Nutrition in Neonatal Pulmonary Disease

Chapter
Part of the Nutrition and Health book series (NH)

Abstract

This chapter provides an overview of the most common pulmonary conditions encountered in the newborn infant population for which there are nutritional implications, the goals of nutrition management, and evidence-based interventions to achieve these goals. The pulmonary diseases and conditions covered in this chapter include neonatal respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTNB), meconium aspiration syndrome (MAS), bronchopulmonary dysplasia (BPD), and chylothorax.

Keywords

Prematurity Later preterm infant Low birth weight Respiratory distress syndrome Transient tachypnea of the newborn Meconium aspiration syndrome Bronchopulmonary dysplasia Chylothorax 

Keypoints

  • The preterm infant, already at high nutritional risk due to insufficient nutrient stores along with increased nutritional demands, is further compromised by chronic respiratory disease.

  • Infants with severe BPD have respiratory difficulties which interfere with oral feeding, so standard feeding regimens may not provide adequate protein or energy intake.

  • Nutritional strategies used to prevent BPD include optimizing nutrient delivery including vitamin A and antioxidants to support healthy growth and development of lung tissue.

  • Nutritional management in the newborn infant with chronic pulmonary diseases should accommodate the different needs of infants born at varying weeks of gestation.

  • Also requiring correction is the nutritional abnormalities which often accompany drugs such as diuretics, corticosteroids, bronchodilators, and antibiotics which are frequently used in these infants.

Introduction

This chapter provides an overview of the most common pulmonary conditions encountered in the newborn infant population for which there are nutritional implications, the goals of nutrition management, and evidence-based interventions to achieve these goals. The pulmonary diseases and conditions covered in this chapter include neonatal respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTNB), meconium aspiration syndrome (MAS), bronchopulmonary dysplasia (BPD), and chylothorax.

Because the occurrence of RDS and BPD is related to degree of premature birth, references to prematurity and birth weight are found throughout this chapter. The definitions of these terms include:
  • Term: 40 weeks of gestation (range 37–42 weeks)

  • Early term: 37–38 weeks of gestation

  • Late preterm: 34–36 6/7 weeks of gestation

  • Preterm: 28–34 weeks of gestation

  • Extremely preterm: 22–28 weeks of gestation

  • Low birth weight: less than 2.5 kg at birth

  • Very low birth weight: less than 1.5 kg at birth

  • Extremely low birth weight: less than 1 kg at birth

Brief descriptions of fetal lung development, pathophysiology and complications of lung diseases in this population as they relate to nutrition in this population are included in the overview to provide initial perspective. Specific nutrition recommendations are given for prevention of complications or progression of respiratory distress to chronic lung disease (CLD), support of normal growth and development, and additional considerations of medical treatments for respiratory disease that may potentially compromise nutritional status.

Overview

Respiratory compromise is one of the most common causes of morbidity and mortality in neonates [1, 2, 3]. Because respiratory compromise is most often associated with premature birth, a brief description of fetal lung development provides initial perspective. During the first 3–7 weeks of gestation, the main structures of the trachea, bronchi, and pulmonary arteries develop. Structural anomalies such as pulmonary agenesis, arteriovenous malformations, congenital cysts, and tracheo-esophageal atresia or fistulas may occur during this phase of development. From 7 to 16 weeks’ gestational age, the conducting airways and bronchioles are formed and membranes between pleural and peritoneal cavities are closed. Structural anomalies such as pulmonary hypoplasia, lymphangiectasia (which causes chylothorax when postnatal feedings commence), and diaphragmatic hernia may occur during this phase of fetal development [4, 5].

The next 10 weeks, from 16 to 26 weeks’ gestational age, involves maturation of both structure and function. If fetal lung development is interrupted by premature birth during this phase, severe respiratory compromise is likely to occur due to underdeveloped structures of peripheral airways, capillary beds, and alveoli as well as lower levels of surfactant and protective antioxidants. At birth, capillary beds and alveoli must provide an adequate gas exchange surface area to accept oxygen into circulation. Alveoli surface area is a function not only of anatomical size, but also the ability to expand, a function enhanced by the presence of surfactant which is not produced in sufficient quantities until later in gestation. After birth, lung tissue is exposed to higher levels of oxygen, causing oxidative stress and triggering inflammation which can further disrupt alveolar development [4, 5].

Between 26 and 36 weeks’ gestational age, peripheral airways, capillary beds, and alveoli continue to mature, increasing gas exchange surface area, surfactant, and antioxidant levels. Surface area is estimated to be 1–2 m2 at 30–32 weeks compared to 3–4 m2 at term. Lung volume at 30 weeks’ gestational age is only 34 % of lung volume at term, but alveoli growth and development continues into the second year of life [4].

Reports indicate that preterm infants may have reduced pulmonary function well into childhood even if they did not exhibit respiratory symptoms during the first few months of life [4]. The cause for this finding is not known, but during fetal development, lung tissue is exposed to an oxygen concentration of only 3–10 %. After birth, inhaled oxygen concentrations are significantly different, even in room air, which may cause oxidative and inflammatory tissue changes, later affecting pulmonary growth and function even in infants who do not develop respiratory compromise.

Respiratory Distress Syndrome

The definition of RDS most commonly used is that of the Vermont Oxford Neonatal Network: “classic ground-glass appearance of lung tissue on X-ray and arterial blood oxygen level less than 50 mmHg in room air, central cyanosis in room air, or need for supplemental oxygen to maintain arterial blood oxygen level of 50 mmHg.” [6] This impairment of ability to oxygenate is caused by the immature structure and function of the alveoli as well as their decreased number in preterm infants, with the net result being a decreased gas exchanging surface area and increased risk for atelectasis [5].

Morbidity reports vary by site, but for infants who survive to at least 12 h of age, 61–100 % of those born at 22–26 weeks’ gestational age are reported to develop RDS [3]. At 26–28 weeks’ gestational age, the incidence of RDS is 55–100 % and gradually decreases to 2–9 % by 34–36 weeks’ gestational age [3, 7, 8]. Term infants are much less likely to develop RDS (0.6–4 %), but when they do, it is more likely to be due to transient tachypnea or MAS, than to immature lung development [7, 8, 9, 10].

Most efforts to prevent or treat RDS are focused on improving the maturity and function of lung tissue: preventing or delaying premature birth, providing corticosteroids prenatally, and providing surfactant [6]. The effects of fetal nutrition on lung growth and development have been studied in animals. These studies show that lung tissue size and surface area are decreased when nutrition is inadequate during fetal development, though when compared to the overall effect on body weight, some sparing of lung tissue accretion seems to occur. Evidence is conflicting regarding the extent to which fetal undernutrition impairs tissue maturation and what effect this may have on respiratory function later in life [11, 12]. These studies also indicate that catch-up growth of lung tissue occurs when adequate fetal nutrition is restored [11], although morphologic changes, such as reduced alveolar number, may occur and may be exacerbated if postnatal nutrition is then inadequate [13]. Human studies of postnatal nutrition during this phase of development primarily focus on the relationship of early nutrient intake with overall growth and neurodevelopmental outcome, but early nutrition has also been shown to affect the severity of respiratory illness [14, 15].

Transient Tachypnea of the Newborn

Transient tachypnea, by definition, is of short duration, usually 12–48 h. Fluid that is normally present in the alveoli during fetal development must be removed at birth so that air can fill the alveoli to provide oxygen delivery. This fluid gradually decreases in volume as the fetus progresses to term, and is removed as the chest is compressed in the vaginal canal during birth and by resorption into the lymphatic vessels and blood capillaries with the first few breaths after birth. When this fluid is not cleared adequately, TTNB may occur. Factors that increase the risk for development of TTNB include birth by Caesarian-section, maternal diabetes, maternal hypertension, and late preterm birth [7, 8, 16]. Fluid management is an important nutrition related factor in treating TTNB.

Meconium Aspiration Syndrome

Meconium is the fetal gastrointestinal contents, comprises various gastrointestinal secretions and substances swallowed during fetal development. Meconium may be passed into the amniotic fluid in response to stress such as hypoxia, placental insufficiency, maternal hypertension, or exposure to nicotine or cocaine. When meconium is present in amniotic fluid, there is greater risk of aspiration. Aspirated meconium may initially cause airway obstruction, but may also cause inflammation and inactivate surfactant resulting in severe hypoxia.

Because meconium is not often found in amniotic fluid until 34 weeks’ gestational age, MAS occurs primarily in late preterm and term infants. Infants at higher risk for MAS include those with thicker meconium, or those who aspirate meconium deeper into the respiratory tract, require intubation, or are less vigorous at birth [10]. Meconium may be present in the amniotic fluid of as many as 20 % of all newborns, but only 2–9 % of those infants develop MAS, and only 30 % of those who develop MAS experience severe hypoxia and require mechanical ventilation.

Nutrition becomes an important factor in the management of MAS only when hypoxia is severe and extracorporeal membrane oxygenation (ECMO) is required. Meeting nutritional needs early, particularly protein needs, using parenteral nutrition if necessary, is important in the care of these infants [10, 17].

Bronchopulmonary Dysplasia

BPD, now referred to as CLD is a complication of RDS. Although both BPD and CLD are terms used for this condition, BPD is the preferred nomenclature to distinguish this from adult chronic lung conditions. BPD was first described by Northway et al. in 1967 [18]. This description was based on changes in lung function and the radiologic appearance of the lungs, with positive pressure mechanical ventilation and exposure to high amounts supplemental oxygen sited as causative factors. The stages of severity were based on radiographic changes in the lung, pulmonary function tests, and the continued need for mechanical ventilation or supplemental oxygen [18]. Due primarily to changes in medical management of RDS, and the resulting changes in the progression of lung disease, the definition of BPD has changed over time. The pulmonary fibrosis and cystic changes, radiologic appearance, and emphysema typical of BPD in the past have become rare with the advent of antenatal steroid use, which enhances lung development and neonatal pulmonary surfactant administration, which supports alveolar stability. Changes in mechanical ventilation using lower airway pressures, gas volumes, and oxygen concentrations have reduced lung tissue damage. Pulmonary changes most commonly seen with current treatment modalities include dilated alveolar ducts, with reduced alveolar surface area and capillary development [19, 20, 21].

Because diagnostic criteria and stratification of severity of disease have evolved over time, reported incidence varies depending upon the definition used:
  • Traditional definition: Supplemental oxygen required at 36 weeks’ gestational age [22]

  • National Institute of Child Health and Human Development (NICHD) definition: At 36 weeks’ gestational age or discharge home, whichever comes first and based on a history of required oxygen supplementation of >21 % for at least 21 days
    • Mild BPD: no further supplemental oxygen requirements

    • Moderate BPD: need for supplemental oxygen of <30 %

    • Severe BPD: need for supplemental oxygen of ≥30 % and/or positive pressure [22]

  • Physiologic definition: Need for mechanical ventilation, continuous positive airway pressure, or supplemental oxygen to maintain oxygen saturation ≥88 % for 1 h

Due to these variations in the definition of BPD, incidence reports are often difficult to compare. The NICHD reported incidence of respiratory morbidity for infants born at 28 weeks’ gestational age or less between January 1, 2003 and December 31, 2007 using the traditional definition was 42 %; using the NICHD definition, the incidence was 68 %; and using the physiologic definition, the incidence was 40 %. In other reports which use the traditional definition of BPD and stratify infants by birth weight, incidence is reported as 42–52 % of infants 501–750 g, 25–34 % of infants 751–1,000 g, 11–15 % of infants 1,001–1,250 g, and 5–7 % of infants 1,251–1,500 g [23, 24]. Two recent studies using the NICHD definition report the incidence of BPD as 26–28 % of infants 501–1,500 g birth weight (Horbar) and 28 % of infants 28 weeks’ gestational age and less [25].

Nutritional strategies used to prevent BPD include optimizing nutrient delivery to support normal growth and development of lung tissue and optimizing vitamin A status. BPD and the medical therapies used to treat BPD may affect protein, energy, electrolyte, and mineral needs.

Chylothorax

Chylothorax is a condition rather than a specific diagnosis. Chylothorax occurs when there is a disruption in the function of the thoracic duct. Long-chain triglycerides from enteral feedings are picked up from the lacteals of the small intestine, and are carried as chyle—an emulsion of chylomicrons in lymph—through the lymphatic system to the thoracic duct, where they are delivered into the general circulation. If the thoracic duct is obstructed or damaged, chyle leaks into the pleural space and may lead to respiratory failure. Congenital causes of chylothorax are rare with an estimated prevalence of 1 in 10,000–15,000 births [26]. Diagnoses include lymphatic dysplasia or intrauterine conditions that cause obstruction and ultimately fistulas or rupture of the thoracic duct. The occurrence of chylothorax at birth may occur more frequently in infants with Noonan, Turner, or Down syndromes [27]. Acquired causes of chylothorax are usually complications from thoracic surgery to repair congenital cardiac defects especially those that involve the aortic arch, or surgical repair of tracheo-esophageal fistulas or diaphragmatic hernias [28].

Symptoms may appear within the first 24 h of birth or may not present until 7–10 days of life when feedings are well established and fat intake is significant [27]. Although spontaneous recovery occurs in more than 50 % of neonatal cases of chylothorax, many neonates with chylothorax require at least conservative medical treatment, which may include thoracentesis and mechanical ventilation to prevent respiratory failure. If chyle output exceeds 50 mL/kg/day for more than 3 days despite maximum medical therapy, surgical intervention is usually considered [29, 30]. Nutritional strategies are designed to provide optimal nutrition either parenterally or enterally, the latter without increasing the production of chylous leakage into the pleural cavity.

Nutrition Management

At birth, the placental supply of nutrients is lost. For the healthy term infant, who has been gradually “outgrowing” his intrauterine environment, this is not problematic. He has been swallowing amniotic fluid throughout his gestation to prepare his gastrointestinal tract for its role in the digestion and absorption of nutrients after birth. He has also accrued a rich store of vitamins, minerals, and even energy during his third trimester of intrauterine life. These stores will help meet his nutrient needs until his mother’s milk supply is fully established. As he begins to nurse at his mother’s breast, she will produce colostrum, which is rich in protein, vitamin A, carotenoids, vitamin E, minerals, and electrolytes as well as many immunologically derived components from her circulation [31]. During the next 10–14 days, his mother’s milk supply will increase in volume and mature in nutrient content to provide all the nutrients he needs to support his rapid growth and development.

The normal continuity of this transitional process is interrupted when respiratory compromise precludes oral feeding. Enteral feeding tolerance may be slow to progress, and nutrients may need to be delivered parenterally. The mother needs encouragement and support to establish lactation so that her milk can be used in her baby’s nutritional management [32]. When respiratory disease is accompanied by prematurity, there are additional confounding factors. Nutrient stores are not sufficient. Gastrointestinal enzymes are present in significant amounts early in gestation, but premature birth places demands on the gastrointestinal tract which often stretch beyond its capabilities, particularly when hindered by other conditions or treatments that accompany premature birth.

The goals of nutritional management in the newborn infant with respect to pulmonary conditions and diseases are to:
  • Support normal overall growth and development, including pulmonary tissues, accommodating the different needs of infants born at varying weeks of gestation.

  • Adjust for differences in nutritional demands related to pulmonary compromise.

  • Protect pulmonary tissues from oxidative damage inherent in respiratory support and correct nutritional abnormalities or potential abnormalities which accompany treatment of pulmonary conditions or diseases.

Recommended intakes for parenterally delivered nutrients are given in Table 4.1. Recommendations for enterally or orally delivered nutrients are given in Table 4.2. Depending upon the route of nutrient delivery, specific lab work is assessed at regular intervals to insure nutritional adequacy and safety [47, 48]. Adequacy of intake is also assessed by measuring weight, length and head circumference, and comparing growth progress to established norms. The Fetal-Infant Growth Chart for Preterm Infants is used to assess the growth of infants born at less than 37 weeks’ gestational age, from 22 weeks’ gestational age through term, up to 10 weeks past term [49]. The growth of term infants is compared to growth charts for infant boys and infant girls, 0–24 months of age, published by the World Health Organization [50].
Table 4.1

Recommended daily parenteral nutrient intakesa,b

Nutrient

Initial dose (days 1–3)

Transition dose (week 1–2)

Growing preterm infant

Growing term infant

Maximum dose

Fluidc (mL/kg)

 <1 kg BW

50–120

90–140

120–150

  

 1–1.5 kg BW

70–90

90–140

120–150

  

 >1.5 kg BW

60–120

120–150

120–150

120–150

 

 Term infantsd

40–60

↑ 20 mL/kg/day

 

150–180

 

Energy (kcal/kg)

40–60

60–85

90–115

90–108

 

Dextrose (mg/kg/min)

5

5–10

5–15

5–15

18

Carbohydrate (g/kg)

7

8–15

10–20

8–20

25

Protein (g/kg)

2.5–3.5

3.5–4

3.2–3.8

2.5–3

4

Fat (g/kg)

0.5–3

1–3

0.5–3

0.5–3

4

Sodium (mEq/kg)

0–1

2–5

2–4

2–4

20

Potassium (mEq/kg)

0

0–2

2–3

2–3

9

Chloride (mEq/kg)

0–1

2–7

2–7

2–7

 

Acetate (mEq/kg)

As needed

As needed

As needed

As needed

6

Calcium (mEq/kg)

1–3

2–3

3

2

4

Phosphorus (mMol/kg)

0–0.6

1.3–2

1.3–2

1–1.5

2

Magnesium (mEq/kg)

0

0.2–0.3

0.2–0.3

0.25–0.5

1

Iron (mg/kg)e

(0.1–0.2)

(0.1)

1

Zinc (μg/kg)

150

150

400

250

 

Copper (μg/kg)

20

20

20

20

 

Manganese (μg/kg)

0–1

0–1

1

1

 

Chromium (μg/kg)

0–0.1

0–0.1

0.05–0.3

0.1–0.2

 

Selenium (μg/kg)

0–1.3

0–1.3

1.5–4.5

2

 

Pediatric multivitaminf

 <1 kg

30 % dose

30 % dose

30 % dose

 

1 dose

 1–2.5 kg

65 % dose

65 % dose

65 % dose

65 % dose

 <2.5 kg

1 dose

1 dose

1 dose

1 dose

Vitamin Ag (IU)

 <1 kg BW

5,000 × 12

 

aReference [33]

bReference [34]

cReference [35]

dReference [36]. Fluid restriction may be used in the management of transient tachypnea in late preterm or term infants

eIron is not usually given parenterally due to incompatibility with other nutrients in the admixture; iron is not indicated during sepsis or in patients with multiple blood transfusions

fVitamin A content of pediatric multivitamin products is 2,300 IU/dose; recommended intake is 700–1,500 IU/kg for preterm infants and 2,300 IU/d for term infants. Vitamin E content is 10 IU/dose; recommended intake 2.8–3.5 IU/kg/day for preterm infants and 7 IU/d for term infants

gRecommendations for additional vitamin A for extremely low birth weight are intramuscular doses of 5,000 IU, given 3 times weekly for 4 weeks (12 doses total) [37]. Due to drug shortages, vitamin A is not currently available in this dosage form

Table 4.2

Recommended daily enteral nutrient intake for selected nutrients

Nutrient

Preterm infantsa,b,c,d,e,f

Term infantsc,g,h,i,j

Per kg

Per 100 kcal

Per kgg or per dayh

Formula per 100 kcali

Breast milk per 100 kcalc

Fluid (mL)

See Table 4.1

 

150–180/kg, See Table 4.1

125–150

143

Energy (kcal) (A)

110–135

100

115/kg

100

100

Proteind (g)

 <1 kg weight

3.8–4.2

3.6–4.1

   

 1–1.8 kg weight

3.4–4

2.8–3.3

   

 1.8–2.5 kg weight

2.8–3.4

2.4–2.8

   

 >2.5 kg weightg

  

1.8–2.2

1.7–3.4

1.28

Lipide (g) (A)

5.3–8.4

4.4–6.2

31/day

4.4–6.4

6

 LA (mg)

385–1,540

350–1,400

 

350–2,240

432

 LNA (%kcal)

0.7–2.1 %

0.7–2.1 %

 

77–256 mg

60 mg

 DHA (mg)

12–30

11–27

 

Varies

 AA (mg)

18–42

16–39

 

Varies

Carbohydratea,b (g)

11.6–13.2

9.6–12.5

12/day

9–13

10.4

Sodiuma (mg)

69–115

63–105

120/day

25–50

26

Potassiuma,b (mg)

66–132

60–160

400/day

60–160

83

Calciuma,b (mg)

120–230

123–185

210/day

50–140

40

Phosphorusa,b (mg)

60–90

55–109

100/day

20–70

21

Magnesiuma,b (mg)

7.9–15

6.8–17

30/day

4–17

4.2

Irona (mg)

2–3

1.8–2.7

0.27/day

0.2–1.65

0.057

Zinca (mg)

1.1–2

1–1.8

2/day

0.4–1

0.17

Seleniuma,b,f (μg)

1.3–10

1.8–9

7/day

1.5–5

2.9

Vitamin Aa,b (IU)

1,332–3,330

700–2,460

1,332/day

100–500

319

Vitamin Da,b (IU)

800–1,000/d

75–270

400/dayj

40–100

2.8

Vitamin Ea (IU)

6–12j

2–10

6/dayj

0.5–5

0.45

Cholinea (mg)

8–55

7–50

125/day

7–30

14

Inositola (mg)

4.4–53

4–48

4–40

22

aReference [38]

bReference [39]

cReference [40]

dReferences [41, 42]

eLA linoleic acid, LNA α-linolenic acid, DHA docosahexaenoic acid, AA arachadonic acid. Breast milk content of DHA and ARA varies with maternal diet

fReference [43]

gReference [44]

hReference [45]

iReference [46]

jReference [34]

Respiratory Distress Syndrome

The goal of specific nutritional strategies for infants with RDS is primarily to promote normal growth and development of lung tissue and prevent progression to BPD. See Table 4.3.
Table 4.3

Grades of recommendations for nutritional management of neonatal pulmonary disease

Nutritional management strategy

Gradea

Respiratory distress syndrome

Fluids: start intravenous fluids at 70 to 80 mL/kg/d and individualize to allow 2.5–4 % weight loss (total of 15 % weight loss) within the first 5 days. Increase fluids to prevent dehydration and allow adequate nutrient delivery [6, 35]

D

Electrolytes: restrict sodium intake during the first few days. Begin sodium after the onset of initial diuresis, monitoring fluid balance and serum electrolyte levels to guide administration [6, 51]

B

Protein: provide 2.5 to 3.5 g protein/kg/d within the first 24 to 48 h of life [41, 42, 52]

B

  Subsequent protein needs are 3.5–4 g/kg/day [52, 53]

B

 Energy: initial energy intake should be 40–60 kcal/kg/day, and increased by day 6 to levels that support tissue accretion [14]

A

  Energy needs of ventilated extremely low birth weight infants may be 25 % higher than non-ventilated infants, although intake greater than 110–135 kcal/kg/day may not be beneficial [52, 53, 54]

D

Parenteral lipid and multivitamin preparations (MVP): if administered as a total nutrient admixture, protecting infusion from light exposure is associated with a decrease in BPD [55, 56, 57]

C

  Co-administration of lipids with MVP separately from dextrose/amino acid solution may protect lung tissue from oxidative damage [58]

C

Vitamin A: extremely low birth weight infants may benefit from 5,000 IU given intramuscularly 3 times weekly for 4 weeks (12 doses total) [37]

A

Transient tachypnea of the newborn

 Term infants: limit fluids to 40 mL/kg/day on day of life 1 and adjust fluids as necessary to prevent dehydration, hypoglycemia, or more than 10 % weight loss from birth weight; increase fluids by 20 mL/kg/day until 150 mL/kg/day or ad libitum feedings are achieved [36]

B

Late preterm infants: limit fluids to 60 mL/kg/day on day of life 1; adjust and increase fluids as for term infants [36]

B

Meconium aspiration (for infants who require extracorporeal membrane oxygenation)

 Parenteral nutrition: initiate 24 to 48 h of birth [17]

C

  Protein: provide 3 g/kg/day [59]

C

  Energy: provide at least 80 kcal/kg/day but not more than 100 kcal/kg/day [59]

C

  Fat: if required, provide through separate venous access [60]

C

 Enteral feedings: begin enteral feedings when infant is medically stable and gradually increase feedings while tapering parenteral nutrition [17]

C

Bronchopulmonary dysplasia

Fluids: although higher early fluid intake and less weight loss during the first 10 days of life may be associated with increased risk of BPD, restriction of fluid does not prevent BPD and may prevent provision of adequate nutrition [35, 61]

B

  Maintenance fluids are 120–150 mL/kg/day [51]

C

Protein: providing an average intake of at least 3.3 g protein during the first 20 days of life to prevent early protein deficits and support fetal growth rates [62]

C

  Intakes of 3.5–4 g/kg/day may be needed to support normal growth [52, 53]

D

Energy: energy needs of preterm infants with chronic lung disease may be 15–25 % higher than healthy preterm infants, although intake greater than 125–135 kcal/kg/day may not be beneficial [51, 52, 53, 54, 63, 64]

C

Feeding problems: reducing noxious stimuli to face and mouth; encourage kangaroo care and nonnutritive suckling at breast, and use hunger and satiety cues for feedings [65]

C

  When fluid restriction is needed in management of pulmonary edema, consider use of nutrient dense feedings, with up to 30 kcal/oz to provide adequate nutrient intake [51, 66, 67]

C

 Drug nutrient interactions

 

  Corticosteroids: insure optimal protein intake during dexamethasone therapy [68]

C

  Diuretics: monitor serum levels of sodium, potassium, chloride, and phosphorus and supplement these nutrients if needed to prevent electrolyte imbalances and osteopenia [69, 70]

D

  Aminoglycosides/vancomycin: as for diuretics [71]

D

Chylothorax

Parenteral nutrition: if chylothorax worsens after initiating feedings, parenteral nutrition prevents further chylous fluid accumulation [72]

D

Fat: when feedings are started, defatted breast milk supplemented with medium chain triglycerides (MCT) or formulas containing MCT may prevent recurring chylothorax [28, 72]

D

 Protein: insure optimal protein intake for gestational age [26]

D

aSupport for grade of recommendation [6]

A at least one high quality meta-analysis of randomized controlled trials or one large sufficiently powered randomized trial, B high quality systematic review of case controlled studies or lower grade randomized controlled trial with high probability of causal relationship, C a well-conducted case controlled study with low risk of bias, D evidence from cohort studies, case reports, expert opinion, or standard of practice

Fluid and Electrolytes

Extracellular water contraction is normal during the first few days of life. Although there is no strong evidence to recommend fluid restriction during this time to prevent chronic lung changes, overhydration may be associated with increased risk of BPD, patent ductus arteriosus (PDA), and necrotizing enterocolitis (NEC) [35, 61, 73, 74]. Daily weight loss of 2.4–4 % up to a total initial weight loss of 8–15 % during the first 3–5 days of life is considered physiological [6]. Greater weight losses may signify dehydration or depletion of energy stores and loss of lean tissue.

Fluid administration must be individualized to prevent over- or underhydration based on gestational age, weight, and clinical condition. Infants of lower gestational age have greater extracellular fluid volumes and disproportionately greater potential fluid losses due to greater body surface area to weight ratios, immature skin tissue, and immature renal function [74, 75]. Infants with lower birth weights have less subcutaneous fat stores are more susceptible to heat losses and the resulting evaporative fluid losses with interruptions in their thermoneutral environment. Infants placed in radiant warmers will lose more fluid due to evaporative losses than infants cared for in double-walled incubators. Fluid status is managed by keeping daily weight changes within the prescribed range, maintaining normal urine output of 1–2 mL/kg/h, and maintaining serum sodium levels within the normal range. Initial, transitional and growth fluid requirements for preterm and term infants are given in Table 4.1.

Sodium needs are minimal during the first few days in preterm infants, in part because initial water losses—from interstitial spaces and insensible losses—exceed sodium losses, and many medications used during the first few days of life are inadvertent sources of sodium [51, 74, 76]. Initial, transitional, and growth sodium requirements for preterm and term infants are also given in Table 4.1. Beyond the first week of life, sodium intake for preterm infants may need to be adjusted frequently. Preterm infants may experience late-onset hyponatremia due to immature renal function and require 5–7 mEq sodium/kg/day to maintain normal serum values.

Energy and Protein

Optimizing energy and protein intake for preterm infants during the first 24–48 h of life and throughout the first week of life improves growth and neurological outcome and has been shown to decrease the odds ratio of adverse outcomes such as NEC, late-onset sepsis, and BPD [14, 15, 77, 78, 79]. Inadequate nutrient intake, particularly during the first few days and weeks of life, may compromise the preterm infant’s ability to resist oxidative damage, barotrauma, and infection due to reduced surfactant synthesis, and decreased growth, development, and repair of lung tissue [80, 81]. Respiratory effort may be compromised by increased ribcage compliance and decreased intercostal muscle strength associated with inadequate protein and energy intake, and with osteopenia associated with vitamin D insufficiency, calcium and phosphorus depletion [82]. Optimizing early nutrient intake reduces postnatal cumulative nutrient deficits, improves growth outcomes, and reduces subsequent morbidity [41, 83]. Nutrient intake, specifically the intake of energy and protein is adjusted to promote normal growth. Energy intake of 140–150 kcal/kg/day along with protein intake of 4–4.5 g/kg/day may be needed if deficits accrue early in the course of care [38].

Human milk is the optimal enteral feeding choice for both term and preterm infants, but the nutrient content of human milk does not match the placental supply of nutrients for infants who are born prematurely. Human milk fortifiers can be added to mother’s own milk or donor breast milk to meet the nutrient needs of the rapidly growing preterm infant. Not all human milk fortifiers provide the total recommended amount of protein or the recommended protein: energy ratio depending upon the protein content of an individual mother’s milk. Human milk fortifier manufacturers’ nutrient content tables use 1.4–1.6 g protein/dL (2–2.3 g/100 kcal) as the protein content of human milk. Early milk contains this level of protein, but protein content decreases rapidly during the first week postpartum. Mature milk is generally present by 2–4 weeks postpartum and is likely to contain 1.05 ± 0.2 g protein/dL (1.5 ± 0.3 g/100 kcal) [40]. (Lawrence) A liquid protein fortifier (Liquid Protein Fortifier®, Abbott Nutrition, which contains 1 g extensively hydrolyzed protein/6 mL) may be used to individualize protein supplementation when mother’s milk contains less than 1.4–1.6 g protein/dL. Product labels for powdered protein supplements indicate intended use for children over 3 years of age. When human milk is not available, preterm infant formulas may be used to meet the specific needs of prematurely born infants, and standard term infant formulas may be used for term infants.

Antioxidants

At birth, lung tissue is exposed to oxygen, which may cause oxidative stress, trigger inflammation, and disrupt alveolar development. Medical management efforts to reduce the effects of oxygen toxicity include lower targeted oxygen saturation levels, gentler ventilation techniques, and nasal continuous positive airway pressure ventilation [20]. Peroxides generated by the exposure of intravenous lipid emulsions and multivitamin preparations to light have also been implicated in the progression of lung disease due to oxidative stress. Protecting total nutrient admixtures from exposure to light by covering the infusion bag and tubing with foil or using tinted tubing is associated with a decrease in the production of peroxides and a decrease in the progression of RDS to CLD [55, 57]. Lipid and vitamin peroxidation as well as the inflammatory response to high levels of oxygen exposure may be significantly reduced when multivitamins are co-administered with parenteral lipids, but infused separately from dextrose and amino acids, whether or not they are shielded from light exposure [58]. In addition, several nutrients may function as antioxidants and have been studied with respect to their potential ability to further protect lung tissue from oxidative damage: vitamin A, vitamin E, and selenium.

Vitamin A plays a role in airway epithelial cell differentiation and repair. Preterm infants have lower plasma concentrations at or shortly after birth. These levels are often in the range indicating marginal or deficient status. The risk for RDS progressing to CLD may be increased in preterm infants with low vitamin A status [84]. Vitamin A administered parenterally in total nutrient admixtures or dextrose/amino acid solutions is often inefficient, with as little as 20 % of the vitamin A content actually administered due to adsorption onto plastic containers and tubing. Administering vitamin A in the lipid emulsion increases actual delivery to 90 % [85]. Enterally administered vitamin A, either from human milk or formula may not adequately improve vitamin A status, as enterally administered supplemental doses of as much as 5,000 IU/kg/day from postnatal day 1 through 28 did not increase plasma levels by day 7 or day 28, nor were there significant differences in survival, oxygen requirement at 28 days or 36 weeks’ gestational age, or survival without BPD [86]. The current recommendation is to provide a 5,000 IU intramuscular dose three times per week for 4 weeks (12 doses total) for infants ≤1,500 g birth weight or <32 weeks’ gestational age [37, 87]. A confounding factor exists at this time in that vitamin A is not currently available due to drug industry shortages.

Although vitamin E deficiency may be associated with oxygen toxicity, there currently is no evidence that supplementing vitamin E beyond sustaining normal serum levels has benefit. Vitamin E deficiency is characterized by mild hemolytic anemia (>10 % erythrocyte hemolysis in hydrogen peroxide) and a serum vitamin E level of <0.6 mg/dL [88]. Risk of sepsis and NEC may be increased if serum levels exceed 3.5 mg/dL [89]. Earlier reports of vitamin E deficiency in preterm infants occurred when formulas had high concentrations of polyunsaturated fatty acids and low levels of vitamin E. Current vitamin E content of infant formulas and human milk fortifiers as well as parenteral multivitamin preparations provide adequate intake without additional supplementation [88, 89].

Selenium plays a role in the enzyme system glutathione peroxidase and superoxide dismutase. Both function as intracellular antioxidants in the lung and other organs, thus selenium may theoretically play a role in protecting lung tissue from oxidative damage. Selenium deficiency has not been described in preterm infants, although low serum concentrations of selenium and glutathione peroxidase have been reported in infants on selenium-free parenteral nutrition. Although animal studies show increased risk of oxidative lung injury with low selenium level, reported symptoms of selenium deficiency in humans include cardiac and skeletal myopathy, but not respiratory compromise [43, 51]. One study reported that preterm infants who developed chronic lung changes had lower serum levels of selenium (38.5 ± 14.1 μg/L) at 30 days of age than infants who did not (45.5 ± 18.7 μg/L), although diet was not reported [90]. Normal serum selenium levels are 45–90 μg/L in infants 0–2 months of age [91]. Supplementation of selenium above the amounts available in breast milk and infant formula has not been shown to reduce the risk of BPD [92].

Inositol

Inositol is a component of membrane phospholipids and plays a role in lung epithelial cell differentiation and the synthesis of lung surfactant during fetal development [51]. Earlier studies showed reduction in death or progression of lung disease in infants with RDS who were supplemented with parenterally administered inositol in doses of 80 mg/kg/day for 5 days or 120 mg/kg/day for 10 days, or enterally administered inositol doses of 160 mg/kg/day for 10 days [93, 94, 95]. Subsequent studies have not been reported, perhaps because the production of endogenous surfactant is not as critical since the advent of surfactant replacement therapy. Inositol content of current parenteral nutrient admixtures is 1.6–2 mg/dL; colostrum of mothers of preterm infants is 35–45 mg/dL; colostrum of mothers of term infants is 18–48 mg/dL; and mature milk is 12–31 mg/dL [96, 97]. Current recommendations for intake and formula content are given in Table 4.2. Although plasma levels of inositol decline during the first month of life, particularly in infants who receive most of their nutrition parenterally, clinical outcomes do not correlate with plasma levels and inositol is not currently added to parenteral nutrition admixtures [98].

Transient Tachypnea of the Newborn

Because TTNB is caused by inadequately cleared alveolar fluid, it is reasonable that fluid management might impact respiratory outcome. During the first 3 days after birth, a healthy breast fed term infant receives between 2 and 20 mL per feeding, or about 100 mL of breast milk per day [31]. This intake provides approximately 25–40 mL/kg/day of fluid. Although TTNB usually resolves within the first 72–96 h, nipple feedings may be delayed if respiratory support is required, and intake may include parenteral as well as enteral fluids. In one study report, the standard of care for combined parenteral and enteral fluid administration for term infants was 60 mL/kg/day and for late preterm infants 80 mL/kg/day. When fluids were restricted to 40 mL/kg/day and 60 mL/g/day, respectively, mimicking low fluid intakes normally taken at breast, the duration of respiratory support required for infants with severe TTNB was significantly decreased, and was safe for all patients studied. Urine output did not fall below 1 mL/kg/h, weight loss did not exceed 10 % of birth weight, and there was no difference between the standard and restricted fluid groups for incidence of hypoglycemia or need for phototherapy [36].

Meconium Aspiration Syndrome

Nutrition becomes an important factor in the management of MAS only when the severity of respiratory compromise requires treatment with ECMO [10, 17]. The use of high frequency ventilation (HFV) and nitric oxide (iNO) in combination has proved very successful in treating severe hypoxemia associated with MAS, and has reduced the need for ECMO. In geographical areas where HFV and iNO are not available, or when hypoxemia is severe and does not respond to other therapies, ECMO may still be required.

Infants receiving ECMO have markedly elevated levels of C-reactive protein and demonstrate significant, though quite variable negative nitrogen balance. Reported average protein losses of 2.3 ± 0.6 g/kg/day translate to a significant reduction in total body protein over a typical 8 day ECMO course of therapy due to increased protein turnover, increased protein degradation, and increased amino acid oxidation [59]. Although both protein and energy intake affect nitrogen balance, excess energy intake may increase carbon dioxide production and further complicate respiratory support. Current nutrition recommendations for infants receiving ECMO are to start nutrition support as soon as possible, provide 2.5–3 g protein/kg/day, and also provide at least 80 kcal/kg/day to minimize amino acid oxidation, but not more than 100 kcal/kg/day to prevent increased carbon dioxide production [17, 59]. Increased protein needs due to increased protein degradation may continue for 3 or more weeks after weaning from ECMO therapy [99].

Parenteral nutrition is the primary initial source of nutrition for infants receiving ECMO, to provide an immediate source of adequate nutrition and provide a period of time to assess gastrointestinal tract perfusion and motility. Provision of parenteral lipids using the ECMO circuit may increase the frequency of clot development and disruption of normal ECMO blood flow. The current recommendation is to administer parenteral lipids through a separate intravenous access to avoid increased risk of clot formation [60]. When the infant is clinically stable, enteral feedings can generally be started and are well tolerated without complication. Infants who cannot advance to full oral feedings within 1 month are more likely to require longer hospitalization and tube feedings at discharge [17, 100].

Bronchopulmonary Dysplasia

The nutritional strategies for preventing BPD are discussed in the RDS section of this chapter. Infants with RDS who develop BPD have additional nutritional challenges. These infants may be less likely to achieve reference growth during the first year after discharge or beyond [101, 102]. Nutrient needs during convalescence may be greater than their healthy counterparts, yet they are also are more likely to experience feeding difficulties [67, 85, 102, 103]. Drugs frequently used in this population may also affect nutritional status, including diuretics, corticosteroids, bronchodilators, and antibiotics.

Nutrient Intake and Growth

Numerous reports are available documenting impaired growth and growth recovery, with deficits in total body fat and fat free mass in infants with BPD [51, 101, 102, 104]. The growth of infants with BPD has improved during the past 10 years, particularly with improved nutrition during the 1–3 weeks of life, but also with improved nutrient intake throughout hospitalization and after discharge [62, 66, 67, 85, 105]. Very low birth weight infants whose documented weight gain is at least 21 g/kg/day during initial weeks of hospitalization demonstrate better growth and developmental outcomes at 18–22 months’ corrected age [83]. Although rapid weight gain during infancy may be a risk factor for increased adiposity later in life, infants who demonstrate postnatal growth delay between 4 and 36 months’ corrected age are more likely to have smaller physical size, lower cognitive scores, and lower academic achievement at age 8 [53, 106].

Infants who receive at least 3.3 g protein/kg/day protein during the first 20 days of life and receive energy intakes of 120 kcal/kg/day earlier are more likely to achieve intrauterine growth rates than those who receive less protein and take longer to reach feeding goals [62]. Energy needs of preterm infants with CLD may be 15–25 % higher than healthy preterm infants due to increased work of breathing or recurrent infections. Providing 3.5–4 g protein/kg/day and 110–135 kcal/kg/day appear to be necessary to support normal growth in this population, although intakes greater than 135 kcal/kg/day may not provide additional benefit [51, 52, 54, 63, 64]. When energy needs are greater due to increased work of breathing or recurrent infections, or if fluid volume tolerance is less than 150 mL/kg/day, standard feeding regimens may not provide adequate protein or energy intake. Deficits begin to accrue, causing growth lag. Although the effect on weight is most readily observed, the head circumference is more likely to fall below the 10th percentile when growth does not keep pace with intrauterine rates and is associated with poor long-term developmental outcome [62, 83].

Most ready-to-use human milk fortifiers and preterm infant formulas provide 20, 22, or 24 cal per ounce. All are enriched in protein, mineral, and vitamin content to approximate established guidelines [39]. Ready-to-use preterm formulas that contain 30 cal per ounce and 3 g protein/100 kcal may be used during hospitalization alone or in combination with other standard caloric strength feedings to provide recommended intake of nutrients when fluid tolerance is less than 150 mL/kg/day and energy needs are 120 kcal/kg/day or greater.

Studies reporting nutritional strategies for the discharged infant with BPD are less definitive. Providing human milk fortification or formulas enriched with protein, vitamins, and minerals is associated with improved growth, bone mineralization, and increased lean body mass in preterm infants [98, 107, 108]. This may not be as evident in infants with BPD [67]. Infants with BPD are more likely to experience nutrient deficits and growth delay early in their neonatal course, which may confound results from studies that focus primarily on intake after discharge.

Nutrition strategies for discharge that include the use of modular products such as glucose polymers, vegetable oil, or medium chain triglyceride oil to increase energy intake when fluid tolerance is limited often do not provide adequate protein, mineral, or vitamin intake. Adding powdered formula to human milk in place of commercially available fortifiers does not provide the recommended intake of protein, minerals, and vitamins. Some infants may benefit from continued use of human milk fortification or preterm formula after discharge, depending upon weight at discharge. Product literature guidelines discourage intakes exceeding 20 packets of human milk fortifier per day or 355–540 mL per day of preterm infant formulas to prevent excessive intake of individual nutrients. Manufacturers’ guidelines also include information regarding use, storage, and preparation. Preterm infant discharge formulas are available for use through 9–12 months of age, and may be concentrated to 22, 24, or higher caloric density using product literature guidelines. Standard pediatric formulas have been used with some success, although these may require vitamin supplementation, as these products are intended for older children [109].

Feeding Problems

Feeding difficulties for infants with BPD may be related to several factors. Successful feeding requires the ability to efficiently coordinate a pattern of suck—swallow—breathe for a long enough period of time to allow consumption of an adequate volume of feeding to support normal growth and development. Infants with severe BPD may have poor feeding coordination and endurance. These infants may need to breathe more frequently, stop breathing for a longer period of time to swallow, suck less frequently with weaker pressures, and swallow less often than infants without BPD or with mild to moderate BPD [110]. Mild to moderate oxygen desaturation may continue to be a problem for infants with moderate to severe BPD up to 2–6 months corrected age, a factor that may also be linked to growth lag [111]. Oral aversion may develop in infants with BPD who require prolonged need for ventilator equipment, orogastric feeding tube placement, or tape placed near the mouth. Feeding therapists can design strategies to reduce noxious oral–facial stimulation and develop individual feeding plans to help pace feedings and increase oral feeding success. When infants continue to require tube feedings after hospital discharge, dietitians can provide a feeding plan that accommodates hunger and satiety cues, and provide guidelines for increments in feeding volumes to support growth but prevent overfeeding [112]. Spoon feedings may be started at 4 months’ corrected age. These foods are of thicker consistency than milk or formula, so they may be swallowed more easily and can provide pleasant oral stimulation for the infant with residual respiratory problems [51].

Drugs That Affect Nutrition

Several drugs frequently used in the treatment of BPD may affect nutritional status. Glucocorticoids have been used for their anti-inflammatory effect since lung tissue inflammation plays a key role in the pathogenesis of BPD. Dexamethasone is the most widely studied glucocorticoid, with numerous reports documenting efficacy in down-regulating lung inflammation, reducing pulmonary edema, facilitating extubation, and reducing the risk of CLD. However, dexamethasone given in doses of approximately 0.5 mg/kg/day at or before 7 days of age has also been associated with short-term adverse outcomes such as gastrointestinal bleeding, intestinal perforation, hyperglycemia, and growth failure [113]. All parameters of physical growth are negatively affected by high dose dexamethasone administration, but growth resumes off treatment, and protein intake correlates positively with weight gain [68]. Doses of 0.35 mg/kg/day are associated with decreased weight gain and increased proteolysis, though not decreased protein synthesis. These differences are no longer apparent when the dexamethasone dose is weaned to 0.1 mg/kg/day [114]. However, early high dose dexamethasone is no longer recommended due to long-term adverse outcomes of neurodevelopmental compromise and cerebral palsy [113]. Hydrocortisone, another corticosteroid currently used in the treatment of infants with BPD, is not associated with adverse neurodevelopmental or growth outcomes, although gastrointestinal perforation remains a significant risk [113]. Betamethasone is a corticosteroid given to mothers who are at risk for delivering before 34 weeks’ gestational age to reduce infant mortality and decrease severity of RDS [20]. Multiple courses of antenatal corticosteroids are associated with decreased fetal growth in weight, length, and head circumference. The long-term implication of these findings and whether or not postnatal protein needs are affected remains unknown [115].

Diuretics are useful in the management of pulmonary edema, which is characteristic of both early and later stages of BPD. The diuretics most commonly used in neonates are furosemide, chlorothiazide, and spironolactone. Furosemide is associated with hyponatremia, hypokalemia, hypochloridemia, and hypercalciuria. Chronic use may cause nephrocalcinosis and bone demineralization, which may be attenuated by concurrent use of chlorothiazide. Hypokalemia is more common with chlorothiazide, often requiring potassium supplementation unless used concurrently with spironolactone, which is potassium sparing. Electrolyte abnormalities occurring with any diuretic may be associated with growth failure. Monitor electrolyte levels regularly and supplement as needed. When diuretics are being used, optimize calcium and phosphorus intake for preterm infants by using preterm infant formula or preterm follow-up formula, and use human milk fortifier for preterm infants receiving their mothers’ milk or donor milk. All diuretics may increase renal calcium and phosphorus losses in preterm infants and may lead to osteopenia [69, 70]. If use of other formulas is indicated for reasons of intolerance or allergy, mineral supplements may be needed to prevent osteopenia. Standard infant formulas may not provide adequate amounts of vitamin D for infants who have not reached term.

Aminoglycosides and vancomycin are antibiotics that may be used frequently for the treatment of infections in ELBW infants, who are also at highest risk for developing BPD. These antibiotics, particularly when used in tandem, may alter renal function, causing increased tubular losses of potassium and phosphorus during drug therapy and for 1–2 weeks after cessation of treatment. Calciuria may also be present, although increased calcium excretion may be due to phosphorus depletion and decreased bone deposition. Potassium and phosphorus supplements may be needed to normalize serum levels [71].

Chylothorax

When chylothorax does not resolve spontaneously, nutritional strategies are designed to provide optimal nutrition either parenterally or enterally, the latter without increasing the production of chylous leakage into the pleural cavity. Parenteral nutrition may be required to reduce the flow of lymph and insure adequate nutrient intake, particularly of protein, fat (thus energy), fat soluble vitamins, and electrolytes. If chyle accumulation increases when feedings are started, using medium chain triglycerides in place of long chain triglycerides may reduce the flow of lymph from the thoracic duct and prevent reaccumulation of chyle [26, 28].

Repeated thoracentesis may cause protein, energy, and electrolyte depletion. Protein intake recommendations are based on standards for gestational age and non-edematous body weight. When long chain triglycerides must be restricted, mother’s milk can be defatted, the fat replaced with medium chain triglycerides, and protein increased with fortification. Several commercially available formulas contain at least a portion of the fat content as medium chain triglycerides. See Table 4.4 for strategies using breast milk or formula to treat chylothorax.
Table 4.4

Nutrient content of various feeding regimens to limit long chain fatty acid intake for treatment of chylothorax

Nutrient

Standard infant 20 kcal/oz

Preterm infant formulaa 24 kcal/oz

Pregestimil®b 20 kcal/oz

Enfaport®b 30 kcal/oz

Defatted human milkc

Defatted human milkc/Enfaport®d

Defatted human milkc/SHMFe

Defatted human milkc/soy/MCTf

Volume (mL)

148

124

148

100

100

147

143

148

Energy (kcal)

100

100

100

100

33–36

100

100

100

Protein (g)

2.1–2.5

3.3

2.8

3.5

0.9

3.2

2.9

2.9

Fat (g)

5.3–5.5

5.4

5.6

5.4

0–0.35

4–4.2

4.8–5.1

5.1–5.5

MCT oil (%)

0

50

55

84

79–84

80–87

76–88

Linoleic acid (mg)

860–1,000

700

940

350

0–50

257–294

356–389

330–395

Carbohydrate (g)

10–11

10

10.2

10.2

7.3

12.8

10.6

9.5

Calcium (mg)

78

180

94

94

28

90

112

37

Vitamin A (IU)

300

1,250

350

350

257

401

Vitamin D (IU)

60

150

50

50

37

78

Vitamin E (IU)

2

4

4

4

2.9

2.1

Vitamin K (IU)

9

12

12

12

8.8

5.4

Zinc (mg)

0.75–1

1.5

1

1

0.24–0.38

0.9

1

0.3

aSimilac® Special Care® 24 high protein (Abbott Nutrition). Other preterm formulas contain less MCT and more long chain triglycerides

bPregestimil® and Enfaport® (Mead Johnson & Company)

cDescription of the process to remove fat from human milk is described elsewhere. Residual fat after processing was reported by the authors to be zero [28]. After a similar defatting process at Bronson Mothers’ Milk Bank, fat content of milk was 0.35 g/100 mL (Duff C. Bronson Mothers’ Milk Bank, Bronson Children’s Hospital, Kalamazoo, MI. 20 Nov 2012, Personal communication). Other nutrient values are representative [28, 116, 117]

dDefatted human milk/Enfaport® is a 1:1 mixture of defatted human milk and Enfaport®

eDefatted human milk/SHMF is 100 mL of defatted human milk + 2 packets of Similac® human milk fortifier (Abbott Nutrition) + 0.4 mL soy oil + 3.5 mL MCT oil + 5 mL Liquid Protein Fortifier® (Abbott Nutrition). Fat content of Similac® human milk fortifier is MCT. Other human milk fortifiers contain long chain triglycerides. Liquid Protein Fortifier® contains 1 g extensively hydrolyzed casein, 4 kcal, and 5 g water per 6 mL

fDefatted human milk/soy/MCT is 100 mL of defatted human milk + 0.5 mL soy oil + 4 mL MCT oil + 8 mL Liquid Protein Fortifier®. This feeding requires fat soluble vitamin supplementation. See text

Summary

Nutrition plays an important role in the health and well-being of the newborn infant, particularly when respiratory disease occurs and interrupts the normal initiation and progression of breast or bottle feedings. This chapter provides guidelines for the nutritional management of infants who develop respiratory compromise during the their first weeks of life, to minimize the nutritional impact of preterm birth, and adjust for the different nutritional demands related to pulmonary compromise and the medical therapies used to treat pulmonary diseases in this population.

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© Springer Science+Business Media, LLC 2014

Authors and Affiliations

  1. 1.SchoolcraftUSA

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