Matthew A. Haemer, MD, MPH
Laura E. Primak, RD, CNSD, CSP
Nancy F. Krebs, MD, MS
NUTRITION & GROWTH
The nutrient requirements of children are influenced by (1) growth rate, (2) body composition, and (3) composition of new growth. These factors vary with age and are especially important during early postnatal life. Growth rates are higher in early infancy than at any other time, including the adolescent growth spurt (Table 11–1). Growth rates should normally decline rapidly starting in the second month of postnatal life (proportionately later in the premature infant).
Table 11–1. Changes in growth rate, energy required for growth, and body composition in infants and young children.
Nutrient requirements also depend on body composition. In the adult, the brain, which accounts for only 2% of body weight, contributes 19% to the total basal energy expenditure. In contrast, in a full-term neonate, the brain accounts for 10% of body weight and for 44% of total energy needs under basal conditions. Thus, in the young infant, total basal energy expenditure and the energy requirement of the brain are relatively high.
Composition of new tissue is a third factor influencing nutrient requirements. For example, fat should account for about 40% of weight gain between birth and 4 months but for only 3% between 24 and 36 months. The corresponding figures for protein are 11% and 21%; for water, 45% and 68%. The high rate of fat deposition in early infancy has implications not only for energy requirements but also for the optimal composition of infant feedings.
Because of the high nutrient requirements for growth and the body composition, the young infant is especially vulnerable to undernutrition. Slowed physical growth rate is an early and prominent sign of undernutrition in the young infant. The limited fat stores of the very young infant mean that energy reserves are modest. The relatively large size and continued growth of the brain render the central nervous system (CNS) especially vulnerable to the effects of malnutrition in early postnatal life.
The major determinants of energy expenditure are (1) basal metabolism, (2) metabolic response to food, (3) physical activity, and (4) growth. The efficiency of energy use may be a significant factor, and thermoregulation may contribute in extremes of ambient temperature if the body is inadequately clothed. Because adequate data on requirements for physical activity in infants and children are unavailable and because individual growth requirements vary, recommendations have been based on calculations of actual intakes by healthy subjects. Suggested guidelines for energy intake of infants and young children are given in Table 11–2. Also included in this table are calculated energy intakes of infants who are exclusively breast-fed, which have been verified in a number of centers. Growth velocity of breast-fed infants during the first 3 months equals and may exceed that of formula-fed infants, but from 6 to 12 months breast-fed infants typically weigh less than formula-fed babies and may show a decrease in growth velocity. The World Health Organization has developed growth standards derived from an international sample of healthy breast-fed infants and young children raised in environments that do not constrain growth. These are considered to represent physiologic growth for infants and young children. (See also section Pediatric Undernutrition.)
After the first 4 years, energy requirements expressed on a body weight basis decline progressively. The estimated daily energy requirement is about 40 kcal/kg/d at the end of adolescence. Approximate daily energy requirements can be calculated by adding 100 kcal/y to the base of 1000 kcal/d at age 1 year. Appetite and growth are reliable indices of caloric needs in most healthy children, but intake also depends to some extent on the energy density of the food offered. Individual energy requirements of healthy infants and children vary considerably, and malnutrition and disease increase the variability. Premature infant energy requirements can exceed 120 kcal/kg/d, especially during illness or when catch-up growth is desired.
One method of calculating requirements for malnourished patients is to base the calculations on the ideal body weight (ie, 50th percentile weight for the patient’s length-age, 50th percentile weight-for-length, or weight determined from current height and the 50th percentile body mass index [BMI] for age), rather than actual weight.
Grummer-Strawn LM et al: Use of World Health Organization and CDC growth charts for children aged 0–59 months in the United States. Centers for Disease Control and Prevention (CDC). MMWR Recomm Rep. 2010 Sep 10;59(RR-9):1–15 [PMID: 20829749].
World Health Organization: Report of a Joint FAO/WHO/UNO Expert Consultation: Energy and Protein Requirements. WHO Tech Rep Ser No. 724, 1985;724.
Table 11–2. Recommendations for energy and protein intake.
Only amino acids and ammonium compounds are usable as sources of nitrogen in humans. Amino acids are provided through the digestion of dietary protein. Nitrogen is absorbed from the intestine as amino acids and short peptides. Absorption of nitrogen is more efficient from synthetic diets that contain peptides in addition to amino acids. Some intact proteins are absorbed in early postnatal life, a process that may be important in the development of protein tolerance or allergy.
Because there are no major stores of body protein, a regular dietary supply of protein is essential. In infants and children, optimal growth depends on an adequate dietary protein supply. Relatively subtle effects of protein deficiency are now recognized, especially those affecting tissues with rapid protein turnover rates, such as the immune system and the gastrointestinal (GI) mucosa.
Relative to body weight, rates of protein synthesis and turnover and accretion of body protein are exceptionally high in the infant, especially the premature infant. Eighty percent of the dietary protein requirement of a premature infant is used for growth, compared with only 20% in a 1-year-old child. Protein requirements per unit of body weight decline rapidly during infancy as growth velocity decreases. The recommendations in Table 11–2 are derived chiefly from the Joint FAO/WHO/UNO Expert Committee and are similar to the Recommended Dietary Allowances (RDAs). They deliver a protein intake above the quantity provided in breast milk. The protein intake required to achieve protein deposition equivalent to the in utero rate in very low-birth-weight infants is 3.7–4.0 g/kg/d simultaneously with adequate energy intake. Protein requirements increase in the presence of skin or gut losses, burns, trauma, and infection. Requirements also increase during times of catch-up growth accompanying recovery from malnutrition (approximately 0.2 g of protein per gram of new tissue deposited). Young infants experiencing rapid recovery may need as much as 1–2 g/kg/d of extra protein. By age 1 year, the extra protein requirement is unlikely to be more than 0.5 g/kg/d.
The quality of protein depends on its amino acid composition. Infants require 43% of protein as essential amino acids, and children require 36%. Adults cannot synthesize nine essential amino acids: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine. Cysteine and tyrosine are considered partially essential because their rates of synthesis from methionine and phenylalanine, respectively, are limited and may be inadequate in infants, the elderly, and those with malabsorption. In young infants, synthetic rates for cysteine, tyrosine, and, perhaps, taurine are insufficient for needs. Taurine, an amino acid used to conjugate bile acids, may also be conditionally essential in infancy. Lack of an essential amino acid leads to weight loss within 1–2 weeks. Wheat and rice are deficient in lysine, and legumes are deficient in methionine. Appropriate mixtures of vegetable protein are therefore necessary to achieve high protein quality.
Because the mechanisms for removal of excess nitrogen are efficient, moderate excesses of protein are not harmful and may help to ensure an adequate supply of certain micronutrients. Adverse effects of excessive protein intake may include increased calcium losses in urine and, over a life span, increased loss of renal mass. Excessive protein intake of more than 4 g/kg/day in older children and adolescents may also cause elevated blood urea nitrogen, acidosis, hyperammonemia, and, in the premature infant more than 6g/kg/day has caused failure to thrive, lethargy, and fever. Impaired capacity to deaminate proteins from liver insufficiency or to excrete excess nitrogen as urea from renal insufficiency can further limit tolerable protein intake.
Hay WW, Thureen P: Protein for preterm infants: how much is needed? How much is enough? How much is too much? Pediatr Neonatol. 2010 Aug;51(4):198–207. doi: 10.1016/S1875-9572(10)60039-3 [PMID: 20713283].
Fats are the main dietary energy source for infants and account for up to 50% of the energy in human milk. Over 98% of breast milk fat is triglyceride (TG), which has an energy density of 9 kcal/g. Fats can be stored efficiently in adipose tissue with a minimal energy cost of storage. This is especially important in the young infant. Fats are required for the absorption of fat-soluble vitamins and for myelination of the central nervous system. Fat also provides essential fatty acids (EFAs) necessary for brain development, for phospholipids in cell membranes, and for the synthesis of prostaglandins and leukotrienes. The EFAs are polyunsaturated fatty acids, linoleic acid (18:2ω6) and linolenic acid (18:3ω3). Arachidonic acid (20:4ω6) is derived from dietary linoleic acid and is present primarily in membrane phospholipids. Important derivatives of linolenic acid are eicosapentaenoic acid (20:6ω3) and docosahexaenoic acid (DHA, 22:6ω3) found in human milk and brain lipids. Visual acuity and possibly psychomotor development of formula-fed premature infants is improved in formulas supplemented with DHA (22:6ω3) and ARA (20:4ω6). The benefits of long-chain polyunsaturated fatty acid supplementation in formulas for healthy term infants are unclear (though safety has been established).
Clinical features of EFA omega-6 deficiency include growth failure, erythematous and scaly dermatitis, capillary fragility, increased fragility of erythrocytes, thrombocytopenia, poor wound healing, and susceptibility to infection. The clinical features of deficiency of omega-3 fatty acids are less well defined, but dermatitis and neurologic abnormalities including blurred vision, peripheral neuropathy, and weakness have been reported. Fatty fish are the best dietary source of omega-3 fatty acids. A high intake of fatty fish is associated with decreased platelet adhesiveness and decreased inflammatory response.
Up to 5%–10% of fatty acids in human milk are polyunsaturated, with the specific fatty acid profile reflective of maternal dietary intake. Most of these are omega-6 series with smaller amounts of long-chain omega-3 fatty acids. About 40% of breast milk fatty acids are monounsaturates, primarily oleic acid (18:1), and up to 10% of total fatty acids are medium-chain triglycerides (MCTs) (C8 and C10) with a calorie density of 7.6 kcal/g. In general, the percentage of calories derived from fat is a little lower in infant formulas than in human milk.
The American Academy of Pediatrics recommends that infants receive at least 30% of calories from fat, with at least 2.7% of total fat as linoleic acid, and 1.75% of total fatty acids as linolenic. It is appropriate that 40%–50% of energy requirements be provided as fat during at least the first year of life. Children older than 2 years should be switched gradually to a diet containing approximately 30% of total calories from fat, with no more than 10% of calories either from saturated fats or polyunsaturated fats.
β-Oxidation of fatty acids occurs in the mitochondria of muscle and liver. Carnitine is necessary for oxidation of the fatty acids, which must cross the mitochondrial membranes as acylcarnitine. Carnitine is synthesized in the human liver and kidneys from lysine and methionine. Carnitine needs of infants are met by breast milk or infant formulas. In the liver, substantial quantities of fatty acids are converted to ketone bodies, which are then released into the circulation as an important fuel for the brain of the young infant.
MCTs are sufficiently soluble that micelle formation is not required for transport across the intestinal mucosa. They are transported directly to the liver via the portal circulation. MCTs are rapidly metabolized in the liver, undergoing β-oxidation or ketogenesis. They do not require carnitine to enter the mitochondria. MCTs are useful for patients with luminal phase defects, absorptive defects, and chronic inflammatory bowel disease. The potential side effects of MCT administration include diarrhea when given in large quantities; high octanoic acid levels in patients with cirrhosis; and, if they are the only source of lipids, deficiency of EFA.
Lapillonne A et al: Lipid needs of preterm infants: updated recommendations. J Pediatr. 2013 Mar;162(3 Suppl):S37–S47. doi: 10.1016/j.jpeds.2012.11.052 [PMID: 23445847].
The energy density of carbohydrate is 4 kcal/g. Approximately 40% of caloric intake in human milk is in the form of lactose, or milk sugar. Lactose supplies 20% of the total energy in cow’s milk. The percent of total energy in infant formulas from carbohydrate is similar to that of human milk.
The rate at which lactase hydrolyzes lactose to glucose and galactose in the intestinal brush border determines how quickly milk carbohydrates are absorbed. Lactase levels are highest in young infants, and decline with age depending on genetic factors. About 20% of nonwhite Hispanic and black children younger than 5 years of age have lactase deficiency. White children typically do not develop symptoms of lactose intolerance until they are at least 4 or 5 years of age, while nonwhite Hispanic, Asian American, and black children may develop these symptoms by 2 or 3 years of age. Lactose-intolerant children have varying symptoms depending on the specific activity of their intestinal lactase and the amount of lactose consumed. Galactose is preferentially converted to glycogen in the liver prior to conversion to glucose for subsequent oxidation. Infants with galactosemia, an inborn metabolic disease caused by deficient galactose-1-phosphate uridyltransferase, require a lactose-free diet starting in the neonatal period.
After the first 2 years of life, 50%–60% of energy requirements should be derived from carbohydrates, with no more than 10% from simple sugars. These dietary guidelines are, unfortunately, not reflected in the diets of North American children, who typically derive 25% of their energy intake from sucrose and less than 20% from complex carbohydrates.
Children and adolescents in North America consume large quantities of sucrose and high-fructose corn syrup in soft drinks and other sweetened beverages, candy, syrups, and sweetened breakfast cereals. A maximum intake of 10% of daily energy from sucrose has been recommended by the World Health Organization, but typical intakes have been reported to far exceed this recommended level. A high intake of these sugars, especially in the form of sweetened beverages, may predispose to obesity and insulin resistance, is a major risk factor for dental caries, and may be associated with an overall poorer quality diet, including high intake of saturated fat. Sucrase hydrolyzes sucrose to glucose and fructose in the brush border of the small intestine. Fructose absorption through facilitated diffusion occurs more slowly than glucose absorption through active transport. Fructose does not stimulate insulin secretion or enhance leptin production. Since both insulin and leptin play a role in regulation of food intake, consumption of fructose (eg, as high-fructose corn syrup) may contribute to increased energy intake and weight gain. Fructose is also easily converted to hepatic triglycerides, which may be undesirable in patients with insulin resistance/metabolic syndrome and cardiovascular disease risk.
Dietary fiber can be classified in two major types: nondigested carbohydrate (β1–4 linkages) and noncarbohydrate (lignin). Insoluble fibers (cellulose, hemicellulose, and lignin) increase stool bulk and water content and decrease gut transit time. Soluble fibers (pectins, mucilages, oat bran) bind bile acids and reduce lipid and cholesterol absorption. Pectins also slow gastric emptying and the rate of nutrient absorption. Few data regarding the fiber needs of children are available. The Dietary Reference Intakes recommend 14 g of fiber per 1000 kcal consumed. The American Academy of Pediatrics recommends that children older than 2 years consume in grams per day an amount of fiber equal to 5 plus the age in years. Fiber intakes are often low in North America. Children who have higher dietary fiber intakes have been found to consume more nutrient-dense diets than children with low-fiber intakes. In general, higher fiber diets are associated with lower risk of chronic diseases such as obesity, cardiovascular disease, and diabetes.
Ambrosini GL et al: Identification of a dietary pattern prospectively associated with increased adiposity during childhood and adolescence. Int J Obes (Lond). 2012 Oct;36(10):1299–1305. doi: 10.1038/ijo.2012.127 [Epub 2012 Aug 7] [PMID: 22868831].
Brannon PM et al: Lactose intolerance and health. NIH Consens State Sci Statements 2010 Feb 24;27(2):1–17 [PMID: 20186234]. http://consensus.nih.gov.
de Ruyter JC, Olthof MR, Seidell JC, Katan MB. A trial of sugar-free or sugar-sweetened beverages and body weight in children. N Engl J Med. 2012 Oct 11;367(15):1397–1406. doi: 10.1056/NEJMoa1203034 [Epub 2012 Sep 21] [PMID: 22998340].
Dietary sources, absorption, metabolism, and deficiency of the major minerals are summarized in Table 11–3. Recommended intakes are provided in Table 11–4.
Table 11–3. Summary of major minerals.
Table 11–4. Summary of Dietary Reference Intakes for selected minerals and trace elements.
Trace elements with a recognized role in human nutrition are iron, iodine, zinc, copper, selenium, manganese, molybdenum, chromium, cobalt (as a component of vitamin B12), and fluoride. Information on food sources, functions, and deficiencies of the trace elements is summarized in Table 11–5. Supplemental fluoride recommendations are listed in Table 11–6. Dietary Reference Intakes of trace elements are summarized in Table 11–4. Iron deficiency is discussed in Chapter 30.
Table 11–5. Summary of trace elements.
Table 11–6. Supplemental fluoride recommendations (mg/d).
Brown KH et al: Dietary intervention strategies to enhance zinc nutrition: promotion and support of breastfeeding for infants and young children. Food Nutr Bull 2009 Mar;30(Suppl 1): S144–S171 [PMID: 19472605].
Krebs NF et al: Effects of different complementary feeding regimens on iron status and enteric Microbiota in breastfed infants. J Pediatr 2013 Aug;163(2):416–23. Epub 2013 Feb 26 [PMID: 23452586].
Because they are insoluble in water, the fat-soluble vitamins require digestion and absorption of dietary fat and a carrier system for transport in the blood. Deficiencies in these vitamins develop more slowly than deficiencies in water-soluble vitamins because the body accumulates stores of fat-soluble vitamins; but prematurity and some childhood conditions can place infants and children at risk (Table 11–7). Excessive intakes carry a considerable potential for toxicity (Table 11–8). A summary of reference intakes for select vitamins is found in Table 11–9. Dietary sources of the fat-soluble vitamins, absorption/metabolism, and causes and clinical features of deficiency are summarized in Table 11–10, and vitamin deficiency and related diagnostic laboratory findings and treatment are detailed in Table 11–11.
Table 11–7. Circumstances associated with risk of vitamin deficiencies.
Table 11–8. Effects of vitamin toxicity.
Table 11–9. Summary of Dietary Reference Intakes for select vitamins.
Table 11–10. Summary of fat-soluble vitamins.
Table 11–11. Evaluation and treatment of deficiencies of fat-soluble vitamins.
Recent recognition of low levels of 25-OH-vitamin D in a relatively large percentage of the population and the broad range of functions beyond calcium absorption have led many experts including the American Academy of Pediatrics to recommend a daily intake of at least 400 IU (10 mcg)/d for all infants, including those who are breast-fed, beginning shortly after birth.
Cesur Y et al: Evaluation of children with nutritional rickets. J Pediatr Endocrinol Metab 2011;24(1-2):35−43 [PMID: 21528813].
IOM: Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: The National Academies Press; 2011.
Pludowski P et al: Vitamin D supplementation and status in infants: a prospective cohort observational study. J Pediatr Gastroenterol Nutr 2011 Jul;53(1):93−99 [PMID: 21694542].
Taylor CE, Camargo CA Jr: Impact of micronutrients on respiratory infections. Nutr Rev 2011 May;69(5):259−269 [PMID: 21521228].
Deficiencies of water-soluble vitamins are generally uncommon in the United States because of the abundant food supply and fortification of prepared foods. Cases of deficiencies (eg, scurvy) in children with special needs have been reported in the context of sharply restricted diets. Most bread and wheat products are fortified with B vitamins, including the mandatory addition of folic acid to enriched grain products since January 1998. There is conclusive evidence that folic acid supplements (400 mcg/d) during the periconceptional period protect against neural tube defects. Dietary intakes of folic acid from natural foods and enriched products also are protective. Biological roles of water-soluble vitamins are listed in Table 11–12.
Table 11–12. Summary of biologic roles of water-soluble vitamins.
The risk of toxicity from water-soluble vitamins is not as great as that associated with fat-soluble vitamins because excesses are excreted in the urine. However, deficiencies of these vitamins develop more quickly than deficiencies in fat-soluble vitamins because of limited stores, with the exception of Vitamin B12.
Major dietary sources of the water-soluble vitamins are listed in Table 11–13. Additional salient details are summarized in Tables 11–7, 11–14, and 11–15.
Table 11–13. Major dietary sources of water-soluble vitamins.
Table 11–14. Causes of deficiencies in water-soluble vitamins.
Table 11–15. Clinical features of deficiencies in water-soluble vitamins.
Carnitine is synthesized in the liver and kidneys from lysine and methionine. In certain circumstances (see Table 11–14), synthesis is inadequate, and carnitine can then be considered a vitamin. A dietary supply of other organic compounds, such as inositol, may also be required in certain circumstances.
Breast-feeding provides optimal nutrition for the normal infant during the early months of life. The World Health Organization recommends exclusive breast-feeding for approximately the first 6 months of life, with continued breast-feeding along with appropriate complementary foods through the first 2 years of life. Numerous immunologic factors in breast milk (including secretory immunoglobulin A [IgA], lysozyme, lactoferrin, bifidus factor, and macrophages) provide protection against GI and upper respiratory infections.
In developing countries, lack of refrigeration and contaminated water supplies make formula feeding hazardous. Although formulas have improved progressively and are made to resemble breast milk as closely as possible, it is impossible to replicate the nutritional or immune composition of human milk. Additional differences of physiologic importance continue to be identified. Furthermore, the relationship developed through breast-feeding can be an important part of early maternal interactions with the infant and provides a source of security and comfort to the infant.
Breast-feeding has been reestablished as the predominant initial mode of feeding young infants in the United States. Unfortunately, breast-feeding rates remain low among several subpopulations, including low-income, minority, and young mothers. Many mothers face obstacles in maintaining lactation once they return to work, and rates of breast-feeding at 6 months are considerably less than the goal of 50%. Skilled use of a breast pump, particularly an electric one, can help to maintain lactation in these circumstances.
Absolute contraindications to breast-feeding are rare. They include tuberculosis (in the mother) and galactosemia (in the infant). Breast-feeding is associated with maternal-to-child transmission of human immunodeficiency virus (HIV), but the risk is influenced by duration and pattern of breast-feeding and maternal factors, including immunologic status and presence of mastitis. Complete avoidance of breast-feeding by HIV-infected women is presently the only mechanism to ensure prevention of maternal–infant transmission. Current recommendations are that HIV-infected mothers in developed countries refrain from breast-feeding if safe alternatives are available. In developing countries, the benefits of breast-feeding, especially the protection of the child against diarrheal illness and malnutrition, outweigh the risk of HIV infection via breast milk. In such circumstances, mixed feeding should be avoided because of the increased risk of HIV transmission with mixed feeds.
In newborns less than 1750 g, human milk should be fortified to increase protein, calcium, phosphorus, and micronutrient content, as well as caloric density. Breast-fed infants with cystic fibrosis can be breast-fed successfully if exogenous pancreatic enzymes are provided. If normal growth rates are not achieved in breast-fed infants with cystic fibrosis, energy or specific macronutrient supplements may be necessary. All infants with cystic fibrosis should receive supplemental vitamins A, D, E, K, and sodium chloride.
Eidelman AI, Schanler RJ, Johnston M, Landers S: Breastfeeding and the Use of Human Milk. Pediatrics 2012 Mar;129(3):e827–e841 [PMID: 22371471].
Jansson LM: Academy of Breastfeeding Medicine Protocol Committee ABM clinical protocol #21: guidelines for breastfeeding and the drug-dependent woman. Breastfeed Med 2009 Dec;4(4):225–228 [PMID: 19835481].
Zachariassen G et al: Nutrient enrichment of mother’s milk and growth of very preterm infants after hospital discharge. Pediatrics 2011 Apr;127(4):e995–e1003. [Epub 2011 Mar 14] [PMID: 21402642].
Support of Breast-Feeding
In developed countries, health professionals are now playing roles of greater importance in supporting and promoting breast-feeding. Organizations such as the American Academy of Pediatrics and La Leche League have initiated programs to promote breast-feeding and provide education for health professionals and mothers.
Perinatal hospital routines and early pediatric care have a great influence on the successful initiation of breast-feeding by promoting prenatal and postpartum education, frequent mother-baby contact after delivery, one-on-one advice about breast-feeding technique, demand feeding, rooming-in, avoidance of bottle supplements, early follow-up after delivery, maternal confidence, family support, adequate maternity leave, and advice about common problems such as sore nipples. A 2011 CDC Morbidity and Mortality Report found that most US hospitals do not have policies that optimally support breast-feeding. Medical providers can modify their own practice patterns and advocate for hospital policies that support breast-feeding.
Very few women are unable to nurse their babies. The newborn is generally fed ad libitum every 2–3 hours, with longer intervals (4–5 hours) at night. Thus, a newborn infant nurses at least 8–10 times a day, so that a generous milk supply is stimulated. This frequency is not an indication of inadequate lactation. In neonates, a loose stool is often passed with each feeding; later (at age 3–4 months), there may be an interval of several days between stools. Failure to pass several stools a day in the early weeks of breast-feeding suggests inadequate milk intake and supply.
Expressing milk may be indicated if the mother returns to work or if the infant is premature, cannot suck adequately, or is hospitalized. Electric breast pumps are very effective and can be borrowed or rented.
Technique of Breast-Feeding
Breast-feeding can be started after delivery as soon as both mother and baby are stable. Correct positioning and breast-feeding technique are necessary to ensure effective nipple stimulation and optimal breast emptying with minimal nipple discomfort.
If the mother wishes to nurse while sitting, the infant should be elevated to the height of the breast and turned completely to face the mother, so that their abdomens touch. The mother’s arms supporting the infant should be held tightly at her side, bringing the baby’s head in line with her breast. The breast should be supported by the lower fingers of her free hand, with the nipple compressed between the thumb and index fingers to make it more protractile. The infant’s initial licking and mouthing of the nipple helps make it more erect. When the infant opens its mouth, the mother should rapidly insert as much nipple and areola as possible.
The most common early cause of poor weight gain in breast-fed infants is poorly managed mammary engorgement, which rapidly decreases milk supply. Unrelieved engorgement can result from inappropriately long intervals between feeding, improper infant suckling, a nondemanding infant, sore nipples, maternal or infant illness, nursing from only one breast, and latching difficulties. Poor maternal feeding technique, inappropriate feeding routines, and inadequate amounts of fluid and rest all can be factors. Some infants are too sleepy to do well on an ad libitum regimen and may need waking to feed at night. Primary lactation failure occurs in less than 5% of women.
A sensible guideline for duration of feeding is 5 minutes per breast at each feeding the first day, 10 minutes on each side at each feeding the second day, and 10–15 minutes per side thereafter. A vigorous infant can obtain most of the available milk in 5–7 minutes, but additional sucking time ensures breast emptying, promotes milk production, and satisfies the infant’s sucking urge. The side on which feeding is commenced should be alternated. The mother may break suction gently after nursing by inserting her finger between the baby’s gums.
Individualized assessment before discharge should identify mothers and infants needing additional support. All mother-infant pairs require early follow-up. The onset of copious milk secretion between the second and fourth postpartum days is a critical time in the establishment of lactation. Failure to empty the breasts during this time can cause engorgement, which quickly leads to diminished milk production.
Nipple tenderness requires attention to proper positioning of the infant and correct latch-on. Ancillary measures include nursing for shorter periods, beginning feedings on the less sore side, air drying the nipples well after nursing, and use of lanolin cream. Severe nipple pain and cracking usually indicate improper infant attachment. Temporary pumping may be needed.
Breast-feeding jaundice is exaggerated physiologic jaundice associated with inadequate intake of breast milk, infrequent stooling, and unsatisfactory weight gain. (See Chapter 2.) If possible, the jaundice should be managed by increasing the frequency of nursing and, if necessary, augmenting the infant’s sucking with regular breast pumping. Supplemental feedings may be necessary, but care should be taken not to decrease breast milk production further.
In a small percentage of breast-fed infants, breast milk jaundice is caused by an unidentified property of the milk that inhibits conjugation of bilirubin. In severe cases, interruption of breast-feeding for 24–36 hours may be necessary. The mother’s breast should be emptied with an electric breast pump during this period.
The symptoms of mastitis include flulike symptoms with breast tenderness, firmness, and erythema. Antibiotic therapy covering β-lactamase–producing organisms should be given for 10 days. Analgesics may be necessary, but breast-feeding should be continued. Breast pumping may be helpful adjunctive therapy.
Centers for Disease Control and Prevention (CDC): HIV-2 Infection Surveillance—United States, 1987–2009. MMWR Morb Mortal Wkly Rep 2011 Aug 5;30(60):1009–1044 [PMID: 21796096].
Centers for Disease Control and Prevention (CDC). Vital signs: hospital practices to support breastfeeding—United States, 2007 and 2009. MMWR Morb Mortal Wkly Rep. 2011 Aug 5;60(30):1020–5 [PMID: 21814166].
U.S. Department of Health and Human Services. The Surgeon General’s Call to Action to Support Breastfeeding. Washington, DC: U.S. Department of Health and Human Services, Office of the Surgeon General; 2011.
Maternal Drug Use
Factors playing a role in the transmission of drugs in breast milk include the route of administration, dosage, molecular weight, pH, and protein binding. Generally, any drug prescribed to a newborn can be consumed by the breast-feeding mother without ill effect. Very few drugs are absolutely contraindicated in breast-feeding mothers; these include radioactive compounds, antimetabolites, lithium, diazepam, chloramphenicol, antithyroid drugs, and tetracycline. For up-to-date information, a regional drug center should be consulted.
Maternal use of illicit or recreational drugs is a contraindication to breast-feeding. Expression of milk for a feeding or two after use of a drug is not an acceptable compromise. The breast-fed infants of mothers taking methadone (but not alcohol or other drugs) as part of a treatment program have generally not experienced ill effects when the daily maternal methadone dose is less than 40 mg.
United States National Library of Medicine Drugs and Lactation Database (Lactmed): http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?LACT.
The nutrient composition of human milk is summarized and compared to that of cow’s milk and formulas in Table 11–16. Outstanding characteristics include (1) relatively low but highly bioavailable protein content, which is adequate for the normal infant; (2) generous but not excessive quantity of essential fatty acids; (3) long-chain polyunsaturated fatty acids, of which DHA is thought to be especially important; (4) relatively low sodium and solute load; and (5) lower concentration of highly bioavailable minerals, which are adequate for the needs of normal breast-fed infants for approximately 6 months.
The American Academy of Pediatrics and the World Health Organization recommend the introduction of solid foods in normal infants at about 6 months of age. Gradual introduction of a variety of foods including fortified cereals, fruits, vegetables, and meats should complement the breast milk diet. Meats provide an important dietary source of iron and zinc, both of which are low in human milk by 6 months, and pureed meats may be introduced as an early complementary food. Single-ingredient complementary foods are introduced one at a time at 3–4 day intervals before a new food is given. Fruit juice is not an essential part of an infant diet. Juice should not be introduced until after 6 months; should only be offered in a cup; and the amount should be limited to 4 oz/d. Delaying the introduction of complementary foods beyond 6 months has not been shown to prevent atopic disease. Breast-feeding should ideally continue for at least 12 months, and thereafter for as long as mutually desired. Whole cow’s milk can be introduced after the first year of life.
Breast-fed infants or toddlers on a vegetarian diet are at particular risk for inadequate intake of iron and zinc because of relatively high requirements during these periods of rapid growth and because animal-based foods are best sources of these minerals.
While breast milk, dairy, soy, legume, and other vegetable sources of protein can provide adequate protein for growth, vegetarian foods are impractical as sources of iron or zinc. To meet requirements, infants and toddlers consuming vegetarian diets should be offered fortified foods including cereals and formula or daily supplementation of iron and zinc. A vegan diet that omits all animal protein sources will require supplementation of vitamin B12 in addition to iron and zinc. Guidance from a pediatric registered dietitian is suggested for families seeking for their infant or toddler to follow a vegetarian or vegan diet to ensure adequate protein, calorie, vitamin, and micronutrient intakes.
Fleischer DM, Spergel JM, Assa’ad AH, Pongracic JA: Primary prevention of allergic disease through nutritional interventions. J Allergy Clin Immunol: In Practice 2013;1:29–36 [PMID: 24229819].
Table 11–16. Composition of human and cow’s milk and typical infant formula (per 100 kcal).
Jonsdottir OH et al: Timing of the introduction of complementary foods in infancy: a randomized controlled trial. Pediatrics 2012;130(6):1038–1045 [PMID: 23147979].
Krebs NF et al: Comparison of complementary feeding strategies to meet zinc requirements of older breastfed infants. Am J Clin Nutr 2012;96:30–35 [PMID: 22648720].
SPECIAL DIETARY PRODUCTS FOR INFANTS
Soy Protein Formulas
Historically, a common rationale for the use of soy protein formulas was the transient lactose intolerance after acute gastroenteritis. Lactose-free cow’s milk protein-based formulas are also now available. The medical indications for soy formulas are rare: galactosemia and hereditary lactase deficiency. Soy formulas provide an option when a vegetarian diet is preferred. Soy protein formulas are often used in cases of suspected intolerance to cow’s milk protein, though cow’s milk hydrolysate formulas are preferred because 30%–40% of infants intolerant to cow’s milk protein will also react to soy protein. In contrast to this T-cell mediated protein intolerance, those infants will less commonly documented IgE-mediated allergy to cow’s milk protein do not typically cross-react to soy formula. The estrogenic properties of isoflavones from soy formula has raised concern about potential reproductive system effects, but an Expert Committee of the National Toxicology program found minimal concern for potential harm based on an extensive review of available evidence in their 2011 report.
Semi-Elemental & Elemental Formulas
Semi-elemental formulas include protein hydrolysate formulas. The major nitrogen source of most of these products is casein hydrolysate, supplemented with selected amino acids, but partial hydrolysates of whey are also available. These formulas contain an abundance of EFA from vegetable oil; certain brands also provide substantial amounts of MCTs. Elemental formulas are available with free amino acids and varying levels and types of fat components.
Semi-elemental and elemental formulas are invaluable for infants with a wide variety of malabsorption syndromes. They are also effective in infants who cannot tolerate cow’s milk and soy protein. Controlled trials suggest that for infants with a family history of atopic disease, partial hydrolysate formulas may delay or prevent atopic disease. For specific product information, consult standard pediatric reference texts, formula manufacturers, or a pediatric dietitian.
McCarver G et al: NTP-CERHR expert panel report on the developmental toxicity of soy infant formula. Birth Defects Res B Dev Reprod Toxicol 2011 Oct;92(5):421–468 [PMID: 21948615].
Occasionally it may be necessary to increase the caloric density of an infant feeding to provide more calories or restrict fluid intake. Concentrating formula to 24–26 kcal/oz is usually well tolerated, delivers an acceptable renal solute load, and increases the density of all the nutrients. Beyond this, individual macronutrient additives (Table 11–17) are usually employed to achieve the desired caloric density (up to 30 kcal/oz) based on the infant’s needs and underlying condition(s). A pediatric nutrition specialist can provide guidance in formulating calorically dense infant formula feedings. The caloric density of breast milk can be increased by adding infant formula powder or any of the additives used with infant formula. Because of their specialized nutrient composition, human milk fortifiers are generally used only for premature infants.
Table 11–17. Common infant formula additives.
Special formulas are those in which one component, often an amino acid, is reduced in concentration or removed for the dietary management of a specific inborn metabolic disease. Also included under this heading are formulas designed for the management of specific disease states, such as hepatic failure, pulmonary failure with chronic carbon dioxide retention, and renal failure. These condition-specific formulas were formulated primarily for critically ill adults and are even used sparingly in those populations; thus, their use in pediatrics should only be undertaken with clear indication and caution.
Complete information regarding the composition of these special formulas, the standard infant formulas, specific metabolic disease formulas, and premature infant formulas can be found in standard reference texts and in the manufacturers’ literature.
Koletzko S et al: Diagnostic approach and management of cow’s-milk protein allergy in infants and children: ESPGHAN GI Committee practical guidelines. European Society of Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr 2012 Aug;55(2):221–229. doi: 10.1097/MPG.0b013e31825c9482 [PMID: 22569527].
NUTRITION FOR CHILDREN 2 YEARS & OLDER
Because of the association of diet with the development of such chronic diseases as diabetes, obesity, and cardiovascular disease, learning healthy eating behaviors at a young age is an important preventative measure.
Salient features of the diet for children older than 2 years include the following:
1. Consumption of three regular meals per day, and one or two healthful snacks according to appetite, activity, and growth needs.
2. Inclusion of a variety of foods. Diet should be nutritionally complete and promote optimal growth and activity.
3. Fat less than 35% of total calories (severe fat restriction <10% may result in an energy deficit and growth failure). Saturated fats should provide less than 10% of total calories. Monounsaturated fats should provide 10% or more of caloric intake. Trans-fatty acids, found in stick margarine and shortening, and in many processed foods, should provide less than 1% of total calories.
4. Cholesterol intake less than 100 mg/1000 kcal/d, to a maximum of 300 mg/d.
5. Carbohydrates should provide 45%–65% of daily caloric intake, with no more than 10% in the form of simple sugars. A high-fiber, whole-grain-based diet is recommended.
6. Limitation of grazing behavior, eating while watching television, and the consumption of soft drinks and other sweetened beverages.
7. Limitation of sodium intake by limiting processed foods and added salt.
8. Consumption of lean cuts of meats, poultry, and fish should be encouraged. Skim or low-fat milk, and vegetable oils (especially canola or olive oil) should be used. Whole-grain bread and cereals and plentiful amounts of fruits and vegetables are recommended. The consumption of processed foods, juice drinks, soft drinks, desserts, and candy should be limited. The American Academy of Pediatrics has endorsed use of low-fat milk in children after 12 months of age.
Lifestyle counseling for children should also include maintenance of a BMI in the healthy range; regular physical activity, limiting sedentary behaviors; avoidance of smoking; and screening for hypertension. The optimal target populations for cholesterol screening in childhood has been a topic of scientific debate. Current recommendations from the National Heart Lung and Blood Institute are to routinely screen all children once at age 9–11, and to consider screening children at younger ages who have additional risk factors (obesity, diabetes, family history of premature cardiovascular disease). The preferred time for screening occurs before puberty, a period in which hormonal changes render lipids unreliable in predicting persistent levels in adulthood.
Daniels SR et al: Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary Report. Pediatrics 2011 Dec 1;128(Suppl 5):S213–S256 [PMID: 22084329].
Liang L, Meyerhoefer C, Wang J: Obesity counseling by pediatric health professionals: an assessment using nationally representative data. Pediatrics 2012 Jul;130(1):67–77. doi: 10.1542/peds. 2011-0596 [Epub 2012 Jun 4] [PMID: 22665411].
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Poor weight gain or weight loss.
Loss of subcutaneous fat, temporal wasting.
Most commonly related to inadequate caloric intake.
Often associated in toddlers with marginal or low iron and zinc status.
Pediatric undernutrition is usually multifactorial in origin, and successful treatment depends on accurate identification and management of those factors. The terms “organic” and “nonorganic” failure to thrive, though still used by many medical professionals, are not helpful because any systemic illness or chronic condition can cause growth impairment and yet may also be compounded by psychosocial problems.
Failure to thrive is a term used to describe growth faltering in infants and young children whose weight curve has fallen by two major percentile channels from a previously established rate of growth, or whose weight for length decreases below the 5th percentile. (See Chapter 9.) The World Health Organization growth charts (http://www.who.int/childgrowth/en/) should be used to evaluate the growth of breast-fed infants, as these charts reflect the slower velocity of weight gain for healthy breast-fed infants without formula supplementation. Differences in weight gain are particularly notable after 6 months of age, and a lower weight for age on the Centers for Disease Control growth references should not necessarily be interpreted to reflect undernutrition. The acute loss of weight, or failure to gain weight at the expected rate, produces a condition of reduced weight for height known as wasting. The reduction in height for age, as is seen with more chronic malnutrition, is termed stunting.
The typical pattern for mild pediatric undernutrition is decreased weight, with normal height and head circumference. In more chronic malnutrition, linear growth will slow relative to the standard for age, although this should also prompt consideration of nonnutritional etiologies. Significant calorie deprivation produces severe wasting, called marasmus. Significant protein deprivation in the face of adequate energy intake, possibly with additional insults such as infection, may produce edematous malnutrition called kwashiorkor.
B. Risk Factors
A discussion of the multiple medical conditions that can cause pediatric undernutrition is beyond the scope of this chapter. However, the most common cause is inadequate dietary intake. In young but otherwise healthy breast- or bottle-fed infants, a weak or uncoordinated suck may be the causative factor; evaluation for congenital heart disease, breathing problems (eg, laryngomalacia), and other physical problems that may interfere with normal feeding. Inappropriate formula mixing or a family’s dietary beliefs may lead to hypocaloric or unbalanced dietary intakes. Diets restricted because of suspected food allergies or intolerances may result in inadequate intake of calories, protein, or specific micronutrients. Iron and zinc are micronutrients that are marginal in many older infants and young children with undernutrition. Deficiencies occur in older breast-fed infants whose diets are low in meats, and in toddlers who are not on any fortified formula and also do not consume good dietary sources. Cases of severe malnutrition and kwashiorkor have occurred in infants of well-intentioned parents who substitute “health food” milk alternatives (eg, rice milk or unfortified soy milk) for infant formula.
1. Measurement of weight for age; length/height for age; occipital frontal circumference (OFC) for age (for < 2 years age), weight for length; and calculation of percent ideal body weight (current weight/median [50th percentile] weight for current length). Assess for downward crossing of growth percentiles (acute malnutrition) and for linear growth stunting (chronic malnutrition).
2. History should include details of diet intake and feeding patterns (including restrictive intake, grazing feeding pattern, inappropriate foods for age and development, excessive juice, sugar-sweetened beverages, or water intake); past medical history, including birth and developmental history; family history; social history; and review of systems.
3. Physical examination should include careful examination of skin (for rashes), mouth, eyes, nails, and hair for signs of micronutrient and protein deficiencies, as well as for abnormal neurologic function (eg, loss of deep tendon reflexes, abnormal strength and tone).
4. Laboratory studies are generally of low yield for diagnosis for growth faltering in the absence of other findings, and should be reserved for moderately severe cases of malnutrition. In such cases, risk of and suspicion for nutrient deficiencies and systemic pathology should guide studies ordered. Typical screening laboratories include chemistry panel; complete blood count; and iron panel, including ferritin. Thyroid function testing is indicated with linear growth faltering. Serology for celiac disease may also be warranted for toddlers. Guidelines for screening for inborn errors of metabolism have recently been published.
5. Some infants are naturally small and have weight for age percentile values below the 5th percentile and may have length and head circumferences at higher percentiles. Such infants are often called “constitutionally small,” as their thinness was present from birth, there was no evidence of intrauterine growth restriction, their mothers had small stature and usually thinness, and the family growth pattern is similar. Mothers of such normally small children should not be discouraged from breast-feeding and should not be counseled to prematurely add food supplements. Workup for failure to thrive is not indicated in these infants and evaluations or referrals for growth failure or child abuse from underfeeding are not warranted.
When providing nutritional rehabilitation to infants/children with severe malnutrition, refeeding syndrome may occur. Monitoring for hypophosphatemia, hypokalemia, hypomagnesemia, and hyperglycemia is prudent, and calorie intake should be slowly increased to avoid metabolic instability.
Poor eating is often a learned behavior. Families should be counseled regarding choices of foods that are appropriate for the age and developmental level of the child. Increasing the caloric density of foods is associated with increased daily caloric intake and improved weight gain, but such weight gain usually is due to fat gain unless the calorie supplements include significant protein. Micronutrient deficiencies should be corrected. For repletion of iron, 2–4 mg/kg/d, divided BID, can be initiated. For zinc, 1 mg/kg/d for 1–2 months, administered several hours apart from iron supplement is typically adequate. Children should have structured meal times (eg, three meals and two to three snacks during the day), ideally at the same time other family members eat. Consultation with a pediatric dietitian can be helpful for educating the families. Poor feeding may be related to family dysfunction. Children whose households are chaotic and children who are abused, neglected, or exposed to poorly controlled mental illness may be described as poor eaters, and may fail to gain. Careful assessment of the social environment of such children is critical, and disposition options may include support services, close medical follow-up visits, family counseling, and even foster placement while a parent receives therapy.
Ficicioglu C, Haack K: Failure to thrive: when to suspect inborn errors of metabolism. Pediatrics 2009;124:972–979 [PMID:19706585].
Jaffe AC: Failure to thrive: current clinical concepts. Pediatr Rev 2011 Mar;32(3):100–107; quiz 108 [PMID: 21364013].
PEDIATRIC OVERWEIGHT & OBESITY (SEE ALSO Chapter 3 FOR OBESITY IN ADOLESCENTS)
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Excessive rate of weight gain; upward change in BMI percentiles.
BMI for age between the 85th and 95th percentiles indicates overweight.
BMI for age > 95th percentile indicates obesity and is associated with increased risk of secondary complications.
BMI for age > 99th percentile indicates severe obesity and a higher risk of complications.
The prevalence of childhood and adolescent obesity has increased rapidly in the United States and many other parts of the world. Currently in the United States, approximately 17% of 6- to 19-year-olds are obese, with even higher rates among subpopulations of minority and economically disadvantaged children. The increasing prevalence of childhood obesity is related to a complex combination of socioeconomic, genetic, and biologic factors.
Childhood obesity is associated with significant comorbidities, which, if untreated, are likely to persist into adulthood. The probability of obesity persisting into adulthood has been estimated to increase from 20% at 4 years to 80% by adolescence. Rates of persistence from early childhood are much higher when one or both parents are obese. Obesity is associated with cardiovascular and endocrine abnormalities (eg, dyslipidemia, insulin resistance, and type 2 diabetes), orthopedic problems, pulmonary complications (eg, obstructive sleep apnea), and mental health problems (Table 11–18).
Table 11–18. Selected complications of childhood obesity.
Huang TT et al: Pediatricians’ and family physicians’ weight-related care of children in the U.S. Am J Prev Med 2011 Jul;41(1):24–32 [PMID: 21665060].
Nadeau KJ, Maahs DM, Daniels SR, Eckel RH: Childhood obesity and cardiovascular disease: links and prevention strategies. Nat Rev Cardiol 2011 Jun 14;8(9):513–525 [PMID: 21670745].
Ross MM et al: Multidisciplinary treatment of pediatric obesity: nutrition evaluation and management. Nutr Clin Pract 2010 Aug;25(4):327–334 [PMID: 20702836].
BMI is the standard measure of obesity in adults and children. BMI is correlated with more accurate measures of body fatness and is calculated with readily available information: weight and height (kg/m2). Routine plotting of the BMI on age- and gender-appropriate charts (http://www.cdc.gov/growthcharts) can identify those with excess weight. Definitions were outlined in 2007 by an expert committee representing numerous professional organizations. BMI between the 85th and 95th percentiles for age and sex identifies those who are overweight. Obese is defined as BMI at or above 95% and is associated with increased risk of secondary complications. Severe obesity is characterized by BMI for age and sex at or above the 99th percentile and is associated with greatly increased risk of comorbidity. An upward change in BMI percentiles in any range should prompt evaluation and possible treatment. An annual increase of more than 2 kg/m2 is almost always an indicator of a rapid increase in body fat. For children younger than 2 years, weight for length greater than 95th percentile indicates overweight and warrants further assessment, especially of energy intake and feeding behaviors.
B. Risk Factors
There are multiple risk factors for developing obesity, reflecting the complex relationships between genetic and environmental factors. Family history is a strong risk factor. If one parent is obese, the odds ratio is approximately 3 for obesity in adulthood, but if both parents are obese, the odds ratio increases to greater than 10 compared to children with two nonobese parents.
Risk factors in the home environment offer targets for intervention. Consumption of sugar-sweetened beverages, lack of family meals, large portion sizes, foods prepared outside the home, television viewing, video gaming, poor sleep, and lack of activity are all associated with risk of excessive weight gain.
Early recognition of rapid weight gain or high-risk behaviors is essential. Anticipatory guidance or intervention earlier in childhood and before weight gain becomes severe is more likely to be successful than delayed intervention. Routine evaluation at well-child visits should include:
1. Measurement of weight and height, calculation of BMI, and plotting all three parameters on age- and sex-appropriate growth charts (http://www.cdc.gov/growthcharts). Evaluate for upward crossing of BMI percentile channels.
2. History regarding diet and activity patterns (Table 11–19); family history, and review of systems. Physical examination should include careful blood pressure measurement, distribution of adiposity (central vs generalized); markers of comorbidities, such as acanthosis nigricans, hirsutism, hepatomegaly, orthopedic abnormalities; and physical stigmata of genetic syndromes (eg, Prader-Willi syndrome).
2. Laboratory studies are recommended as follows for children beginning by age 10 years or at onset of puberty. Consider testing at younger ages with severe obesity but not younger than 2 years:
Overweight with personal or family history of heart disease risk factors—fasting lipid profile, fasting glucose, alanine aminotransferase (ALT).
Obese—fasting lipid profile, fasting glucose, ALT.
Table 11–19. Suggested areas for assessment of diet and activity patterns.
Other studies should be guided by findings in the history and physical.
Barton M: Screening for obesity in children and adolescents: US Preventive Services Task Force recommendation statement. Pediatrics 2010 Feb;125(2):361–367 [PMID: 20083515].
Treatment should be based on risk factors, including age, severity of obesity, and comorbidities, as well as family history. For children with uncomplicated obesity, the primary goal is to achieve healthy eating and activity patterns, not necessarily to achieve ideal body weight. For children with a secondary complication, improvement of the complication is an important goal. In general, weight goals for obese children range from weight maintenance up to 1 lb/mo weight loss for those younger than 12 years to 2 lb/wk for those older than 12 years. More rapid weight loss should be monitored for pathologic causes that may be associated with nutrient deficiencies and linear growth stunting (Table 11–20).
Treatment focused on behavior changes in the context of family involvement has been associated with sustained weight loss and decreases in BMI. Clinicians should assess the family’s readiness to take action. Motivational interviewing techniques can be helpful with resistant or ambivalent families to promote readiness. These techniques include open-ended questioning, exploring and resolving the family’s ambivalence toward changes, and accepting the family’s resistance nonjudgmentally. Providers should engage the family in collaborative decision making about which behavior change goals will be targeted. Improving dietary habits and activity levels concurrently is desirable for successful weight management. The entire family should adopt healthy eating patterns, with parents modeling healthy food choices, controlling foods brought into the home, and guiding appropriate portion sizes. The American Academy of Pediatrics recommends no television for children younger than 2 years old, a maximum of 2 h/d of television and video games for older children, with lower levels recommended for children during attempts at BMI reduction.
Table 11–20. Weight management goals.
A “staged approach” for treatment has been proposed, with the initial level depending on the severity of overweight, the age of the child, the readiness of the family to implement changes, the preferences of the parents and child, and the skills of the health care provider.
1. Prevention plus: Counseling regarding problem areas identified by screening questions (see Table 11–19); emphasis on lifestyle changes, including healthy eating and physical activity patterns.
2. Structured weight management: Provides more specific and structured dietary pattern, such as meal planning, exercise prescription, and behavior change goals. This may be done in the primary care setting. Generally referral to at least one ancillary health professional will be required: dietitian, behavior specialist, and/or physical therapist. Monitoring is monthly or tailored to patient and family’s needs.
3. Comprehensive multidisciplinary: This level further increases the structure of therapeutic interventions and support, employs a multidisciplinary team, and may involve weekly group meetings.
4. Tertiary care intervention: This level is for patients who have not been successful at the other intervention levels or who are severely obese. Interventions are prescribed by a multidisciplinary team, and may include intensive behavior therapy, specialized diets, medications, and surgery.
Pharmacotherapy can be an adjunct to dietary, activity, and behavioral treatment, but by itself it is unlikely to result in significant or sustained weight loss. Only one medication is approved for obesity treatment in adolescents: orlistat, a lipase inhibitor, is approved for patients older than 12 years. For severely obese adolescents, particularly with comorbidities, bariatric surgery is performed in some centers. In carefully selected and closely monitored patients, surgery can result in significant weight loss with a reduction in comorbidities.
Barlow SE: Expert Committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: summary report. Pediatrics 2007;120(Suppl 4):S164 [PMID: 18055651].
Haemer M, Ranade D, Baron A, Krebs NF: A clinical model of obesity treatment is more effective in preschoolers and Spanish speaking families. Obesity 2013 May;21(5):1004–12 [PMID: 23784904].
Pratt JS et al: Best practice updates for pediatric/adolescent weight loss surgery. Obesity (Silver Spring) 2009 May;17(5):901–910 [PMID: 19396070].
Enteral nutrition support is indicated when a patient cannot adequately meet nutritional needs by oral intake alone and has a functioning GI tract. This method of support can be used for short- and long-term delivery of nutrition. Even when the gut cannot absorb 100% of nutritional needs, some enteral feedings should be attempted. Enteral nutrition, full or partial, has many benefits:
1. Maintaining gut mucosal integrity
2. Preserving gut-associated lymphoid tissue
3. Stimulation of gut hormones and bile flow
Nasogastric feeding tubes can be used for supplemental enteral feedings, but generally are not used for more than 6 months because of the complications of otitis media and sinusitis. Initiation of nasogastric feeding usually requires a brief hospital stay to ensure tolerance to feedings and to allow for parental instruction in tube placement and feeding administration.
If long-term feeding support is anticipated, a more permanent feeding device, such as a gastrostomy tube, may be considered. Referral to a home care company is necessary for equipment and other services such as nursing visits and dietitian follow-up.
Table 11–21. Guidelines for the initiation and advancement of tube feedings.
Table 11–21 suggests appropriate timing for initiation and advancement of drip and bolus feedings, according to a child’s age. Clinical status and tolerance to feedings should ultimately guide their advancement.
Monitoring the adequacy of enteral feeding depends on nutritional goals. Growth should be frequently assessed, especially for young infants and malnourished children. Hydration status should be monitored carefully at the initiation of enteral feeding. Either constipation or diarrhea can be problems, and attention to stool frequency, volume, and consistency can help guide management. When diarrhea occurs, factors such as infection, hypertonic enteral medications, antibiotic use, and alteration in normal gut flora should be addressed.
In medically stable patients, the enteral feeding schedule should be developmentally appropriate (eg, 5–6 small feedings/d for a toddler). When night drip feedings are used in conjunction with daytime feeds, it is suggested that less than 50% of goal calories be delivered at night so as to maintain a daytime sense of hunger and satiety. This will be especially important once a transition to oral intake begins. Children who are satiated by tube feedings will be less likely to take significant amounts of food by mouth, thus possibly delaying the transition from tube to oral nutrition.
ASPEN Board of Directors: Clinical guidelines for the use of enteral nutrition in adult and pediatric patients, 2009. JPEN 2009 May–Jun;33(3):255–259 [PMID: 19398611].
2. PARENTERAL NUTRITION
A. Peripheral Parenteral Nutrition
Peripheral parenteral nutrition is indicated when complete enteral feeding is temporarily impossible or undesirable. Short-term partial intravenous (IV) nutrition via a peripheral vein is a preferred alternative to administration of dextrose and electrolyte solutions alone. Because of the osmolality of the solutions required, it is usually impossible to achieve total calorie and protein needs with parenteral nutrition via a peripheral vein.
B. Total Parenteral Nutrition
Total parenteral nutrition (TPN) should be provided only when clearly indicated. Apart from the expense, numerous risks are associated with this method of feeding (see the section Complications). Even when TPN is indicated, every effort should be made to provide at least a minimum of nutrients enterally to help preserve the integrity of the GI mucosa and of GI function.
The primary indication for TPN is the loss of function of the GI tract that prohibits the provision of required nutrients by the enteral route. Important examples include short bowel syndrome, some congenital defects of the GI tract, and prematurity.
In recent years, an increasing number of injectable essential nutrients have been in short supply in the US pharmaceutical market. Shortages have included intravenous lipids, multi-vitamins mixtures, and trace minerals. Deficiencies of these micronutrients have led to significant medical morbidity. Nutrition support teams or quality improvement committees are encouraged to develop clinical guidelines to ensure provision of available injectable micronutrients to those patients who have the greatest need, eg, preterm infants and children with long-term exclusive dependence upon parenteral nutrition. Policies to promote use of enteral micronutrient preparations can also help to reduce the reliance on parenteral supplies.
Norton SA: Notes from the field: zinc deficiency dermatitis in cholestatic extremely premature infants after a nationwide shortage of injectable zinc, Washington, DC, December 2012. MMWR 2013 Feb 22;62(7):136–137 [PMID: 23425963].
Catheter Selection & Position
An indwelling central venous catheter is preferred for long-term IV nutrition. For periods of up to 3–4 weeks, a percutaneous central venous catheter threaded into the superior vena cava from a peripheral vein can be used. For the infusion of dextrose concentrations higher than 12.5%, the tip of the catheter should be located in the superior vena cava. Catheter positioning in the right atrium has been associated with complications, including arrhythmias and right atrial thrombus. After placement, a chest radiograph must be obtained to check catheter position. If the catheter is to be used for nutrition and medications, a double-lumen catheter is preferred.
A. Mechanical Complications
1. Related to catheter insertion or to erosion of catheter through a major blood vessel—Complications include trauma to adjacent tissues and organs, damage to the brachial plexus, hydrothorax, pneumothorax, hemothorax, and cerebrospinal fluid penetration. The catheter may slip during dressing or tubing changes, or the patient may manipulate the line.
2. Clotting of the catheter—Addition of heparin (1000 U/L) to the solution is an effective means of preventing this complication. If an occluded catheter does not respond to heparin flushing, filling the catheter with recombinant tissue plasminogen activator may be effective.
3. Related to composition of infusate—Calcium phosphate precipitation may occur if excess amounts of calcium or phosphorus are administered. Factors that increase the risk of calcium phosphate precipitation include increased pH and decreased concentrations of amino acids. Precipitation of medications incompatible with TPN or lipids can also cause clotting.
Doellman D: Prevention, assessment, and treatment of central venous catheter occlusions in neonatal and young pediatric patients. J Infus Nurs 2011 Jul-Aug;34(4):251–258 [PMID: 21734521].
B. Septic Complications
Septic complications are the most common cause of non-elective catheter removal, but strict use of aseptic technique and limiting entry into the catheter can reduce the rates of line sepsis. Fever over 38–38.5°C in a patient with a central catheter should be considered a line infection until proved otherwise. Cultures should be obtained and IV antibiotics empirically initiated. Removing the catheter may be necessary with certain infections (eg, fungal), and catheter replacement may be deferred until infection is treated.
C. Metabolic Complications
Many of the metabolic complications of IV nutrition are related to deficiencies or excesses of nutrients in administered fluids. These complications are less common as a result of experience and improvements in nutrient solutions. However, specific deficiencies still occur, especially in the premature infant. Avoidance of deficiencies and excesses and of metabolic disorders requires attention to the nutrient balance, electrolyte composition, and delivery rate of the infusate and careful monitoring, especially when the composition or delivery rate is changed.
Currently the most challenging metabolic complication is cholestasis, particularly common in premature infants of very low birth weight. The causes of cholestasis associated with TPN may be multifactorial: related to lack of enteral intake, toxicity of TPN constituents or contaminants, and interaction with underlying disease processes requiring IV nutrition. Patient and medical risk factors include prematurity, sepsis, hypoxia, major surgery (especially GI surgery), absence of enteral feedings, and small bowel bacterial overgrowth. Risk factors related to IV nutrition include amino acid excess or imbalance, use of IV omega-6-fatty-acid-rich soybean oil-based lipid emulsions, and prolonged duration of PN administration. Amino acid solutions with added cysteine decrease cholestasis. Practices that may minimize cholestasis include initiating even minimal enteral feedings as soon as feasible, avoiding sepsis by meticulous line care, avoiding overfeeding, using cysteine- and taurine-containing amino acid formulations designed for infants, preventing or treating small bowel bacterial overgrowth, protecting TPN solutions from light, and avoiding hepatotoxic medications. Substitution of omega-3 fatty acids for omega-6 lipid emulsions can prevent or reverse TPN associated cholestasis in children. Data also support the beneficial effect of restricting use of soy oil-based lipid emulsions to the minimum that is required to prevent essential fatty acid deficiency.
Kurvinen A et al: Effects of long-term parenteral nutrition on serum lipids, plant sterols, cholesterol metabolism, and liver histology in pediatric intestinal failure. J Pediatr Gastroenterol Nutr 2011 Oct;53(4):440–6 [PMID: 21543999].
Nehra D et al: The prevention and treatment of intestinal failure-associated liver disease in neonates and children. Surg Clin North Am 2011 Jun;91(3):543–563 [PMID: 21621695].
Tillman EM: Review and clinical update on parenteral nutrition–associated liver disease. Nutr Clin Pract 2013 Feb;28(1):30–39 [ PMID: 23087263].
Wheeler DS et al: A hospital-wide quality-improvement collaborative to reduce catheter-associated bloodstream infections. Pediatrics 2011 Oct;128(4):e995–e1004; quiz e1004-7. doi: 10.1542/peds.2010-2601 [Epub 2011 Sep 19] [PMID: 21930547].
NUTRIENT REQUIREMENTS & DELIVERY
When patients are fed intravenously, no fat and carbohydrate intakes are unabsorbed, and no energy is used in nutrient absorption. These factors account for at least 7% of energy in the diet of the enterally fed patient. The intravenously fed patient usually expends less energy in physical activity because of the impediment to mobility. Average energy requirements may therefore be lower in children fed intravenously, and the decrease in activity probably increases this figure to a total reduction of 10%–15%. Caloric guidelines for the IV feeding of infants and young children are outlined below.
The guidelines are averages, and individuals vary considerably. Factors significantly increasing the energy requirement estimates include exposure to cold environment, fever, sepsis, burns, trauma, cardiac or pulmonary disease, and catch-up growth after malnutrition.
With few exceptions, such as some cases of respiratory insufficiency, at least 50%–60% of energy requirements are provided as glucose. Up to 40% of calories may be provided by IV fat emulsions.
The energy density of IV dextrose (monohydrate) is 3.4 kcal/g. Dextrose is the main exogenous energy source provided by total IV feeding. IV dextrose suppresses gluconeogenesis and provides a substrate that can be oxidized directly, especially by the brain, red and white blood cells, and wounds. Because of the high osmolality of dextrose solutions (D10W yields 505 mOsm/kg H2O), concentrations greater than 10%–12.5% cannot be delivered via a peripheral vein or improperly positioned central line.
Dosing guidelines: The standard initial quantity of dextrose administered will vary by age (Table 11–22). Tolerance to IV dextrose normally increases rapidly, due primarily to suppression of hepatic production of endogenous glucose. Dextrose can be increased by 2.5 g/kg/d, by 2.5%–5%/d, or by 2–3 mg/kg/min/d if there is no glucosuria or hyperglycemia. Standard final infusates for infants via a properly positioned central venous line usually range from 15% to 25% dextrose, though concentrations of up to 30% dextrose may be used at low flow rates. Tolerance to IV dextrose loads is markedly diminished in the premature neonate and in hypermetabolic states.
Problems associated with IV dextrose administration include hyperglycemia, hyperosmolality, and glucosuria (with osmotic diuresis and dehydration). Possible causes of unexpected hyperglycemia include the following: (1) inad-vertent infusion of higher glucose concentrations than ordered, (2) uneven flow rate, (3) sepsis, (4) a stress situation (including administration of catecholamines or corticosteroids), and (5) pancreatitis. If these causes have been addressed to the degree possible and severe hyperglycemia persists, use of insulin may be considered. IV insulin reduces hyperglycemia by suppressing hepatic glucose production and increasing glucose uptake by muscle and fat tissues. It usually increases plasma lactate concentrations, but does not necessarily increase glucose oxidation rates; it may also decrease the oxidation of fatty acids, resulting in less energy for metabolism. Use of IV insulin also increases the risk of hypoglycemia. Hence, insulin should be used very cautiously. A standard IV dose is 1 U/4 g of carbohydrate, but much smaller quantities may be adequate and, usually, one starts with 0.2–0.3 U/4 g of carbohydrate.
Table 11–22. Pediatric macronutrient guidelines for total parenteral nutrition.
Hypoglycemia may occur after an abrupt decrease in or cessation of IV glucose. When cyclic IV nutrition is provided, the IV glucose load should be decreased steadily for 1–2 hours prior to discontinuing the infusate. If the central line must be removed, the IV dextrose should be tapered gradually over several hours.
Maximum oxidation rates for infused dextrose decrease with age. It is important to note that the ranges for dextrose administration provided in Table 11–22 are guidelines and that individual patient tolerance and clinical circumstances may warrant administration of either less or more dextrose. Quantities of exogenous dextrose in excess of maximal glucose oxidation rates are used initially to replace depleted glycogen stores; hepatic lipogenesis occurs thereafter. Excess hepatic lipogenesis may lead to a fatty liver (steatosis). Lipogenesis results in release of carbon dioxide, which when added to the amount of carbon dioxide produced by glucose oxidation (which is 40% greater than that produced by lipid oxidation) may elevate the Paco2 and aggravate respiratory insufficiency or impede weaning from a respirator.
The energy density of lipid emulsions (20%) is 10 kcal/g of lipid or 2 kcal/mL of infusate. The lipids are derived from either soybean or safflower oil. All commonly available formulations consist of more than 50% linoleic acid and 4%–9% linolenic acid. It is recognized that this high level of linoleic acid is not ideal due to the pro-inflammatory potential of omega-6 fatty acids, except when small quantities of lipid are being given to prevent an EFA deficiency. Ultimately, improved emulsions are anticipated, including an omega-3 fish oil based product that is currently available in Europe and in clinical trials or available for compassionate use for children with TPN-associated cholestatic liver disease in the US. Because 10% and 20% lipid emulsions contain the same concentrations of phospholipids, a 10% solution delivers more phospholipid per gram of lipid than a 20% solution. Twenty percent lipid emulsions are preferred. IV lipid is often used to provide 30%–40% of calorie needs for infants and up to 30% of calorie needs in older children and teens.
The level of lipoprotein lipase (LPL) activity is the rate-limiting factor in the metabolism and clearance of fat emulsions from the circulation. LPL activity is inhibited or decreased by malnutrition, leukotrienes, immaturity, growth hormone, hypercholesterolemia, hyperphospholipidemia, and theophylline. LPL activity is enhanced by glucose, insulin, lipid, catecholamines, and exercise. Heparin releases LPL from the endothelium into the circulation and enhances the rate of hydrolysis and clearance of triglycerides. In small premature infants, low dose heparin infusions may increase tolerance to IV lipid emulsion.
In general, adverse effects of IV lipid can be avoided by starting with modest quantities and advancing cautiously in light of results of triglyceride monitoring and clinical circumstances. In cases of severe sepsis, special caution is required to ensure that the lipid is metabolized effectively. Monitoring with long-term use is also essential.
IV lipid dosing guidelines: Check serum triglycerides before starting and after increasing the dose. Commence with 1 g/kg/d, given over 12–20 hours or 24 hours in small preterm infants. Advance by 0.5–1.0 g/kg/d, every 1–2 days, up to goal (see Table 11–22).
As a general rule, do not increase the dose if the serum triglyceride level is above 250 mg/dL during infusion (150 mg/dL in neonates) or if the level is greater than 150 mg/dL 6–12 hours after cessation of the lipid infusion.
Serum triglyceride levels above 400–600 mg/dL may precipitate pancreatitis. In patients for whom normal amounts of IV lipid are contraindicated, 4%–8% of calories as IV lipid should be provided (300 mg linoleic acid/100 kcal) to prevent essential fatty acid deficiency. Neonates and malnourished pediatric patients receiving lipid-free parenteral nutrition are at high risk for EFA deficiency because of limited adipose stores.
A.S.P.E.N. Position Paper: Clinical Role for Alternative Intravenous Fat Emulsions. Nutr Clin Pract 2012 Apr;27(2):150–192 [PMID: 22378798].
Park KT, Nespor C, Kerner J Jr: The use of Omegaven in treating parenteral nutrition-associated liver disease. J Perinatol 2011 Apr;31(Suppl 1):S57–S60 [PMID: 21448206].
One gram of nitrogen is yielded by 6.25 g of protein (1 g of protein contains 16% nitrogen). Caloric density of protein is equal to 4 kcal/g.
A. Protein Requirements
Protein requirements for IV feeding are the same as those for normal oral feeding (see Table 11–2).
B. Intravenous Amino Acid Solutions
Nitrogen requirements can be met by one of the commercially available amino acid solutions. For older children and adults, none of the standard preparations has a clear advantage over the others as a source of amino acids. For infants, however, including premature infants, accumulating evidence suggests that the use of TrophAmine (McGaw) is associated with a more normal plasma amino acid profile, superior nitrogen retention, and a lower incidence of cholestasis. TrophAmine contains 60% essential amino acids, is relatively high in branched-chain amino acids, contains taurine, and is compatible with the addition of cysteine within 24–48 hours after administration. The dose of added cysteine is 40 mg/g of TrophAmine. The relatively low pH of TrophAmine is also advantageous for solubility of calcium and phosphorus.
C. Dosing Guidelines
Amino acids can be started at 1–2 g/kg/d in most patients (see Table 11–22). In severely malnourished infants, the initial amount should be 1 g/kg/d. Even in infants of very low birth weight, there is evidence that higher initial amounts of amino acids are tolerated with little indication of protein “toxicity.” Larger quantities of amino acids in relation to calories can minimize the degree of negative nitrogen balance even when the infusate is hypocaloric. Amino acid intake can be advanced by 0.5–1.0 g/kg/d toward the goal. Normally the final infusate will contain 2%–3% amino acids, depending on the rate of infusion. Concentration should not be advanced beyond 2% in peripheral vein infusates due to osmolality.
Monitoring for tolerance of the IV amino acid solutions should include routine blood urea nitrogen. Serum alkaline phosphatase, γ-glutamyltransferase, and bilirubin should be monitored to detect the onset of cholestatic liver disease.
Minerals & Electrolytes
A. Calcium, Phosphorus, and Magnesium
Intravenously fed premature and full-term infants should be given relatively high amounts of calcium and phosphorus. Current recommendations are as follows: calcium, 500–600 mg/L; phosphorus, 400–450 mg/L; and magnesium, 50–70 mg/L. After 1 year of age, the recommendations are as follows: calcium, 200–400 mg/L; phosphorus, 150–300 mg/L; and magnesium, 20–40 mg/L. The ratio of calcium to phosphorous should be 1.3:1.0 by weight or 1:1 by molar ratio. These recommendations are deliberately presented as milligrams per liter of infusate to avoid inadvertent administration of concentrations of calcium and phosphorus that are high enough to precipitate in the tubing. During periods of fluid restriction, care must be taken not to inadvertently increase the concentration of calcium and phosphorus in the infusate. These recommendations assume an average fluid intake of 120–150 mL/kg/d and an infusate of 25 g of amino acid per liter. With lower amino acid concentrations, the concentrations of calcium and phosphorus should be decreased.
Standard recommendations are given in Table 11–23. After chloride requirements are met, the remainder of the anion required to balance the cation should be given as acetate to avoid the possibility of acidosis resulting from excessive chloride. The required concentrations of electrolytes depend to some extent on the flow rate of the infusate and must be modified if flow rates are unusually low or high and if there are specific indications in individual patients. IV sodium should be administered sparingly in the severely malnourished patient because of impaired membrane function and high intracellular sodium levels. Conversely, generous quantities of potassium are indicated. Replacement electrolytes and fluids should be delivered via a separate infusate.
Table 11–23. Electrolyte requirements for parenteral nutrition.
C. Trace Elements
Recommended IV intakes of trace elements are as follows: zinc 100 mcg/kg, copper 20 mcg/kg, manganese 1 mcg/kg, chromium 0.2 mcg/kg, selenium 2 mcg/kg, and iodide 1 mcg/kg. Of note, IV zinc requirements may be as high as 400 mcg/kg for premature infants and can be up to 250 mcg/kg for infants with short bowel syndrome and significant GI losses of zinc. When IV nutrition is supplemental or limited to fewer than 2 weeks, and preexisting nutritional deficiencies are absent, only zinc need routinely be added.
IV copper requirements are relatively low in the young infant because of the presence of hepatic copper stores. These are significant even in the 28-week fetus. Circulating levels of copper and manganese should be monitored in the presence of cholestatic liver disease. If monitoring is not feasible, temporary withdrawal of added copper and manganese is advisable.
Copper and manganese are excreted primarily in the bile, but selenium, chromium, and molybdenum are excreted primarily in the urine. These trace elements, therefore, should be administered with caution in the presence of renal failure.
Two vitamin formulations are available for use in pediatric parenteral nutrition: MVI Pediatric and MVI-12 (Astra-Zeneca). MVI Pediatric contains the following: vitamin A, 0.7 mg; vitamin D, 400 IU; vitamin E, 7 mg; vitamin K, 200 mcg; ascorbic acid, 80 mg; thiamin, 1.2 mg; riboflavin, 1.4 mg; niacinamide, 17 mg; pyridoxine, 1 mg; vitamin B12, 1 mcg; folic acid, 140 mcg; pantothenate, 5 mg; and biotin, 20 mcg. Recommended dosing is as follows: 5 mL for children weighing more than 3 kg, 3.25 mL for infants 1–3 kg, and 1.5 mL for infants weighing less than 1 kg. Children older than 11 years can receive 10 mL of the adult formulation, MVI-12, which contains the following: vitamin A, 1 mg; vitamin D, 200 IU; vitamin E, 10 mg; ascorbic acid, 100 mg; thiamin, 3 mg; riboflavin, 3.6 mg; niacinamide, 40 mg; pyridoxine, 4 mg; vitamin B12, 5 mcg; folic acid, 400 mcg; pantothenate, 15 mg; and biotin, 60 mcg. MVI-12 contains no vitamin K.
IV lipid preparations contain enough tocopherol to affect total blood tocopherol levels. The majority of tocopherol in soybean oil emulsion is α-tocopherol, which has substantially less biologic activity than the α-tocopherol present in safflower oil emulsions.
A dose of 40 IU/kg/d of vitamin D (maximum 400 IU/d) is adequate for both full-term and preterm infants.
Vanek VW et al; Novel Nutrient Task Force, Parenteral Multi-Vitamin and Multi–Trace Element Working Group; American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors: A.S.P.E.N. position paper: recommendations for changes in commercially available parenteral multivitamin and multi-trace element products. Nutr Clin Pract 2012 Aug;27(4):440–491. doi: 10.1177/0884533612446706 [Epub 2012 Jun 22] [PMID: 22730042].
The initial fluid volume and subsequent increments in flow rate are determined by basic fluid requirements, the patient’s clinical status, and the extent to which additional fluid administration can be tolerated and may be required to achieve adequate nutrient intake. Calculation of initial fluid volumes to be administered should be based on standard pediatric practice. Tolerance of higher flow rates must be determined on an individual basis. If replacement fluids are required for ongoing abnormal losses, these should be administered via a separate line.
Vital signs should be checked on each shift. With a central catheter in situ, a fever of more than 38.5°C requires that peripheral and central-line blood cultures, urine culture, complete physical examination, and examination of the IV entry point be made. Instability of vital signs, elevated white blood cell count with left shift, and glycosuria suggest sepsis. Removal of the central venous catheter should be considered if the patient is toxic or unresponsive to antibiotics.
A. Physical Examination
Monitor especially for hepatomegaly (differential diagnoses include fluid overload, congestive heart failure, steatosis, and hepatitis) and edema (differential diagnoses include fluid overload, congestive heart failure, hypoalbuminemia, and thrombosis of superior vena cava).
B. Intake and Output Record
Calories and volume delivered should be calculated from the previous day’s intake and output records (that which was delivered rather than that which was ordered). The following entries should be noted on flow sheets: IV, enteral, and total fluid (mL/kg/d); dextrose (g/kg/d or mg/kg/min); protein (g/kg/d); lipids (g/kg/d); energy (kcal/kg/d); and percent of energy from enteral nutrition.
C. Growth, Urine, and Blood
Routine monitoring guidelines are given in Table 11–24. These are minimum requirements, except in the very long-term stable patient. Individual variables should be monitored more frequently as indicated, as should additional variables or clinical indications. For example, a blood ammonia analysis should be ordered for an infant with lethargy, pallor, poor growth, acidosis, azotemia, or abnormal liver test results.
Table 11–24. Summary of suggested monitoring for parenteral nutrition.
American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors: Clinical guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients, 2009. JPEN J Parenter Enteral Nutr 2009 May-Jun;33(3):255–259. doi: 10.1177/0148607109333115 [PMID:19398611].
Greene HL et al: Guidelines for the use of vitamins, trace elements, calcium, magnesium, and phosphorus in infants and children receiving total parenteral nutrition: report of the Subcommittee on Pediatric Parenteral Nutrient Requirements from the Committee on Clinical Practice Issues of the American Society for Clinical Nutrition. Am J Clin Nutr 1988;48:1324 [PMID: 3142247].
Joffe A et al: Nutritional support for critically ill children. Cochrane Database Syst Rev 2009 Apr 15;(2):CD005144 [Review] [PMID: 19370617].