic. The interpretation of this finding is problematic, however, as it is difficult to know whether the occurrence of sepsis is the result of bacterial translocation from bowel ischemia, and as such is the harbinger of NEC, or whether sepsis from a nonbowelrelated source triggers hemodynamic compromise and thus the mesenteric vascular insufficiency that leads to NEC. It was not possible to sort out this dilemma in our patient population. Major feeding problems led to the need for gastrostomy tube placement in 18% of our patients, and extended hospitalization to master oral feeding in many others. We speculate that these GI problems and poor oromotor coordination observed by other investigators may be related to surgical manipulation and trauma to the left vagus nerve, which is in the area of dissection when constructing the neoaorta. Recent work presented by Skinner and coworkers [20] documented a 36% incidence of poor oromotor coordination among 25 patients routinely studied after the Norwood procedure. In addition, 24% were shown to be aspirating, although left vocal cord paralysis was found in only 8% of their patients. In our study population, 3 patients had left vocal cord paralysis (3%), and these children required gastrostomy tube placement for nutritional support. Although we attempt to avoid trauma to the nerve, avoiding it in the dissection is difficult. Other factors that could contribute to feeding problems include suboptimal cardiac function or neurologic injury. We found no evidence that these were significant contributing factors in our population. After surgical palliation, we use a nutritional support protocol in the care of our neonates with single ventricle physiology. Parenteral nutritional support is initiated in the first 24 to 48 hours after surgery. Enteral nutrition is started only after hemodynamic stability is achieved. In addition, feeding is advanced over 3 to 5 days. Then the formula concentration is incrementally increased to achieve a caloric intake of 110 to 130 kcal/kg daily as directed by our dedicated cardiac dietician. If feeding (as directed by our specialized occupational therapy team) is progressing poorly after 7 to 10 days, we proceed with a GI work-up. That includes a swallowing study, upper GI barium study, or a nuclear medicine scan to rule out important gastroesophageal reflux. We then proceed to
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either percutaneous or surgical gastrostomy tube placement depending on the child’s anatomy and the need for an antireflux procedure. The incidence of gastroesophageal reflux in our study was 9% (n ⫽ 11), and 7 of these children underwent a surgical antireflux procedure. Whereas other programs frequently discharge patients with a nasogastric tube to provide supplemental feedings, our family demographics have made us reluctant to use this method owing to concern over unrecognized tube displacement leading to aspiration with feedings. Optimally, the care of GI complications in neonates after congenital heart repair would be managed by a multidisciplinary team that includes the occupational therapy feeding specialist, the pediatric gastroenterologist, and pediatric surgeon. Early recognition and work-up of problematic feedings with appropriate action has the potential to shorten the hospital stay and conserve resources. It is hoped that such an approach will also lead to the early diagnosis of impending NEC at a point at which bowel rest and aggressive antibiotic therapy has the potential to salvage this otherwise potentially devastating problem. Finally, the creation and implementation of a nutritional support protocol may serve to further decrease the incidence of NEC. Future work will need to be done to determine whether the placement of a right ventricle to pulmonary artery conduit will reduce the incidence of NEC. In addition, the development of a feeding protocol may also serve to decrease the incidence of NEC.
The authors wish to thank Fred Dorey for providing statistical assistance.
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11. Hofner G, Behrens R, Koch A, Singer H, Hofbeck M. Enteral nutritional support by percutaneous endoscopic gastrostomy in children with congenital heart disease. Pediatr Cardiol 2000;21:341– 6. 12. Pollack MM, Ruttimmann UE, Getson PR. Pediatric risk of mortality (PRISM) score. Crit Care Med 1988;16: 1110 – 6. 13. Shore S, Nelson DP, Pearl JM, et al. Usefulness of corticosteroid therapy in decreasing epinephrine requirements in critically ill infants with congenital heart disease. Am J Cardiol 2001;88:591– 4. 14. Wernovsky G, Wypij D, Jonas RA, et al. Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. Circulation 1995;92: 2226 –35. 15. Walsh MD, Kleigman RM. Necrotizing enterocolitis: treatment based on staging criteria. Pediatr Clin 1986;33:179 – 201.
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16. Cheung TF, Ho MH, Cheng VY. Mesenteric blood flow response to feeding after systemic-to-pulmonary arterial shunt palliation. Ann Thorac Surg 2003;75:947–51. 17. del Castillo SL, Moromisato DY, Ludwick J, et al. Mesenteric blood flow velocities in the newborn with single ventricle physiology: modified Blalock-Taussig shunt versus right ventricle-pulmonary artery conduit. Pediatr Crit Care Med. In press. 18. Lequier LL, Nikaidoh H, Leonard SR, et al. Preoperative and postoperative endotoxemia in children with congenital heart disease. Chest 2000;117:1706 –12. 19. Fatica C, Gordon S, Mossad E, McHugh M, Mee R. A cluster of necrotizing enterocolitis in term infants undergoing open heart surgery. Am J Infect Contr 2000;28:130 –2. 20. Skinner ML, Halstead LA, Rubinstein CS, Atz AM, Bradley SM. Laryngopharyngeal dysfunction following the Norwood procedure [Abstract]. 85th Annual Meeting of the American Association for Thoracic Surgery, April 2005:116.
Southern Thoracic Surgical Association: Fifty-Third Annual Meeting The Fifty-Third Annual Meeting of the Southern Thoracic Surgical Association (STSA) will be held November 9 –11, 2006, in Tucson, Arizona. Members wishing to participate in the Scientific Program should submit an abstract by April 7, 2006, 12:00 Midnight, Central Daylight Time. Abstracts must be submitted electronically. Instructions for the abstract submission process can be found on the STSA Web site
© 2006 by The Society of Thoracic Surgeons Published by Elsevier Inc
at www.stsa.org; on the CTSNet Web site at www. ctsnet.org; or in the back of the issue of The Annals of Thoracic Surgery. Manuscripts accepted for the Resident Competition must be submitted to the STSA headquarters office no later than September 15, 2006. The Resident Award will be based on abstract, presentation, and manuscript.
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