In the contemporary era, marked by advancements in perinatal medicine, the survival rates of infants afflicted by BPD have witnessed an upward trajectory. Nonetheless, BPD persists as a pervasive challenge, standing out as one of the most prevalent and consequential sequelae affecting preterm infants. The ramifications extend beyond the individual to cast a substantial burden on both families and society at large. A burgeoning body of research underscores the pivotal role of early nutritional support in mitigating the risk of BPD among preterm infants. This investigation seeks to unravel the intricate interplay between BPD occurrence and the nuanced domains of nutritional and fluid management. The overarching aim is to refine and elevate the standards of nutritional and fluid management for the betterment of preterm infants.
Calories:
This investigation reveals a noteworthy distinction in caloric provisioning between the non-BPD and BPD groups during the initial postnatal week. The findings underscore the protective role of heightened caloric intake in preterm infants against BPD development. Notably, children grappling with BPD exhibit an augmented demand for calories attributable to heightened metabolic requisites and increased respiratory workload. Consequently, a keen focus on caloric supply is imperative. Experimental animal models have corroborated that caloric restriction diminishes alveolar count and reduces the effective alveolar surface area [15]. Additionally, Ehrenkranz et al. [16] established a correlation wherein a 2% reduction in BPD prevalence per 1 Kca/kg-d increase in weekly total energy intake was observed in neonates. National expert consensus advocates a tailored approach, suggesting an initial daily energy intake of 80–100 kcal/kg in the first week, progressively scaling to 120–150 kcal/kg daily over the initial four weeks, thereby mitigating the BPD risk [17].
Fluids
Body fluids, integral conveyors of nutrients and metabolites, wield significant influence on postpartum BPD genesis. Deviations in fluid supply during this critical period can precipitate abnormal fluid status, contributing to BPD onset. Striking a balance is paramount; fluid restriction impairs energy intake, fostering malnutrition and stunted growth [18]. Conversely, elevated fluid volume may culminate in pulmonary edema, compromised lung compliance, heightened airway resistance, impaired gas exchange, and escalated reliance on mechanical ventilation [19–21]. Intriguingly, our study renders fluid loading and BPD development statistically non-significant. This may stem from inherent heterogeneity within our study cohort. The expert consensus urges caution, recommending a capped initiation of postnatal fluid in high-risk BPD infants at 80–100 mL/kg daily, with a stringent fluid volume ceiling of 120–150 mL/kg daily for the initial week [17].
Protein
Emerging research posits that protein deficiency in preterm infants intensifies lung tissue oxidation, precipitating alveolar thinning and hastening BPD progression [22]. Our study corroborates a statistically significant difference in protein provisioning during the first postnatal week between BPD and non-BPD groups. Augmented protein supply emerges as a protective factor against BPD development in preterm infants, underscoring the imperative of prioritizing heightened protein intake during early postnatal stages.
Lipid
The salutary role of fat in providing ample calories, curbing oxidative stress, and bolstering tissue growth is underscored in our study. Clinical trials demonstrate that neonates administered parenteral nutrition infused with fish oil fat emulsion manifest a reduced likelihood of severe BPD [23]. Furthermore, fat emulsions exhibit potential in attenuating inflammatory responses and enhancing immune function [24]. Ensuring adequate calorie intake to diminish BPD risk mandates the early incorporation of lipids into intravenous nutritional solutions [25]. Our study echoes this sentiment, elucidating that fat milk supply in the non-BPD group significantly surpasses that in the BPD group during the postnatal week. This observation reinforces the pivotal role of fat milk in furnishing preterm infants with requisite calories and reducing BPD susceptibility. Consequently, vigilant attention to fat milk intake in intravenous nutrition is advocated.
Carbohydrate:
Carbohydrates stand as the primary energy source for preterm infants during the early postnatal phase, with glucose serving as the principal substrate for carbohydrate utilization. Glucose, a ubiquitous metabolic fuel, caters to the energy demands of vital organs. Al-Jebawi et al. discerned a significant reduction in carbohydrate intake within the moderate to severe BPD cohort during the initial week of life compared to the non-BPD and mild BPD groups [12]. Thiess [26] further affirms that carbohydrate intake fosters pulmonary development, aligning with our study's findings. Emphasis on meticulous attention to carbohydrate intake in preterm infants is warranted. Simultaneously, a heightened carbohydrate load may elevate basal oxygen consumption and carbon dioxide production, posing pulmonary stress risks [27]. Careful control of glucose supply rate is crucial, ensuring a per-minute glucose administration of less than 12 mg/kg to avert undue speed-associated complications.
Transition to Full Enteral Feeding
Prolonged reliance on intravenous nutrition may precipitate atrophy of intestinal mucosal villi, rendering children susceptible to cholestasis and related ailments. Our study reveals a markedly abbreviated duration of parenteral nutrition in the non-BPD group and a significantly prolonged period of total enteral feeding in the BPD group in comparison to the non-BPD group. This underscores the protective role of expeditious realization of total enteral feeding against BPD development. Hence, early implementation of enteral nutrition, contingent on conducive conditions, and expeditious removal of central venous catheters assume paramount significance in BPD prevention and management.
Compared to preceding meta-analyses [28], our study encompasses a more extensive array of pertinent research, integrating additional macronutrient impact indicators while imposing more stringent inclusion criteria and undertaking further subgroup analyses. Nevertheless, inherent limitations persist: 1. Discrepancies exist in prevailing clinical guidelines and consensuses on nutritional management of bronchopulmonary dysplasia in preterm infants both domestically and internationally. Divergent nutritional guidelines among the incorporated literature may yield clinical heterogeneity, potentially compromising systematic evaluation efficacy. 2. Adequacy of study effect indicators is not uniformly realized, necessitating statistical transformations for certain analyses.