Higher Fluid and Lower Caloric Intakes: Associated Risk of Severe Bronchopulmonary Dysplasia in ELBW Infants

doi:10.21203/rs.3.rs-3408262/v1

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Higher Fluid and Lower Caloric Intakes: Associated Risk of Severe Bronchopulmonary Dysplasia in ELBW Infants

https://doi.org/10.21203/rs.3.rs-3408262/v1

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Journal Publication

published 08 Mar, 2024

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Objective

To examine nutritional intake profiles and growth trajectories of extremely low birth weight (ELBW) infants who develop severe bronchopulmonary dysplasia (BPD).

Study Design

Case-control study using multiple logistic regression analysis with generalized estimating equations (GEE) to adjust for matching.

Results

Cumulative and mean fluid intakes were higher (p=0.003) and caloric intakes lower (p<.0001)through week two in infants who developed severe BPD (n=120) versus those without severe BPD (n=104). Mean caloric intake through week 12 was lower in infants who developed severe BPD (102±10.1 vs. 107±8.5 kcal/kg/day, p<0.0001). In logistic regression models, lower mean caloric intake through week 12 was associated with increased risk of developing severe BPD. Linear growth reduced the odds of BPD by ~30% for each Z-score point.

Conclusions

Higher fluid and lower total caloric intakes and reductions in linear growth were independently associated with an increased risk of developing severe BPD in ELBW infants.

Health sciences/Health care/Paediatrics

Health sciences/Diseases/Respiratory tract diseases

Biological sciences/Physiology/Respiration

Bronchopulmonary dysplasia (BPD) remains an important morbidity of prematurity without a change in its incidence despite advances in perinatal care and improved survival of extremely low birth weight (ELBW) infants (1). Although the pathogenesis of BPD is multifactorial including multiple prenatal and postnatal risk factors such as gestational age, birth weight, severity of lung disease, and the level of respiratory support (2, 3), postnatal malnutrition is an additional important factor that could be associated with the development of BPD.

Inadequate nutrition has been shown to reduce lung weight and alveolar number in animal models (4, 5). A number of retrospective studies have sought to evaluate nutritional intake in preterm infants who develop BPD with conflicting results. Wemhoner, et al. evaluated parenteral and enteral nutritional intakes in the first two weeks of life in 95 preterm infants and showed no differences in total fluid, caloric, or protein intake between the group of infants who developed BPD and controls who did not develop BPD (3). In contrast, Malikiwi, et al. examined nutritional intake in 66 preterm infants with and without BPD and showed that infants who developed BPD received lower calorie and in addition to lower fluid intakes in the first month of life (6). Both groups demonstrated that enteral intake was significantly lower in infants who subsequently develop BPD. Although inadequate nutritional intake has previously been associated with the subsequent development of BPD, less is known regarding the impact of reduced nutritional intake on the development of severe BPD.

Infants who develop severe chronic respiratory disease represent a distinct population with complex medical needs who have not as yet received much attention in the literature. Therefore, optimal management strategies to attenuate morbidity and optimize outcomes remain to be determined (7). In particular, there is a paucity of information regarding profiles of nutritional intake in ELBW infants and their association with the incidence of severe BPD. The present study was performed to examine nutritional intake profiles and growth trajectories of ELBW infants who develop severe BPD, and to test the hypothesis that infants with severe BPD have lower nutritional intake and delayed growth compared to control infants who do not develop severe BPD.

The present study was a retrospective observational case-control study involving infants weighing ≤ 1,000 g at birth admitted to the neonatal intensive care unit (NICU) at Women & Infants Hospital of Rhode Island between August 2011 and December 2017. Index cases (severe BPD) were identified using the definition of severe BPD delineated by the National Institutes of Health (NIH) consensus guidelines of 2001 (8). This included infants at 36 weeks postmenstrual age (PMA) who continued to require significant respiratory support, which included mechanical ventilation, non-invasive positive pressure ventilation (NiPPV), continuous positive airway pressure (CPAP), high flow nasal canula > 2 L/min, and/or FiO2 ≥ 0.3.

The control group was defined as a group of infants who did not develop severe BPD, and included a combination of infants without BPD, mild BPD, and moderate BPD. These infants were matched by date of birth within 24 months, birth weight within 380 g, gestational age within 9 days, and gender. These distance measures represent the maximum closeness allowed with our cohort as a result of the high prevalence of BPD in ELBW infants. Furthermore, given the increased likelihood of severe BPD at lower gestational ages, infants born at gestational ages 23 to 26 6/7 weeks were matched two cases to one control, whereas infants born at gestational ages ≥ 27 weeks were matched one case to two controls. Infants with major congenital anomalies and death prior to discharge were excluded. Sample size and power calculations were not performed because the study was designed to include a specific historical cohort, who had developed severe BPD. Institutional Review Board of Women & Infants Hospital of Rhode Island approved the study.

Variables explored for associations with severe BPD included the following: (a) maternal variables, including maternal race/ethnicity, hypertension, antenatal steroids, and mode of delivery; (b) infant characteristics, including gestational age, birth weight, sex, small for gestational age (SGA), and hospitalization days; (c) respiratory variables, including surfactant administration, ventilator days (both high frequency and conventional), supplemental oxygen therapy days, management with postnatal steroids and/or chronic diuretic therapy, defined as oral administration of Diuril and/or Aldactone for greater than one week, and presence of tracheostomy; (d) morbidity variables, including severe intraventricular hemorrhage (IVH, grade III/IV), necrotizing enterocolitis (NEC, Bell stage II or higher), patent ductus arteriosus (PDA), late onset sepsis, retinopathy of prematurity (ROP) requiring treatment, and surgical gastrostomy tube placement. It is important to note that standard practice at Women & Infants NICU during the study period was routine use of prophylactic indomethacin for infants born ≤ 28 weeks.

All nutritional and growth variables were obtained from the Women & Infants NICU Nutritional Database, which was established in July 2005 as a quality improvement initiative (9). After this date, NICU nutritionists prospectively recorded the daily parenteral and enteral intakes of all ELBW infants who survived to discharge at prespecified time points. Nutritional variables examined for associations with severe BPD included parenteral nutrition exposure days, cumulative exposure to mother’s breastmilk, mean and cumulative total fluid intake (ml/kg/day), mean and cumulative total energy intake (kcal/kg/day), and mean and cumulative total protein intake (g/kg/day). Protein and caloric intake in maternal breast milk were estimated based on average reported values of 1.54 grams of protein/100 kcal, 1.05 grams of protein/100 ml. Donor human milk was not utilized during the study period. Although there were not fixed standardized protocols for feeding and fluid management, early enteral nutrition with mothers’ own breast milk was encouraged and guidelines suggested limiting fluid intake wherever feasible. The fat and carbohydrate content of enteral nutrition were not prospectively recorded within the database, and therefore were not included. Growth variables included weight gain velocity (g/kg/day) calculated according to the Patel exponential model (10), anthropometric measures of weight, length, and head circumference at various time points in Z-scores, and Z-score change from birth to 36 weeks PMA.

Bivariate comparisons were made between groups using t-tests or Wilcoxon tests for continuous variables or Chi-squared tests for categorical variables. Significant variables in bivariate tests were considered for inclusion in regression modeling. Predictors of BPD were identified using multiple logistic regression with generalized estimating equations (GEE) to adjust for matching. Three separate models were estimated, each including a different measure of anthropometric growth. Statistical significance was defined as p < 0.05 on two-tailed tests. The analysis was performed using SAS version 9.4 statistical software.

Our study cohort consisted of 224 infants: 120 who developed severe BPD and 104 infants who did not develop severe BPD. We had a minimum detectable difference in means between two groups of 0.4 standard deviation at 80% power and an alpha of p = 0.05 available from our final existing sample. Infants with severe BPD were born at lower gestational ages and weights and had more days of hospitalization compared with infants without severe BPD; there were no differences in maternal characteristics, mode of delivery, or gender at delivery (Table 1).

Table 1

Maternal & Infant Demographics
	Control (n = 104)	Severe BPD (n = 120)	p value
Maternal Data
Race/Ethnicity, n (%) White Hispanic African American Asian Other	59 (57.3) 22 (21.4) 17 (16.5) 1 (1.0) 4 (3.9)	64 (54.2) 20 (17.0) 23 (19.5) 3 (2.5) 8 (6.8)	0.64
Hypertension (chronic, gestational, pre-eclampsia), n (%)	38 (36.5)	35 (29.2)	0.24
Antenatal steroids (any), n (%)	79 (77.5)	82 (78.1)	0.91
C-section, n (%)	81 (77.9)	84 (70.6)	0.22
Infant Data
Gestational age, weeks	26.5 ± 1.85	25.4 ± 1.71	< .0001
Birth weight, kg	0.83 ± 0.118	0.71 ± 0.153	< .0001
Male, n (%)	61 (58.7)	73 (60.8)	0.74
SGA, n (%)	17 (16.4)	29 (24.2)	0.15
Hospitalization days	90 ± 26.9	135 ± 30.8	< .0001
Data are mean ± standard deviation or number and percentage (in parentheses). SGA: small for gestational age.

Infants with severe BPD had an increased number of ventilator and total oxygen days, and were more likely to receive treatment with surfactant, postnatal steroids, and chronic diuretic therapy (all p < 0.0001, Table 2). Furthermore, infants with severe BPD were more likely to have a tracheostomy placed and develop late onset sepsis and retinopathy of prematurity (ROP) requiring treatment. There was no difference in the incidence of other neonatal morbidities including severe intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), or patent ductus arteriosus (PDA) (Table 2).

Table 2

Respiratory Variables & Neonatal Morbidities
	Control (n = 104)	Severe BPD (n = 120)	p value
Surfactant, n (%)	74 (71)	113 (94)	< .0001
Conventional ventilator days	2 (0–42)	19 (0–196)	< .0001
High frequency ventilator days	0 (0–36)	5.5 (0–55)	< .0001
Supplemental oxygen therapy days	65 (3–170)	129 (66–214)	< .0001
Postnatal steroids (dexamethasone, hydrocortisone, and/or prednisone), n (%)	7 (6.7)	66 (55.0)	< .0001
Chronic diuretic therapy, n (%)	9 (8.7)	85 (70.8)	< .0001
Tracheostomy, n (%)	0 (0.0)	13 (10.8)	0.0005
IVH – Grade III/IV, n (%)	6 (5.8)	10 (8.3)	0.46
NEC, n (%)	4 (3.9)	9 (7.5)	0.24
PDA, n (%)	2 (1.9)	6 (5)	0.22
Late onset sepsis, n (%)	19 (18.3)	50 (41.7)	0.0002
ROP requiring treatment (laser therapy and/or Avastin), n (%)	4 (3.9)	26 (21.7)	< .0001
Surgical gastrostomy tube, n (%)	2 (1.9)	7 (5.8)	0.14
Data are median (range) or number (percentage).

Infants with severe BPD had significantly more days of parenteral nutrition exposure compared to those infants without severe BPD (35 ± 28.9 vs. 22 ± 19.5, p < 0.0001). Furthermore, there was a significant difference in total breastmilk received throughout the hospitalization between the two groups. Infants with severe BPD received significantly less cumulative breastmilk from day 1 through week 2 (66 ± 69.4 vs. 102 ± 75.4 ml/kg, p = 0.0002) as well as day 1 though week 12 (573 ± 390.8 vs. 424.6 ± 368.2 ml/kg, p = 0.0062) compared to infants who did not develop severe BPD.

Total nutritional intake was assessed both in terms of cumulative intake and mean daily intake (Table 3). Cumulative total fluid intake (ml/kg) was significantly higher in infants who developed severe BPD in the first two weeks of life and from day one through week 12 compared to infants who did not develop severe BPD. The mean total fluid intake (ml/kg/day) was significantly higher day one to week two for infants who developed severe BPD, but not significantly different when assessed day one to week 12.

Table 3

Nutritional Intake
	Control (n = 104)		Severe BPD (n = 120)
	Cumulative Intake	Mean Intake	Cumulative Intake	Mean Intake
Total Fluid Intake	ml/kg	ml/kg/day	ml/kg	ml/kg/day
Day 1 to Week 2	513 ± 45.4	128 ± 11.3	538 ± 76.9*	135 ± 19.2*
Day 1 to Week 12	1385 ± 161.3	136 ± 5.6	1488 ± 114.8*	136 ± 9.5
Total Caloric Intake	kcal/kg	kcal/kg/day	kcal/kg	kcal/kg/day
Day 1 to Week 2	324 ± 33.8	81 ± 8.5	298 ± 39.2*	74 ± 9.8*
Day 1 to Week 12	1084 ± 141.6	107 ± 8.5	1111 ± 112.7	102 ± 10.1*
Total Protein Intake	g/kg	g/kg/day	g/kg	g/kg/day
Day 1 to Week 2	12.4 ± 1.36	3.1 ± 0.34	12.2 ± 1.45	3.0 ± 0.36
Day 1 to Week 12	35.6 ± 4.53	3.5 ± 0.26	38.0 ± 3.13*	3.5 ± 0.27
Data are mean ± standard deviation, *p < 0.05 versus control group

Cumulative total caloric intake (kcal/kg) was significantly lower in the first two weeks of life in infants who developed severe BPD compared to infants without severe BPD. No significant difference was observed between the groups in cumulative caloric intake through week 12. The mean total caloric intake (kcal/kg/day) through week 2 and through week 12 was lower in infants with severe BPD compared to infants without severe BPD (Table 3, Fig. 1A, p < 0.0001). Mean total caloric intake was significantly lower on day four (74 ± 12.5 vs. 80 ± 10.9 kcal/kg/day), day seven (85 ± 15.8 vs. 96 ± 16.1 kcal/kg/day), and at week 4 (112 ± 23.4 vs. 125 ± 17.4 kcal/kg/day) in infants with severe BPD compared to those without severe BPD (all p < 0.0001, Fig. 1A). There was no difference observed in total caloric intake between the groups on day 1 and at 36 weeks PMA.

Cumulative total protein intake through week 12 was significantly higher in infants with severe BPD compared to those without, but protein intake was otherwise not significantly different between the two groups (Table 3).

Weight gain velocity was lower in infants with severe BPD than in those without severe BPD (13.3 ± 1.64 vs. 14.6 ± 1.63 g/kg/day, p < 0.0001). Weight, length, and head circumference Z-score changes between birth and 36 weeks PMA or discharge, whichever came first, were lower in severe BPD infants (Fig. 1B, p < 0.001).

Increasing caloric intake through week 12 reduced the odds of developing severe BPD by approximately four percent for each one kcal/kg in the logistic regression models with the effect size consistent across models (p < 0.001, Table 4). On the other hand, reducing fluid intake through week 12 reduced the odds of severe BPD by approximately four percent for each one ml/kg in the length model, and by approximately three percent for each one ml/kg in the head circumference model. Growth, measured by Z-score change, was significant for weight, reducing the odds of BPD by approximately 23% for each Z-score point, and for length, reducing the odds of BPD by approximately 30% for each Z-score point.

Table 4

Logistic Regression Models for Predictors of Severe BPD
Variable	Weight model OR, 95% CI P	Length model OR, 95% CI P	Head circumference model OR, 95% CI P
Birth Z-score	1.04, 0.85–1.28 0.6868	0.76, 0.62–0.97 0.0232	0.91, 0.75–1.09 0.2987
Surfactant	3.14, 1.84–5.36 < .0001	2.98, 1.67–5.33 0.0002	3.07, 1.76–5.33 <.0001
Z-score change, birth to 36 weeks	0.77, 0.60-1.00 0.0473	0.70, 0.52–0.94 0.0179	0.89, 0.72–1.09 0.2570
Mean fluid intake to 12 weeks (per ml/kg)	1.02, 1.00-1.05 0.0522	1.04, 1.01–1.07 0.0033	1.03, 1.00-1.06 0.0093
Mean caloric intake to 12 weeks (per kcal/kg)	0.96, 0.95–0.98 < .0001	0.96, 0.94–0.98 < .0001	0.96, 0.94–0.97 < .0001
Adjusted for age, birth weight, gestation, sex. Matching was adjusted for with generalized estimating equations (GEE).

The present study demonstrates an independent association between severe BPD and lower caloric intake and higher total fluid intake during the first two weeks of life. Cumulative total fluid intake was higher and mean total caloric intake lower in infants with severe BPD through week 12 compared to those without severe BPD. Therefore, it appears that early fluid and nutritional management in the first two weeks of life may predispose to the subsequent development of severe BPD. In contrast, nutritional intake through week 12 is more likely to reflect the effects of the development and presence of established chronic lung injury including efforts by clinicians to increase nutritional intakes, and the potential for increased energy expenditure resulting from increased work of breathing (11).

Many prior studies have focused on the potential for higher total fluid intake predisposing to the development of BPD. Oh et al. (12) demonstrated that less postnatal weight loss and higher fluid intake during the first ten days of life were significantly associated with a higher risk of developing BPD in a cohort of ELBW infants. A Cochrane review analyzing 5 RCTs of varying water intake in premature infants indicated restricted fluid intake was associated with increased postnatal weight loss, as well as reduced risk of patent ductus arteriosus and necrotizing enterocolitis. However, restricted fluid intake was only associated with a trend towards a reduced risk of BPD but this was not statistically significant (13). The present findings can be interpreted to suggest that early restriction of fluid intake is critical to attenuate the development of severe BPD because higher cumulative and mean total fluid intakes during the first two weeks of life were significantly associated with an increased risk of developing severe BPD.

More recent reports have addressed the influence of nutritional intakes on the development of BPD (6, 14, 15). Al-Jebawi, et al. recently reported that low caloric intakes in the first week of life were associated with an increased risk of developing moderate to severe BPD (OR 0.94, 0.91–0.97) (14). However, ELBW infants in this study were exclusively parenterally fed during the first week of life (14). In contrast, although our study is consistent with these findings, the infants in our study received a combination of parenteral and enteral nutrition. Furthermore, our findings examine the role of caloric deficit in the early management through week 2 as well as through 12 weeks PMA, demonstrating that both are associated with the development of severe BPD.

Malikiwi, et al. demonstrated that the odds of developing BPD was lower after receiving a higher four-week average daily caloric intake (OR = 0.89) in a retrospective case-control study consisting of 66 infants (6). Likewise, another cohort of 296 infants born less than 27 weeks of gestation exhibited reduced risk of developing BPD after receiving higher energy intakes from postnatal days seven to 27 (15). However, the definition of BPD utilized in the aforementioned studies described infants requiring supplemental oxygen at 36 weeks postmenstrual age, which would be consistent with a definition of moderate to severe BPD as defined by National Institutes of Health (NIH) consensus guidelines of 2001 (8).

The nutritional evaluation in our study examined a subgroup of infants with complex medical needs who developed severe BPD, in contrast to the previous reports (6, 14, 15). In addition, the current study represents a retrospective analysis of prospectively collected nutritional and growth profiles. There is a paucity of previous studies that have examined the contribution of nutritional profiles specifically to the development of severe BPD. The present study emphasizes the importance of early higher caloric intake in infants who are more likely to develop severe BPD. Moreover, higher caloric intake through week 12 reduced the odds of developing severe BPD by approximately four percent for each one kcal/kg. Nonetheless, the current study along with the previous findings (6, 14, 15) represent retrospective analysis of low-birth-weight infants that were destined to develop BPD at 36 weeks of age. In addition, we cannot rule out the possibility that factors known to contribute to the development of BPD including gestational age, birth weight, severity of lung disease, and the level of respiratory support, did not also influence the nutritional intake of the infants who were destined to develop severe BPD.

The infants with severe BPD also received a higher cumulative total protein intake through week 12. This is most likely because of the longer duration of exposure to parenteral nutrition in the infants who developed severe BPD compared with the control infants. The control infants also received more breast milk, which has a lower protein content than parenteral alimentation.

A Cochrane meta-analysis (16) from 2006 attempted to explore randomized trials that assessed the effects of increased energy intake on outcomes of preterm infants with or destined to develop chronic lung disease (CLD)/BPD, but eligible trials were not identified, thus emphasizing the need for future randomized controlled trials to prospectively examine the benefits of more optimal nutritional intakes in reducing the severity of BPD.

The present study also demonstrated an association between the development of BPD and reduced weight, length, and head circumference growth trajectories. It has long been recognized infants with BPD demonstrate poor postnatal growth (17). Vohr et al. (17) originally showed that infants with BPD were more likely to have poor weight gain with weight less than the third percentile at 4 and 12 months postnatal age compared with infants without BPD. The lower postnatal weight gain was suggested to be associated with poor nutritional intake and greater expenditure of energy (17). Subsequently, Ehrenkranz et al. (18) examined a cohort of ELBW infants divided into quartiles of in-hospital growth velocity rates. Fifty six percent of infants in the lowest growth quartile (mean weight gain of 12.0 g/kg/day) developed BPD, compared to 31% of infants in the highest growth quartile (mean weight gain of 21.2 g/kg/day), p < 0.001.

The results of the current study agree with the results in the prior studies that demonstrate poor postnatal weight gain in infants with severe BPD, but also emphasizes growth failure across anthropometric measures in these infants, including length and head circumference. The present study also accentuates the importance of the association between linear growth and the development of severe BPD. It is well documented that height is an important predictor of lung function both in children and adults (19). Moreover, the importance of length as it relates to lung growth in preterm infants is becoming increasingly recognized (20). Sanchez-Solis et al. (21) showed in a multivariate analysis that lung function in preterm infants with and without BPD was associated with gain in height velocity, but not specifically with increases in weight gain. These findings are consistent with the results of our logistic regression analysis, in which the anthropometric measure of strongest significance was the length trajectory. These findings suggest that future efforts to prevent BPD should include an emphasis on the evaluation of linear growth, as well as weight gain velocity.

We also observed that head circumference Z-score changes between birth and 36 weeks PMA (or discharge if sooner) were lower in infants with severe BPD. Head circumference is often utilized as an indirect measure of postnatal brain growth, and the literature has shown an association between suboptimal brain growth and subsequent neurodevelopmental impairment (22–24). Nesterenko, et al. demonstrated a correlation between oxygen exposure and delays in head growth at six months corrected age in infants with moderate to severe BPD with birth head circumference less than the 50th percentile (25). However, it remains to be determined whether the oxygen exposure is directly related to the pathogenesis of delayed head growth or is simply a marker of clinical illness severity. Additional studies are required to elucidate the significance of head growth as it relates to BPD and neurodevelopmental outcomes.

There are several limitations to the present study. Although the nutritional and fluid intakes and growth parameters were prospectively collected, a major limitation is the retrospective nature of analysis of the study. Furthermore, given the patient population in this study included only ELBW infants, it was difficult to identify infants without BPD. Consequently, the infants who did not develop severe BPD included some infants with an oxygen requirement at discharge, but who did not develop severe BPD as this was the population of interest for our study. Further, despite our best efforts to match the populations with and without severe BPD, the group with severe BPD had significantly lower weights and gestational ages at birth compared with those without severe BPD, though within our defined measures of closeness. A larger cohort may allow for more precise matching. Moreover, as this is a single center study, our findings may not be generalizable to other centers because the incidence of BPD varies widely among centers (26).

In conclusion, higher fluid and lower total caloric intakes and reductions in linear growth were independently associated with an increased risk of developing severe BPD in ELBW infants.

BPD: bronchopulmonary dysplasia

CLD: chronic lung disease

CPAP: continuous positive airway pressure

ELBW: extremely low birth weight

IVH: intraventricular hemorrhage

NEC: necrotizing enterocolitis

NICU: neonatal intensive care unit

NIH: National Institutes of Health

NiPPV: non-invasive positive pressure ventilation

PDA: patent ductus arteriosus

PMA: postmenstrual age

ROP: retinopathy of prematurity

SGA: small for gestational age

Conflict of Interest: The authors have no conflicts of interest to disclose.

Funding source: No funding was secured for this study.

Author Contributions:

Dr. Kolitz conceptualized and designed the study, designed the data collection instruments, collected data, carried out the initial analyses, and drafted the initial manuscript.

Lynn Przystac conceptualized and designed the study, designed the data collection instruments, and reviewed and revised the manuscript.

Richard Tucker conceptualized and designed the study, designed the data collection instruments, carried out the initial analyses, and reviewed and revised the manuscript.

Dr. Oh conceptualized and designed the study and critically reviewed the manuscript for important intellectual content.

Dr. Stonestreet conceptualized and designed the study, coordinated and supervised data collection, and critically reviewed the manuscript for important intellectual content.

All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

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There is NO conflict of interest to disclose.

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Editorial decision: revise
21 Nov, 2023
Review #2 received at journal
17 Nov, 2023
Reviewer #2 agreed at journal
06 Nov, 2023
Review #1 received at journal
30 Oct, 2023
Reviewer #1 agreed at journal
12 Oct, 2023
Reviewers invited by journal
11 Oct, 2023
Submission checks completed at journal
04 Oct, 2023
Editor assigned by journal
03 Oct, 2023
First submitted to journal
03 Oct, 2023

You are reading this latest preprint version

Higher Fluid and Lower Caloric Intakes: Associated Risk of Severe Bronchopulmonary Dysplasia in ELBW Infants

Status:

Journal Publication

Version 1

Abstract

Figures

Introduction

Methods

Results

Discussion

Abbreviations

Declarations

References

Additional Declarations

Status:

Journal Publication

Version 1