Nutrition is fundamental for ensuring adequate energy for basal metabolism, growth, and physical activity. Infants and children possess high metabolic rates and limited reserves of endogenous substrates at baseline, and are at risk for developing deficiencies of energy during episodes of acute or chronic illness. 1 Infants and children with congenitally malformed hearts are at significant risk for developing such energetic imbalance due to increased expenditure of energy, and poor or inadequate nutrition. 2 Energetic imbalance leads to the development of malnutrition, which can adversely affect somatic growth, along with cognitive and motor development. 3 Failure of growth alters the metabolic response to injury and, for children with congenitally malformed hearts, increases the risk of post-operative morbidity and mortality, contributing to longer lengths of hospitalisation and times needed for recovery. 1
MALNUTRITION
Malnutrition is defined as a state of poor nutrition and failure of growth ( Table 66-1 ). Failure of growth exists when weight, or weight for height, is less than 2 standard deviations below the mean for sex and age, weight is less than the third centile, or weight for age has a z value of less than −2.0. 4 Criterions for the diagnosis of malnutrition also apply to children whose curve for gain in weight crosses more than 2 centiles from baseline on the growth charts created by the National Center for Health Statistics after having previously achieved a stable pattern. The baseline centile is the maximum weight achieved between 4 and 8 weeks of age, as studies have shown that the gain in weight during this time period correlates with the weight at the age of 12 months. 4
| Range | Acute Malnutrition (Wasting) (% Median of Weight for Height) | Chronic Malnutrition (Stunting) (% Median of Height for Age) |
|---|---|---|
| Normal | >90 | >95 |
| Mild | 80–90 | 90–95 |
| Moderate | 70–80 | 85–90 |
| Severe | <70 | <85 |
Malnutrition is a well-known consequence of congenital cardiac disease. It is estimated that four-fifths of hospitalised infants with congenitally malformed hearts suffer from acute or chronic malnutrition. 5 Prior to the 1980s, when such children underwent surgical correction at an older age, those with acyanotic and cyanotic lesions exhibited failure of growth at birth that persisted well into childhood. 6 In the current era of neonatal surgery, there has been a shift in the severity of pre-operatively delayed growth from the infants with cyanotic lesions to those having congestive cardiac failure. This is due primarily to the earlier age at surgical intervention. 7 The cause of malnutrition in these children is multi-factorial, albeit that the magnitude of the disturbed growth appears to be related to the anatomical lesion. 1
Significance of Malnutrition in Those with Congenitally Malformed Hearts
Malnutrition, specifically failure of growth, has been reported in more than half the children with congenitally malformed hearts. 2 The amount and type of retardation in somatic growth varies depending on the haemodynamic impact of the defect. In one study, 8 factors impacting on the extent of malnutrition included gender, the type of cardiac disease, weight at birth, thickness of the subscapular and triceps muscles, and cephalic circumference. The index of weight for length was found rapidly to decrease in those with cyanotic lesions, albeit that no differences in anthropometric measurements were noted between those having cyanotic and acyanotic lesions. Boys showed greater deterioration in weight for age, suggesting more acute malnutrition, while girls had lower linear growth for age, indicative of more chronic malnutrition. In another study, 9 somatic growth was shown to be most affected in patients with large ventricular septal defects and tetralogy of Fallot, improving after operative repair, but failing to normalise. Catch-up growth for length was strongly correlated with severity of pre-operative growth failure, but not with age at operation. 9 In yet another study, 10 weight was found to be below the third centile in half of those studied, height in one-third, and skin fold thicknesses in from one-eighth to one-fifth, thus endorsing the findings of Chen and colleagues. 2
MECHANISMS OF FAILURE TO GROW
Congenital Cardiac Disease
As discussed already, at birth, infants with both cyanotic and acyanotic cardiac lesions are more likely to have low weight. 2,8 The Baltimore-Washington Infant Study 11 found that infants with tetralogy of Fallot, atrioventricular septal defects, ventricular septal defects, and hypoplastic left heart syndrome had the lowest weights at birth, even when corrected for gestational age, findings endorsed in another study, this one showing also that those with transposition had normal weights at birth. 12
Failure to grow after birth is dependent on the haemodynamic effects of the cardiac lesion. The growth curve of neonates with mild malformations may be minimally affected, while those with severe cyanotic disease are at highest risk for malnutrition. 13 Pulmonary hypertension appears to be an important risk factor for failing growth in those with both acyanotic and cyanotic lesions, such children tending to suffer severe growth failure. 14
Congestive cardiac failure causes a hypermetabolic state and subsequent growth failure. 1 Cardiac lesions commonly resulting in congestive cardiac failure include hypoplastic left heart syndrome, patency of the arterial duct, totally anomalous pulmonary venous connection, critical valvar aortic stenosis, coarctation of the aorta, and ventricular septal defects. 15,16 With large and unrestrictive left-to-right shunts, excessive flow of blood to the lungs causes increased pulmonary and left heart pressures, along with elevated left ventricular end-diastolic pressures, resulting in a high-output state and failure to grow. 14
Children with cyanotic defects frequently have decreased weight and height compared to healthy infants. 15 Cyanotic lesions such as transposition and tetralogy of Fallot with and without pulmonary atresia usually have right-to-left shunting resulting in hypoxaemia. The duration of hypoxaemia in years is directly related to the retardation of growth. 2 Children who are both hypoxaemic and have congestive cardiac failure are more severely affected. 2
Children with multiple anomalies, in addition to congenital cardiac disease, are at the highest risk for acute and chronic malnutrition. 2 Genetic syndromes frequently associated with congenital cardiac disease, including trisomies 21, 13, and 18, Turner’s syndrome, Williams syndrome, Noonan’s syndrome, and DiGeorge syndrome, may also impact the rate of growth due to alterations in caloric intake, gastrointestinal absorption, metabolism, and expenditure of energy. 1,2
Inadequate Caloric Intake
Inadequate caloric intake is believed to be the main cause of infants with congenital cardiac disease failing to grow. The feeding patterns of such children have been compared to matched subgroups of normal infants. 1,17 For infants with congenitally malformed hearts, feeding is equivalent to an exercise test, demanding increased amounts of energy. Intolerance of feeding can be attributed to an inability to expend sufficient energy on feeding, as exhibited by tachycardia, tachypnoea, shortness of breath, and vomiting. Other contributing factors include early satiety, decreased gastric capacity caused by hepatosplenomegaly, delayed gastric emptying time secondary to low cardiac output and an uncoordinated suck, and abnormal patterns of swallowing and breathing due to tachypnoea. Additionally, fluid restrictions and diuretic therapy as part of the medical management may limit caloric intake.
Hypermetabolism
Energetic imbalance is a major contributing factor to failure of growth and malnutrition in children with congenitally malformed hearts. 18 The energy available for metabolism is the sum of total energy expenditure and energy stored. Basal metabolic rate represents the major component of total energy expenditure and metabolisable energy. In general, children have a higher metabolic rate, placing them at high risk for energetic deficiencies during episodes of acute illness. 1 The basal metabolic rate of infants is almost twice that of an adult per kilogram of body weight.
Children with congestive cardiac failure have been reported to have up to five times higher basal metabolic rates than children without cardiac disease. 18 The elevated basal metabolic rate may be due to the increased workload of the cardiac and respiratory systems. Resting expenditure of energy represents consumption of oxygen per kilogram of body weight, and has been shown to be increased in malnourished infants with congestive cardiac failure. 1 This increase has been attributed to a dilated or hypertrophied cardiac muscle, which can use up to one-third of the total oxygen consumed by the body, compared to one-tenth used by the healthy child. 10 Other conditions which have been attributed to an elevation in the total body metabolic rate in children with congestive cardiac failure include increased activity of the sympathetic nervous system, haematopoietic tissue, and respiratory muscles. 1
Frequent respiratory infections and fever will also contribute to a state of hypermetabolism and failure of growth. In infants, total expenditure of energy is increased due to an increase in physical activity from 5% of total metabolisable energy intake at 6 weeks of age to 34% at 12 months of age. 19 A marked rise in total energy expenditure relative to resting energy expenditure occurs in 3- to 5-month-olds with left-to-right shunting lesions due to increased cardiac workload, increased work of breathing, diminished myocardial efficiency, and increased stimulation of the sympathetic nervous system. 1
Malabsorption
Malabsorption is another condition which contributes to the malnutrition seen in children with congenitally malformed hearts. This can result from gastrointestinal tissue hypoxia, and causes feeding intolerance, limits caloric intake, and decreases absorption of nutrients. 13 The presence of hepatosplenomegaly may cause decreased gastric capacity and altered oral intake of nutrients. Those with cardiac lesions resulting in right-sided cardiac failure and increased systemic venous pressure due to right-to-left shunting may develop oedema of the intestinal wall and mucosal surfaces. These changes in the intestinal wall will lead to impaired nutrient extraction and malabsorption, affecting the timing, volume, and caloric density of feedings. 13
Growth Factor Hormone
Endocrine factors have been investigated as a possible cause for the growth delay in children with congenital heart disease. 20 Others found a positive correlation between low saturations of oxygen and levels of IGF-1 in the serum, indicating that hypoxaemia may be an independent factor contributing to growth failure. 21–23
ASSESSMENT OF GROWTH DELAY
Physical Growth
Physical growth is a direct reflection of nutritional well-being and is the single most important parameter used in assessing nutritional growth. Periodic assessments should be made to determine whether weight, height, length, and head circumference are within normal limits for age and gender. Anthropometric measurements can assess the longitudinal speed of growth. Length is the most useful indicator, and is most reliable after 2 years of age due to the difficulty in obtaining accurate measurements in infants. 4 Weight for height, the ratio of true weight to the ideal weight for height, is used to differentiate stunted growth from wasting independent of age. Stunting caused by chronic malnutrition, chronic illness, and genetic or endocrine abnormalities results in a child who is small for age but proportional for weight to height. 4 Body mass index is the best indicator of excess weight and obesity in children and adolescents. Children with an index between the 85th and 95th centiles are considered at risk for being overweight, whilst those with an index greater than or equal to the 95th centile are considered obese. 24 Head circumference is a useful tool until the child reaches 3 years of age. It is particularly important for children who have undergone a bidirectional Glenn procedure, and may provide information regarding the patency of the shunt. Measurements of the skinfolds at the triceps and the suprailiac crest are useful for estimating total body fat. Their application is limited in infants and young children, however, due to their lack of validity. 4 Other tools exist, but are rarely used routinely in children, again due to lack of validity, coupled with lack of accessibility, invasiveness, or cost.
Anthropometry
For children who are hospitalised, anthropometry may occur on a daily or biweekly basis to track tolerance of oral feedings, or effectiveness of breast-feedings, high-calorie diet, or anti-congestive therapy. Standard guidelines point to a target gain of weight of 10 to 35 grams per day for infants, depending on their age in months 25 ( Table 66-2 ). Infants who are undernourished have weights that plot at 2 standard deviations below the mean for gender and age on the growth charts compiled by the National Center for Health Statistics. 4 The rate of gain in weight of children with congenitally malformed hearts is typically affected more than the height. If the nutritional deficit is severe and long term, weight and height are equally affected. 8 Currently, there are no standard measurements which have been established for the population with congenitally malformed hearts. Interpreting data collected for this population, and evaluating any delayed growth on the basis of standards derived from healthy children, therefore, may exaggerate the degree of malnutrition.
| Age | Weight (g/day) | Length (cm/mo), Crown to Heel |
|---|---|---|
| Newborns (gestational age) | ||
| 31 wk | 24 | 3.2–4.4 |
| 34 wk | 35 | |
| >36 wk | 30 | |
| Infants | ||
| 0–3 mo | 25–35 | 2.6–3.5 |
| 4–6 mo | 15–21 | 1.6–2.5 |
| 7–12 mo | 24 | 1.2–1.7 |
| Children | ||
| 1–3 yr | 4–10 | 0.7–1.1 |
| 4–6 yr | 5–8 | 0.5–0.8 |
| 7–10 yr | 5–12 | 0.4–0.6 |
Prealbumin
Prealbumin, also known as thyroxine-binding prealbumin, or transthyretin, is a sensitive marker for assessing the severity of illness in children who have critical or chronic disease, and correlates with outcomes and recovery. 26 Specifically, levels of prealbumin have been shown to be a sensitive indicator of protein-calorie nutrition. The marker is more sensitive than either albumin or transferrin in measuring intake of protein and calories. 26 Being a negative acute phase reactant, its levels will decrease in presence of inflammation. It also decreases in the presence of hepatic dysfunction, since it reflects the ability of the liver to synthesise protein. Due to the accessibility of the test, and the rapid turnover in results, measuring levels of prealbumin allows for a more accurate and timely assessment of change in diet. 26 Serial levels obtained once or twice a week can assist in identifying nutritional adequacy. 27 The test should be used when there is suspicion of subclinical or marginal levels of protein-calorie nutrition, to assess the nutritional response to diet, including parenteral nutrition, and as a biochemical marker of nutritional adequacy in premature infants.
NUTRITIONAL MANAGEMENT
Requirements of Nutrients in Infancy
There are six classes of nutrients that influence the patterns of growth in infants and children: carbohydrates, fats, proteins, vitamins, minerals, and water, which in combination provide optimal nutrition and allow somatic growth ( Table 66-3 ). Nutritional options in infancy include breast-feeding along with a host of commercial formulas prepared specifically for premature and term infants, as well as for specific medical conditions. For healthy infants up to 6 months of age, the recommended dietary allowance in terms of calories is from 108 to 117 kilocalories per kilogram of body weight (kcal/kg) per day. 25 The need for protein during early infancy is high, due to rapid muscular and skeletal growth, and approximately 2.2 grams per kilogram of body weight 4 (see Table 66-3 ). Neonates with haemodynamically significant congenital cardiac malformations require substantially more nutritional support to sustain and catch up growth than do their healthy counterparts. 1 Those with mild to moderate disease may require from 130 to 150 kcal/kg per day, while those having moderate to severe lesions may require as much as 175 to 180 kcal/kg per day. 2 Diets that contain a deficient amount of carbohydrates, fats, and protein will result in poor weight gain, while linear growth is retarded when the dietary intake of protein is deficient. 4
| Component | Function | Recommended Daily Intake | Special Considerations for CHD |
|---|---|---|---|
| Calories | Provides energy for all metabolic processes and to support growth. |
|
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| Protein | Major structural component of all cells, acts as transport carrier. |
|
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| Carbohydrate | Calorie source to maintain body weight. Primary source of energy for the brain. |
| Carbohydrate modular use for caloric supplementation may cause increased fecal output due to high osmolarity. |
| Fat |
|
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| Fluids/Water | Essential for maintaining vascular volume. |
|
|
Vitamins
| Antioxidant, important in protecting mitochondria and cells from reactive oxygen intermediates. Essential for normal vision, gene expression, embryonic development, growth and immune function. |
|
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| B 1 , thiamine | Coenzyme for carbohydrate metabolism and maintenance of myelin for nerve and muscle function. |
| Endogenous antioxidants include enzymatic antioxidants (zinc in superoxide dismutase or selenium in glutathione peroxidase), free radical scavengers (vitamins A, C, and E) and metal chelators. |
| B 3 , niacin | Functions in intracellular respiration, fatty acid synthesis, and glucose oxidation. Decreases cholesterol and lipoprotein levels. |
| During stress, free radical production exceeds normal clearance. Antioxidants limit deleterious effect of free radicals. |
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| B 12 | Improves endothelial function by reducing homocysteine levels. |
| |
| Vitamin C | Antioxidant. Helps maintain tissue levels of vitamins A and E. |
| |
| Vitamin D | Essential for calcium absorption from the intestine. | 0 mo–18 yr, 5 μg | |
| Vitamin E | Antioxidant working to prevent propagation of lipid peroxidation. |
| |
| Vitamin K | Promotes liver synthesis of clotting factors (II, VII, IX, X). |
| |
| Folate | Necessary for DNA synthesis and replication. |
| Inadequate concentrations may decrease circulating levels of homocysteine. |
Minerals
| Essential for bone metabolism and muscle contraction. |
| |
| Chromium | Potentiates the action of insulin. Plays role in protein and lipid metabolism. Required for growth. |
| Decrease intake in presence of renal dysfunction. |
| Copper |
|
| |
| Iron | Necessary for ATP to be synthesized. |
| |
| Magnesium | Active component of antioxidant enzymes. |
| |
| Manganese | Cofactor in many enzyme functions. Stimulates synthesis of cholesterol and fatty acids in liver. Influences mucopolysaccharide synthesis. |
| |
| Phosphorus | Antioxidant that works in concert with vitamin E to protect cells from peroxidase damage. Required in all cellular reproduction and protein synthesis. |
| Vital to the structure of bones and teeth. Primary constituents of cellular membranes. Required for the production of ATP, the major physiologic molecule used in the storage and transport of energy. Key buffering system used to ensure acid-base balance. |
| Selenium | Antioxidant component of glutathione peroxidase that protects cell components from oxidative damage. |
| |
| Zinc | Needed for DNA and RNA synthesis and other enzyme functions. Necessary for optimal wound healing. |
| |
Other
| Essential for transport of long-chain fatty acids from cytoplasm to β-oxidation sites within the mitochondrial matrix. |
| |
| Taurine | Nonessential amino acid that participates in controlling cellular calcium levels. | No established RDA | |
| Fiber | Assists in maintaining normal glucose levels and bowel regularity. |
|
Fluid requirements for the normal neonate are 120 mL/kg per day for those weighing less than 3 kilograms, and 100 mL/kg per day for heavier neonates. 28 Once intravenous access is secured, intravenous fluids are started at 80 mL/kg per day, and generally advanced to a goal of 100 mL/kg per day over the course of 72 hours for all neonates except those with functionally univentricular circulations, or those with excessive insensible losses, fluids in these latter cases generally being started at 100 mL/kg per hour. 29 Neonates with congestive heart failure have losses of fluids up to one-sixth greater than those of a normal neonate due to their increased work of breathing, vomiting, and diuretics. 29 Achieving an optimal fluid balance in children with congenitally malformed hearts, therefore, is challenging, in part because of their insensible losses, but also because of the potential for protein imbalance and the role it plays in the retention of fluid.
Management of In-patients
It is axiomatic that timely nutritional support is needed for patients with congenitally malformed hearts so as to maintain an adequate nutritional state, and to minimise the physiologic consequences of undernutrition. Goals for neonates considered to be at risk, therefore, are to provide adequate nutrition to promote growth, and to correct nutrient deficiency. Goals for children include providing adequate nutrition to meet current metabolic demands, as well as for catch-up growth. 30 The challenge is to calculate energy requirements to maintain metabolism, this requiring 40 to 70 kcal/kg per day, as well as synthesis of tissues and storage of energy for growth, requiring an additional 50 to 70 kcal/kg per day, and to cope with routine losses of approximately 20 kcal/kg per day as well as any further expenditures related to illness. 28 A compromised nutritional state may delay surgical intervention and increase the risk of post-operative complications. In the neonate, poor nutrition negatively impacts cerebral development, cognitive function, and attainment of motor skills. 29
Types of Nutrition
Parenteral Nutrition
Parenteral nutrition and intralipids should be started when the initiation of enteral feedings is not an option for ensuring metabolic needs. 28 Due to the high incidence of respiratory problems, limited gastric capacity, and intestinal hypomotility of premature infants, enteral feeds should be initiated and advanced in slow fashion. 29 Parenteral nutrition supplements the calories provided by limited enteral feedings to ensure the nutritional needs. The nutritional content of the parenteral supply is limited by the type of vascular access available. The content of dextrose in peripheral parenteral nutrition should not exceed 12.5%, and amino acids should not exceed 2%, because of the potential of producing venous irritation. Lipid tolerance of 20% solutions is superior to that of 10% solutions due to their lower content of phospholipid emulsifiers. 28 For term infants born with low weight, parenteral nutrition should be instituted within the initial 3 days of life if enteral feeds are contra-indicated due to concerns of necrotizing enterocolitis or extracardiac anomalies such as tracheoesophageal fistula, duodenal atresia, and gastroschisis. 29 In such infants born with low weight, it has been shown that the average retention of nitrogen improved even when the intake of energy was less than 30 kcal/kg per day when protein, 1.15 g/kg per day, was initiated on the first day of life. 28
The rate of glomerular filtration, and the distal and proximal tubular function, are decreased in infants of less than 34 weeks of gestation. Premature infants have a decreased ability to concentrate urine compared to those born at term. 4 This produces a risk for hyperkalaemia during the first few days of life. Electrolytes, therefore, are generally not added to intravenous fluids for the first 24 hours of life. 4 Neonates born at term may require supplementation of calcium over the first 24 to 48 hours after birth due to the sudden cessation of placental delivery of calcium, the decreased release of parathyroid hormone, and elevated levels of calcitonin. 30 Infants who are premature, infants who required phototherapy or were exposed to anticonvulsants during fetal life, and infants of diabetic mothers or mothers with a history of hyperparathyroidism are all at risk for prolonged periods of hypocalcaemia. Preventative therapy consists of doses of 25 to 75 mg/kg per day of intravenous elemental calcium added to intravenous fluid or parenteral nutrition. 30
For children and adolescents, parenteral nutrition and intralipids should be initiated when a delay of up to 1 week is anticipated before enteral feedings can be started. 4 Parenteral nutrition should be implemented in children who exhibit signs of malnutrition pre-operatively to avoid deficiencies of fatty acids and to promote optimal nutrition. 30 If a delay of longer than 1 week is anticipated before the initiation of enteral feedings, consideration should be given to placing a central venous line so as to optimise the caloric density of the parenteral solution. 4
Prolonged administration of parenteral nutrition is associated with cholestasis, hepatocellular necrosis, and in advanced cases, hepatic disease or cirrhosis. 4 After 2 to 3 weeks of parenteral nutrition, infants are at risk for developing cholestasis as evidenced by hyperbilirubinaemia and elevated transaminaemia. 28 Older children and adolescents develop steatosis and steatohepatitis. 30 The severest hepatic pathological changes are found in patients with the poorest enteral intake. Enteral feedings, therefore, should be commenced as soon as possible, even if only as trophic feeds, to minimise the risk of hepatic dysfunction. 4
Infant Nutrition
Breast Milk
The Department of Health and Human Services of the United States and the American Academy of Pediatrics recommend exclusive breast-feeding during the first year of life. 31,32 Human milk provides optimal fat, protein, and carbohydrates for the infant born at term. Breast milk possesses anti-infective properties, reducing the incidence of acute illness, pathogenic bacterial faecal flora, necrotizing enterocolitis, otitis media, and infections of the lower respiratory and urinary tracts. 32 It has been suggested that immune-mediated diseases, such as diabetes mellitus, Crohn’s disease, eczema, asthma, and allergic gastroenteritis, are lower among breast-fed infants. 32 The bond between mother and infant is enhanced, and cognitive scores consistently improve in direct relation to the duration of breast-feeding. 33 When the mother is unable to produce sufficient supply, or when breast-feeding is contra-indicated due to maternal health reasons, banked donor breast milk is available. Possible reasons for using donor breast milk may include prematurity, allergies, inborn errors of metabolism, and renal disease. Despite the well-known benefits of breast-feeding, infants with congenitally malformed hearts are often unable to meet their caloric needs by this method. Despite this caveat, parents should be educated about the benefits of breast milk, provided either by bottle or a supplemental device.
Commercial Formulas
Iron fortified formulas are indicated as substitutes for human milk when the mother chooses not to breast-feed or use banked donor breast milk, when breast-feeding is medically contra-indicated, and as a supplement when the intake of breast milk is inadequate. 33 Formulas based on cow’s milk contain up to half more protein than does human milk. Fats are derived from vegetable oils, or a mixture of vegetable and animal fat, and the major carbohydrate source is lactose. 4 Soy-based formulas are indicated when the family is vegetarian or the infant has a history of lactase deficiency, galactosaemia, immunoglobulin E–associated cow milk protein reaction, or suspected intolerance to cow milk–based formula as exhibited by colic, loose stools, and vomiting. 4 The concentration of protein in soy milk–based formula is supplemented with methionine, and sucrose is the major source of carbohydrates. 4 Protein hydrolysate formulas are designed for infants who are severely intolerant to intact cow milk or soy proteins, and for those with significant malabsorption due to gastrointestinal or hepatobiliary disease. This type of formula has the advantage that the protein is extensively hydrolysed, resulting in peptides that do not elicit an immunologic response. The disadvantages include taste, cost, and higher osmolality. 4
Maximizing Calories
Optimizing caloric intake to meet increased hypermetabolic needs of children with cardiovascular disease can be achieved by increasing either the volume or the caloric density of the feeds, and by implementing medical and surgical interventions to manage symptoms associated with their cardiac disease. If the infant with congestive cardiac failure feeds on demand, without change in baseline symptoms and vital signs, limiting feeds is typically not warranted. If restriction of fluids is not a concern, then breast milk, or commercial formula which provides 20 calories per ounce, can be offered at an increased volume. If intake of fluid is a concern, increasing caloric density of either pumped breast milk or commercial formula should be provided ( Table 66-4 ). Studies have reported that weight gains of infants following cardiac surgery are suboptimal and that outcomes are improved by rapid advancement of calories. 34 Caution is needed when increasing caloric density, however, since it can lead to decreased free water, increased osmolarity, and increased solute load, resulting in an increase in output of stool and disturbed electrolytes. 4 Renal solute load, that is, excess accumulation of nitrogen due to metabolism of proteins, may also be altered when the concentration of the formula is changed. Dehydration may then occur as the body the attempts to compensate, drawing out excess water to dilute the solute load.
