Bronchopulmonary dysplasia, or BPD, is a chronic lung disease that develops when the fragile, immature lungs of very preterm infants are damaged by mechanical ventilation, oxygen therapy, and inflammation during the first weeks of life. Infants who develop BPD often require prolonged respiratory support and hospitalization, and they face elevated risks of rehospitalization, neurodevelopmental impairment, and long-term respiratory problems such as asthma-like symptoms and reduced lung function well into childhood and adulthood. Because survival rates for extremely preterm infants have climbed steadily over recent decades, BPD has become one of the most common long-term consequences of prematurity, making effective prevention strategies a major priority for neonatal medicine.

Caffeine is already a workhorse of neonatal care. A methylxanthine compound that crosses the blood-brain barrier readily, caffeine acts primarily as a respiratory stimulant by antagonizing adenosine receptors in the brainstem, increasing the drive to breathe and improving diaphragmatic contractility. Since a landmark 2006 international trial demonstrated that caffeine therapy shortened the duration of mechanical ventilation and reduced the rate of BPD among extremely low-birth-weight infants, caffeine citrate has become standard treatment for apnea of prematurity in neonatal intensive care units worldwide. However, that trial initiated caffeine only once apnea developed or clinicians judged treatment necessary—what neonatologists call therapeutic administration. Whether giving the drug prophylactically, within hours of birth to all very preterm infants regardless of symptoms, could prevent BPD more effectively remained unresolved, and prior smaller studies had produced mixed and inconclusive results.

To address this gap, researchers led by Fangfang Tao and Jiang-Qin Liu of Shanghai First Maternity and Infant Hospital, together with colleagues at Children’s Hospital of Fudan University and the University of Alberta, enrolled 372 very preterm neonates born before 32 weeks and 0 days of gestation between September 2016 and January 2024. In this single-center, randomized clinical trial, infants were assigned to one of two strategies. The prophylactic caffeine administration group received caffeine citrate shortly after birth, beginning with a loading dose of 20 milligrams per kilogram of body weight followed by a daily maintenance dose of 10 milligrams per kilogram. The comparison group received therapeutic caffeine administration, meaning the same drug at the same doses, but only after a diagnosis of apnea was made. The primary endpoint was the composite of BPD at 36 weeks postmenstrual age and/or death before hospital discharge.

The results favored early treatment. BPD or death occurred in 37.1 percent of infants in the prophylactic group—69 of 186 infants—compared with 47.3 percent in the therapeutic group, or 88 of 186. That difference corresponds to a relative risk of 0.77 with a 95 percent confidence interval of 0.62 to 0.95, and a P value of 0.013, meaning the reduction was statistically significant and unlikely to be due to chance alone. In practical terms, for roughly every ten very preterm infants treated prophylactically rather than reactively, one fewer infant would be expected to die before discharge or leave the hospital requiring oxygen for chronic lung disease.

The effect proved robust across five different sensitivity analysis models designed to test whether the finding depended on particular statistical assumptions. Notably, the benefit appeared more pronounced in several clinically meaningful subgroups: female infants, infants whose mothers had received antenatal corticosteroids to accelerate fetal lung maturation, infants who were not intubated in the delivery room, and infants who required only noninvasive ventilation after birth. This pattern is biologically plausible, since these are infants whose lungs were less severely compromised at the outset and who therefore stood to gain the most from protecting the airways and respiratory drive before injury could accumulate.

Caffeine’s protective mechanism in the context of BPD is thought to extend beyond simple respiratory stimulation. Experimental work suggests that caffeine exerts anti-inflammatory effects, modulates cytokine responses, improves diaphragmatic and intercostal muscle function, and enhances respiratory pattern stability, all of which can reduce the need for invasive mechanical ventilation and high oxygen concentrations—the principal drivers of lung injury in preterm infants. By stabilizing breathing from the first hours of life, prophylactic caffeine may prevent the cascade of apnea episodes, desaturations, and escalation of ventilatory support that culminates in chronic lung disease.

The trial was not without signals of potential harm, and the authors were careful to report them. Infants in the prophylactic group received a higher number of blood transfusions than those in the therapeutic group, with a mean difference of 0.42 transfusions (95 percent confidence interval, 0.05 to 0.79; P = 0.027). The clinical significance of this small increase is uncertain, but it aligns with earlier observations that early caffeine use has been associated with more frequent phlebotomy-related blood sampling and transfusion in previous trials. Importantly, no significant differences were observed between the two groups in the incidence of other serious complications of prematurity, including necrotizing enterocolitis, intraventricular hemorrhage, retinopathy of prematurity, and late-onset sepsis, nor in the duration of mechanical or noninvasive ventilation, oxygen exposure, length of hospital stay, or medical costs.

The researchers emphasized that the study had limitations inherent to its design. As a single-center trial, its findings may reflect the specific practices and patient population of one institution, and confirmation in multicenter settings is needed before the results can be generalized universally. The trial was registered retrospectively in the Chinese Clinical Trial Registry, a point the authors acknowledged transparently. In addition, the composite primary outcome of BPD or death, while standard in neonatal trials, combines two distinct events, and a larger sample would be required to separately power each component. Still, the trial’s seven-and-a-half-year enrollment window, its randomized design, and the consistency of the effect across sensitivity analyses lend considerable weight to the conclusion.

For neonatologists, the study raises the prospect of shifting practice: rather than waiting for apnea to declare itself, starting caffeine citrate routinely within the first hours of life in infants born before 32 weeks could prevent a substantial share of BPD cases and deaths. Prophylactic caffeine is already inexpensive, well tolerated, and familiar to every neonatal unit, which means that if the findings are confirmed, implementation barriers would be minimal compared with entirely new therapies. As BPD continues to burden a growing population of preterm survivors, an intervention this simple—administering earlier a drug already sitting in the NICU pharmacy—represents exactly the kind of low-cost, high-reach strategy that could reshape outcomes for the most vulnerable newborns. The study was funded through the CHINA-CANADA Clinical Research program, and the full open-access article is available in BMC Pediatrics.

Subject of Research: Prophylactic caffeine administration to prevent bronchopulmonary dysplasia in very preterm infants

Article Title: Prophylactic administration of caffeine reduces bronchopulmonary dysplasia in very preterm infants: a single center, randomized controlled trial

Article References: Tao, F., Zhou, M., Fu, Y., Zhou, J., Wang, M., Duan, Y., Li, M., Hua, J., Wang, Y., Chen, C., Cheung, P.-Y., Yuan, L., Yan, W., & Liu, J.-Q. (2026). Prophylactic administration of caffeine reduces bronchopulmonary dysplasia in very preterm infants: a single center, randomized controlled trial. BMC Pediatrics. https://doi.org/10.1186/s12887-026-07625-5

Image Credits: AI Generated

DOI: 10.1186/s12887-026-07625-5

Keywords: caffeine, bronchopulmonary dysplasia, very preterm infants, prophylactic administration, randomized controlled trial, apnea of prematurity, neonatal intensive care, caffeine citrate, chronic lung disease, mechanical ventilation, Prophylactic, administration

Surfactant therapy, a cornerstone intervention for preterm infants struggling with respiratory distress syndrome (RDS), is well known for its life-saving properties. Typically administered early after birth, surfactant helps reduce the surface tension within the lungs, allowing for better gas exchange and oxygenation. However, the timing and influence of surfactant administration later in the neonatal period—referred to as late surfactant therapy—have been subjects of ongoing investigation. The question arises as to whether the presence of other complicated neonatal conditions, such as PDA, modulates the efficacy of late surfactant treatment.

PDA, a common congenital cardiac anomaly in preterm infants, involves the persistence of a fetal blood vessel called the ductus arteriosus that normally closes soon after birth. Its persistence can lead to significant hemodynamic disturbances, increasing the risk of morbidity and mortality via pulmonary overcirculation and systemic hypoperfusion. Given these physiological complexities, it has been hypothesized that PDA status might influence the outcomes of interventions aimed at ameliorating respiratory conditions like bronchopulmonary dysplasia (BPD).

The study in question undertakes a secondary analysis of a randomized clinical trial involving ventilated preterm infants receiving inhaled nitric oxide (iNO), an agent used to improve oxygenation, to explore whether PDA status modifies the therapeutic effect of late surfactant administration. The primary outcome examined was survival without BPD at 36 and 40 weeks’ postmenstrual age (PMA), a critical milestone for assessing long-term pulmonary function in preterm infants.

Remarkably, the findings demonstrate that the presence or absence of PDA did not significantly influence the outcome efficacy of late surfactant treatment. This suggests that the physiological challenges posed by PDA do not diminish or enhance the potential benefits of surfactant administered later in the clinical course. Moreover, secondary outcomes related to respiratory support parameters, duration of ventilation, and other morbidity indices corroborated the lack of effect modification by PDA status.

These insights carry profound implications for clinical practice. They suggest that clinicians may not need to tailor surfactant administration based on PDA status, streamlining treatment protocols and potentially simplifying decision-making processes in the neonatal intensive care unit (NICU). It also underscores the resilience and independent mechanism of action of surfactant therapy, unaffected by the hemodynamic perturbations caused by PDA.

From a pathophysiological perspective, this uncoupling between PDA status and surfactant efficacy highlights the distinct therapeutic pathways these conditions traverse. While PDA primarily affects cardiovascular dynamics and pulmonary blood flow, surfactant therapy primarily targets alveolar mechanics and pulmonary compliance. This distinction perhaps explains why their interplay does not yield a compounded or mitigated clinical effect when combined.

Further, the study’s utilization of a robust randomized clinical trial framework lends credence to the reliability of the findings. Rigorous randomization and controlled conditions ensure that confounding variables were minimized, bolstering confidence in the interpretation that PDA does not modulate late surfactant treatment effects. This methodological strength is critical given the complex and multifactorial nature of neonatal morbidities.

In addition, the sample population—ventilated preterm infants receiving iNO—represents a clinically high-risk cohort, further emphasizing the significance of these results. Ventilation and iNO therapy are indicators of severe respiratory compromise; thus, demonstrating efficacy or lack of modification in this subset suggests broad applicability of the findings across various neonatal care scenarios.

Beyond immediate clinical implications, these results invite further research into tailored therapies for preterm infants with PDA. Although PDA may not influence late surfactant efficacy, it remains a significant contributor to neonatal morbidity. Future studies might explore adjunctive or alternative therapies that target PDA-related complications without impacting surfactant administration strategies.

Moreover, understanding the molecular and cellular pathways involved in surfactant metabolism and PDA pathogenesis may illuminate new therapeutic targets. For instance, investigations into how inflammation, oxidative stress, or endothelial dysfunction associated with PDA influence lung development and function could open avenues for combination therapies that enhance overall outcomes in these vulnerable infants.

This research also adds a new layer to the ongoing discourse regarding the timing and indications for surfactant therapy. While early administration remains the gold standard, late surfactant use may have a nuanced role in mitigating long-term pulmonary sequelae. Clarity on factors that do not modify its efficacy, such as PDA, refines this therapeutic landscape and supports more evidence-based guidelines and protocols.

The collaborative efforts of Peebles, Eickhoff, Elgin, and colleagues underscore the importance of multidisciplinary and multicenter approaches to neonatal research. Their work illustrates how secondary analyses of clinical trials, when rigorously designed and executed, can yield important findings beyond the initial study questions, influencing clinical paradigms and patient care.

In summary, the current investigation provides compelling evidence that the presence of patent ductus arteriosus does not alter the therapeutic benefit of late surfactant administration in ventilated preterm infants receiving inhaled nitric oxide. This clarity informs NICU protocols, optimizes treatment pathways, and directs future research toward exploring novel interventions for PDA management without concern for interference with surfactant therapy outcomes. The study represents a significant step forward in refining neonatal respiratory care and enhancing survival and quality of life for some of the most vulnerable patients.

As neonatology strives to evolve with precision medicine, such findings highlight the intricate balance of interventions that may be administered concurrently yet operate through independent mechanisms. Integrating these nuanced insights into clinical practice will ensure that emerging therapies are implemented with maximal efficacy and safety, ultimately improving the prognosis of preterm infants worldwide.

The publication of this research is a testament to the relentless pursuit of knowledge and continuous improvement in neonatal care, showing that even in the face of complex cardiac and respiratory comorbidities, targeted therapies can maintain their intended benefits. With ongoing advancements, the future holds promise for even more personalized and effective treatments that cater to the diverse needs of preterm infants.

Subject of Research: The interaction between late surfactant therapy and patent ductus arteriosus status in ventilated preterm infants receiving inhaled nitric oxide, focusing on survival without bronchopulmonary dysplasia and related secondary outcomes.

Article Title: Effect modification of late surfactant treatment by patent ductus arteriosus status in ventilated preterm infants: a secondary analysis of a randomized clinical trial.

Article References:
Peebles, P.J., Eickhoff, J.C., Elgin, T.G. et al. Effect modification of late surfactant treatment by patent ductus arteriosus status in ventilated preterm infants: a secondary analysis of a randomized clinical trial. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02705-x

Image Credits: AI Generated

DOI: 20 April 2026

Surfactant deficiency in preterm infants results in impaired lung function and escalating respiratory failure, conditions that SRT effectively mitigates by restoring alveolar stability and improving oxygenation. However, in infants with CHD, the scenario acquires layers of complexity due to the altered hemodynamics inherent to cardiac malformations. The authors emphasize that while optimizing lung mechanics through surfactant administration promotes pulmonary recruitment, this intervention can inadvertently precipitate major air leaks or destabilize the delicate pulmonary-systemic circulation balance.

Accurate diagnosis of RDS is paramount before surfactant therapy is considered, as misdiagnosis can expose infants to unnecessary risks without therapeutic benefit. The hallmark signs of RDS—manifesting as classic radiologic features on chest radiographs or confirmed via increasingly accessible lung ultrasound—must be clearly identified. This precision ensures that surfactant therapy is judiciously employed, tailored specifically to infants suffering from surfactant deficiency rather than those whose respiratory symptoms might stem from cardiac pathophysiology alone.

The physiological rationale guiding surfactant administration becomes particularly instructive when considering the unique circulatory dynamics in CHD. Notably, infants with duct-dependent pulmonary blood flow may derive significant benefits from surfactant therapy. In these cases, left-to-right shunting through the ductus arteriosus maintains crucial pulmonary perfusion, and optimizing lung function can support life-sustaining oxygenation. Herein, the interplay between cardiac lesion physiology and lung mechanics underscores the necessity for a personalized, case-by-case clinical evaluation.

Pulmonary overdistension caused by aggressive ventilation post-surfactant administration has the potential to alter pulmonary vascular resistance, sometimes compromising cardiac output or exacerbating shunt physiology unfavorable to systemic circulation. The authors highlight these risks, advocating for cautious titration of surfactant and vigilant respiratory support to mitigate air leaks and hemodynamic instability. This approach reflects an evolving understanding of the interdependence between respiratory interventions and cardiovascular function in neonates.

Communication between neonatologists and pediatric cardiologists emerges as a critical factor in optimally navigating surfactant therapy decisions. The article underscores the invaluable role of collaborative, multidisciplinary care in balancing respiratory benefits against cardiac risks, encouraging active dialogue that incorporates detailed cardiac lesion assessment, real-time monitoring, and dynamic treatment planning. Such partnerships are essential for tailoring interventions that reflect both pulmonary necessities and cardiac realities in this high-risk cohort.

The authors raise pointed awareness of existing knowledge gaps, underscoring that the evidence base guiding surfactant use in the context of CHD remains preliminary and incomplete. Despite decades of advancing neonatal care and surfactant technology, the specificities of neonates with cardiac defects require focused investigation. The call to action within the article is evident: rigorous scientific enquiry and innovative research strategies are necessary to unravel these complexities and develop evidence-based guidelines.

Supplementary materials appended to the study catalog these research priorities, reinforcing the urgency for detailed physiological studies, clinical trials, and outcome analyses. Questions linger regarding optimal timing of surfactant administration, dosage customization, respiratory support strategies, and the interplay of pharmacologic adjuncts in CHD populations. Addressing these gaps would illuminate pathways to reduce morbidity and mortality, enhancing survival prospects for these vulnerable patients.

Moreover, the technological evolution of diagnostic imaging, particularly bedside lung ultrasound, offers promising avenues for refining diagnosis of neonatal RDS. Non-invasive and repeatable, ultrasound may facilitate earlier and more accurate identification of surfactant deficiency, enabling timely and precise therapeutic interventions. The integration of such monitoring tools aligns perfectly with the tailored, multidisciplinary care paradigm advocated by the authors.

In discussing the therapeutic considerations, the article highlights surfactant therapy not as a panacea but as a component of comprehensive clinical management. Attention to ventilatory strategies that minimize barotrauma and volutrauma, alongside cardiovascular monitoring that detects hemodynamic perturbations, is crucial. The delicate interplay between ventilation and cardiac function in CHD warrants protocols that are adaptable and responsive to individual patient response trajectories.

Physiological concepts elucidated in the article remind clinicians of the dual pulmonary and systemic circulatory burdens in CHD infants. Corrections or palliations of structural defects alter the baseline physiology dynamically, and any respiratory intervention, including surfactant, must be conceptualized within this shifting landscape. The authors advance the perspective that nuanced understanding of these interdependencies enhances decision-making quality, optimizing therapeutic efficacy and safety.

This article, published in the Journal of Perinatology in April 2026, constitutes a significant contribution to neonatal medicine, merging physiological insights with clinical pragmatism. By articulating the challenges and identifying research lacunae, Sehgal and colleagues set the stage for future investigations designed to elevate standards of care for premature infants grappling with intertwined respiratory and cardiac pathologies. Their work beckons the neonatal community toward concerted, evidence-driven innovation.

The ultimate message resonates with both caution and optimism: surfactant replacement therapy, when judiciously applied and carefully managed through collaborative expertise, holds potential to improve outcomes in one of the most precarious patient populations. As neonatal science pushes boundaries, this article acts as both a guidepost and a catalyst, inspiring enhanced diagnostic precision, therapeutic refinement, and interdisciplinary synergy.

In light of the complexity and gravity of decisions surrounding surfactant use in premature infants with CHD, this study serves as an essential reference. It highlights the necessity for individualized treatment frameworks and continuous research, underscoring the delicate balance between achieving pulmonary stability and maintaining cardiovascular equilibrium. The neonatal care landscape stands to benefit profoundly from these insights as efforts intensify toward optimizing survival and long-term health in this vulnerable group.

The convergence of technological advances, collaborative clinical practices, and rigorous scientific inquiry will undoubtedly shape the future of surfactant therapy in this intricate context. The article leaves clinicians and researchers alike with both a roadmap and a challenge — to translate theoretical knowledge into practical strategies that improve lives and fulfill the promise of modern neonatal medicine.

Subject of Research: Surfactant replacement therapy in premature infants with congenital heart disease, focusing on physiological mechanisms, clinical decision-making complexity, and therapeutic considerations.

Article Title: Surfactant replacement therapy in preterm infants with congenital heart disease: Physiological concepts and therapeutic considerations.

Article References:
Sehgal, A., McNamara, P.J., & Menahem, S. Surfactant replacement therapy in preterm infants with congenital heart disease: Physiological concepts and therapeutic considerations. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02654-5

Image Credits: AI Generated

DOI: 20 April 2026

Keywords: Surfactant replacement therapy, congenital heart disease, preterm infants, respiratory distress syndrome, neonatal intensive care, pulmonary hemodynamics, neonatal cardiology, respiratory therapy, lung ultrasound, neonatal ventilation.

A groundbreaking study led by Limpose et al., recently published in the Journal of Perinatology, delves deeply into this very issue. The researchers undertook the ambitious task of dissecting the relationship between GT insertion and VPS infection rates, particularly focusing on neonatal patients with hydrocephalus. This investigation bridges a significant knowledge gap by exploring not just the occurrence rates but also identifying the responsible pathogens and, importantly, recommending an optimal timeline for these invasive procedures to reduce life-threatening complications.

Central to this study was a cohort of infants diagnosed with hydrocephalus requiring VPS placement. Historically, the presence of a GT has been implicated as a risk factor for VPS infection, yet comprehensive data specifying the meningitis incidence in this particular population remained sparse. Limpose and colleagues’ meticulous work establishes the infection rate percentages by comparing infants who had both devices implanted against those with VPS alone. The results unequivocally confirmed that the concomitant presence of a GT significantly elevates the risk of meningitis, underscoring the necessity for precision in clinical decision-making.

Beyond just quantifying infection rates, the team pursued the crucial task of pathogen identification. Comprehensive microbial analysis was undertaken to catalog the meningeal invaders responsible for VPS infections in the context of GT presence. Intriguingly, this research revealed a predominance of gram-negative organisms, a finding that challenges previous assumptions centered mostly on gram-positive cocci such as Staphylococcus epidermidis. This revelation has profound implications for surgical prophylaxis protocols and antibiotic stewardship in neonatal intensive care units.

The study’s analytical depth extended to evaluating whether the sequence of device placements—whether the GT precedes the VPS or vice versa—bears influence on infection rates. The data emerged with compelling evidence supporting the notion that delaying GT placement until a significant postoperative window following VPS insertion notably reduces infection risk. Conversely, placing a GT prior to VPS installation was associated with a marked increase in meningitis incidence, suggesting the former order as suboptimal for patient outcomes in this sensitive demographic.

Understanding the mechanistic rationale behind these findings, the authors postulate that early GT insertion disrupts the peritoneal environment crucial for VPS function and infection resistance. Additionally, GT placement potentially facilitates bacterial translocation and biofilm formation around the VPS catheter, a critical pathway to infectious complications. These biological insights reinforce the clinical recommendation for strategic scheduling of these procedures to optimize neonatal care and reduce morbidity.

The implications of this study ripple across clinical protocols worldwide. Neonatologists and neurosurgeons are urged to integrate these findings into multidisciplinary care plans, emphasizing cautious scheduling and rigorous monitoring of post-procedural infection signs. The study further advocates for stringent infection control measures during and after both surgeries to mitigate identified risks. Enhanced surveillance for meningitis pathogens and tailored antimicrobial therapies based on identified organisms must become part of the standard care regimen.

Importantly, this research also highlights the vital need for parental counseling and interdisciplinary communication. Families of infants requiring VPS and GT should be apprised of the infection risks and the rationale behind procedural timing, thus aligning expectations and fostering participatory decision-making. Beyond the immediate clinical impact, this approach promotes comprehensive care models enhancing both short-term recovery and long-term neurological outcomes.

Critically, the study encourages future research avenues, such as exploring novel antimicrobial-impregnated VPS catheters or investigating alternative nutritional support methods that might obviate or delay GT necessity. Temporal and spatial mapping of biofilm formation dynamics on implanted devices could yield transformative insights into preventative strategies. Moreover, expanding cohorts with diverse demographic characteristics and multi-center collaborations could validate and generalize these findings globally.

While this study significantly advances our understanding, it acknowledges inherent limitations in patient selection bias and retrospective data interpretation. Hence, ongoing prospective, randomized controlled trials are warranted to refine these recommendations further. The intricate balance between managing hydrocephalus and providing nutritional support in neonates remains a delicate clinical puzzle, but this research lights a promising path toward safer interventions.

In essence, Limpose et al.’s work represents a seminal advance in neonatal neurosurgical care paradigms. By rigorously delineating the association between GT placement timing and VPS-associated meningitis, it equips clinicians with vital evidence to reduce devastating infectious complications. The translation of these findings into practice holds the promise of enhancing survival rates and quality of life for neonates navigating the dual challenges of hydrocephalus and nutritional compromise.

As neonatal intensive care continues to evolve with technological and procedural innovations, studies like this stand at the forefront, reminding us that even subtle modifications in surgical timing can yield profound clinical dividends. The impact of gastrostomy tube placement on the neurological and overall health trajectories of infants with VPS cannot be overstated, and safeguarding these infants through informed procedural strategies is now an attainable goal fostered by this landmark research.

The medical community awaits further validation studies to consolidate these findings, but the current evidence empowers a shift toward more nuanced, evidence-based scheduling of device placements. This shift promises to attenuate the burden of VPS infections—one of the most feared complications in this high-risk group—thereby transforming clinical outcomes and reinforcing the commitment to precision medicine in neonatal care.

In conclusion, this pioneering investigation couples detailed microbiological insights with pragmatic surgical timing recommendations, marking a crucial step forward in managing infants with hydrocephalus who require both VPS and GT. The interplay between device-associated infection risk and procedural strategies elucidates a path to safer, more effective care, ultimately striving to improve survival and developmental prospects for our most fragile patients.

Subject of Research: The impact of gastrostomy tube placement on the rate and microbial profile of meningitis in neonates with hydrocephalus implanted with ventriculoperitoneal shunts, focusing on timing and sequence of device insertion to reduce infection risks.

Article Title: Impact of gastrostomy tube placement on meningitis in infants with hydrocephalus requiring ventriculoperitoneal shunt.

Article References:
Limpose, K.L., Piazza, A.J., He, Z. et al. Impact of gastrostomy tube placement on meningitis in infants with hydrocephalus requiring ventriculoperitoneal shunt. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02625-w

Image Credits: AI Generated

DOI: 10.1038/s41372-026-02625-w (19 March 2026)

Keywords: hydrocephalus, ventriculoperitoneal shunt, gastrostomy tube, meningitis, neonatal infection, surgical timing, neonatal care, device-associated infection, shunt infection, microbial pathogens