Congenital heart disease (CHD) is

June 2013 ICAN: Infant, Child, & Adolescent Nutrition Clinical Research Reports Malnutrition in Congenital Heart Disease Management to Improve Outc...
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June 2013

ICAN: Infant, Child, & Adolescent Nutrition

Clinical Research Reports

Malnutrition in Congenital Heart Disease Management to Improve Outcomes Lilly Erna Hubschman, MSN, RN, NNP-BC

Abstract: Advanced corrective and palliative cardiovascular surgical procedures have significantly reduced mortality related to congenital heart disease. However, in infants with congenital heart disease, inadequate nutrient intake, insufficient nutrient absorption, and increased energy needs limit the ability to grow and develop. Infants with congenital heart disease have a high prevalence of malnutrition. Nutrition provides an opportunity to optimize growth, development, and quality of life in an era of increased survival. Early intervention and identification of at-risk patients has the potential to decrease morbidity and mortality related to malnutrition in infants with congenital heart disease. Currently, a paucity of research prohibits practitioners from providing comprehensive evidence-based care and compromises the care of the growing population of patients with congenital heart disease who survive infancy. The purpose of this article is to examine existing evidence that could contribute to guidelines for improving outcomes and data gaps that can be filled. This article establishes a malnutrition prevention/growth promotion protocol using

risk assessments, estimation of resting energy expenditure, calorie and protein administration recommendations, growth charts, discharge planning, and follow-up care. Keywords: congenital heart disease; malnutrition; neonates; infants

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ongenital heart disease (CHD) is the largest contributor to neonatal mortality in the United States,

more patients with CHD survive the neonatal period, the focus must shift toward long-term management and outcome optimization. Nutritional management provides a unique opportunity to impact survival, development, and quality of life in patients with CHD. This article will review the etiology of malnutrition in patients with CHD, recommendations and management of malnutrition in patients with CHD, and future research needs.

“As more patients with CHD [congenital heart disease] survive the neonatal period, the focus must shift toward long-term management and outcome optimization.” accounting for more neonatal deaths than all other birth defects combined. Historically, infant mortality accounted for 48.1% of CHD-related deaths. However, refined surgical palliation and continuing medical and surgical innovation in treatment of CHD allowed for a 2.8% annual decrease in CHD-related infant mortality from 1999 to 2006.1 As

Etiology of Malnutrition in Patients With Congenital Heart Disease Congenital heart disease is a structural problem in the walls, valves, chambers, and arteries or veins near the heart that is present at birth. These defects disrupt normal hemodynamics, causing a

DOI: 10.1177/1941406413485906. From Columbia University School of Nursing, New York, New York. Address correspondence to Lilly Erna Hubschman, RN, BSN, NNPs, 150 East 93rd Street, Apartment 9B, New York, NY 10128; e-mail: [email protected]. For reprints and permissions queries, please visit SAGE’s Web site at http://www.sagepub.com/journalsPermissions.nav. Copyright © 2013 The Author(s)

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pathophysiology responsible for inadequate nutrient intake, insufficient nutrient absorption, and increased metabolic demands. Total energy requirements in the neonate are comprised of energy needed to maintain metabolism and energy required for growth. The neonate with CHD must contend with potential hypermetabolism, decreased mesenteric perfusion, delayed enteral feeding, and inherent difficulty in estimating their nutritional needs. Providing optimal nutrition in this population can improve surgical outcomes by establishing a solid baseline from which to correct or palliate the pathophysiology associated with CHD. Moreover, postoperative nutritional management that provides adequate protein, fat, and electrolytes can speed recovery, lower hospital costs, and prevent the long-term developmental sequelae of malnutrition. Increased Energy Needs

In addition to insufficient nutrient absorption, delayed enteral feeding, and increased metabolic demands, neonates with CHD have higher energy expenditures than previously perceived. Infants with CHD have higher resting energy expenditures preoperatively compared with healthy control infants.2 Postoperatively, a hypermetabolic state, characterized by high VO2, VCO2, and energy expenditure is sustained for 8 hours3 and resting energy expenditure normalizes to control group levels within a week after surgery.2 During the immediate postoperative period, pediatric patients undergoing surgical correction of CHD experience a state of hypermetabolism that is often unmatched by calorie and protein intake.3 Limitations in calorie and protein intake may be attributed to postoperative fluid intake restriction and use of resting energy expenditure predictive equations. Energy expenditure may be estimated using predictive equations or measured by indirect calorimetry. Numerous recent studies have cited the inaccuracy of commonly used predictive equations in estimating energy expenditures in postoperative neonates with CHD. De Wit et al4 determined that the mean measured energy expendi-

ICAN: Infant, Child, & Adolescent Nutrition

ture of CHD patients 0-7 days postoperative who required cardiopulmonary bypass was 73.6 ± 15.11 kcal/kg/d versus 58.3 ± 10.88 kcal/kg/d in nonbypass patients. The difference between measured energy expenditure in bypass and nonbypass patients was statistically significant; however, none of the currently used predictive equations for estimating energy expenditures in pediatric patients correlated with these findings. The Schofield, pediatric intensive care unit–specific White, and World Health Organization (WHO) equations all underestimated the resting energy expenditure of postoperative pediatric patients with CHD. Despite a 18.39% to 36.35% mean difference4 in estimation of energy expenditures between the Schofield, White, and WHO equations and energy expenditures measured by De Wit et al,4 these equations are commonly used to prescribe feeding protocols used in this population. Although indirect calorimetry may more accurately determine energy requirements, its cost and availability may be prohibitive. Existing feeding protocols based on imprecise estimates grossly fail to meet energy demands of postoperative patients.3,4 Inadequate Nutrient Intake

Patients with congenital heart defects also experience delayed feeding milestones and gastrointestinal morbidity that contribute to inadequate nutrient intake. Among patients who undergo stage I palliation for hypoplastic left heart syndrome, up to 41% will develop gastrointestinal complications. The most common complications include discharge home with feeding tubes, necrotizing enterocolitis, and prolonged hospital stay for additional nutritional support. Moreover, delayed feeding cues, enteral feeding and oromotor coordination, as well as oropharyngeal dysphagia significantly contribute to delayed feeding milestones.5 Infants who had longer intubation times, lower preoperative weight, vocal cord injury, open chest on return from surgery, and more complex surgery—as measured by Risk Adjusted Congenital Heart Surgery score (RACHS)—were more likely to not achieve full oral feeding on discharge.6,7

Vocal cord dysfunction strongly correlates with feeding difficulties in children who undergo surgery for CHD. Cardiovascular surgery that requires manipulation of the aortic arch or left pulmonary artery can compromise the left recurrent laryngeal nerve, which runs parallel to the ductus arteriosus. Moreover, surgery involving the carotid sheath can also damage the vagus nerve, which innervates the right vocal cord. Among patients who undergo manipulation of the aortic arch or left pulmonary artery, 1.7% experience vocal cord dysfunction, and 89% of the population with vocal cord dysfunction display clinical signs of swallow dysfunction. Only a very small portion of these patients will achieve full oral feedings at the time of discharge.8 Despite significant barriers among patients with CHD, conventional wisdom in neonatology encourages oral and enteral feeding. At the Children’s Hospital of Philadelphia, postoperative patients with single-ventricle physiology are fed 20 cal/oz formula or expressed breast milk via nasogastric tubes. Over a 48- to 72-hour period feed volumes are advanced to 100 to 120 mL/ kg/d, at which point parenteral nutrition is discontinued and caloric density of feeds is increased to 24 to 27 cal/ oz. Subsequently, bolus nasogastric and oral feeds are attempted. This protocol is modified for biventricular patients, who are permitted to feed orally with supplemental nasogastric feeds as needed. A retrospective chart review at the Children’s Hospital of Philadelphia established that despite aggressive nutritional monitoring and management, enteral feeding does not provide adequate nutrition for growth immediately after neonatal surgery for complex CHD.9 Insufficient Nutrient Absorption

Congenital heart defects and postoperative physiology that impose a considerable volume load on the right ventricle decrease cardiac output and amplify the risk for decreased splanchnic perfusion. Congestive heart failure that ensues from increased right ventricular pressure predispose the patient to 171

June 2013

ICAN: Infant, Child, & Adolescent Nutrition

decreased end-organ perfusion, thereby decreasing the blood flow available to the digestive organs for nutrient absorption. Furthermore, decreased cardiac output may contribute to feeding intolerance and feeding fatigue.10 Up to 50% of infants with circulation that compromises splanchnic perfusion experience severe malnutrition on readmission for further cardiovascular surgery. These malnourished patients experience longer admissions, more readmissions, longer stays in the intensive care unit, and higher diuretic doses.10 Management and Recommendations To prevent the morbidity and latestage mortality associated with malnutrition in infants with CHD, aggressive evidence-based management must be enacted. Neonatal CHD patients who previously could not be saved are now living into adulthood and require extensive integrated care to optimize growth, developmental outcomes, and quality of life. Nutrition management provides an exceptional opportunity to significantly affect these parameters. A comprehensive, evidence-based protocol that includes use of appropriate growth charts, risk assessments, enteral and parenteral nutrition, preoperative management, accurate estimation of energy requirements, and timing of surgical intervention should be in place in neonatal intensive care units that treat patients with congenital heart defects. Use of Growth Charts

In practice, most practitioners use growth charts as standards against which patients may be measured for optimal or suboptimal growth. Historically, American practitioners have used the Centers for Disease Control and Prevention (CDC) growth charts to graph weight for age, length for age, weight for length, and body mass index for age. In 2006, however, the CDC, National Institutes of Health, and American Academy of Pediatrics determined that the 2006 WHO Growth Charts should be used for children younger than 24 months and that 172

CDC growth charts should be used for children 24 months to 20 years old. The WHO growth charts compare the patient with growth standards and reflect optimal growth, whereas the CDC growth charts compare the patient with growth references.11 Although infants with CHD do not often experience optimal growth, use of WHO growth charts provides an opportunity to identify abnormal growth patterns and guides the practitioner to investigate the modifiable causes of these growth anomalies. Optimize Preoperative Feeding

Preoperative optimization of caloric intake is a modifiable risk factor associated with greater weight gain in the first 14 months of life.12 Although preoperative oral feeding does not contribute to an infant’s ability to orally feed postoperatively,7 postponing enteral feeds until after surgery may instigate nutritional deficiencies that persist through the immediate postoperative period and beyond. Possible contraindications to preoperative feeding include the presence of umbilical catheters and continuous infusions of prostaglandin E1. However, neither of these treatments can be considered categorical contraindications. Among the various studies consulted in preparing these guidelines, each institution bore its own protocols with respect to feeding with indwelling umbilical catheters. A case–control study by McElhinney et al13 cites prostaglandin E1 doses greater than 0.05 µg/kg/min as a significant risk factor for necrotizing enterocolitis among neonates with CHD. Interestingly, prostaglandin E1 infusions were only statistically significant risk factors for necrotizing enterocolitis in this study’s univariable analysis, and not its multivariate analysis. Moreover, the study by McElhinney et al13 found no correlation between necrotizing enterocolitis and history, timeline, or substrate of enteral feeding. A 2008 retrospective chart review from the Children’s Hospital of Denver further suggests that enteral feeding of prostaglandin-dependent neonates may be a reasonable practice. The retrospective chart review found that only one out of 34 patients displayed signs of

feeding intolerance while on a continuous prostaglandin E1 infusion. Feeding intolerance was defined as large volume or bilious emesis, increased abdominal girth of >3 cm over 8 hours, hemoccult positive stools, bowel dysmotility, pneumatosis, pneumoperitoneum, portal venous air, gasless abdomen, and/or abnormal bowel distension on abdominal x-ray.14 These hypothetical complications of enteral feeding while continuously infusing prostaglandin E1 in the ductal-dependent CHD patient must be reweighed on a case-by-case basis against the recognized advantages of enteral feeding in light of the studies’ findings.13,14 Given the opportunity to optimize preoperative nutrition, patients at risk for malnutrition establish a baseline from which to benefit postoperatively. Although weight is only one measure of nutritional status, higher preoperative weights correlate with higher postoperative weight-for-age Z scores. This indicates that patients who are nutritionally optimized preoperatively are more nutritionally prepared for the hypermetabolism and other factors that contribute to postoperative malnutrition.12 Moreover, patients who achieve full enteral feeds prior to surgery have lower postoperative mortality rates and are less likely to be discharged on gavage feeds.15 CHD patients with higher preoperative weights are also more likely to achieve full postoperative oral feedings on discharge.7 Timing Surgical Intervention

Patients who must undergo surgical correction or palliation of CHD are at risk for nutritional consequences. Although timing surgical intervention is determined by the cardiac lesion and the surgeon’s judgment, several growth studies of infants with CHD have found that prompt surgical correction or palliation may improve postoperative weight gain and survival. Patients with single-ventricle physiology who experienced greater postoperative catch-up growth were, on average, younger at the time of stage I hypoplastic left heart palliative surgery. Furthermore, height and weight-for-age Z scores may be decreased in neonates who undergo palliative or corrective

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surgery after 10 days of life as compared to neonates who undergo surgery before 10 days of life.2 Among patients who require multiple surgeries, such as those with hypoplastic left heart syndrome, close nutritional surveillance can reduce interstage mortality by up to 15%. At approximately 150 days of life, patients with hypoplastic left heart syndrome experience a growth plateau that correlates with interstage mortality. Patients in the surveillance cohort of a study by Ghanayem et al16 were instructed to seek medical advice for >30 g/d weight loss or 55 cal/kg/d and protein >1 g/ kg/d in infants requiring cardiac surgery. Likewise, Bechard et al17 found that anabolism correlated with administration of >57 cal/kg/d and protein >1.5 g/kg/d in critically ill pediatric patients requiring mechanical ventilation. However, hypermetabolic patients may require a minimum of 2.8 g/kg/d of protein to maintain the positive nitrogen balance associated with anabolism.17 Perhaps the most promising breakthrough in preventing malnutrition in infants with CHD is a rapid feeding advancement protocol of calorie concentrated formula. Francy Pillo-Blocka and her colleagues at the Hospital for Sick Children in Toronto, Ontario, conducted a double-blind randomized control trial in postoperative CHD patients younger than 1 year to assess the effect of advancement to higher calorie formulas on weight gain and length of hospital stay. The study protocol determined

energy requirements based on percentage of actual compared with ideal weight-for-height. Study patients whose weight-for-height was >85% of the ideal were prescribed the recommended daily allowances for age according to Nutrition Recommendations: The Report of the Scientific Review Committee—95 to 120 cal/kg/d.21 Study patients whose weight-for-height was