Chronic Lung Disease (CLD) or Bronchopulmonary Dysplasia (BPD) is a disease of premature babies who required prolonged support with their breathing and supplemental oxygen. These babies are at high risk of many short and long term problems with their breathing, growth and development, including death in infancy or childhood. Studies have shown that these babies have higher energy expenditure and lower energy intake compared with babies without CLD/BPD. Increasing energy intake for these babies beyond standard levels may therefore seem beneficial. However, setting high targets for energy intake for these babies may not be achievable. Furthermore, methods of increasing energy intake, like increasing the milk volume or concentration, or giving intravenous nutrition, may lead to complications of their own. We planned to examine whether increasing energy intake for these babies improves their breathing status, their growth and development, and reduces their risk of death without producing significant complications. Having found no suitable study to date that answers these questions, we are currently unable to provide any evidence on whether increasing the energy intake for babies with (or developing) CLD/BPD is overall beneficial.
Infants with CLD have increased energy expenditure compared to preterm infants without CLD (Denne 2001).This has been attributed to persistent airway inflammation secondary to lung injury from various aetiologies (Pierce 1995), leading to disordered pulmonary mechanics and increased work of breathing (Lui 2000). However, work of breathing cannot completely account for the higher energy expenditure in these infants (Kurzner 1988a). The demonstration of increased pulmonary oxygen consumption has provided new insights into the possible sources of energy expenditure (Schulze 2001). In spite of this increased expenditure in energy, decreased intake is often observed in these infants, as a result of poor sucking and iatrogenic fluid restriction (Wilson 1991). Increased energy expenditure and decreased nutrient accretion may account for the perpetuation of their respiratory morbidity, and worsen the growth deficits already experienced by preterm infants after the first few weeks (Embleton 2001). In the long term, CLD is a risk factor for growth failure (Kurzner 1988b), respiratory morbidities (Northway 1990) and neurodevelopmental disabilities (Singer 1997). These morbidities are compounded by the use of corticosteroids, which have been shown to have at least a temporary growth retarding effect during the course of treatment (Leitch 1999) and a possible association with increased rates of abnormal neurological examination and cerebral palsy (Halliday 2004a).
Along with other treatments, the addition of certain nutrients or an increase in the overall energy intake for infants with CLD may be beneficial in decreasing these adverse effects and improving outcomes. There are now many studies assessing the role of specific nutrients like vitamin A and antioxidants in CLD (Darlow 2004; Suresh 2004). Less clear is the role of an increase in overall energy intake; there has not been any evidence-based recommendation on the optimal energy intake for infants with CLD (Atkinson 2001).
To increase energy intake enterally, one can increase the energy content and/or the volume of feed. In infants with CLD, increasing fluid volume is an issue of concern, as there is evidence that restricted fluid intake early in life in very low birth weight infants possibly reduces the risk of developing CLD, compared with liberal fluid intake (Bell 2004). Parenteral nutrition alone does not provide adequate energy to meet the needs of preterm infants, and there have been reports associating the use of parenteral nutrition with the development and worsening of CLD (Hammerman 1988; Cooke RW 1991). Compared with fat-based supplements, feeding infants at increased energy level with carbohydrate as the main non-protein fuel confers benefits in better weight gain and net protein accretion, but also produces some less desirable metabolic consequences, including higher energy expenditure and O2 consumption, higher CO2 production and increased cardiorespiratory work (Kashyap 2001). Other reported complications with various strategies to provide increased energy feeding were feed intolerance, necrotising enterocolitis, symptomatic PDA and sepsis (Sutphen 1988; Hallstrom 2003; Lucas 1996; Donnell 2002; Schiff 1993).
Although the definition of optimal growth for preterm infants is still subject to debate (Cooke RJ 2003), recommendations have been made on their energy intake. Currently, the standard energy intake for a newborn is commonly accepted as 120 kcal/kg/day, and recommendations for preterm infants from different authorities range from 98 kcal/kg/day to 135 kcal/kg/day (Klein 2002). This range of energy values was found by different studies to be required to cover for variations in the energy expenditure of preterm infants, while providing sufficient energy to approximate intrauterine growth rates (Klein 2002), and could hence be regarded as standard range of energy intakes. Energy levels beyond this range were used to achieve greater growth than intrauterine rates or to compensate for deficits, and could be considered as increased intakes. Currently the maximum achievable energy intake for preterm infants with positive benefit-risk balance is not known (Klein 2002). The definition of "standard" and "increased" intakes will probably change with changes in the definition of standard growth for preterm infants. A fluid limit of 150 ml/kg/day is assumed when making nutritional recommendations, although some in practice raise the limits up to 180 to 200 ml/kg/day (Klein 2002). The differences in the energy contents of feed and in fluid regimes lead to variations in the working definitions of standard and increased energy intakes. These intakes may not be consistently achieved in practice (Carlson 1998).
This review aims to examine the effect of increased energy intake on mortality and respiratory, growth and neurodevelopmental outcomes for preterm babies with (or developing) CLD. We also assess whether increased energy intake in these infants is associated with significant complications.
In these infants, is increased energy intake associated with any significant complication compared to standard energy intake?
Subgroup analysis will be performed if available for the following:
i) Trials using enteral and/or parenteral methods of delivering increased energy intake
ii) Trials using standard fluid volumes and increased fluid volumes to achieve increased energy intake
iii) Trials providing additional energy using predominantly protein, carbohydrate or fat, or mixtures of equal proportions (in terms of caloric values)
iv). Infants with established CLD/BPD and those considered as developing CLD/BPD (as detailed in Types of Participants)
Infants considered as having BPD/CLD should fulfil the following criteria:
Oxygen dependence at 28 days after birth or at 36 weeks postmenstrual age and/or typical chest x-ray changes.
Infants considered as developing BPD/CLD should fulfill the following
criteria:
i) Less than 14 days of life at recruitment
ii) Oxygen dependent
including those who are ventilated
These criteria are set so there will be sufficient periods of intervention for the assessment of clinically important outcomes, such as days on oxygen and CLD at day 28 or at 36 weeks corrected age.
Increased energy feedings may include any of the following approaches:
i) Enteral feeding using energy-enriched formula or fortified breast milk with the same feed volume as the control group. Energy-enriched formula or fortified breast milk should contain energy value higher than that of the standard preterm formula (80 kcal/100 ml)
ii) Enteral feeding using higher feed volume than the control group, with either energy-enriched formula, standard preterm formula, fortified or unfortified breast milk or standard term formula, alone or in any combination. The targeted feed volume in the experimental group should exceed 150 ml/kg/day
iii) Enteral feeding using nutrient supplements to boost energy intake in addition to the standard feeding regime. Nutrient supplement can be given in the forms of protein, carbohydrate, fat or a mixture
iv) Parenteral feeding alone
v) Enteral and parenteral feeding combined, in any proportion
The targeted level of increased energy intake will be accepted as variously defined by the authors of the included trials, but must be greater than 135 kcal/kg/day.
Standard energy feeding:
The targeted level of standard energy intake will be accepted as variously defined by the authors of the included trials. However a range between 98 to 135 kcal/kg/day will be set to avoid the inclusion of studies with unusual practices.
The intervention may commence as soon as the infant is considered to be developing BPD/CLD, as detailed in "Types of participants". For trials assessing long term outcomes like growth and neurodevelopment, the intervention may commence before or after discharge. The intervention should be given for at least one month.
1. Number of infants with CLD at 28 days after birth or at 36 weeks postmenstrual age
2. Neonatal mortality (mortality within 28 days of life)
3. Number of infants with CLD or neonatal mortality
Secondary outcome measures
4. Other short term respiratory
outcomes including:
i) Days on oxygen
ii) Days of assisted ventilation
iii) Number of
extubation failures (re-intubation within 24 hours of prior extubation)
iv)
Number of infants with pneumothorax
v) Number of infants needing additional
treatment for BPD/CLD (steroid, bronchodilators)
vi) Number of infants
needing home oxygen
5. Combination of relevant outcomes including:
i) Days on oxygen in survivors beyond 28 days of life
ii) Days of assisted
ventilation in survivors beyond 28 days of life
iii) Number of infants with
pneumothorax and/or neonatal mortality
iv) Number of infants needing
additional treatment for BPD/CLD (steroid, bronchodilators) or neonatal
mortality
v) Number of infants needing home oxygen or neonatal mortality
6. Long term respiratory outcomes, including the likelihood of wheeze or asthma (assessed during the follow-up periods of the included studies)
7. Growth: weight, length and head circumference at term and at discharge, and longer term growth including weight, height and head circumference assessed at 6-12 months of corrected age, or at 12 - 18 month of corrected age and beyond
8. All-cause mortality (during the follow-up periods of the included studies)
9. Neurodevelopmental disabilities at or after 12 months of corrected age, assessed using validated tools like Bayley Scales of Infant Development, including diagnosed cerebral palsy, blindness or deafness
10. Mortality or neurodevelopmental disabilities
11. Cognitive and educational outcomes at school age (more than five years old), assessed using intelligence quotient and/or indices of educational achievement measured using validated assessment tools, including school examination results
Possible complications associated with increased energy intake, as follows:
12. Feed intolerance, including gastroesophageal reflux (diagnosed clinically, or via upper GI contrast studies or pH probe studies)
13. Necrotising enterocolitis - any stage, as defined by Bell criteria (Bell 1978)
14. Sepsis (bacterial and fungal - proven by blood culture)
15. Patent ductus arteriosus (echocardiographically proven or clinically diagnosed and treated)
16. All other parenteral nutrition and central line associated complications, including thromboembolism, pericardial tamponade (diagnosed with doppler ultrasound and echocardiography respectively), TPN extravasation and thrombophlebitis (diagnosed clinically).
The following words and MeSH terms were included:
<bronchopulmonary
dysplasia> or <chronic lung disease>, preterm, prem$, low birth weight,
feed$, nutrition, energy, intake, calorie, enteral, parenteral, increased
energy, high energy, formula, milk, volume. Search output will be limited to
clinical trial (PT), human, all infants: birth - 23 months (children), with no
language restriction.
The studies were accepted whether published or unpublished, in full article or abstract form, as long as assessment of study quality was possible and where the other inclusion criteria were fulfilled. If studies were published as abstracts, the authors would be contacted for further information.
Authors of all studies identified to be relevant would be contacted where possible to clarify details of reported follow-up studies where necessary, or to obtain any information about long-term follow-up where none had been reported, and to enquire about additional studies potentially suitable for inclusion.
We examined references cited in previous relevant Cochrane reviews, in other relevant studies, review articles, standard textbooks and manuals of neonatal medicine. Hand search results from the Cochrane Neonatal Review Group were also assessed. Relevant information from expert informants on additional published and unpublished studies was also sought.
2. Two reviewer authors (LNM and KTAN) would independently assess the methodological quality of the included trials, using the standard methods of the Cochrane Neonatal Review Group. Specifically, the trials would be assessed on the following: allocation concealment, blinding of intervention, completeness of follow up, intention to treat analysis, blinding of outcome measurement and other information like being single or multicentred. The authors of the relevant trials would be contacted if additional information was needed to assess the methodological quality.
3. Both reviewer authors (LNM and KTAN) would independently enter individual data from each included trial using a standardised data collection form. The data entered would be compared, and differences resolved by consensus. The authors of the relevant trials would be contacted if additional data was required.
4. Statistical analysis would follow the procedures of the Cochrane Neonatal Review Group. For categorical data, relative risk, risk difference and NNT would be used with their respective 95% confidence intervals. For continuous data, weighted mean difference would be used with 95% confidence interval. Meta-analysis of the included trials would be performed with RevMan 4.2, using a fixed effects model.
5. The treatment effects of individual trials and the heterogeneity between trial results would be assessed by inspecting the forest plots. I2 test would be used to measure inconsistency in the studies' results. If significant heterogeneity was detected, the causes would be explored (for example, difference in study quality, participants, intervention or outcome assessment) via post hoc sub group analyses.
Atkinson 1999 randomized 70 premature infants with birth weight < 1800 g to either a nutrient-enriched formula or standard formula just prior to discharge, with follow up to 12 months of corrected age. Although not explicitly stated, infants with CLD/BPD were excluded, as inferred by the exclusion criteria of "severe lung disease".
Brunton 1998a randomized 60 preterm infants with bronchopulmonary dysplasia to either nutrient enriched formula (90 kcal/100 ml, high-protein, high mineral) or standard formula with the same energy density, with outcome assessment performed at three months corrected age. The study took place between January 1991 and November 1994. Brunton 1998b, although published one year earlier (1997) in abstract form, was a follow-up study to Brunton 1998a. In this study, the same group of infants were followed up until 12 months of corrected age, after their nutritional intervention ceased at three months corrected age. The two groups of infants were not allocated to receive different feed volumes, hence their overall energy intakes were not designed to be different. During the follow up-period after three months of corrected age, the overall energy intakes for the participants were also not controlled or compared.
Fewtrell 1997 randomized 60 preterm infants who were still in oxygen at 28 days of age to either high-density formula (100 kcal/100 ml) at 145 ml/kg/day or standard preterm formula (80 kcal/100 ml) at 180 ml/kg/day. Although the results showed a difference in the mean total energy intakes between the high energy group and the standard-energy group (143.3 kcal/kg/day vs 130.5 kcal/kg/day), the intended energy intake for both groups was 145 kcal/kg/day.
Sosenko 1993 randomly assigned 133 ventilator-dependent premature infants to either early intralipid (< 12 hours of life) or to control group (intralipid after day seven). The study was not designed to compare different levels of energy intake.
Wilson 1997 randomized 125 sick VLBW babies to either a standard nutritional regimen or a more aggressive intervention: either earlier and/or more rapid increment of parenteral carbohydrate, amino acids, lipid and enteral feeds. The study was not designed to compare different levels of energy intake. Although the results showed a difference between two groups in their mean energy intakes, the intakes for all babies were consistently lower than 120 kcal/kg/day.
The other studies identified during our search include Alwaidh 1996; Brownlee 1993; Carlson 1996; Guzman 2001; O'Connor 2003 and Pereira 1994. They are listed with the reasons of their exclusion in "Characteristics of excluded studies".
In Brunton 1998a, VLBW infants with CLD/BPD who reached 37 weeks postmenstrual age were randomized to receive one of two formulas, both with identical high energy content at 90 kcal/100 ml but one enriched with protein and minerals. The enrolled infants were fed the assigned formulas according to the nursery protocol while still in hospital, and were fed ad libitum after discharge home until three months of corrected age. Outcome assessments were performed at one and three months of corrected age. It was found that the experimental group with enriched protein and minerals in their feed had significantly higher daily intakes of protein, calcium, phosphorus and zinc at one and three months. They also had greater length, lean body mass and bone mineral content, with greater nitrogen and mineral retention. This study focused on growth, nutrient intake and retention as its primary and secondary outcomes, with no assessment on respiratory outcomes. In fact, one infant was excluded from analysis due to death from respiratory complications. The same was true for the follow-up study (Brunton 1998b), in which growth, nutrient intake and retention at six and 12 months of corrected age were assessed, although the results showed that the growth advantages of the experimental group at one and three months were lost by 12 months of age.
In Fewtrell 1997, infants with CLD/BPD were randomized at four to eight postnatal weeks to receive either a formula of standard energy density (24 kcal/oz) or a formula enriched with energy (30 kcal/oz), protein, carbohydrate, fat, minerals and vitamins. However, the feed volumes were reciprocally adjusted to provide the same overall nutrient and energy intakes for both groups (145 kcal/kg/day). The participants were fed the assigned formula until discharge home, or until three months of corrected age. Although there was a significant difference in the total energy consumed per day between the two groups [143.3 kcal/kg/day (high-energy group) vs 130.5 kcal/kg/day (standard energy group)], the differences between two groups in the energy and protein intakes from the trial formulas failed to reach statistical significance (energy: 133.6 kcal/kg/day vs 126.7 kcal/kg/day; protein: 3.6 g/kg/day vs 3.4 g/kg/day). Neither group achieved the pre-designated energy intake of 145 kcal/kg/day, as both groups were unable to feed to the targeted volumes. The standard formula group received 155.5 ml/kg (target 180 ml/kg/day). This volume of intake significantly exceeded that of the high-energy-density group (mean daily volume: 131.3 ml/kg). The mean total fluid intake of the standard formula group (combining the trial formula, expressed breast milk and intravenous fluid) was 164.7 ml/kg/day, compared to the high-energy-density group with 148.3 ml/kg/day. There was no difference between the two groups in growth, respiratory outcomes, oedema and diuretic requirements.
The authors tested two main hypotheses. First, nutrient intake and growth of infants with CLD would be improved by providing nutrients in a more concentrated form. It was unclear how nutrient intake could be tested in this study, since by adjusting the targeted feed volumes according to the energy density of the assigned formulas, the energy and nutrient intakes for both groups were set at identical level. The second hypothesis was that lower volume of intake would improve respiratory status. Although both groups were unable to achieve the targeted feed volumes, the mean daily volume of intake for the high-energy group was significantly lower than that of the standard-energy group. There was no difference found between the two groups in respiratory status. The failure to achieve the targeted feed volume was not attributed to feed intolerance, as the formulas were well-tolerated by both groups, with no significant differences between the groups in the incidence of vomiting, abdominal distension and the volume of gastric aspirate. The authors suggested that the difference between the targeted and achieved volumes of intake might be explained by the subconscious reluctance of the attending staff to make up missed or incomplete feeds, or to replace gastric aspirates for fear of "fluid overload" in the high-volume group. In addition, since one-third of the infants received expressed maternal breast milk and 18% received intravenous fluid on top of their assigned formulas, it was possible that the assigned formulas were not advanced to the full targeted volumes, as caregivers might have thought that breast milk and/or intravenous fluid were providing sufficient additional fluids.
Important points for future studies could be gleaned from this study. First, setting high target feed volumes to increase energy intake might not be clinically realistic for infants with CLD/BPD. Instead, to examine the effects of increased energy intake, it might be more realistic to keep the feed volume constant for both groups and vary the energy density of the trial formula. A possible fluid volume to be targeted would be 165 ml/kg/day, which was shown by this study to be potentially achievable, without increased adverse effects on respiratory function or feed tolerance compared to lower fluid volumes. Second, it is important to ensure that the pre-specified volumes of the trial formulas be achieved where clinically possible, regardless of the contribution of the other sources of energy intake, like breast milk or intravenous fluid.
| Study | Reason for exclusion |
| Alwaidh 1996 | No comparison between different energy intake. |
| Atkinson 1999 | Infants with CLD/BPD were excluded. |
| Brownlee 1993 | No comparison between different energy intake. |
| Brunton 1998a | No comparison between different energy intake. |
| Brunton 1998b | Follow-up study to Brunton 1998a. No comparison between different energy intake. |
| Carlson 1996 | No comparison between different energy intake. |
| Fewtrell 1997 | Comparison made between formula of high and standard energy densities, but feed volumes were adjusted in the study so both groups were designated to receive identical total energy intake of 145 kcal/kg/day. |
| Guzman 2001 | Non-randomised study. |
| O'Connor 2003 | No comparison between different energy intake. |
| Pereira 1994 | Single group of premature infants were examined. |
| Sosenko 1993 | No comparison between different energy intake. |
| Wilson 1997 | No comparison between different energy intake. |
Alwaidh MH, Bowden L, Shaw B, Ryan SW. Randomised trial of effect of delayed intravenous lipid administration on chronic lung disease in preterm neonates. Journal of Pediatric Gastroenterology and Nutrition 1996;22:303-6.
Atkinson 1999 {published data only}
Atkinson SA, Randall-Simpson J, Chang M, Paes B. Randomised trial of feeding nutrient-enriched versus standard formula to premature infants during the first year of life. Pediatric Research 1999;45:276A.
Brownlee 1993 {published data only}
Brownlee KG, Kelly EJ, Ng PC, Kendall-Smith SC, Dear PR. Early or late parenteral nutrition for the sick preterm infants? Archives of Disease in Childhood 1993;69:281-3.
Brunton 1998a {published data only}
Brunton JA, Saigal S, Atkinson S. Growth and body composition in infants with bronchopulmonary dysplasia up to 3 months corrected age: a randomized trial of a high-energy nutrient-enriched formula fed after hospital discharge. Journal of Pediatrics 1998;133:340-5.
Brunton 1998b {published data only}
Brunton JA, Saigal S, Atkinson SA. Nutrient intake similar to recommended values does not result in catch-up growth by 12 months of age in very low birth weight infants (VLBW) with bronchopulmonary dysplasia (BPD). American Journal of Clinical Nutrition 1997;66:221.
Carlson 1996 {published data only}
Carlson SE, Werkman SH, Tolley EA. Effect of long-chain n-3 fatty acid supplementation on visual acuity and growth of preterm infants with and without bronchopulmonary dysplasia. American Journal of Clinical Nutrition 1996;63:687-97.
Fewtrell 1997 {published data only}
Fewtrell MS, Adam C, Wilson DC, Cairns P, McClure G, Lucas A. Randomized trial of high nutrient density formula versus standard formula in chronic lung disease. Acta Paediatrica 1997;86:577-82.
Guzman 2001 {published data only}
Guzman JM, Jaraba MP, De La Torre MJ, Ruiz-Gonzalez MD, Huertas MD, Alvarez R et al. Parenteral nutrition and immature neonates. Comparative study of neonates weighing under 1000 and 1000 - 1250 g at birth. Early Human Development 2001;65 Suppl:S133-44.
O'Connor 2003 {published data only}
O'Connor DL, Jacobs J, Hall R, Adamkin D, Auestad N, Castillo M et al. Growth and development of premature infants fed predominantly human milk, predominantly premature infant formula, or a combination of human milk and premature formula. Journal of Pediatric Gastroenterology and Nutrition 2003;37:437-46.
Pereira 1994 {published data only}
Pereira GR, Baumgart S, Bennett MJ, Stallings VA, Georgieff MK, Hamosh M, Ellis L. Use of high-fat formula for premature infants with bronchopulmonary dysplasia: metabolic, pulmonary, and nutritional studies. Journal of Pediatrics 1994;124:605-11.
Sosenko 1993 {published data only}
Sosenko IR, Rodriguez-Pierce M, Bancalari E. Effect of early initiation of intravenous lipid administration on the incidence and severity of chronic lung disease in premature infants. Journal of Pediatrics 1993;123:975-82.
Wilson 1997 {published data only}
Wilson DC, Cairns P, Halliday HL, Reid M, McClure G, Dodge J. Randomised controlled trial of an aggressive nutritional regimen in sick very low birthweight infants. Archives of Disease in Childhood 1997;77:F4-11.
* indicates the primary reference for the study
Atkinson S. Special nutritional needs of infants for prevention of and recovery from bronchopulmonary dysplasia. Journal of Nutrition 2001;131:942S-6S.
Bell MJ, Ternberg JL, Feigin RD, Keating JP, Marshall R, Barton L et al. Neonatal necrotizing enterocolitis. Therapeutic decisions based upon clinical staging. Annals of Surgery 1978;187:1-7.
Bell EF, Acarregui MJ. Restricted versus liberal water intake for preventing morbidity and mortality in preterm infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Carlson SJ, Ziegler EE. Nutrient intakes and growth of very low birth weight infants. Journal of Perinatology 1998;18:252-8.
Cooke RJ. Nutrient requirements in preterm infants. Pediatric Research 2003;53:2.
Cooke RW. Factors associated with chronic lung disease in preterm infants. Archives of Disease in Childhood 1991;66:776-9.
Darlow BA, Graham PJ. Vitamin A supplementation for preventing morbidity and mortality in very low birth weight infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Denne SC. Energy expenditure in infants with pulmonary insufficiency: is there evidence for increased energy needs? Journal of Nutrition 2001;131:935S-7S.
Donnell SC, Taylor N, van Saene HK, Magnall VL, Pierro A, Lloyd DA. Infection rates in surgical neonates and infants receiving parenteral nutrition: a five year prospective study. Journal of Hospital Infection 2002;52:273-80.
Embleton NE, Pang N, Cooke RJ. Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants? Pediatrics 2001;107:270-3.
Halliday HL, Ehrenkranz RA, Doyle LW. Early postnatal (<96 hours) corticosteroids for preventing chronic lung disease in preterm infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Halliday HL, Ehrenkranz RA, Doyle LW. Delayed (> 3 weeks) postnatal corticosteroids for chronic lung disease in preterm infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Hallstrom M, Koivisto Am, Janas M, Tammela O. Frequency of and risk factors for necrotising enterocolitis in infants born before 33 weeks of gestation. Acta Paediatrica 2003;92:111-3.
Hammerman C, Aramburo MJ. Decreased lipid intake reduces morbidity in sick neonates. Journal of Pediatrics 1988;113:1083-8.
Horbar JD, Badger GJ, Carpenter JH, Fanaroff AA, Kilpatrick S, LaCorte M et al. Trends in mortality and morbidity for very low birth weight infants, 1991-1999. Pediatrics 2002;110:143-51.
Kashyap S, Ohira-Kist K, Abildskov K, Towers HM, Sahni R, Ramakrishnan R et al. Effects of quality of energy intake on growth and metabolic response of enterally fed low-birth-weight infants. Pediatric Research 2001;50:390-7.
Klein CJ. Nutrient requirements for preterm infant formulas. Journal of Nutrition 2002;132:1395S-1577S.
Kurzner SI, Garg M, Bautista DB, Sargent CW, Bowman CM, Keens TG. Growth failure in bronchopulmonary dysplasia: elevated metabolic rates and pulmonary mechanics. Journal of Pediatrics 1988;112:73-80.
Kurzner SI, Garg M, Bautista DB, Bader D, Merritt RJ, Warburton D, Keens TG. Growth failure in infants with bonchopulmonary dysplasia: nutrition and elevated resting metabolic expenditure. Pediatrics 1988;81:379-84.
Leitch CA, Ahlrichs J, Karn C, Denne SC. Energy expenditure and energy intake during dexamethasone therapy for chronic lung disease. Pediatric Research 1999;46:109-13.
Lucas A, Fewtrell MS, Morley R, Lucas PJ, Baker BA, Lister G, Bishop NJ. Randomized outcome trial of human milk fortification and developmental outcome in preterm infants. American Journal of Clinical Nutrition 1996;64:142-51.
Lui K, Lloyd J, Ang E, Rynn M, Gupta JM. Early changes in respiratory compliance and resistance during the development of bronchopulmonary dysplasia in the era of surfactant therapy. Pediatric Pulmonology 2000;30:282-90.
Ng GYT, da Silva O, Ohlsson A. Bronchodilators for the prevention and treatment of chronic lung disease in preterm infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Northway WH Jr, Moss RB, Carlisle KB, Parker BR, Popp RL, Pitlick PT et al. Late pulmonary sequelae of bronchopulmonary dysplasia. New England Journal of Medicine 1990;323:1793-9.
Parker RA, Lindstrom DP, Cotton RB. Improved survival accounts for most, but not all, of the increase in bronchopulmonary dysplasia. Pediatrics 1992;90:663-8.
Pierce MR, Bancalari E. The role of inflammation in the pathogenesis of bronchopulmonary dysplasia. Pediatric Pulmonology 1995;19:371-8.
Schiff DE, Stonestreet BS. Central venous catheters in low birth weight infants: incidence of related complications. Journal of Perinatology 1993;13:153-8.
Schulze A, Abubakar K, Gill G, Way RC, Sinclair JC. Pulmonary oxygen consumption: a hypothesis to explain the increase in oxygen consumption of low birth weight infants with lung disease. Intensive Care Medicine 2001;27:1636-42.
Singer L, Yamashita T, Lilien L, Collin M, Baley J. A longitudinal study of developmental outcome of infants with bronchopulmonary dysplasia and very low birth weight. Pediatrics 1997;100:987-93.
Suresh GK, Davis JM, Soll RF. Superoxide dismutase for preventing chronic lung disease in mechanically ventilated preterm infants. In: The Cochrane Database of Systematic Reviews, Issue 3, 2004.
Sutphen JL, Dillard VL. Effect of feeding volume on early postcibal gastroesophageal reflux in infants. Journal of Pediatric Gastroenterology and Nutrition 1988;7:185-8.
Wilson DC, McClure G, Halliday HL, Reid MM, Dodge JA. Nutrition and bronchopulmonary dysplasia. Archives of Diseases in Childhood 1991;66:37-8.
Dr Kenneth Tan
Assistant Professor
Department of
Paediatrics
McMaster University
Division of Neonatology, Room 4G37
1200
Main Street West
Hamilton
Ontario CANADA
L8N 3Z5
Telephone 1: 1 905
521 2100 ext: 76486
Facsimile: 1 905 521 5007
E-mail: ktan@mcmaster.ca
| This review is published as a Cochrane review in The
Cochrane Library, Issue 3, 2006 (see http://www.thecochranelibrary.com for
information). Cochrane reviews are regularly updated as new evidence emerges
and in response to feedback. The Cochrane Library should be consulted for
the most recent version of this review. |